S2HY

Allergy&Immunology Allergy&Immunology
Niket Sonpal,MD
ChiefResident LenoxHillHospitalNSLIJ AssistantClinicalProfessor Touro CollegeofMedicine
Anaphylaxis Angioedema Urticaria AllergicRhinitis PrimaryImmunodeficiency Disorders
Anaphylaxis Worst form of acute allergic reaction Synonymous with immediate hypersensitivity Pathogenesis
Initial sensitization to antigen with subsequent reexposure Upon re-exposure, IgE binds to mast cells leading to release of their granules (e.g., histamine, prostaglandins, and leukotrienes) Results in abnormalities that essentially define anaphylaxis
Anaphylaxis Sensitization
Initial sensitization to antigen
Re-exposure Anaphylaxis
Upon re-exposure, IgE binds to mast cells leading to release of their granules
LEUKOTRIENES
DEATH
HISTAMINE
PROSTAGLANDINS
MTBS2CK p.41
MTBS2CK p.41
Hives Itching Constriction of airways Swollen tongue Wheezing Dyspnea Tachycardia Nausea, vomiting, or diarrhea Dizziness or fainting Hypotension
Anaphylaxis Anaphylactoid Reactions

No presensitization to antigen
Anaphylaxis/Etiology
Causes of anaphylaxis = causes of any allergic event

Insect bites and stings Medications: penicillin, phenytoin, lamotrigine, quinidine, rifampin, and sulfa Foods Latex is a very important cause of anaphylaxis in healthcare workers
Identical Tx
Non-IgE related
MTBS2CK p.41
MTBS2CK p.41
Anaphylaxis/Presentation
Anaphylaxis/Treatment
Characterized by Hypotension Tachycardia Respiratory: stridor Rash
The best initial treatment is A Airway Protection

Intubation Cricothyroidodotomy
B Breathing g C - Circulation
Epinephrine Antihistamines H1 and H2 Glucocorticoids
MTBS2CK p.42
Source: Fashad Bagheri. MD
MTBS2CK p.4142
Angioedema Angioedema is sudden swelling of

Face Tongue Eyes Airway
Look for recent start of ACE inhibitors preceding symptoms
Angioedema/Presentation
Hereditary angioedema is a genetic disorder Glucocorticoids dont work
This can be from deficiency of C1 esterase inhibitor Characteristic association of onset with minor physical trauma Angioedema often idiopathic
Source: commons.wikimedia.org
MTBS2CK p.42
MTBS2CK p.43
Angioedema/Tests The best initial test...

C2 and C4 levels in complement pathway
Will be decreased
Angioedema/Treatment Airway Acute Tx Long Term Tx
C1 esterase inhibitor
Also decreased
3 types of hereditary angioedema

Type I - decreased levels of C1INH (85%) Type II - normal levels but decreased function of C1INH (15%) Type III - no detectable abnormality in C1INH
Ensure airway protection first
Fresh frozen plasma Ecallantide E ll tid
Androgens Danazole And Stanazole
MTBS2CK p.43
MTBS2CK p.43
Urticaria Form of allergic reaction that causes sudden swelling of superficial skin layers Can be caused by
Insects Medications Pressure Cold Vibration
Urticaria/Treatment 1. Antihistamines
Hydroxyzine, diphenhydramine, fexofenadine, loratidine, cetirizine, or ranitidine
2 L 2. Leukotriene k ti receptor t antagonists

Montelukast or zafirlukast
MTBS2CK p.43
MTBS2CK p.44
AllergicRhinitis
AllergicRhinitis/DiagnosticTests
IgE-dependent triggering of mast cells Seasonal allergies such as hay fever are common Presents with recurrent episodes of Watery y eyes, y , sneezing, g, itchy y nose, , and itchy eyes Inflamed, boggy nasal mucosa Pale or violaceous turbinates Nasal polyps
MTBS2CK p.44
Diagnosed clinically Skin testing and blood testing IgE levels may be elevated Nasal smear with eosinophils
MTBS2CK p.44
AllergicRhinitis/Treatment
CommonVariableImmunodeficiency(CVID)
1. Prevention & avoidance 2. Intranasal corticosteroid sprays 3. Antihistamines H1 blockers 4. Intranasal anticholinergic medications 5. Desensitization to allergens
B cells are present but decreased Igs Decrease in all Ig subtypes

IgG, IgM, and IgA
LOW B cells output, normal T cells
MTBS2CK p.44
MTBS2CK p.45
CommonVariableImmunodeficiency(CVID) Recurrent sinopulmonary infections Frequent episodes of

Bronchitis Pneumonia Sinusitis And Otitis media
Other manifestations are

Giardiasis Sprue-like intestinal malabsorption
Clue to CVID is a decrease in the output of B lymphocytes with a normal number of B cells as well as normal amounts of lymphoid tissue (e.g., nodes, adenoids, and tonsils)
MTBS2CK p.45
MTBS2CK p.45
Immunoglobulin levels
Decreased
Antigen Stimulation Decreased response

Normal Number of B Cells
Treatment Antibiotics are used for each infection as it develops Chronic maintenance
Regular Reg lar inf infusions sions of IVIG
MTBS2CK p.45
MTBS2CK p.45
Xlinked(Bruton)Agammaglobulinemia Low B, normal T in males Male children with increased sinopulmonary infections B cells and lymphoid tissues are diminished T cells are normal Treatment: Abx for infections as they arise Long-term regular administration of IVIG keeps children healthier
SevereCombinedImmunodeficiency LOW B AND LOW T The word combined in severe combined immunodeficiency (SCID) means that there is deficiency in both B and T cells
Results in infections related to both deficiencies
LOW B cells and LOW T cells. Analogous to HIV LOW B cells, normal T cells in young male children
MTBS2CK p.45 MTBS2CK p.46
SevereCombinedImmunodeficiency
IgADeficiency These patients present with recurrent sinopulmonary infections The difference with this syndrome is: Atopic diseases Anaphylaxis to blood transfusion when blood donor has normal levels of IgA Sprue-like condition with fat malabsorption Increase in risk of vitiligo, thyroiditis, and rheumatoid arthritis
B cells Decreased Ig production T cells Markedly decreased numbers of T cells Long-Term Treatment Bone marrow transplant
MTBS2CK p.46
MTBS2CK p.46
IgADeficiency
HyperIgE Syndrome Presents with recurrent skin infections due to Staphylococcus Treat infections as they arise Consider prophylactic antibiotics (e.g., dicloxacillin or cephalexin)
Source:wikimedia commons
Treat infections as they arise Washed blood transfusions otherwise anaphylaxis IVIG injections will not work The Th t trace amounts t of fI IgA Ai in IVIG may provoke anaphylaxis
MTBS2CK p.46
MTBS2CK p.46
WiskottAldrichSyndrome Normal T cells normal B cells decline with age Immunodeficiency combined with thrombocytopenia and eczema T lymphocytes markedly deficient in blood and lymph nodes Bone marrow transplantation is only definitive treatment
ChronicGranulomatousDisease(CGD)
CGD is genetic disease resulting in extensive inflammatory reactions Leads to lymph nodes with purulent material leaking out
Normal T cells normal B cells decline with age
MTBS2CK p.46
MTBS2CK p.46
Aphthous ulcers And Inflammation of nares is common
Granulomas may become obstructive in the GI or urinary tract Look for infections with odd combination of:
Staphylococcus Burkholderia Nocardia Aspergillus
Source:commons.wikimedia.org
MTBS2CK p.46
MTBS2CK p.4647
PrimaryImmunodeficiencyDisorders
CVID LOW B cell output Normal T cells Hyper IgE Syndrome Skin infections Staphylococcus X-linked (Bruton) Agammaglobulinemia LOW B cells normal T cells in young male children SCID IgA Deficiency Atopic Anaphylaxis
Abnormal nitroblue tetrazolium testing

This is a decrease in NADPH oxidase, which generates superoxide CGD test is negative
LOW B & T cells Analogous to HIV
Wiskott-Aldrich Syndrome
Normal T cells Normal B cells Low Platelets Eczema
CGD Lymph nodes with purulent material Infections, combined with Staphylococcus Burkholderia Nocardia Aspergillus
MTBS2CK p.47
MTBS2CK p.4547
TheCardiovascularSystem
ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity
CoronaryArtery Disease Part1

Definition D fi iti RiskFactors ClinicalPresentation
CoronaryArteryDisease(CAD)/Definition
Can be used interchangeably with:

Atherosclerotic heart disease Ischemic heart disease
All imply insufficient perfusion of coronary arteries Abnormal narrowing of vessels Insufficient oxygen delivery to myocardial tissue
MTBS2CK p.49
48-year-old woman in office with chest pain for several weeks. Pain isn't reliably related to exertion. No pain now. The pain is retrosternal and sometimes associated with nausea. No SOB and no radiation beyond chest. She has no past medical history. What is the most likely diagnosis? a. Gastroesophageal reflux disease (GERD) b. Unstable angina Acute, severe pain in ED c. Pericarditis Pain worse with lying down, better when sitting up d. Pneumothorax Sharp, pleuritic pain, tracheal deviation e. Prinzmetal angina Nonexertional chest pain,
MTBS2CK p.49
early in morning, ST segment elevation
RiskFactorsforCAD Menstruating women virtually never have MIs Which of the following is most likely to benefit a patients risk of coronary disease?
Estrogen simply does NOT help CAD
Risk factors are most important with equivocal or uncertain histories
a. Administration of estrogen replacement at time of menopause b Stopping tamoxifen Tamoxifen unrelated to CAD b. c. Stopping aromatase inhibitors Zero relationship to CAD d. Regular exercise e. Relaxation methods (e.g., meditation) Good, but
Women > men eventually die of heart disease

immeasurable, no evidence of proven benefit
RiskFactorsforCAD
RiskFactorsforCAD
Clear ones:
Diabetes mellitus Tobacco smoking HTN Hyperlipidemia Family history of premature CAD Age > 45 men; > 55 women
Diabetes (worst risk) HTN Defined as > 140/90 More common than diabetes 20% of total population (60 million people) with HTN 50% unaware theyre hypertensive
MTBS2CK p.50
MTBS2CK p.50
RiskFactorsforCAD
Family history not a risk if CAD developed in elderly relatives Relatives were grandparents, cousins, or aunts and uncles Family y history y is a risk ONLY if First-degree relatives (siblings/parents) Premature disease: Defined as:
Male relative < 55 Female relative < 65
MTBS2CK p.5051
Which of the following is the most dangerous to a patient in terms of risk for CAD?
Triglycerides not as dangerous as elevated LDL
a. Elevated triglycerides b. Elevated total cholesterol Its not the TOTAL cholesterol or low l HDL HDL, it its LDL! c. Decreased D d HDL d. Elevated LDL e. Obesity The danger of obesity is from its association
with high LDL, DM, and HTN
MTBS2CK p.51
RiskFactorsforCAD
Less clear Physical inactivity Excess alcohol Insufficient fruits & vegetables Emotional stress CT scan calcium scores Positron emission tomography (PET) scanning
MTBS2CK p.51
Postmenopausal woman develops chest pain immediately on hearing news of her sons death. She develops chest pain, dyspnea, and ST segment elevation in leads V2 to V4. Troponin levels rise with MI. Coronary angiography is normal including an absence of vasospasm. Echocardiography: Apical LV ballooning Whats the presumed mechanism of this disorder? a. Absence of estrogen g Its not absent estrogen g only y causing g MI b. Massive catecholamine discharge c. Plaque rupture There were no plaques on angiography d. Platelet activation Platelets cause MI from CAD, not emotions e. Emboli to coronary arteries It wouldve been seen
MTBS2CK p.52
RiskFactorsforCAD Unreliable (Unproven) Risk Factors for CAD Homocysteine Chlamydia infection C-reactive protein No clear benefit in therapeutic intervention on these factors Theyre the wrong answers
RiskFactorsforCAD
The Most Common Wrong Answer If risk factor question involves: Family history Mistaking CAD in elderly relatives as a risk for patient
Frequently used wrong answers are just as important to learn as right answers
ChestPain/Presentation Correcting which of the following risk factors for CAD results in the most immediate benefit?
What Is the Most Likely Diagnosis? Ischemic pain

Dull /Sore Squeezing (Pressure-like)
a. b. c c. d. e.
Diabetes mellitus Tobacco smoking Hypertension Hyperlipidemia Weight loss
Fixing all of them is good. But Not as fast as smoking cessation!
Like any muscle thats starved for oxygen Produces sore-muscle type pain when ischemic Qualities that go against ischemia
Sharp (knifelike) or pointlike Lasts for few seconds
MTBS2CK p.53
MTBS2CK p.53
ChestPain/Presentation
Three features help tell whether or not the pain is ischemic in nature:
1. Changes with respiration (pleuritic) 2. Changes with position of body 3. Changes with touch of chest wall (tenderness)
< 10% with chest pain in ED end up having an MI 50% have no cardiac disease at all MCC of chest pain that isnt isn t ischemic in nature is GI related
Each (pleuritic, positional, tender) excludes ischemia with 95% negative predictive value (NPV)
MTBS2CK p.53
MTBS2CK p.53
Characteristics of Ischemic Pain
CausesofChestPain
Location Substernal
Ifthecase describes. Chestwalltenderness Radiationtoback, unequalblood pressurebetween arms
Answerasmost likelydiagnosis Costochondritis Aorticdissection
Answerasmost accuratetest Physicalexamination ChestXray withwidened mediastinum,chest CTA,MRA,orTEE confirmsdisease EKGwithSTelevation everywhere,PR depression
Duration Stable angina: > 2 - < 10 min ACS: > 10 - 30 min
Provoking factors Physical activity, activity cold cold, emotional stress
Quality Squeezing, tightness, heaviness, pressure, burning, aching NOT: sharp, pins, stabbing, or knifelike
Alleviating factors Rest
NOT tender NOT positional NOT pleuritic
Associated symptoms SOB, nausea, diaphoresis, dizziness, lightheadedness, fatigue
Radiation Neck, lower jaw and teeth, arms, shoulders
Painworsewithlying flat,betterwhen sittingup
Pericarditis
MTBS2CK p.54
CausesofChestPain
Ifthecase describes. Epigastricdiscomfort, painrelatedtoeating Answerasmost likelydiagnosis Duodenalulcer disease Answerasmost accuratetest Endoscopy Ifthecase describes. Suddenonset,SOB, tachycardia,hypoxia Sharp,pleuriticpain, trachealdeviation
CausesofChestPain
Answerasmost likelydiagnosis Pulmonaryembolus Answerasmost accuratetest SpiralCT,V/Qscan
Pneumothorax
ChestXray
,cough, g , Badtaste, hoarseness
p g Gastroesophageal reflux
Response p toPPIs; ;or liquidantacids
Cough,sputum, hemoptysis
Pneumonia
ChestXray
MTBS2CK p.54
MTBS2CK p.54
Features that DONT help answer the diagnosis question Nausea Fever SOB (dyspnea) (d ) Sweating (diaphoresis) Anxiety

Diagnosis
MTBS2CK p.54
DiagnosticTests/Electrocardiogram
DiagnosticTests/Enzymes(CKMB/Troponin)
The best initial test for all forms of chest pain is certainly an electrocardiogram (EKG) In office-based setting:
Expect normal EKG
Cardiac enzymes are not the answer in Office/ambulatory case Chronic or stable chest pain If the patient has acute chest pain then the answer is:
Transfer
But You cant do other testing until you know the EKG
MTBS2CK p.55
to the emergency department
MTBS2CK p.55
DiagnosticTests/Enzymes(CKMB/Troponin)
DiagnosticTests/StressTesting Exercise tolerance testing (ETT) is the answer when: Etiology is unclear and EKG is not diagnostic Answer Stress test ETT without nuclear isotopes: when: Etiology
1. Read EKG 2 Exercise 2.
Enzymes are the answer when: Acute cases of chest pain Emergency department
uncertain & EKG not diagnostic
Exercise means heart rate > 80% of maximum Maximum heart rate = 220 patient age
MTBS2CK p.55 MTBSCK p.55
DiagnosticTests/StressTesting Thallium (Nuclear) Stress Normal myocardium picks up thallium like potassium via Na/K-ATPase Myocardium alive & perfused? Nuclear isotopes will be picked up Abnormalities/Ischemia or Infarction? Decreased thallium or nuclear uptake Stress or Dobutamine Echo Normal myocardium moves on echo Abnormalities decrease wall motion Dyskinesis, Akinesis, or Hypokinesis
MTBSCK p.56
DiagnosticTests/StressTesting
Ischemia versus infarction: Ischemia = Reversible decreased perfusion Reversal of decrease in thallium uptake or wall motion It returns to normal after a period of rest Infarction = Irreversible
Ischemia is reversible wall motion or thallium uptake between rest and exercise. Infarction is irreversible or fixed.
MTBSCK p.56
Cant exercise?
UseofExerciseToleranceTesting Test
Exercisetolerance
Indication
Ischemiadetected
Persantine (dipyridamole) or adenosine with nuclear isotopes (e.g., thallium or sestamibi) Or

Dobutamine in combination with echocardiography Dobutamine increases myocardial oxygen consumption Dobutamine provokes ischemia Ischemia decreases wall motion on echocardiogram
Determinepresence STsegmentdepression ofischemia CantreadEKG Decreaseduptakeof p nuclearisotope Decreasedwallmotion Decreaseduptakeof nuclearisotope Decreasedwallmotion
Exercisethallium
Exerciseecho
CantreadEKG
Dipyridamolethallium Cantexercise
Dipyridamole may provoke bronchospasm. Avoid in asthmatics.

MTBSCK p.56
Dobutamineecho
MTBS2CK p.56
Cantexercise
Chest pain (likelihood of CHD is high)

Resting EKG abnormalities?
Nuclear and Echo:
No Able to exercise? Yes No Chemical stress test (dipyridamole thallium or dobutamine echo)
Yes
Sensitivity = Specificity
Exercise Thallium = Exercise Echo Dipyridamole Thallium = Dobutamine Echo
Exercise stress test
+
ANGIOGRAPHY
Stress echocardiogram or nuclear stress test
1 or 2 vessel disease
3 vessel disease, left main or 2 vessel disease in diabetics CABG
MTBSCK p.56
Stent placement
DiagnosticTests/CoronaryAngiography
DiagnosticTests/CoronaryAngiography
Detects anatomic location of disease Determines surgery, angioplasty, or other methods of revascularization Sometimes used if noninvasive tests are equivocal
Stenosis (narrowing) < 50% of diameter is insignificant Surgery or angioplasty is done for at least 70% stenosis
MTBSCK p.5657
MTBSCK p.57
DiagnosticTests/HolterMonitoring
Continuous ambulatory EKG monitor Records rhythm Usually for 24-hour period May be for 48 to 72 hours Holter monitor detects rhythm disorders: A-fib, atrial flutter Ectopy (e.g., premature beats) V-tach Holter monitor does not detect ischemia Not accurate for evaluating the ST segment
MTBSCK p.57
48-year-old woman comes to office with chest pain occurring over several weeks. Pain isnt reliably related to exertion. Shes comfortable now. The pain is retrosternal. Past medical history and the EKG is normal. What is the most appropriate next step in management?
a. CK-MB Cardiac enzymes evaluate ACS b. Troponin Evaluate valve function, function wall motion motion, EF c. Echocardiogram E h di d. Exercise tolerance testing Detect the anatomic location of stenosis; e. Angiography f. CT angiography determines method of revascularization CT Angiogram and MRI not accurate enough g. Cardiac MRI h. Holter monitor Used for rhythm evaluation
CAD/Treatment USMLE Step 2 CK is most concerned that you know:

Treatment
Medications that lower mortality

Chronic angina (not an acute coronary syndrome)
Aspirin Beta blockers Nitroglycerin
Step 2 will not test dosing Route of administration is tested

MTBS2CK p.57
CAD/Treatment
CAD/Treatment
Nitroglycerin: Chronic Stable Angina Oral Transdermal patch Acute Coronary Syndrome Sublingual Paste Intravenous
Nonspecific beta blockers (e.g.. propranolol) are not used routinely in cardiology Clopidogrel
Acute MI (all forms) Aspirin intolerance (e.g., allergy) Recent angioplasty with stenting Adverse effect
Rare thrombotic thrombocytopenic purpura
MTBS2CK p.58
MTBS2CK p.58
Treatment/Prasugrel
Treatment/ACEInhibitors
Thienopyridine - same class as clopidogrel and ticlopidine Prasugrel: Antiplatelet medication for use in: Angioplasty & stenting All acute MI Intolerant of aspirin 75 increased hemorrhagic stroke
MTBS2CK p.58
Low EF/systolic dysfunction (best mortality benefit) Regurgitant valvular disease Most M t common adverse d effect: ff t Cough
7% of patients Switch to ARBs
MTBS2CK p.58
Treatment/LipidManagement
64-year-old man starts lisinopril for CAD with EF of 24%, and symptoms of breathlessness. He sometimes has rales, but is asymptomatic today. Physical reveals minimal edema of lower extremities. Potassium level is elevated and its present on a repeat measurement. EKG is unchanged. How would you best manage the patient?
Remove K from the body;You y; should eliminate the cause
Statins (HMG-CoA reductase inhibitors)
CAD with LDL > 100 mg/dL
a. b. c. d. e.
Add kayexalate (potassium-binding resin) Insulin and glucose Drive K into the cell, given in acute situation He should get an alternative drug Stop lisinopril Switch lisinopril to candesartan ARBs lead to hyperkalemia Switch lisinopril to hydralazine and nitrates
MTBS2CK p.5859
MTBS2CK p.59
Treatment/LipidManagement
CADEquivalents
LDL > 70: Treat when patient has Coronary disease AND diabetes
Youre tested on national guidelines from nonbiased federal organizations g Not private organizations (e.g., ACC) Everyone will agree: With CAD, goal of LDL at least < 100 mg/dL
CAD equivalents Statins to bring LDL down if > 100:

Peripheral artery disease (PAD) Carotid disease (not stroke) Aortic disease (aortic artery, not valve) Diabetes mellitus
MTBS2CK p.59
MTBS2CK p.59
OtherLipidLoweringTherapies Which is the most common adverse effect of statin medications? a. Rhabdomyolysis b. Liver dysfunction c Renal failure c. d. Encephalopathy e. Hyperkalemia Niacin, gemfibrozil, cholestyramine, and ezetimibe all have beneficial effects on lipid profiles None is Best initial therapy None has clear mortality benefit statins provide Niacin and fibric acid derivatives such as gemfibrozil have some mortality benefit benefit, but not as much as statins Statins: Antioxidant effect on endothelial lining of coronary arteries Gives benefit transcending lowering LDL number
MTBS2CK p.60
The most common wrong answer
They arent adverse effects of statins
MTBS2CK p.60
Niacin
Gemfibrozil
Associated with: Glucose intolerance Elevation of uric acid Uncomfortable itchiness from histamine Niacin is excellent to add to statins if full lipid control not achieved with statins Although statins, exercise, and cessation of tobacco use will all raise HDL level, niacin will raise HDL somewhat more
MTBS2CK p.60
Fibric acid derivatives: Lower triglyceride levels > statins Benefit of lowering triglycerides alone not proven as useful as straightforward mortality benefit of statins Use caution combining fibrates with statins
Fibrates + Statins= Increased myositis
MTBS2CK p.60
Cholestyramine
Ezetimibe
Bile acid sequestrant Significant interactions with medications in gut Potentially blocking their absorption Cholestyramine Ch l t i associated i t d with ith uncomfortable GI complaints Constipation & flatus
Definitely lowers LDL
No clear benefit to patient

LDL levels are an imperfect marker of benefit with cholesterol-lowering therapies Ezetimibe: No better than placebo No Change in MI, stroke, or death
MTBS2CK p.60
MTBS2CK p.60
LipidLoweringTherapy
LipidLoweringMedsandAdverseEffects
Agent Adverseeffect
Lipid-lowering therapy: What is clear? Statins lower mortality the most Questions about adverse effects Besides the benefit of statins in CAD with LDL levels > 100 mg/dL, the only truly clear aspect t of f other th therapies th i i is th their i adverse d effects
Statins
Elevationsoftransaminases(LFTs), myositis Elevationinglucoseanduricacidlevel, Pruritus Increasedriskofmyositiswhencombined withstatins Flatusandabdominalcramping Welltoleratedandnearlyuseless
Niacin
Fibric acid derivatives Cholestyramine Ezetimibe

MTBS2CK p.61
Check AST & ALT with statins

MTBS2CK p.61
CalciumChannelBlockers(CCBs)
Dihydropyridine CCBs:
Nifedipine Nitrendipine Nicardipine Nimodipine Ni di i
May increase mortality with CAD because of raising heart rate
CCBs are: Negative inotropes Should decrease myocardial oxygen consumption Increased heart rate in the aggregate gg g will increase myocardial oxygen consumption Bottom line:
Do not routinely use CCBs in CAD
None of the calcium-channel blockers have been shown to lower morality in CAD
MTBS2CK p.61
MTBS2CK p.61
Verapamil and diltiazem, which do not increase heart rate, are used in those who cannot tolerate beta blockers because of severe asthma 70% with reactive airway diseases (e (e.g., g asthma) still tolerate beta-1 specific BBs
Use CCBs (verapamil/diltiazem) in CAD only with: Severe asthma precluding the use of beta blockers Prinzmetal variant angina Cocaine-induced chest pain Adverse Effects of CCBs Edema You must know adverse effects Constipation Heart block (rare)
MTBS2CK p.6162
MTBS2CK p.61
10
Revascularization
CoronaryArteryBypassGrafting(CABG)
Angiography: Evaluates possibility of revascularization Either coronary bypass surgery or angioplasty Symptoms alone cannot tell the number of vessels involved
Lowers mortality only with: Three vessels with > 70% stenosis in each Left main occlusion Two-vessel T l di disease with ith di diabetes b t Persistent symptoms despite maximal medical therapy
MTBS2CK p.62
MTBS2CK p.62
CoronaryArteryBypassGrafting(CABG)
PercutaneousCoronaryIntervention(PCI)
Benefit greatest with left ventricular dysfunction Internal mammary artery grafts last 10 years Saphenous vein grafts last 5 years
Percutaneous coronary intervention (PCI) (angioplasty) Intervention best therapy in acute coronary syndromes Particularly those with ST segment elevation Mortality benefit of PCI Much harder to demonstrate in chronic stable angina
MTBS2CK p.62
MTBS2CK p.62
PercutaneousCoronaryIntervention(PCI)
Max medical therapy with aspirin, beta blockers, ACEi/ ARBs, and statins has proven benefit thats PCI in stable CAD PCI decreases dependence on medication Decreasing frequency of angina episodes
PCI: Best in acute coronary syndromes, particularly with ST segment elevation. PCI doesnt provide clear mortality benefit for stable patients.
MTBS2CK p.62
AcuteCoronary Syndromes Part1

Definition Presentation Diagnosis
11
AcuteCoronarySyndromes(ACS)
Definition Impossible to determine precise etiology of (ACS) from history & physical alone Risk factors (e (e.g., g hypertension hypertension, diabetes mellitus, tobacco) same for CAD
Acute Coronary Syndrome

EKG ST elevation No ST elevation Cardiac Biomarkers
+
STEMI
UA
NSTEMI
NSTEMI(Ischemia)
STEMI
S4Gallop 70-year-old woman in ED with crushing substernal chest pain for last hour. Pain radiates to left arm and is associated with anxiety, diaphoresis, and nausea. Pain is sore and dull and clenches fist in front of chest. History of hypertension. Pulsus paradoxus, Which is most likely in this patient? tamponade p a. >10 mmHg decrease in BP on inhalation b. Increase in jugular venous pressure on inhalation Kussmaul sign: constrictive friction rub: pericarditis c. Triphasic scratchy sound Pericardial pericarditis d. Continuous machinery murmur PDA (patent ductus) e. S4 gallop LVH/dilated cardiomyopathy f. Point of maximal impulse displaced to axilla
MTBS2CK p.63
12
AcuteCoronarySyndromes Increased jugulovenous pressure on inhalation Kussmaul sign Constrictive pericarditis Triphasic scratchy sound: Pericardial friction rub Dressler syndrome: Not until several days after MI Much rarer Everyone is on aspirin already!
MTBS2CK p.63
AcuteCoronarySyndromes Continuous machinery murmur Patent ductus arteriosus Displaced point of maximal impulse (PMI) LVH as well as dilated cardiomyopathy Displaced p PMI is an anatomic abnormality y Could not occur with ACS
Dont walk into Step 2 without knowing when you will expect each cardiac physical findings
MTBS2CK p.63
No specific physical finding allows you to answer a most likely diagnosis question in terms of ST elevation or depression without an EKG
70-year-old woman in ED with crushing substernal chest pain for the last hour. Which EKG finding gives the worst prognosis? a. ST elevation in leads II, III, aVF IWMI better prognosis than AWMI b. PR interval >200 milliseconds First degree AV block c ST elevation in leads V2-V4 c. V2 V4 d. Frequent premature ventricular complexes (PVCs) e. ST depression in leads V1 and V2 Posterior MI f. Right bundle branch block (RBBB)
Benign compared to LBBB
MTBS2CK p.6364
PVCs should not be treated, even with acute infarction
70-year-old woman comes to ED with crushing substernal chest pain for the last hour. EKG shows ST segment elevation in V2 to V4. What is the next step in management? a. CK-MB level Neither of them would be elevated b. Oxygen All of them should be given, c. Nitroglycerin sublingual but neither lowers mortality d. Aspirin e. Thrombolytics All will be done, but first aspirin f. Metoprolol Sh ld b Should be given, i ti time d doesnt t matter tt g. Atorvostatin Not in acute settings h. Angioplasty Never the right answer i. Consult cardiology j. Transfer patient to intensive care unit Start treatment first k. Troponin level l. Morphine m. Angiography
MTBS2CK p.6465
AcuteCoronarySyndromes
70-year-old woman comes to ED with crushing substernal chest pain for last hour. EKG shows ST segment elevation in V2 to V4. Aspirin has been given to chew. What is next step in this patient? a. CK-MB level Neither of them would be elevated b. Oxygen All of them should be given, c. Nitroglycerin sublingual but none lowers mortality d. Morphine Angioplasty is superior to thrombolytics e. Thrombolytics BBs and statins should be given, but they are f. Metoprolol not critically dependent upon time g. Atorvostatin h. Angioplasty i. Troponin level j. Lisinopril
Learn the order in which to do things. You must know what is first.
MTBS2CK p.65
MTBS2CK p.65
13
AcuteCoronarySyndromes
ACS/DiagnosticTests
Test Timetobeing abnormal Durationofabnormality
On USMLE Step 2 CK, consultation is almost never the correct choice. Do everything yourself.
In ACS:
Does the treatment lower Which is most important to do
EKG
Immediatelyat onsetofpain
STelevationprogresses toQwavesoverdays toaweek 12days 12days 1014days
Myoglobin
14hours 46hours 46hours
mortality? first?
CKMB Troponin
MTBS2CK p.65
MTBS2CK p.66
ACS/DiagnosticTests
DiagnosticTests/Reinfarction
Troponin Cant distinguish reinfarction several days after the first event Renal insufficiency gives false positive tests Troponin: excreted through the kidney
New episode of pain within a few days of the first? EKG detects new ST segment abnormalities Check CK-MB levels After 2 days, y , the CK-MB level from the initial infarction returns to normal CK-MB elevated several days after initial MI indicates a new ischemic event
MTBS2CK p.66
MTBS2CK p.66
IntensiveCareUnitMonitoring
After initial management patient should be in ICU Continuous rhythm monitoring is essential Monitoring and rapid cardioversion improves survival
Most common cause of death first several days after myocardial infarction is ventricular arrhythmia (ventricular tachycardia, ventricular fibrillation) Rapid electrical cardioversion or defibrillation
MTBS2CK p.66
AcuteCoronary Syndromes Part2

Treatment
14
Treatment/STEMI Angioplasty versus Thrombolytics Angioplasty (PCI) superior to thrombolytics

Better survival and mortality Less bleeding Complications of MI decreased Less arrhythmia, less CHF, fewer ruptures of septum, free wall [tamponade] and papillary muscles [valve rupture]
Treatment/STEMI
Complications of PCI Rupture of coronary artery Restenosis Hematoma at entry site into artery Only 20% of U.S. hospitals can do primary angioplasty Important to have ability to perform emergency cardiac surgery to repair the vessel
MTBS2CK p.67
Standard of care: PCI within 90 minutes of arriving in emergency department with chest pain Door to balloon time: under 90 minutes
MTBS2CK p.67
Treatment/STEMI Which is most important in decreasing the risk of restenosis of the coronary artery after PCI? a. Multistage procedure (i.e., doing 1 vessel at a time, with multiple procedures) Used only at procedure b Use of heparin for 36 b. 3 6 months after the procedure c. Warfarin use after the procedure For DVT and PE not coronary disease d. Placement of bare metal stent e. Placement of drug-eluting stent (paclitaxel, sirolimus)
Has much more risk for restenosis than drug-eluting stent Doesnt change risk with each vessel done
Restenosis within 6 Months of PCI No stent: 30% 40% Bare metal stent:15% 30% Drug-eluting stent:10% Cant use thrombolytics? Transfer to a facility performing PCI
MTBS2CK p.67
MTBS2CK p.67
Treatment/STEMI
Absolute Contraindications to Thrombolytics Major bleeding:

Bowel (melena), brain
Recent surgery (within the last 2 weeks) Severe hypertension (>180/110) Nonhemorrhagic stroke within the last 6 months Heme-positive brown stool is not an absolute contraindication to the use of thrombolytics
MTBS2CK p.6768
Patient comes to small rural hospital without catheterization lab with chest pain and ST segment elevation. What is the next step in management? a. Transfer for angioplasty Should be done within 90 minutes b. Administer thrombolytics now c. Consult cardiology Never the right answer
Time is muscle. Delay = Death Door to needle time: under 30 minutes

MTBS2CK p.68
15
TreatmentIndicationsandBenefits
Therapy Inwhatcasesiseffectgreatest?
TreatmentIndicationsandBenefits
Therapy Inwhatcasesiseffectgreatest?
Aspirin Clopidogrel
Everyone,bestinitialtherapy AllMIs,undergoingangioplastyand stenting Everyone,effectnotdependenton time;startedanytimeduring admission Everyone,benefitbestwithejection fraction<40%
Statins Oxygen,nitrates Heparin
Everyone,bestwithLDL>100mg/dL Noclearmortalitybenefit Afterthrombolytics/PCItoprevent restenosis,initialtherapywithNSTEMI andunstableangina Cantusebetablockers,cocaine inducedpain,Prinzmetal angina
Betablockers
ACEI/ARBs
MTBS2CK p.68
Calciumchannel blockers
MTBS2CK p.68
Treatment/STSegmentDepressionACS
A man comes to the ED with chest pain for the last hour that is crushing in quality and does not change with respiration or position of his body. EKG: ST segment depression, V2 to V4. Aspirin has been given. What is the next step in this patient? a. Low molecular-weight heparin b. Thrombolytics Benefit only with STEMI c. Glycoprotein IIb/IIIa inhibitor (abciximab) PCI with stenting
d. e. f. g.
Nitroglycerin No clear benefit Morphine Angioplasty Heparin first Metoprolol Should be given, but not urgent
Glycoprotein IIb/IIIa Inhibitors (Abciximab, Tirofiban, Eptifibitide) Used in acute coronary syndromes Those who undergo angioplasty and stenting Not beneficial in acute ST elevation infarctions Inhibits I hibi platelet l l aggregation i Reduction in mortality with ST depression, particularly in patients whose troponin or CK-MB levels rise and then develop an MI requiring PCI with stenting
MTBS2CK p.69
MTBS2CK p.69
SummaryofTreatmentDifferencesbetween CardiacEvents Stableangina UA/NSTEMI STEMI
SummaryofTreatmentDifferencesbetween CardiacEvents Stableangina UA/NSTEMI STEMI
Aspirin Betablockers Nitrates Heparin
Yes Yes Yes No
Yes Yes Yes Yes
Yes Yes Yes Yes,onlyafter thrombolytics
Thrombolytics No
No
Yes,butnotas goodasPCI No No
CCBs Warfarin
No No
No No
GPIIb/IIIa meds No
MTBS2CK p.70
Yes
No
MTBS2CK p.70
16
AcuteCoronarySyndromes/Treatment
Bottom line: 1. tPA (thrombolytics) are beneficial only with STEMI 2. Heparin is best for NSTEMI 3. GPIIb/IIIa inhibitors are best for NSTEMI and those undergoing PCI and stenting
Treatment/STSegmentDepressionACS
In non-ST elevation ACS, when all medications have been given and the patient is not better, urgent angiography and possibly angioplasty (PCI) should be done. Not better means: Persistent pain S3 gallop or CHF developing Worse EKG changes Rising troponin levels
Calcium-channel blockers & warfarin: No mortality benefit in ACS LMW heparin superior to unfractionated heparin for mortality benefit
MTBS2CK p.70
MTBS2CK p.70
Acute Coronary Syndromes STEMI Non-STEMI/UA

Aspirin/Clopidogrel Beta Blockers Statin ACE Morphine p Nitrates
ComplicationsofAcuteMI
Excellent source of: What is the most likely diagnosis? questions, (most common question on Step 2) All MI complications can result in low BP Hypotension: Not help determine diagnosis
PCI
If available <90 min after patient arrives
1. 2. Emergency CABG Failed PCI Ischemia refractory ALL therapy
Thrombolytics
If PCI not available. Use within 12 hrs from start of chest pain

Heparin Early PCI

Absolute contraindications to thrombolytics Major bleeding (bowel/brain) Recent surgery (within last 2 weeks) Severe hypertension (>180/110) Nonhemorrhagic stroke last 6 months
MTBS2CK p.70
MTBS2CK p.71
ComplicationsofAcuteMI/Bradycardia
Heart rate: Key to establishing diagnosis Sinus bradycardia: Very common with MI From ischemia of sinoatrial (SA) node
Third-degree (complete) AV block:
Cannon a waves
Distinguishes 3rd degree block from sinus bradycardia before EKG From atrial systole against closed tricuspid Tricuspid valve closed because essence of third-degree block is atria and ventricles contracting separately Atria/ventricles out of coordination with each other
MTBS2CK p.71
MTBS2CK p.71
17
ComplicationsofAcuteMI/Tachycardia
Cannon is jugulovenous wave bouncing up into the neck Look for: right ventricular infarction and third-degree AV block All symptomatic bradycardias: 1. Treated first with atropine 2. Then place pacemaker if the atropine is not effective 3. Pace all permanent 3rd degree blocks
MTBS2CK p.71
Right Ventricular Infarction Look for: New inferior wall MI & clear lungs on auscultation Cant g get blood into lungs g if blood cant enter heart Flip EKG leads from left side to right side of chest Most specific finding: ST elevation in right lead 4 (RV4)
MTBS2CK p.71
Right coronary supplies:
Right ventricle (RV) AV node Inferior wall of the heart

Up to 40% with inferior wall myocardial infarctions (IWMI) have right ventricular infarction Treat RV infarct with high-volume fluid Avoid nitroglycerin (markedly worsens filling)
MTBS2CK p.71
Tamponade/Free Wall Rupture Usually takes several days after infarction for wall to scar & weaken enough for rupture Look for sudden loss of pulse Lungs: Clear Cause of Pulseless Electrical Activity (PEA) Test: Echocardiography Treat: Pericardiocentesis is done on way into operating room for repair
MTBS2CK p.72
ComplicationsofAcuteMI/Tachycardia Valve or Septal Rupture Both present with new onset murmur and pulmonary congestion Mitral regurgitation best heard at apex with radiation to axilla Ventricular septal rupture best heard at lower left sternal border Look for a step-up in oxygen saturation as you go from the right atrium to the right ventricle to hand you the diagnosis of septal rupture
MTBS2CK p.72
Ventricular Tachycardia/Ventricular Fibrillation Both can cause sudden death No way to distinguish without EKG if no pulse Cardiovert/ Defibrillate
These complications are the reason patients with acute MI are monitored in an ICU for the first several days after the infarction
MTBS2CK p.72
18
IntraaorticBalloonPump
Most accurate test: Echocardiogram for both You cant always depend on buzzwords like step-up for oxygenation Often, only numbers are presented: 42% oxygen saturation found on blood from right atrium and 85% saturation found in right ventricular sample
Intraaortic balloon pump (IABP): Answer for pump failure from anatomic problem that can be fixed in operating room IABP contracts & relaxes in sync with natural heartbeat Helps give a push forward to blood IABP is never a permanent device (bridge to surgery)
MTBS2CK p.72
MTBS2CK p.72
ExtensionoftheInfarction/Reinfarction
Aneurysm/MuralThrombus
Second event infarct Look for: Recurrence of pain New rales Bump up in CK-MBs Sudden onset pulmonary edema Actions: Repeat EKG Re-treat with angioplasty or thrombolytics
Continue: aspirin, metoprolol, nitrates, ACE, statins
MTBS2CK p.7273
Detected with echocardiography Most aneurysms dont need specific therapy Mural thrombi are treated with heparin followed by warfarin
MTBS2CK p.73
WhatistheMostLikelyDiagnosis? Diagnosis Keyfeature
WhatistheMostLikelyDiagnosis? Diagnosis Keyfeature
ThirddegreeAV Block Sinusbradycardia Tamponade/wall Rupture RVinfarction
Bradycardia,cannona Waves Nocannonawaves Suddenlossofpulse,JVD
Valverupture
Newmurmur, rales/congestion Newmurmur,increasein oxygensaturationon enteringtherightventricle Lossofpulse,needEKGto answerquestion
Septal rupture
IWMIinhistory,clearlungs, hypotension
Ventricular fibrillation
MTBS2CK p.73
MTBS2CK p.73
19
PreparationforDischargefromHospital
Detection of Persistent Ischemia Stress test prior to discharge Stress test determines if angiography needed Angiography A i h d determines t i need df for revascularization (angioplasty or bypass surgery)
Everyone should go home on: Aspirin Clopidogrel Beta blockers (metoprolol) Statins ACE inhibitors
Best for anterior wall infarctions because of high likelihood of developing systolic dysfunction
MTBS2CK p.74
Dipyridamole is never the right choice for coronary artery disease
MTBS2CK p.73
SexualIssuesPostinfarction
Clopidogrel: All MIs, or intolerant of aspirin, or post-stenting ARBs: those with cough to ACE inhibitor Ticlopidine: for rare person intolerant of both aspirin and clopidogrel
Prophylactic antiarrhythmic medications: Do not use amiodarone, flecainide, or any rhythmcontrolling medication to prevent the development of ventricular tachycardia or fibrillation. Do not be fooled by the question describing frequent PVCs and ectopy. Prophylactic antiarrhythmics increase mortality.
MTBS2CK p.74
The most commonly tested facts are: Dont combine nitrates with sildenafil; hypotension can result because theyre both vasodilators Erectile dysfunction postinfarction is most commonly from anxiety Most common medication is beta blocker
MTBS2CK p.74
SexualIssuesPostinfarction
Wait after MI for sexual activity

2-6 weeks
If post-MI stress test is normal, any form of exercise program can be started including sex
CongestiveHeartFailure
Definition Presentation Diagnosis Treatment
MTBS2CK p.74
20
CongestiveHeartFailure(CHF)/Definition
CHF/CausesofSystolicDysfunction
Shortness of breath (dyspnea) - essential feature of congestive heart failure (CHF) Dysfunction of heart as a pump of blood Insufficient oxygen delivery and fluid in lungs Either from: S t li dysfunction: Systolic d f ti Low Ejection Fraction (EF) and dilation of heart Diastolic dysfunction: EF is preserved Heart cant relax and receive blood
MTBS2CK p.7475
Most Common: Hypertension resulting in cardiomyopathy Initially theres preservation of EF Over time time, the heart dilates resulting in systolic dysfunction and low EF Valvular heart disease of all types results in CHF
MTBS2CK p.75
CHF/CausesofSystolicDysfunction Myocardial infarction (MI) is a very common cause of dilated cardiomyopathy and decreased EF Dead or infarcted heart wont pump CHF most common cause of hospital admission in USA MI death rate down from:
Thrombolytics Beta blockers Angioplasty Aspirin, clopidogrel
CHF/CausesofSystolicDysfunction
Infarction Dilation Regurgitation CHF

MTBS2CK p.75
Many are normal, are living with CHF

MTBS2CK p.75
CHF/CausesofSystolicDysfunction Less common causes are: Alcohol Postviral (idiopathic) myocarditis Radiation Adriamycin (doxorubicin) use Chagas Ch di disease and d other th i infections f ti Hemochromatosis (also causes restrictive cardiomyopathy) Thyroid disease Peripartum cardiomyopathy Thiamine deficiency
MTBS2CK p.75
CHF/Presentation In addition to dyspnea on exertion look for: Orthopnea (worse when lying flat, relieved when sitting up or standing) Peripheral edema Rales on lung exam Jugulovenous distention (JVD) Paroxysmal nocturnal dyspnea (PND)(sudden worsening at night, during sleep) S3 gallop rhythm (Be prepared to identify the sound on Step 2. It may be played.)
MTBS2CK p.7677
21
HeartSoundsTimingintheCardiacCycle
CHF/Presentation
The most frequently asked USMLE Step 2 CK question is: What is the most likely diagnosis?
MTBS2CK p.76
MTBS2CK p.76
WhatistheMostLikelyDiagnosis? forDyspnea
Keyfeature Mostlikelydiagnosisis
Keyfeature Mostlikelydiagnosisis
Suddenonset,clearlungs Suddenonset,wheezing, increasedexpiratoryphase Slower,fever,sputum,unilateral rales/rhonchi Decreasedbreathsounds unilaterally,trachealdeviation

MTBS2CK p.77
Pulmonaryembolus Asthma
Circumoral numbness,caffeine use,historyofanxiety Pallor,gradualoverdaysto weeks k
Panicattack
Anemia
Pneumonia Pulsus paradoxus,decreased heartsounds,JVD Pneumothorax Palpitations,syncope

MTBS2CK p.77
Tamponade
Arrhythmia (ofalmostanykind)
Keyfeature Dullnesstopercussionatbase Longsmokinghistory,barrelchest ,brownblood Recentanestheticuse, notimprovedwithoxygen,clear lungsonauscultation,cyanosis Burningbuildingorcar,wood burningstoveinwinter,suicide attempt
MTBS2CK p.77
MostLikelydiagnosisis Pleuraleffusion COPD g Methemoglobinemia
All of these will lack: Orthopnea/PND S3 gallop
Carbonmonoxidepoisoning
MTBS2CK p.77
22
CHF/DiagnosticTests
CHF/EjectionFraction What is the best initial test? Transthoracic echo
Echocardiography Most important test of CHF There is no OTHER way to distinguish Systolic vs. Diastolic dysfunction Will NOT distinguish by: History Physical Tests (e.g., EKG, chest X-ray, or BNP)
MTBS2CK p.77
Whats the most accurate test? Multiple Multiple-gated gated acquisition scan (MUGA) or nuclear ventriculography Transesophageal echocardiography (TEE): More accurate for valves
MTBS2CK p.78
CHF/DiagnosticTests
CHF/DiagnosticTests
When should you answer nuclear ventriculography? Rarely needed Person receiving chemotherapy with doxorubicin Trying to give max dose to cure lymphoma But not cause cardiomyopathy
MTBS2CK p.78
When should you answer BNP? Acute SOB Etiology unclear You cant wait for echo Normal BNP excludes CHF
MTBS2CK p.78
TestsUsedtoDetermineEtiologyofCHF
TestsUsedtoDetermineEtiologyofCHF Test
T4/TSH
Test
EKG ChestXray Holter monitor Cardiac catheterization CBC
MTBS2CK p.78
Etiology ofCHF
MI,heartblock Dilatedcardiomyopathy
Etiology ofCHF
Bothhighandlowthyroidlevels causeCHF Excludessarcoid,amyloid Rarelyneeded Canbiopsyothersites
Myocardialbiopsy
Paroxysmalarrhythmias Precisevalvediameters, septal defects Anemia

SwanGanz rightheart catheterization
DistinguishesCHFfromARDS;not routine
MTBS2CK p.78
23
CHF/Treatment
CHF/Treatment
Systolic Dysfunction (Low EF) ACE inhibitors or angiotensin receptor blockers (ARBs) Beta blockers Spironolactone, S i l t E l Eplerenone Diuretics Digoxin
ACE/ARBs All patients with systolic dysfunction All stages of disease Beneficial effects: any drug in class When are ARBs Next best step? ACE induced cough
MTBS2CK p.79
MTBS2CK p.79
CHF/Treatment
CHF/Treatment
Beta Blockers Not clearly any drug in class Evidence only for:
Metoprolol Bisoprolol Carvedilol
Beta Blockers are: Anti-ischemic Decrease heart rate Decrease O2 consumption Antiarrhythmic
MTBS2CK p.79
MTBS2CK p.79
CHF/Treatment Which of the following is the MCC of death from CHF? a. b. c c. d. e. Pulmonary edema We can fix this almost all the time Myocardial infarction CHF doesnt cause MI Arrhythmia/sudden death Emboli Clots rare in CHF unless AFib Myocardial rupture This from MI, not CHF
Spironolactone Benefit from inhibition of aldosterone Only proven for more advanced CHF (class III and IV) with dyspnea on minimal exertion or at rest What is the most common adverse effect? Hyperkalemia Gynecomastia
MTBS2CK p.7980
MTBS2CK p.79
24
CHF/Treatment
CHF/Treatment
When is eplerenone the answer? When spironolactone leads to antiandrogenic effects (e.g., gynecomastia)
Diuretics ED: Acute pulmonary edema Office: Combination with ACEi or ARB Furosemide, torsemide, or bumetanide equal Spironolactone, although a diuretic, is not used at doses where it has a diuretic effect Diuretics control symptoms of CHF. They do not lower mortality.
MTBS2CK p.80
MTBS2CK p.80
CHF/Treatment
CHF/Treatment Devices with mortality benefit
Digoxin Digoxin does NOT lower mortality in CHF This is often the single most important question concerning CHF on USMLE Digoxin will: Control symptoms Decrease frequency of hospitalizations No positive inotropic agent (digoxin, milrinone, amrinone, dobutamine) has been proven to lower mortality
MTBS2CK p.80
1. Implantable defibrillator: Ischemic CM & EF < 35%. Remember: Arrhythmia and sudden death are MCC of death in CHF 2. Biventricular pacemaker: EF < 35% & wide QRS > 120 ms with persistent symptoms
MTBS2CK p.8081
CHF/Treatment
CHF/Treatment
Biventricular pacemaker is NOT a dualchamber pacemaker Dual-chamber pacer has wire in right ATRIUM and right VENTRICLE Biventricular pacemaker resynchronizes the heart when theres a conduction defect Defers/delays need for cardiac transplantation Symptoms markedly improved
MTBS2CK p.81
Transplantation Symptoms despite maximal medical therapy (ACE, BB, spironolactone, diuretics, digoxin) and possibly biventricular pacemaker Warfarin Always wrong in absence of clot in heart
MTBS2CK p.81
25
CHF/Treatment
CHF/Treatment
Mortality Benefit in Systolic Dysfunction ACEi/ARBs Beta blockers Spironolactone Hydralazine/nitrates Implantable defibrillator Calcium-channel blockers (CCBs) can actually raise mortality
MTBS2CK p.81
Diastolic Dysfunction (CHF with preserved EF) Less clear Beta blockers have clear benefit No mortality benefit in diastolic dysfunction Digoxin clearly has no benefit
MTBS2CK p.81
CHF/Treatment
Diuretics control symptoms of fluid overload Do not confuse diastolic dysfunction from hypertrophic CM with hypertrophic obstructive cardiomyopathy (HOCM) Diuretics are contraindicated in HOCM because they increase obstruction
AcutePulmonaryEdema
MTBS2CK p.81
AcutePulmonaryEdema
AcutePulmonaryEdema/Presentation How do I answer What is the most likely diagnosis? Acute shortness of breath with: Rales JVD S3 gallop Edema Ed Orthopnea MAY be: Ascites & enlargement of liver/spleen from chronic passive congestion of right side of heart
MTBS2CK p.82
Definition Worst (most severe) form of CHF Rapid fluid accumulation in lungs
MTBS2CK p.82
26
S3GallopRhythm
JVD
PittingEdema
WetCrackles
Whatisthebestinitialtest? Brain Natriuretic Peptide (BNP) is the answer if: Diagnosis not clear Normal BNP excludes CHF Chest X-ray shows: Vascular congestion Filling Filli of f bl blood d vessels l t toward dh head d( (cephalization h li ti of flow) Flow mostly at base because of gravity Enlargement of heart Effusion
MTBS2CK p.82 82
PulmonaryEdema
Pulmonary edema with cephalization of flow and engorged pulmonary veins

Source: Saba Ansari, MD.
MTBS2CK p.83
27
AcutePulmonaryEdema/DiagnosticTests
Oximetry/Arterial Blood Gas (ABG) Hypoxia expected Respiratory alkalosis from hyperventilation CO2 leaves l more easily il than th oxygen enters
AcutePulmonaryEdema/ WhichTestismostlikelytoalteracutemanagement?
Answer!!! EKG A-fib, Atrial flutter, or V-tach What to do first? Synchronized cardioversion Restore atrial systole = Return atrial contribution to cardiac output
MTBS2CK p.83
MTBS2CK p.83
EKG Diseased hearts need atrial systole more than normal hearts Up from 10% to 30 - 40% of cardiac output Diseased hearts means:
Dil Dilated t d cardiomyopathy di th Valvular heart disease
If acute pulmonary edema is from arrhythmia fix it fast with..

Cardioversion!!!!!
MTBS2CK p.83
Echocardiography MUST be done on all patients ONLY WAY to determine systolic or diastolic dysfunction No difference in initial therapy Huge difference in chronic therapy
MTBS2CK p.83
AcutePulmonaryEdema/Treatment 74-woman comes to ED with the acute onset of SOB, RR of 38/minute, rales to apices, S3 gallop, and JVD. What is the best initial step in management?
Will be done, but first you have to treat a. Oximeter Should be done, but not urgently b. Echocardiography c. Intravenous furosemide d. Ramipril Although they are used in CHF, they are not e. Metoprolol Part of the treatment of acute setting f. Nesiritide No mortality benefit. Not better than nitrates
Preload Reduction Initial therapy: Oxygen Loop diuretics (e.g., furosemide or b bumetinide) ti id ) Morphine Nitrates
MTBS2CK p.84
MTBS2CK p.84
28
AcutePulmonaryEdema/Treatment
The majority in acute pulmonary edema can be managed with preload reduction Removing 1 to 2 liters of fluid is best Nesiritide does NOT work better than other agents
What do you do if the questions say: Preload reduction hasnt been effective? Positive Inotropic Agents Dobutamine in ICU Amrinone and milrinone Phosphodiesterase inhibitors that perform the same role
Increase contractility
Decrease afterload
MTBS2CK p.84
MTBS2CK p.84
Positive Inotropic Agents Digoxin too slow! Increases contractility, but Needs several weeks to work No benefit of digoxin in acute setting
Afterload Reduction ACEi and ARBs: Used on discharge Long-term use with systolic dysfunction (low EF) Nitroprusside in ICU Hydralazine alternate for ACE/ARB
Heparin is always wrong for acute pulmonary edema, use for clots
MTBS2CK p.85
MTBS2CK p.85
ValvularHeartDisease/Definition
ValvularHeartDisease
All can be congenital in nature Rheumatic fever can lead to any form and mitral stenosis is most common Aging = Aortic stenosis Regurgitant R it t via i HTN & i ischemia h i Infarction regurgitation Regurgitation dilation
MTBS2CK p.85
29
ValvularHeartDisease/Presentation
ValvularHeartDisease/DiagnosticTests
All forms associated with SOB and CHF Only murmurs are specific for presentation Right-sided heart lesions (tricuspid and pulmonic valve) increase with inhalation Inhalation venous return to right side Left-sided lesions (mitral and aortic valve) with exhalation Exhalation squeezes blood out of lungs into left side
Best initial test: Echocardiogram Transesophageal: more sensitive & specific than transthoracic echo Most accurate test: Catheterization C th t i ti : Catheterization Most precise valvular diameter Most exact pressure gradient across valve
MTBS2CK p.85
MTBS2CK p.85
ValvularHeartDisease/DiagnosticTests
ValvularHeartDisease/Treatment
EKG: Not specific with valvular heart disease Shows hypertrophy of chambers Cannot confirm diagnosis from EKG Chest X X-ray: ray: Shows enlargement chambers Precise anatomic correlation poor X-ray is neither the most accurate test nor the best initial test
MTBS2CK p.85
All forms associated with fluid overload All benefit from diuretics Meds alone cant improve stenotic lesions Mitral Mit l stenosis: t i Dilated Dil t d with ith balloon b ll Aortic stenosis: Surgical replacement
MTBS2CK p.86
Regurgitant lesions Respond best to vasodilators ACEi/ARBs, nifedipine, or hydralazine Surgical replacement must be done before heart dilates too much If heart dilates excessively valve replacement will not be able to correct decrease in systolic function If myocardium stretches too much it wont return to normal size and shape
MTBS2CK p.86
Assess ventricular size based on: End-systolic diameter Ejection fraction Expansion of end-systolic diameter (must replace p the valve) )
Endocarditis prophylaxis is not indicated for any of these valve lesions.
MTBS2CK p.86
30
MitralStenosis (MS)
MitralStenosis
Definition/Etiology Most often from rheumatic fever Extremely uncommon in US Low incidence of acute rheumatic fever Treatment if symptomatic Do not treat asymptomatic MS
Look for: Pregnancy and Immigrant Pregnancy: 50% increase in plasma volume Contraction of uterus squeezes squeezes 500 mL extra into central circulation Most with MS are immigrants to the US Come from places where acute rheumatic fever is still common
MTBS2CK p.86
MTBS2CK p.86
MitralStenosis
MitralStenosis/Presentation
Presentation SOB and CHF AND! Unique features of presentation:

Dysphagia: Left atrium (LA) presses on esophagus Hoarseness: LA presses on laryngeal nerve Atrial fibrillation & stroke from enormous LA MS: Look for Hemoptysis
Enlarged left atrium in mitral stenosis compresses the esophagus causing dysphagia
Source: Andrew Peredo
young adult patients
MTBS2CK p.8687
MTBS2CK p.87
MitralStenosis
MitralStenosis headphonesrequired
Physical findings Diastolic murmur after opening snap Squatting & leg raising increase it! Increased venous return increases murmur
MTBS2CK p.87
MTBS2CK p.87
31
MitralStenosis
Diagnostic tests Echo TTE: Best initial test TEE more accurate than TTE Catheterization: Most accurate test EKG Atrial rhythm disturbance, particularly atrial fibrillation, very common LA hypertrophy: Biphasic P wave: V1 and V2
MTBS2CK p.87
MitralStenosis/DiagnosticTests Diagnostic tests Chest X-ray: Left Atrial Hypertrophy Straightening of left heart border Elevation of left main mainstem bronchus Second bubble behind heart
MitralStenosis/Treatment
Diuretics & sodium restriction: When fluid overload present Balloon valvuloplasty With a catheter Valve replacement Only O l when h a catheter h procedure d cannot b be d done or fails Warfarin A-fib to INR 2 to 3 Rate control: Digoxin, beta blockers, or diltiazem/ verapamil
MTBS2CK p.88
Source : Andrew Peredo
MTBS2CK p.87 88
AorticStenosis
AorticStenosis
Definition/Etiology Congenital bicuspid valve Increasing calcification with age Presentation Angina (most common) Syncope CHF:
Poorest prognosis 2-year average survival
Murmur Systolic, crescendo-decrescendo Peaks in diamond-shape mid-systole Heard best at 2nd right intercostal space Radiates to carotids
Source: Shwan Christian
MTBS2CK p.88
MTBS2CK p.88
32
AorticStenosis
AorticStenosis headphonesrequired
Murmur Valsalva & standing Decrease intensity of murmur Less venous return = Less Murmur Handgrip Softens murmur Less blood ejected = Less murmur
MTBS2CK p.88
MTBS2CK p.88
AorticStenosis/DiagnosticTests TTE, then TEE, then catheterization Chest X-ray

Left ventricular hypertrophy
AorticStenosis/Treatment
EKG LV hypertrophy (LVH)

Source: Nihar Shah, MD.
S V1 + R V5 > 35 mm
MTBS2CK p.89
Cardiac enlargement is defined as a heart greater in diameter than 50% of the total transthoracic diameter
Replacement: Only truly effective therapy for AS Diuretics CHF but dont tolerate volume depletion well Balloon valvuloplasty p y Not routine for AS AS calcification doesnt improve well with balloon valvuloplasty Only if surgery isnt an option Unstable/fragile patients
MTBS2CK p.89
MitralRegurgitation
MitralRegurgitation
Definition/Etiology MR is abnormal backward flow of blood through mitral valve that doesnt fit together Hypertension Endocarditis Myocardial infarction Papillary muscle rupture Any heart dilation leads to MR
MTBS2CK p.89
Presentation Signs/Symptoms of CHF Unique finding: Pansystolic (holosystolic) murmur Obscures S1 and S2 Radiates to axilla Handgrip worsens murmur of MR Handgrip increases afterload Pushes blood backwards Handgrip worsens AR and MR
MTBS2CK p.90
33
MitralRegurgitation/Presentation
MitralRegurgitation headphonesrequired
Squatting & leg raising worsen MR Increase venous return to heart All left-sided murmurs except mitral valve prolapse (MVP) and hypertrophic obstructive cardiomyopathy will increase with expiration MR diagnosed with echo
MTBS2CK p.90
MTBS2CK p.90
MitralRegurgitation
MitralRegurgitation/Treatment
Treatment Vasodilators: ACE or ARBs are best Decrease rate of progression Digoxin & diuretics for symptomatic CHF
Valve replacement: Indicated when heart dilates Dont wait for left ventricular end systolic diameter (LVESD) to become large Replace R l when: h LVESD > 40 mm or EF < 60% Valve repair:
Placing a clip or sutures across valve to tighten
MTBS2CK p.90
MTBS2CK p.90
AorticRegurgitation
AorticRegurgitation
Definition/Etiology AR caused by: Anything that makes the heart or aorta dilate: MI HTN Endocarditis Marfan syndrome or cystic medial necrosis Inflammatory disorders (e.g., Ankylosing spondylitis, Reiter syndrome) Syphilis
MTBS2CK p.9091
Presentation Besides CHF unique physical findings are: Wide pulse pressure Water-hammer (wide, bounding) pulse Quincke pulse (pulsations in nail bed) Hill sign (BP in legs as much as 40 mmHg above arm BP) Head bobbing (de Musset sign)
MTBS2CK p.91
34
AorticRegurgitation
AorticRegurgitation headphonesrequired
Murmur Diastolic, decrescendo murmur Heard best: Lower left sternal border Valsalva & Standing: Softer Handgrip (increases afterload): Worse
MTBS2CK p.91
MTBS2CK p.91
AorticRegurgitation
AorticRegurgitation
Diagnostic tests EKG & Chest X-ray: LVH
Treatment ACEi/ARBs or nifedipine: Vasodilators Increase forward flow of blood Delay progression Digoxin & Diuretics: Little benefit Surgical valve replacement: Acute valve rupture (MI) Replace valve before LV dilates excessively EF < 55% LVESD > 55 mm
MTBS2CK p.91
MTBS2CK p.91
MitralValveProlapse(MVP)
MitralValveProlapse
Common Considered normal anatomic variant 2% to 5% of population Particularly in women Marfan or Ehlers-Danlos syndrome
Presentation Most often asymptomatic When symptoms do occur: Symptoms of CHF usually absent Most common is:
Atypical chest pain Palpitations Panic attack
MTBS2CK p.91
MTBS2CK p.91
35
MitralValveProlapse
MitralValveProlapse headphonesrequired
Murmur Presents with: Midsystolic click When severe associated with murmur Mitral regurgitation Valsalva & Standing worsen MVP Squatting & Handgrip improve (diminish) MVP
MitralValveProlapse Redundant mitral valve leaflet doesnt seal allowing regurgitation
MitralValveProlapse
Diagnostic tests Echocardiography: Best choice Catheterization: Rarely, if ever, done Valve replacement: Rarely needed
MTBS2CK p.92
MTBS2CK p.92
MitralValveProlapse
Treatment Beta blockers: When symptomatic Valve repair With catheter Place clip to tighten valve Stitches valve to tighten leaflets Surgical repair rarely necessary Endocarditis prophylaxis not recommended
MTBS2CK p.92
Cardiomyopathy & PericardialDisease

DilatedCardiomyopathy Hypertrophic h Cardiomyopathy d h RestrictiveCardiomyopathy AcutePericarditis PericardialTamponade ConstrictivePericarditis
36
Cardiomyopathy/Definition
Cardiomyopathy/Etiology
Abnormal function of heart muscle Frequent valve or auscultory abnormalities But! It originates i i t from f an abnormally b ll contracting or relaxing myocardium
Can be dilated, hypertrophic, or restrictive The terms dilated cardiomyopathy, systolic dysfunction, and low EF are often used interchangeably Hypertrophic cardiomyopathy interchangeable with diastolic dysfunction Or!! Cardiac failure with preserved EF
MTBS2CK p.92
MTBS2CK p.93
Cardiomyopathy/Presentation
Cardiomyopathy/DiagnosticTests
All forms give: SOB, particularly worsened by exertion Edema Rales JVD
Echocardiography: Best initial test Often Most accurate test used EKG & Chest X-ray: Should be performed Nothing specific on them confirm the diagnosis Murmurs not increasing with expiration: HOCM MVP
MTBS2CK p.93
MTBS2CK p.93
Cardiomyopathy/Treatment
DilatedCardiomyopathy
All treated with diuretics Other treatments based on type of cardiomyopathy The only real functional difference in management and answers to questions is: TREATMENT
In addition to previous MI and ischemia, dilated cardiomyopathy can be from:

Alcohol Postviral myocarditis Radiation Toxins (e.g., doxorubicin) Chagas disease
MTBS2CK p.93
MTBS2CK p.93
37
DilatedCardiomyopathy
DilatedCardiomyopathy/Treatment
Dyspnea, gallop, edema, testing same as section on CHF
Multiple meds mortality ACEi (or ARBs) Beta blockers (metoprolol, carvedilol) Spironolactone (or eplerenone) Symptom Control ONLY: Diuretics & Digoxin
MTBS2CK p.93
MTBS2CK p.93
DilatedCardiomyopathy/Treatment
HypertrophicCardiomyopathy
QRS wide (> 120 ms) Biventricular pacemaker Improve both symptoms and survival Automated implantable cardioverter/defibrillator di t /d fib ill t h has mortality t lit benefit
HTN - MCC MUST distinguish between hypertrophic cardiomyopathy (HCM) and HOCM HCM: Reaction to BP Heart hypertrophies yp p to carry y load Develops difficulty relaxing in diastole Cant relax = Cant receive blood Patient becomes short of breath
MTBS2CK p.9394
MTBS2CK p.94
HypertrophicObstructiveCardiomyopathy
HypertrophicCardiomyopathy
MTBS2CK p.9495
Genetic disorder Abnormal shape of septum Asymmetrically hypertrophied septum and valve leaflet blocks blood leaving the heart
S4 gallop Fewer signs of right heart failure Less ascites Less enlargement of liver and spleen
MTBS2CK p.94
38
HOCM/Presentation
Dyspnea Chest pain Syncope & lightheadedness Sudden death, particularly in healthy athletes Worsened by heart rate
(e.g., exercise, dehydration, and diuretics)
HOCM/DiagnosticTests
Echo (best initial test) Septum 1.5x thickness of posterior wall

Systolic anterior motion (SAM) of mitral valve is classic for HOCM. It contributes t ib t t to obstruction. b t ti Catheterization is most accurate test to determine precise gradients of pressure across the chamber. Septal Q waves in the inferior and lateral leads are common in HOCM.
Worsened by in left ventricular chamber size

(e.g., ACEi, ARBs, digoxin, hydralazine, valsalva, and standing suddenly)
MTBS2CK p.94
EKG: Nonspecific ST and T wave changes are common. LVH is common. EKG can be normal in a quarter
MTBS2CK p.95
HypertrophicCardiomyopathy/Treatment
HOCM/SpecificTherapy Implantable defibrillator: HOCM with syncope Ablation of septum: Catheter placing absolute alcohol in muscle Causes small infarctions If symptoms t persist: i t Surgical S i l myomectomy t Surgical myomectomy is the therapy only if all medical and catheter procedures fail.
MTBS2CK p.95
Beta blockers: Best initial therapy both HOCM & HCM Diuretics help HCM Diuretics harm HOCM
Digoxin and spironolactone are definitely always wrong in hypertrophic cardiomyopathy.
MTBS2CK p.95
In HOCM, ACEi and diuretics definitely dont help. This is the major difference between HOCM and HCM
RestrictiveCardiomyopathy Hypertrophic versusDilatedCardiomyopathy
Hypertrophic
BetaBlockers Diuretics ACEi/ARB Spironolactone Digoxin
MTBS2CK p.95
Dilated
Yes Yes Yes Yes Yes
Yes Yes Unclearbenefit No No
Combines worst aspects of dilated and hypertrophic cardiomyopathy Heart neither contracts nor relaxes Infiltrated with substances creating immobility
MTBS2CK p.96
39
RestrictiveCardiomyopathy
Causes are: Sarcoidosis Amyloid Hemochromatosis Endomyocardial fibrosis Scleroderma
Presentation Dyspnea: Most common Right heart failure Ascites, edema, JVD Enlargement g of liver & spleen p Pulmonary hypertension: Common Kussmaul sign: jugulovenous pressure on inhalation
MTBS2CK p.96
MTBS2CK p.96
Diagnosis Echocardiography: Initial test EF normal or elevated EKG: Low voltage Amyloid: Speckling of septum on echo or cardiac MRI Most accurate test: Endomyocardial biopsy Rarely done Diagnosis made from biopsies elsewhere
MTBS2CK p.96
Treat underlying cause Diuretics relieve some pulmonary HTN and signs of right heart failure No other clear therapy
MTBS2CK p.96
MurmursandtheEffectsofManeuvers
MurmursandtheEffectsofManeuvers Standing/Valsalva Decreasesboth
Lesion
Squatting/Legraising
Mitralandaortic Increasesboth stenosis Mitralandaortic Increasesboth regurgitation Mitralvalve prolapse HOCM

MTBS2CK p.96
Decreasesboth
More blood increases all murmurs except MVP and HOCM.
Decrease
Increase
Decrease
Increase
MTBS2CK p.96
Less blood decreases all murmurs except MVP and HOCM.
40
EffectsofManeuvers
EffectsofManeuvers
Standing from a squatting position: Opens vessels of legs Decreases venous return to heart Valsalva: Exhalation against a closed glottis Increases intrathoracic pressure Decreases venous return to heart
MTBS2CK p.97
Standing or Valsalva = Diuretic use Stenotic & regurgitant murmurs all treated with diuretics and salt restriction Standing St di & Valsalva V l l will ill i improve th them
MTBS2CK p.97
EffectsofManeuvers
EffectsofManeuvers
MVP & HOCM: Worsen with diuretics Diuretics decrease LV size Diuretics worsen MVP and obstruction of HOCM Standing St di and d valsalva l l worsens th them
Handgrip Handgrip increases afterload Contraction of arm muscles compresses arteries Decreases emptying of heart Opposite of ACE inhibitor Worsens AR and MR
MTBS2CK p.97
MTBS2CK p.97
EffectsofManeuvers Amyl nitrate: Direct arteriolar vasodilator Decreases afterload Simulates ACE inhibitors or ARBs on heart Valvular disease treated with ACEi/ARB will improve with amyl nitrate Improves AR and MR Handgrip = Fuller left ventricle Amyl nitrate = ACEi = Emptier left ventricle
MTBS2CK p.97
EffectofManeuverson Intensity(loudness)ofMurmurs Lesion Aorticstenosis Mitralstenosis A i regurgitation Aortic i i Mitralregurgitation Mitralvalveprolapse HOCM
MTBS2CK p.97
Handgrip Decreases Noeffect I Increases Increases Decreases Decreases
Amylnitrate Increases Noeffect D Decreases Decreases Increases Increases
41
EffectofManeuverson Intensity(loudness)ofMurmurs
PericardialDisease
Handgrip and amyl nitrate have no meaningful effect on mitral stenosis in the same way ACEi stenosis, has no meaningful effect on MS
Causes of pericarditis, pericardial tamponade & constrictive pericarditis overlap If the etiology of pericarditis extravasates fluid, then tamponade can occur If the cause of pericarditis is chronic, fibrosis and calcification of pericardium lead to constrictive pericarditis
MTBS2CK p.97
MTBS2CK p.98
Pericarditis/Etiology
Pericarditis/Etiology
Any Infection Inflammatory disorder Connective tissue disorder Chest trauma or cancer near the heart can cause pericarditis Most common infection is viral
MTBS2CK p.98
Systemic lupus erythematosus: Most common connective tissue disorder But Wegener granulomatosis Goodpasture syndrome Rheumatoid arthritis Polyarteritis nodosa and others can cause pericarditis
MTBS2CK p.98
Pericarditis/Presentation
Pericarditis/DiagnosticTests EKG shows ST segment elevation in all leads, but the most specific finding is PR segment depression
What Is the Most Likely Diagnosis? Sharp chest pain Changes with respiration Changes with position of body Worsened by lying flat Improved by sitting up
MTBS2CK p.98
MTBS2CK p.9899
42
Pericarditis/Treatment
PericardialTamponade/Etiology
Treat cause Majority: Idiopathic

Idiopathic presumed viral Coxsackie B virus
T Treated t d with ith NSAIDs NSAID (e.g., ( ibuprofen, ib f naproxen) Colchisine - recurrences
Any cause of pericarditis can extravasate enough fluid to cause tamponade Compression heart starts on right side Walls are thinner 50 mL acutely y cause tamponade p Over weeks to months, pericardium stretches for 2 L of fluid Can also be from trauma Bleed requires emergent thoracotomy
MTBS2CK p.99
MTBS2CK p.99
PericardialTamponade/Presentation
PericardialTamponade
What Is the Most Likely Diagnosis? Hypotension Tachycardia Distended neck veins Clear lungs
Which of the following physical findings is most likely to be associated with this patient? Pulsus paradoxus Decrease of more than 10 mmHg in systolic blood pressure on inhalation
EKG: Electrical alternans (different heights of QRS complexes between beats)
Chest X-ray: Enlarged cardiac shadow expanding in both directions (globular heart) Echocardiogram: Right atrial and ventricular diastolic collapse Right heart catheterization: Equalization of pressures in diastole
MTBS2CK p.100
MTBS2CK p.100101
43
78-year-old man with lung cancer experiences several days of increasing SOB. Hes lightheaded today. BP 106/70; pulse 112; JVD present; lungs: clear, BP drops to 92/58 on inhalation. Which is most appropriate to confirm the diagnosis?
a. b b. c. d. e.
EKG Low voltage non-specific. Rare alternans y; globular g heart later Chest X-ray X ray Normal acutely; Echocardiogram Most accurate; Right heart catheterization should do echo first Cardiac MRI Not clearly right for
Treatment Pericardiocentesis Needle rapidly reexpands the heart IV fluids A hole or window recurrent cases
Diuretics will decrease intracardiac filling pressure and may markedly worsen collapse of right side of heart
ANYTHING at this time
MTBS2CK p.100
MTBS2CK p.101
ConstrictiveDisease
ConstrictiveDisease
Any cause of pericarditis with calcification and fibrosis Prevents filling of right side of heart Tuberculosis
What Is the Most Likely Diagnosis? Signs of right heart failure such as:
Edema Ascites Enlargement of liver and spleen JVD
Constrictive pericarditis is a combination of physical findings described above with calcification on chest X-ray
ConstrictiveDisease
PericardialKnock headphonesrequired
Which physical findings is most likely associated with this patient? Kussmaul sign: Increase in JVD on inhalation Normally neck veins go down on inhalation Knock: Extra heart sound in diastole From ventricular filling Heart fills to its maximum, it hits the stiff, rigid pericardium with a knock
MTBS2CK p.101
44
ConstrictiveDisease
ConstrictiveDisease
Best initial test Chest X-ray: Calcification & fibrosis
CT scan or MRI more accurate, not 1st Echocardiogram: Excludes RV hypertrophy or cardiomyopathy as cause Myocardium moves normally with constrictive pericarditis
MTBS2CK p.101
Commons.wikimedia.org. Used with permission
MTBS2CK p.101
ConstrictiveDisease
Treatment Diuretics: Decompress filling of heart Relieves edema and organomegaly Surgical removal of pericardium
PeripheralArteryDisease,Aortic Disease,&HeartDisease inPregnancy

Definition Etiology Presentation Diagnosis Treatment
MTBS2CK p.101
PeripheralArteryDisease(PAD)/Etiology
PeripheralArteryDisease/Presentation What Is the Most Likely Diagnosis? Pain in calves on exertion Relieved by rest Walking up or down hills Severe disease causes loss of:
Hair H i f follicles lli l Sweat glands Sebaceous glands
Stenosis of peripheral arteries from: Diabetes mellitus Hyperlipidemia Hypertension Tobacco smoking
Same causes as Coronary Disease!!
The skin becomes smooth and shiny

Spinal stenosis pain is worse when walking down hills because of leaning back
45
PeripheralArteryDisease Diagnostic tests Best initial test = Ankle-brachial index (ABI) ABI: Ratio of BP in ankles to brachial arteries Normally equal or slightly greater in ankles because of gravity If difference between them is > 10% (ABI < 0 0.9), 9) disease is present Most accurate test = angiogram Angiogram not necessary unless revascularization will be done
There is no routine screening for PAD since there is no mortality benefit to be obtained
MTBS2CK p.102
PeripheralArteryDisease
Treatment The best initial therapy is:

Aspirin Smoking cessation Cilostazol
Single most effective medication: Cilostazol Surgery or angioplasty if medical therapy not effective
In all major vascular disease control the following: BP LDL < 100 Diabetes
MTBS2CK p.102103
AorticDissection 67-year-old man in ED with sudden onset chest pain is also felt between his scapulae. He has a history of HTN and tobacco smoking. BP 169/108. What is the best initial test?
a. b. c. d. e. f. g. Chest X-ray Chest CT Dont show specific changes MRA, TEE, and CTA MRA have same accuracy; Transesophageal echocardiogram not most accurate, Transthoracic echocardiogram neither best initial CT angiogram Angiography Most accurate, but not best initial test
Author: J. Heuser; commons.wikimedia.org Used with permission
MTBS2CK p.103
AorticDisease
AorticDisease/Treatment For dissection, Most important step is: Control BP This can be done with:
Beta blockers Nitroprusside
Most frequently tested points in aortic disease Diagnosis & treatment of acute dissection Screening recommendations
Key points for presence of aortic dissection Pain in between the scapulae Difference in blood pressure between the arms
Beta blockade decreases shearing forces that worsens dissection Beta blockers must start before nitroprusside to protect against reflex tachycardia of nitroprusside, which worsens shearing forces
MTBS2CK p.103
MTBS2CK p.104
46
AbdominalAorticAneurysm Which of the following is the most appropriate screening for aortic aneurysm?
a. b. c. d d. e.
Everyone > 50 with CT angiography Men who ever smoked > 65 with ultrasound Everyone > 50 with ultrasound Everyone > 65 with ultrasound Men > 65 with ultrasound
Incidence of AAA is less in both nonsmokers and in women, so there is no recommendation for screening in those groups
MTBS2CK p.104
PeripartumCardiomyopathy Which of the following is most dangerous to a pregnant woman? a. b. c. d. e. Mitral stenosis Peripartum cardiomyopathy Choose this if p peripartum p Ei Eisenmenger phenomenon h cardiomyopathy is not one of the choices Mitral valve prolapse Atrial septal defect
Not as dangerous as choices b and c
Unknown why antibodies are made against the myocardium in some pregnant women LV dysfunction often reversible and short term If LV dysfunction does not improve, then must undergo cardiac transplantation
MTBS2CK p.104
MTBS2CK p.105
PeripartumCardiomyopathy Therapy the same as for dilated cardiomyopathy of any cause:

ACEi/ARB Beta blockers Spironolactone Diuretics Digoxin
EisenmengerSyndrome
Repeat pregnancy with peripartum cardiomyopathy will kill 50-70% of women!! Peripartum cardiomyopathy develops after delivery in most cases; ACEi/ARBs must be used
MTBS2CK p.105
From right-to-left shunt from pulmonary HTN Develops in person with ventricular septal defect with left-to-right shunt that eventually develops pulmonary HTN When pulmonary HTN becomes very severe shunt reverses Right-to-left shunting develops
MTBS2CK p.105
47
EisenmengerSyndrome
EisenmengerSyndrome
If peripartum cardiomyopathy is not one of the choices in asking, What is the worst cardiac disease in pregnant women? then Look for Eisenmenger in the choices
Pregnancy increases plasma volume by 50%. Mitral stenosis will worsen in pregnancy, But not as much as peripartum cardiomyopathy or Eisenmenger
Large left-to-right shunt (congenital heart defect)
P l Pulmonary HTN
Reverse of the shunt: right-to-left shunt
MTBS2CK p.105
MTBS2CK p.105
48
Dermatology Part1 Dermatology Part1

ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity CutaneousMalignancies AtopicDermatitis(Eczema) Psoriasis PityriasisRosea SeborrheicDermatitis(Dandruff) BlisteringDiseases
Cutaneousmalignancies
MalignantMelanoma
Greater with pale skin More sun-exposed areas Diagnosis: Biopsy Treatment: Surgical removal No truly effective chemotherapy
Skin Cancer More sun, more cancer Biopsy Remove
MTBS2CK p. 363
More frequent in sun-exposed areas But! Not exclusive to those areas Benign vs. Malignant Melanoma clinically ABCDE: A: Asymmetry B: Border irregularity C: Color irregularities D: Diameter > 6 mm E: Evolution (changing over time)
MTBS2CK p.363
MalignantMelanoma
DistinctionBetweenBenignandMalignant
Diagnosis? Suspicious?
Benign
Malignant
Biopsy!
Include entire thickness of lesion if possible ibl Worst prognosis!!
Round Evenborders Colorevenlyspread Diameterconstant

MTBS2CK p.364
Asymmetric Bordersuneven Coloruneven Diameterincreases
Growing lesions
MTBS2CK p. 363
BenignLesion
MalignantMelanoma
Diagnostic Test Full thickness biopsy: indispensible Dont perform shave biopsy Treatment/Prognosis Surgical removal Must include normal skin surrounding lesion Interferon injection helpful in widespread disease Melanoma has strong tendency to metastasize to brain
MTBS2CK p.364
MTBS2CK p.364
SquamousCellCancer
SquamousCellCancer
Sunlight
Organ transplant!!!!
Immunosuppressive drugs! Squamous starts looking like ulcer Doesnt heal, grows Biopsy and remove
Source: James Heilman MD
MTBS2CK p.364
MTBS2CK p.364
BasalCellCarcinoma
BasalCellCarcinoma
Most common skin cancer Question describes: Waxy lesion
Shiny like a pearl

U Unlike lik melanoma, l wide id margins i not t necessary Shave biopsy fine! (diagnostic) Recurrence < 5% Basal cell: use Mohs microsurgery
BasalCellCarcinoma/ MohsMicrographicSurgery
BasalCellCarcinoma/ MohsMicrographicSurgery
Remove skin cancer under dissecting microscope Very thin slices of skin Immediate frozen section VERY precise way to treat skin cancer Mohs:
Remove cancer Keep normal
MTBS2CK p.365
Stop resecting when margin is cancerfree No removal of wide margins Mohs Best: Delicate areas Eyelid & Ear
MTBS2CK p.365
KaposiSarcoma(KS)
KaposiSarcoma(KS)
In past, KS seen only in older men of Mediterranean origin Now: AIDS From HHV-8, which is oncogenic Reddish/purplish R ddi h/ li h More vascular than others
MTBS2CK p.365
MTBS2CK p.365
KaposiSarcoma(KS)
KaposiSarcoma/Treatment
Also in GI tract and lung Only from AIDS via sexual contact associated with KS IDU AIDS rarely associated with KS
Unlike other skin cancers, KS not routinely removed surgically 1. Treat AIDS with antiretrovirals 2. Majority disappear as CD4 improves 3 Intralesional 3. I t l i li injections j ti of f vincristine i i ti or interferon 4. If these fail, use chemotherapy with liposomal doxorubicin
MTBS2CK p.366
MTBS2CK p.365
ActinicKeratoses
ActinicKeratoses
Premalignant From high-intensity sun exposure in fairskinned people Very small risk of SCC for each individual lesion
Richard Usatine, M.D. Used with permission.
MTBS2CK p.366
MTBS2CK p.366
ActinicKeratoses
ActinicKeratoses
Many occur in a single person Risk is cumulative Like cervical dysplasia and cervical cancer Slow to progress Remove with:
Curettage Cryotherapy Laser Topical 5-fluorouracil Imiquimod
MTBS2CK p.366
MTBS2CK p.366
ActinicKeratoses
SeborrheicKeratoses
Imiquimod Local immunostimulant Also for molluscum contagiosum Condyloma acuminatum
Extremely common in elderly Hyperpigmented lesions Commonly referred to as liver spots Stuck on appearance May look like melanoma to some people Seborrheic keratoses = Zero malignant potential
MTBS2CK p.366
MTBS2CK p.366
SeborrheicKeratoses
SeborrheicKeratoses
Removed with: Cryotherapy Surgery Laser Removal (cosmetic reasons)
Source: James Heilman MD
MTBS2CK p.366
MTBS2CK p.366
AtopicDermatitis(Eczema)
AtopicDermatitis(Eczema)/Presentation
Common skin disorder Associated with overactivity of mast cells & immune system Look for history of: Asthma Allergic rhinitis Family history of atopic disorders Onset < age 5, very rare to start > 30
From premature and idiosyncratic release of transmitters (e.g., histamine) Pruritus & scratching is most common presentation Scratching leads to scaly rough areas of thickened skin On face, neck & skin folds Popliteal area behind knee
MTBS2CK p.366
MTBS2CK p.366
MTBS2CK p.366
MTBS2CK p.366
AtopicDermatitis(Eczema)/Presentation Itching scratching Scratching more itching Superficial skin infections from Staphylococcus are common Microorganisms driven under epidermis by scratching This, in turn, more itching Skin thickened because of scratching and drying = lichenified
MTBS2CK p.367
AtopicDermatitis(Eczema)/SkinCare
1. Stay moisturized: dry skin is more itchy 2. Use a humidifier, especially in winter 3. Avoid bathing, soap, and washcloths (skin hyperirritable) 4. Avoid brushes, , washcloths, , hot water, , and anything that rubs on skin 5. Cotton less irritating than wool
IgE levels: Elevated in atopic dermatitis
MTBS2CK p.367
Food allergies dont exacerbate atopic dermatitis
AtopicDermatitis(Eczema)/MedicalTherapy
AtopicDermatitis(Eczema)/MedicalTherapy
1. Topical corticosteroids: used in flares of disease (oral steroids only in most severe acute flares) 2. Tacrolimus and pimecrolimus
T cellinhibiting agents L Longer-term t control t l Help get patient off steroids Used systemically in organ transplant recipients Prevent organ rejection Used topically for atopic dermatitis
MTBS2CK p.367
3. Antihistamines:
Mild disease: nonsedating drugs (cetirizine, fexofenadine, loratadine) Severe disease: hydroxyzine, diphenhydramine, doxepine
4. Antibiotics (e.g., cephalexin, mupirocin, retapamulin) when impetigo occurs 5. UV light (phototherapy) for severe recalcitrant disease
MTBS2CK p.367
Psoriasis/Definition/Presentation
Psoriasis/Definition/Presentation
Incredibly common 2 million in US Characterized by silvery, scaly plaques Not itchy most of the time Arthritis < 10% Extensive disease associated with depression
MTBS2CK p.367
MTBS2CK p.368
Psoriasis/Treatment Local Disease 1. Topical high-potency steroids: fluocinonide, amcinolone, betamethasone, clobetasol 2. Vitamin A & Vitamin D ointment Helps get patient off steroids Vitamin D agent is calcipotriene Steroids cause skin atrophy 3. Coal tar preparation 4. Pimecrolimus and tacrolimus Used in delicate areas (e.g., face & penis) Alternative to steroids Less deforming
MTBS2CK p.368
Psoriasis/Treatment
Steroids cause atrophy Inhibit collagen formation and growth Convert AAs glucose Gluconeogenesis
MTBS2CK p.368
Psoriasis/Treatment
Extensive Disease 1.UV light 2.Antitumor necrosis factor (TNF) inhibitors Etanercept Adalimumab Infliximab Miraculous for severe disease 3.Methotrexate: Last because of effects on liver & lung First for psoriatic arthritis
MTBS2CK p.368
TNF inhibitors reactivate TB Screen with PPD prior to use
MTBS2CK p.368
PityriasisRosea
PityriasisRosea
Idiopathic, transient dermatitis Starts with a single lesion (herald patch) Then disseminates Can look like secondary syphilis But spares palms & soles Transient If symptomatic: treat with steroids or UV light
MTBS2CK p.369
MTBS2CK p.368
SeborrheicDermatitis(Dandruff)
SeborrheicDermatitis(Dandruff)
Hypersensitivity reaction Dermal infection Noninvasive dermatophyte organisms Both topical steroids and antifungal agents t (e.g., ( ketoconazole) k t l ) are useful f l
Increased in:
AIDS Parkinsons disease
Seborrheic = Benign
MTBS2CK p.369
MTBS2CK p.369
PemphigusVulgaris
PemphigusVulgaris
Both idiopathic/autoimmune form and Drug induced form Associated with: ACE inhibitors Penicillamine Phenobarbital Penicillin
Autoantibodies split epidermis, resulting in: Bullae that easily rupture Thin-walled Involvement I l t of f mouth th Fluid loss & infection Widespread (acts like burn)
MTBS2CK p.369
MTBS2CK p.369
PemphigusVulgaris
PemphigusVulgaris
Source: phil.cdc.gov
PemphigusVulgaris
PemphigusVulgaris
Characteristic finding: Nikolsky sign Loss or denuding of skin from mild pressure Nikolsky y sign: g Removal of superficial layer of skin Single sheet while pulling on it Fingers worth of pressure
MTB S2CK - p. 370
Most accurate test = biopsy Biopsy shows: autoantibodies on immunofluorescent (IF) studies
Without treatment, pemphigus is fatal
MTBS2CK p.370
PemphigusVulgaris/Treatment
BullousPemphigoid
1. Systemic steroids (prednisone) 2. Azathioprine or mycophenolate to wean patient off steroids 3. Rituximab (anti-CD20 antibodies) or IVIG in refractory cases
Much milder than pemphigus: Bullae stay intact Less loss of fluid Less infection Mouth involvement uncommon
MTBS2CK p.370
MTBS2CK p.370
BullousPemphigoid
BullousPemphigoid
Biopsy with IF stains is Most accurate test Best initial therapy: Prednisone To get patients off steroids, use azathioprine, cyclophosphamide, or mycophenolate Mild bullous p pemphigoid p g responds p to erythromycin, dapsone, and nicotinamide (not niacin)
Nikolsky sign absent in bullous pemphigoid
MTBS2CK p.370
PorphyriaCutaneaTarda
PorphyriaCutaneaTarda
Blistering skin disease Sun-exposed areas With history of: Liver disease Hepatitis C Alcoholism Estrogen use Iron overload (hemochromatosis)
MTBS2CK p.370
Hepatitis C: Most frequently tested association with PCT Look for involvement of: backs of hands & face
MTBS2CK p.370
PorphyriaCutaneaTarda/ DiagnosticTests/Treatment
Most accurate test Increased uroporphyrins on 24-hr urine Deficiency of uroporphyrin decarboxylase activity Treatment Correct underlying cause Stop alcohol Stop estrogens Remove iron with phlebotomy
MTBS2CK p.370
Dermatology Part2
SkinInfections DrugReactions StaphylococcalScaldedSkinSyndromeand ToxicShockSyndrome Acne
Impetigo
Impetigo/Treatment
Most superficial bacterial skin infection Staphylococcus and Streptococcus invade epidermis Results in weeping, crusting, oozing, & draining of skin
Mild disease with topical agents: Mupirocin Bacitracin Retapamulin Severe disease with oral agents: Dicloxacillin or cephalexin Community-acquired MRSA with: Doxycycline Clindamycin Trimethoprim/sulfamethoxazole (TMP/SMZ)
MTBS2CK p.371
MTBS2CK p.371
10
Erysipelas
Erysipelas/Presentation
Much more severe than impetigo Occurs at deeper level in skin Streptococcus > Staphylococcus Invades dermal lymphatics Causes bacteremia, bacteremia leukocytosis leukocytosis, fever fever, and chills Fatal, if untreated
Skin infections can cause glomerulonephritis, but not rheumatic fever.
MTBS2CK p.371
Bright, red, hot swollen Lesion on face Leukocytosis Often systemic disease
MTBS2CK p.371
Erysipelas/Presentation
Erysipelas/Treatment Although erysipelas is more often from Streptococci, you must treat for Staphylococcus as well unless you have a definitive diagnostic test such as blood cultures. Treatment of all skin infections is similar Same answers as for:
Cellulitis Folliculitis Furuncles Carbuncles
Source: Thomas F Sellers
MTBS2CK p.371
Erysipelas/Treatment
Mild disease - oral medications: Dicloxacillin, cephalexin, cefadroxyl Penicillin allergic: erythromycin, clarithromycin, or clindamycin MRSA: Doxycycline, clindamycin, or TMP/SMX
Severe disease (e.g., fever): IV medications: Oxacillin, nafcillin, cefazolin Penicillin allergic: Clindamycin, vancomycin MRSA: Vancomycin, linezolid, daptomycin, tigecycline, ceftaroline
Cross reaction Between penicillin and cephalosporins unusual (< 5%)
MTBS2CK p.372
MTBS2CK p.372
11
Cellulitis
Step 2 CK tests: Route of administration (O l vs Intravenous) (Oral I t )
Soft tissue infection of skin Extends from dermis into subcutaneous tissue Skin: Warm, red, swollen, and tender
MTBS2CK p.372
MTBS2CK p.372
Cellulitis
Cellulitis Involves legs > arms Doesnt have collections of walled-off infection, which is an abscess Cellulitis isnt only at hair follicle; that's folliculitis, furuncles, and carbuncles
Skin infection: Caused by S. aureus
NOT S. epidermidis
S. epidermidis lives on skin as normal flora
Cellulitis/DiagnosticTests
Cellulitis/Treatment
No diagnostic testing needed Most accurate test

Inject sterile saline into skin & aspirate for culture
Yield only 20%
Same as for erysipelas Topical antibiotics will not cover cellulitis Below dermal/epidermal junction Topical T i l antibiotics tibi ti wont t reach h
Staphylococcus > Streptococcus
MTBS2CK p.372
MTBS2CK p.372
12
Folliculitis,Furuncles,Carbuncles
Originate around hair follicles Different terms dont have precise definitions Indistinguishable, no cutoff in size
Severe disease = fever, chills, bacteremia
Folliculitis,Furuncles,Carbuncles/ SizeoftheInfection
Folliculitis: Earliest & mildest Furuncle: Small abscess or collection of infected material Carbuncle: Collection of furuncles
Folliculitis < Furuncle < Carbuncle
Treat: Ox/Clox/Diclox/Naf
Source: cdc.gov
Folliculitis,Furuncles,Carbuncles/ PenicillinAllergy
Reaction - Rash Use cephalosporins Reaction - Anaphylaxis Mild infection: Macrolides, clindamycin, doxycycline, or TMP/SMZ Severe infection: Vancomycin, linezolid, daptomycin, or tigecycline
13
Folliculitis,Furuncles,Carbuncles/ OtherAntistaphylococcal Medications
FungalInfections
Beta-lactam/beta-lactamase combinations
Amoxicillin/clavulanate Ticarcillin/clavulanate Ampicillin/sulbactam Piperacillin/tazobactam
Dermatophyte = superficial fungal infection = tinea For example: Tinea corporis p = body y Tinea manum = hand Tinea pedis = foot Tinea cruris = groin (jock itch)
MTBS2CK p.374
Carbapenems (imipenem, meropenem)
MTBS2CK p.373374
FungalInfections
FungalInfections/DiagnosticTests/Treatment
Best initial test KOH (potassium hydroxide) Dissolves epidermal skin cells Leaves fungi intact Most accurate test Fungal culture
MTBS2CK p.374
FungalInfections/DiagnosticTests/Treatment
FungalInfections/Treatment
Best initial therapy Topical antifungal agent if no hair or nails involved For hair (tinea capitis) and nail (tinea unguium)
Terbinafine Itraconazole
Topical antifungal agents: Clotrimazole Ketoconazole Oral ketoconazole Econazole causes gynecomastia Miconazole Mi l Nystatin Ciclopirox
MTBS2CK p.374
MTBS2CK p.375
14
FungalInfections/OralandVaginalCandidiasis
DrugReactions Hypersensitivity reactions to medications vary in severity When severity of reaction changes, the name of reaction changes Drugs causing hypersensitivity reactions: Penicillins Sulfa drugs (including thiazides, furosemide, and sulfonylureas) Allopurinol Phenytoin Lamotrigine NSAIDs
MTBS2CK p.375
Same answers for both KOH: Best initial test Fungal culture: Most accurate test With clear presentation: Treat Topical antifungal from previous list
MTBS2CK p.375
DrugReactions
MorbilliformRash
Drugs that cause hypersensitivity reactions of the skin are the same that cause: Hemolysis Interstitial I t titi l nephritis h iti Thrombocytopenia
Mildest reaction Skin stays intact No mucous membrane involvement No specific therapy
MTBS2CK p.375
MTBS2CK p.375
MorbilliformRash
ErythemaMultiforme
Widespread Target lesions Mostly on trunk Mucous membrane uninvolved From herpes or mycoplasma Prednisone may benefit
MTBS2CK p.376
MTBS2CK p.375
15
ErythemaMultiforme
StevensJohnsonSyndrome
Erythema multiforme is characterized by multiple small target-shaped l i lesions th that t can b be confluent
Very severe Involves mucous membranes Sloughs off respiratory epithelium May lead to respiratory failure Steroids not beneficial Use intravenous immunoglobulins (IVIG)
MTBS2CK p.375
MTBS2CK p.375
ToxicEpidermalNecrolysis
ToxicEpidermalNecrolysis
Mucous membrane involvement Nikolsky sign Steroids definitely dont help Treat with IVIG
The skin comes off in a sheet, simulating a burn.
MTBS2CK p.375
MTBS2CK p.376
Source: Conrad Fischer, MD
StaphylococcalScaldedSkinSyndrome(SSSS) andToxicShockSyndrome(TSS)
StaphylococcalScaldedSkinSyndromeand ToxicShockSyndrome
Different severities of same event Reaction to toxin in surface of Staphylococcus SSSS looks similar to TEN, including Nikolsky sign life TSS has skin involvement as well as lifethreatening multi-organ involvement:
Hypotension Renal dysfunction ( BUN and creatinine) Liver dysfunction CNS involvement (delirium)
Both treated with: Antistaphylococcal medications Oxacillin or nafcillin are most effective Cefazolin is essentially equal Antibiotics dont reverse disease Kills Staphylococcus that produces toxin
MTBS2CK p.377
MTBS2CK p.377
16
Acne/Treatment
Acne/Treatment
Mild acne Topical antibacterials: Benzoyl peroxide If ineffective add topical antibiotics (e.g., clindamycin or erythromycin)
Moderate acne Add topical vitamin A derivatives: tretinoin, adapalene, or tazarotene to topical antibiotics If no response to topical vitamin A derivatives and antibiotics, use oral antibiotics (e.g., minocycline or doxycycline)
MTBS2CK p.377
MTBS2CK p.377
Acne/Treatment
Severe acne Add oral vitamin A, isotretinoin to oral antibiotics Isotretinoin causes hyperlipidemia
Vitamin A derivatives extremely teratogenic
MTBS2CK p.377
17
EMERGENCYMEDICINE
NiketSonpal,MD
ChiefResident LenoxHillHospitalNSLIJ AssistantClinicalProfessor TouroCollegeofMedicine
Toxicology,Poisoning,& Overdose
TreatmentofOverdose
32-year-old woman with a history of depression comes to ED 30 minutes after taking a bottle of pills in a suicide attempt. BP 118/70, pulse 90, and respirations normal. She refuses to tell you what she took. What is the next step?
Gastric Lavage
OVERDOSE TREATMENTS
a. Induce emesis with ipecac p th way up the b. Gastric lavage c. Psychiatric consultation Consultations are 99% wrong on USMLE Takes too long d. Serum chemistry e. Urine toxicology screen Urine wont show up yet Pills will not make that transit time f. Cathartics/laxatives g. Whole bowel irrigation Doesnt change outcomes We dont know if its opiates h. Naloxone We dont know if its benzos i. Flumazenil
MTBS2CK p.533
It could be caustic and injure on
Cathartics
Bowel Irrigation Fluids and Diuresis
Ipecac
MTBS2CK p.534
InitialManagementofPoisoning
Gastrointestinal Emptying Gastric lavage

Gastric emptying of any kind is always wrong with Caustics (acids and alkali) Altered mental status
Gastric lavage is rarely done. Removes 50% of pills at 1 hour Removes 15% of pills at 2 hours
Ipecac is always a wrong answer in ED
MTBS2CK p.534
MTBS2CK p.534
Ipecac No inpatient benefit 15-20 minutes onset Hinders antidotes
Cathartics Cathartic agents WRONG answer Prokinetics WRONG answer
MTBS2CK p.534
MTBS2CK p.534
Forced Diuresis Fluids and diuretics is always a wrong answer Risk of PE > benefit
Whole Bowel Irrigation
NGT with polyethylene glycol-electrolyte solution is almost always wrong Only for:
Iron ingestion Lithium Drug-filled packets
MTBS2CK p.534
MTBS2CK p.534
When answer is unclear and cause of overdose is asked say:

Acetaminophen 1st Most Common Aspirin 2nd Most Common
Woman comes to ED one hour after taking a bottle of pills. BP 118/70, pulse 90/min, and respirations 14/min. She is confused, disoriented, and lethargic. What is the next step in the management?
Seizure risk too high 2 line a. Flumazenil Dangerous in AMS b. Gastric lavage c. Psychiatric consultation Never get a consult youre an MD d. Naloxone and dextrose Not the first step e. Intubation
nd
What to do is often unclear. What is useless or dangerous (ipecac, forced diuresis, cathartics) is very clear.
MTBS2CK p.535
MTBS2CK p.535
Psychiatric consultation is indicated for suicide attempt, but is a wrong answer on USMLE S2 CK when specific antidotes and diagnostic tests are needed.
Opiate overdose is fatal: Give naloxone immediately Benzodiazepine overdose by itself is not fatal and acute withdrawal causes seizures Dont give flumazenil
MTBS2CK p.535
MTBS2CK p.535
Acetaminophen
Charcoal Charcoal is benign Charcoal is not dangerous Charcoal is superior to lavage and ipecac
When you dont know what to do in toxicology, give charcoal
MTBS2CK p.535536
Legal drugs kill more people in the United States than illegal drugs because theyre less expensive and more available Toxicity of acetaminophen with ingestion > 8 to 10 g Fatality with ingestions > 12 to 15 g
MTBS2CK p.536
Acetaminophen Four Most Common Acetaminophen Overdose Questions: 1. If a clearly toxic amount of acetaminophen has been ingested (> 810 g) Ans er N-acetylcysteine Answer: N acet lc steine 2. If the overdose was > 24 hours ago No therapy
Acetaminophen 3. Amount of ingestion unclear? Drug level 4. Charcoal does not make N-acetylcysteine ineffective Charcoal isnt contraindicated with Nacetylcysteine
MTBS2CK p.536
MTBS2CK p.536
AspirinOverdose
AspirinOverdose
What is the most likely diagnosis?

Renal Toxicity Altered Mental Status
Respiratory Alkalosis Metabolic Acidosis
Aspirin causes diffuse, multisystem toxicity

Increased PT
ARDS
Aspirin Overdose
Tinnitus
Aspirin Overdose
Increased Anion Gap
Respiratory Failure Lactic Acidosis
Increased PTT
Hyperventilation
MTBS2CK p.536
MTBS2CK p.536
AspirinOverdose
Treatment is alkalinizing urine, which increases rate of aspirin excretion Know blood gas in aspirin overdose
Tinnitus, respiratory alkalosis, and metabolic acidosis are the key to diagnosing aspirin overdose.
Which of the following is most likely to be found in aspirin overdose?

(Normal values: pH 7.40, pCO2 40, HCO3 24)
a. pH 7.55 pCO2 50 HCO3 24 pH 7.25 p pCO2 62 HCO3 38 b. p c. pH 7.46 pCO2 22 HCO3 16 d. pH 7.35 pCO2 32 HCO3 20
This is a distracter p overdose never g gives Aspirin respiratory acidosis Metabolic acidosis with respiratory compensation
MTBS2CK p.536
MTBS2CK p.536537
Depressed patient presents with altered mental status from ingesting multiple toxic substances. You know for certain that he took some lorazepam only today, for the first time. There is no response to naloxone or dextrose. The patient is given flumazenil and immediately seizes. What is the most likely cause of the seizure?
What is the best initial test for the patient previously described?
a. Urine toxicology b. Electroencephalogram c. EKG Wont show the cause of the seizure d. Head CT in this patient e. Potassium level
a. Cocaine withdrawal Cocaine toxicity causes seizures, not withdrawal Doesnt cause seizures b. Opiate withdrawal c. Tricyclic antidepressants d. SSRIs SSRIs toxicity causes serotonin syndrome (SS) Causes tinnitus and hyperventilation, not seizures e. Aspirin
MTBS2CK p.537
MTBS2CK p.537
TricyclicAntidepressantToxicity
TricyclicAntidepressants Seizures Arrhythmia
Widened QRS Complex Dry mouth
TCA Toxicity
Urinary retention Constipation
MTBS2CK p.537
MTBS2CK p.538
TricyclicAntidepressants
Caustics
The best initial treatment of TCA overdose is with sodium bicarbonate

Bicarbonate will protect the heart against arrhythmia Bicarbonate does not increase urinary y excretion of TCAs as it does for aspirin
Caustic ingestion of acids and alkalis (e.g., drain cleaner) causes

Mechanical damage to oropharynx Esophageal perforation Stomach perforation
Dont give alkali to reverse acids
MTBS2CK p.538
MTBS2CK p.538
Caustics
CarbonMonoxidePoisoning
Flush out caustics Use water in high volumes Endoscopy is performed to assess degree of damage
Steroids dont prevent injury from caustics
Carbon monoxide (CO) poisoning is the MCC of death in fires
Thermal injury is always the wrong answer
MTBS2CK p.538
MTBS2CK p.538
CO binds oxygen to Hb so tightly that carboxyhemoglobin will not release oxygen to tissues Carboxyhemoglobin acts functionally like anemia
Myocardial infarction Carbon Monoxide
Functional Anemia
Dyspnea
Confusion Seizures
Lightheadedness
Source:cdc.gov
MTBS2CK p.538
MTBS2CK p.538
No functional difference between absence of blood and carboxyhemoglobin; 60% carboxyhemoglobin = loss of 60% of blood The left ventricle cant can t distinguish between anemia, carboxyhemoglobin, and stenosis of coronary arteries.
Which of the following blood gas results would you find in carbon monoxide poisoning?
a. b. c. d. pH 7.55 pCO 50 HCO 24 pH 7.25 pCO 62 HCO 38 pH 7.46 pCO 22 HCO 16 pH 7.35 pCO 26 HCO 18
2 3 2 3 2 3 2 3
Distracter Respiratory acidosis with metabolic alkalosis Respiratory alkalosis with metabolic acidosis
MTBS2CK p.538
MTBS2CK p.538
Diagnostic tests
Carbon monoxide poisoning gives normal pO2 because oxygen doesnt detach from hemoglobin Routine oximetry will be falsely normal Most accurate test is a level of carboxyhemoglobin
Treatment
Remove patient from exposure Give 100% oxygen
MTBS2CK p.538
MTBS2CK p.539
Methemoglobinemia
Treatment Severe disease is treated with hyperbaric oxygen Severe symptoms are defined as:
CNS symptoms Cardiac symptoms Metabolic acidosis
Methemoglobin is oxidized Hb Ferric Ferric = Fe3+ Ferrous = Fe2+ Oxidized hemoglobin is brown and will ill not t carry oxygen Chocolate-brown blood
MTBS2CK p.539
Wikimedia
MTBS2CK p.539
Methemoglobinemia
Methemoglobinemia/Presentation
Methemoglobinemia from idiosyncratic reaction of hemoglobin to drugs such as: Benzocaine and anesthetics Nitrites and nitroglycerin Dapsone p
The effects of methemoglobinemia are similar to carboxyhemoglobin Oxygen isnt delivered to tissues
Metabolic Acidosis Methemoglobinemia Functional Anemia
Ferrous Hemoglobin
Benzocaine Nitrites Dapsone
Methemoglobinemia Ferric Hemoglobin Confusion Seizures Headache

MTBS2CK p.539
Dyspnea Cyanosis
Lightheadness
MTBS2CK p.539
Methemoglobinemia/Presentation
Methemoglobinemia/DiagnosticTests/ Treatment
Carbon monoxide: blood abnormally red Methemoglobinemia: blood abnormally brown
Both methemoglobinemia and carboxyhemoglobin give normal pO2 on blood gas Most accurate test is methemoglobin level Best initial therapy is 100% oxygen Most effective therapy is methylene blue, which half-life of methemoglobin
Cyanosis + normal pO2 = methemoglobinemia

Organophosphate(Insecticide)Poisoningand NerveGas
Organophosphate(Insecticide)Poisoningand NerveGas Bronchospasm Bronchorrhea Organophosphate g p p Poisoning Salivation Respiratory arrest
Organophosphates and nerve gas identical in their effects Nerve gas faster and more severe Massive increase in acetylcholine by i hibiti metabolism inhibiting t b li
Polyuria y
Lacrimation
MTBS2CK p.540
MTBS2CK p.540
Acetylcholine constricts bronchi and increases bronchial secretions
56-year-old military commander attacked with nerve gas. Presents with salivation, lacrimation, urination, defecation, and SOB. Pupils are constricted. What is the first step in management?
a. Atropine p b. Decontaminate (wash) the patient Stabilize first c. Remove his clothing Stabilize first d. Pralidoxime Takes too long e. No therapy is effective Never the right answer
MTBS2CK p.540
MTBS2CK p.540
DigoxinToxicity/Etiology
Nerve gas and organophosphates g p p are absorbed through the skin
Hypokalemia predisposes to digoxin toxicity because potassium and digoxin compete for same site on the Na+/K+ATPase Less potassium is bound, more digoxin is bound
K+ Increased Digoxin Binding
MTBS2CK p.540
MTBS2CK p.540
DigoxinToxicity/Presentation
DigoxinToxicity/Presentation
Confusion
Yellow Halo Vision
Hypokalemia
Digoxin g Toxicity Arrhythmias y
Digoxin toxicity Hyperkalemia
Digoxin toxicity
Hyperkalemia
Nausea Vomiting Abdominal Pain

MTBS2CK p.541
MTBS2CK p.540541
DigoxinToxicity/DiagnosticTests
DigoxinToxicity/DiagnosticTests
Most accurate test: digoxin level Best initial tests: potassium level and EKG EKG: downsloping of ST segment in all leads
Atrial tachycardia with variable AV block is the most common digoxin toxic arrhythmia
Digoxin can produce any arrhythmia

MTBS2CK p.541
DigoxinToxicity/Treatment
LeadPoisoning Renal Tubule Toxicity (ATN) Abdominal pain lead colic
Control potassium and give digoxinspecific antibodies Digoxin-binding antibodies rapidly remove digoxin from circulation
Strongest indication for digoxin-binding antibodies: CNS and cardiac involvement.
Lead Toxicity Sideroblastic Anemia
Memory y loss confusion Peripheral Neuropathy wrist drop
MTBS2CK p.541
MTBS2CK p.541
LeadPoisoning
LeadPoisoning/Treatment
Best initial test: level of free erythrocyte protoporphyrin Most accurate test: lead level
Chelating agents remove lead from body

Succimer: only oral Ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL) are parenteral
Most accurate test for sideroblastic anemia: Prussian blue stain
MTBS2CK p.541
MTBS2CK p.541
MercuryPoisoning Oral ingested Neurological problems Nervous, jittery, twitchy, and sometimes hallucinatory Inhaled Lung toxicity & interstitial fibrosis
MercuryPoisoning
Theres no therapy to reverse pulmonary toxicity Chelating agents such as dimercaprol and succimer are effective in removing mercury from body and decreasing neurological t i it toxicity
MTBS2CK p.541
ToxicAlcohols/MethanolandEthyleneGlycol Methanol Ethylene glycol
DifferencesbetweenMethanoland EthyleneGlycol
Methanol Source Woodalcohol,cleaning solutions,paintthinner Ethyleneglycol Antifreeze
1. Intoxication 1 2. Metabolic Acidosis 3. Increased Anion Gap 4. Osmolar Gap
Treated w/ 1. Fomepizole 2. Dialysis
Toxic metabolite Presentation
Formicacid/formaldehyde Oxalicacid/oxalate
Oculartoxicity
Renaltoxicity Hypocalcemia, envelopeshaped oxalatecrystalsin urine
Initialdiagnostic Retinalinflammation abnormality

MTBS2CK p.542
MTBS2CK p.542
10
ToxicAlcohols/MethanolandEthyleneGlycol Osmolar Gap Osmolar gap = measured serum osmolality - calculated osmolality Serum osmolality = 2(Na+) + BUN/2.8 + Glucose/18
Ex: Measurement 350 - Calculated 300 = gap of 50 osmoles
ToxicAlcohols/MethanolandEthyleneGlycol
Treatment Best initial therapy: fomepizole, which inhibits alcohol dehydrogenase and prevents production of toxic metabolite Only dialysis removes methanol and ethylene glycol
Ordinary alcohol (ethanol) also osmolar gap

SnakeBites
SnakeBites/Treatment
Ineffectiveordangerous treatment Beneficialtherapy
Most common injury from snake bites is local wound Death from snake bites:
Hemolytic toxin: hemolysis, DIC, and damage to endothelial lining of tissues Neurotoxin: can result in respiratory paralysis, ptosis, dysphagia, and diplopia
Tourniquetsblocking arterialflow Ice
Pressure
Immobilizationdecreases movementofvenom Antivenin
Incisionandsuction, especiallybymouth
MTBS2CK p.542543
MTBS2CK p.543
SpiderBites/Presentation
DifferencesbetweenTypesofSpiderBites
Blackwidow Brownrecluse
All spider bites present with a sudden, sharp pain that patient may describe as: 1.I stepped on a nail 2. A piece of glass was in my shoe.
Presentation
Abdominal pain, musclepain Hypocalcemia
Localskin necrosis
Labtest abnormalities Treatment
None
Calcium, antivenin
Debridement, steroids, dapsone
MTBS2CK p.543
MTBS2CK p.543
11
Dog,Cat,andHumanBites
Dog,Cat,andHumanBites
Management of dog, cat, and human bites is essentially identical Theyre managed with:
Amoxicillin/clavulanate Tetanus vaccination booster if > 5 years since last injection
Dog and Cats: Pasteurella multocida Humans: Eikenella corrodens

Human bites are more damaging than dog and cat bites
MTBS2CK p.543
Rabies vaccine only if: Animal has altered mental status/bizarre behavior Attack was unprovoked, by a stray dog that cannot be observed or diagnosed
MTBS2CK p.544
RabiesandBats
HeadTrauma
If a bat was noted to be in the room and the patient was asleep VACCINATE!
MTBS2CK p.544
HeadTrauma
HeadTrauma
Any head trauma resulting in altered mental status or loss of consciousness (LOC) is managed first with a head CT Head CT without contrast is best initial test to detect blood
Contrast detects mass lesions such as cancer and abscess, not blood
LOC = CT Concussion:
No focal neurological abnormalities Normal CT scan
Contusion:
Occasionally (rarely) has focal findings Ecchymoses found on CT (blood mixed in with brain parenchyma)
MTBS2CK p.544
MTBS2CK p.544
12
Contusion
Headtrauma
Subdural and epidural hematomas: usually associated with more severe trauma than a concussion Impossible to distinguish without head CT, epidural hematoma more frequently with skull k ll f fracture t
MTBS2CK p.544
MTBS2CK p.544
EpiduralHematoma
SubduralHematoma
MTBS2CK p.545
Source: Brendan T. Doherty
LucidInterval
Treatment
Lucid interval is a second loss of consciousness occurring several minutes to several hours after initial loss of consciousness
Patient wakes up after initial LOC, but loses consciousness a second time due to accumulation of blood
Concussion: no specific therapy

Wait at least 24 hours before returning to sports
Contusion: vast majority need no specific treatment

Rarely need surgical debridement
Those with concussion safe to go home. Hospitalization isnt necessary. Observe at home for altered mental status.
MTBS2CK p.545
Time between first and second episodes of LOC is lucid interval

Both epidural and subdural hematomas are associated with a lucid interval.
MTBS2CK p.545
13
Treatment
DefinitionofaLargeIntracranialhemorrhage
Subdural and epidural hematoma: Treatment is based on size and signs of compression of brain Small ones are left alone Large L h hematomas t are managed d with: ith
1. Intubation and hyperventilation 2. Mannitol 3. Drainage
MTBS2CK p.545
Compression of ventricles or sulci Herniation with abnormal breathing and unilateral dilation of pupil Worsening mental status or focal findings
MTBS2CK p.546
SummaryofSevereHeadTrauma
Concussion Contusion Subdural Epidural
SummaryofSevereHeadTrauma
Concussion Contusion Subdural Epidural
Nofocal findings Nolucid Interval
Rarelyfocal +/ focal findings Nolucid Interval +/ lucid Interval
+/ focal findings +/ lucid interval
NormalCT
Ecchymoses
Venous, Arterial, crescent biconvexor lensshaped hematoma Drainlarge Drainlarge ones ones
Nospecific treatment; observeat home

MTBS2CK p.546
Nospecific treatment; observein hospital
MTBS2CK p.546
HeadTrauma 25-year-old man sustains head trauma in MVA. A large epidural hematoma is found. Immediately after intubation and mannitol, surgical evacuation is successfully performed. Which of the following will benefit the patient?
a. Repeated doses of mannitol Doesnt reduce mortality Doesnt always work b. Continued hyperventilation c. Proton pump inhibitor (PPI) For SAH only d. Nimodipine e. Dexamethasone Doesnt change outcomes
Steroids dont benefit intracranial bleeding. They decrease edema around mass lesions.
14
Burns
Burns&Hypothermia
Best initial therapy for those caught in a fire is 100% oxygen to treat smoke inhalation and CO poisoning Airway burn is 2nd MCC of death from burns only if theres been airway injury
MTBS2CK p.547
Burns
Burns
Stridor
Burns inside mouth
Burn Victim Indications for Intubation
Burns inside nasopharynx
If airway burn is not present, the 2nd MCC of death is volume loss Fluid replacement is based on percentage of body surface area (BSA) burned
Hoarseness
Wheezing
MTBS2CK p.547
MTBS2CK p.547
VolumeofFluidReplacement
VolumeofFluidReplacement
Replace with Ringer lactate Give one-half in first 8 hours, a quarter in second 8 hours, and a quarter in the third 8 hours Give 4 mL for each percentage of BSA burned (including 2nd and 3rd degree burns) for each kilogram of body weight
Head: 9% BSA Arms: 9% BSA each Legs: 18% BSA each Chest or back: 18% BSA each
MTBS2CK p.547
Patchy burns that arent continuous make the percentage of BSA burned hard to assess. Use the width of patients hand to make an estimate Each hand width is 1% of BSA The short answer is: give the largest amount of Ringer lactate or normal saline listed as a choice; its probably the right answer
Fluid replacement: (4 mL) (% BSA burned) weight (kg)
MTBS2CK p.547
15
HeatDisorders What is the MCC of death several days to weeks after a burn? a. Infection Rhabdomyolysis causes renal failure b. Renal failure c. Cardiomyopathy Not affected so quickly Most common immediate cause of death d Lung injury d. Fluid loss doesnt mean malnutrition e. Malnutrition
Heatcramps/ exhaustion Heatstroke
Risk
Exertion;high outsidetemp Normal Normal
Exertion;high outsidetemp Elevated Elevated
Bodytemp CPKandK+ level Treatment
Oralfluidsand electrolytes
IVfluids; evaporation
MTBS2CK p.547
MTBS2CK p.548
HeatDisorders
Neuroleptic malignantsyndrome Risk Antipsychotic medications Malignant hyperthermia Anesthetics administered systemically Elevated Elevated Dantrolene
Hypothermia
Look for intoxicated person with hypothermia MCC of death: cardiac arrhythmia Best initial step: EKG
Bodytemp CPKandK+ level Treatment
Elevated Elevated Dantroleneor dopamineagonists: bromocriptine,cabergoline
MTBS2CK p.548
MTBS2CK p.548
Hypothermia
Drowning
Manage with airway and administer positive pressure ventilation

Steroids and antibiotics are not beneficial Salt water drowning: acts like CHF with wet, heavy lungs
Wrong answers for drowning include:

Steroids Antibiotics
16
Drowning
Fresh water drowning: causes hemolysis from absorption of hypotonic fluid into vasculature
CardiacRhythmDisorders
RBC RBC
Fresh H20
RBC Hemolysis
MTBS2CK p.549
InitialManagementofCardiacArrest
First step :
Make sure patient is truly unresponsive Call for help: call 911/activate Emergency Medical Services (EMS)
After patient has been shown to be unresponsive, and EMS activated, the next step is:
1. Open airway: head tilt, chin lift, jaw thrust p and start chest compressions p if 2. Check pulse pulseless 3. Give rescue breaths if not breathing
CPR doesnt restart the heart; CPR keeps patient alive until cardioversion can be performed.
MTBS2CK p.549
Truly unresponsive Chest compressions Rescue breaths
MTBS2CK p.549
Pulselessness
When is a precordial thump the answer?

Very recent onset of arrest (<10 minutes) with no defibrillator available You know its recent because you saw it happen (witnessed)
Sudden loss of a pulse can be caused by:

Asystole Ventricular fibrillation (VF) Ventricular tachycardia (VT) Pulseless electrical activity (PEA)
Best initial management of all forms of pulselessness is CPR

MTBS2CK p.549550
MTBS2CK p.549
17
Pulselessness
Pulselessness
Asystole Besides CPR, therapy for asystole is with epinephrine Vasopressin is alternative to epinephrine They both constrict blood vessels in tissues (e.g., skin) Shunts blood into critical central areas (e.g., heart and brain)
MTBS2CK p.550
Ventricular Fibrillation Best initial therapy for VF is an immediate, unsynchronized cardioversion followed by CPR Unsynchronized = defibrillation All electrical cardioversions synchronized except VF and pulseless VT
MTBS2CK p.550
Pulselessness
Ventricularfibrillation
Only VF and VT without a pulse l get t unsynchronized h i d cardioversion.
MTBS2CK p.550
MTBS2CK p.550
Pulselessness
Pulselessness
After defibrillation, then is epinephrine or vasopressin followed by another electrical shock Amiodarone or lidocaine Magnesium
Ventricular Tachycardia (VT) Wide complex tachycardia with regular rate Management entirely based on hemodynamic status
Pulseless VT: manage exactly same way as VF Hemodynamically stable VT: Amiodarone, then lidocaine, then procainamide. If all medical therapy fails, then cardiovert patient
Bretylium is always a wrong answer

MTBS2CK p.550551
MTBS2CK p.551
18
Pulselessness
VentricularTachycardia
Ventricular Tachycardia Hemodynamically unstable VT: Perform electrical cardioversion several times followed by medications (e.g., amiodarone or lidocaine)
VT is managed with shock, drugs, and CPR at all times in between the shocks.
Pulselessness
Pulselessness
Hemodynamic instability is defined as: Chest pain Dyspnea/CHF Hypotension Confusion These qualities of instability are the same for all rhythm disturbances Direct intracardiac medication administration is always a wrong answer
MTBS2CK p.551
Pulseless Electrical Activity (PEA) PEA = electrically normal, but no motor contraction PEA = no cardiac output
MTBS2CK p.551
Pulselessness
Pulselessness/Treatment
PEA treated by correcting underlying cause We synchronize delivery of electricity in cardioversion of VT to prevent worsening of arrhythmia into ventricular fibrillation or asystole asystole. Tamponade
Tension Pneumothorax
Causes of PEA
HYPOvolemia HYPOglycemia HYPO l i HYPOxia HYPOthermia
PEA: look for patient with a normal EKG and no pulse

MTBS2CK p.551552
Massive PE
MTBS2CK p.552
Metabolic acidosis HYPERkalemia HYPOkalemia
19
AtrialArrhythmias
AtrialArrhythmias
Atrial rhythm disturbances rarely associated with hemodynamic compromise Look for :
Palpitations, p , dizziness, , or lightheadedness g Exercise intolerance or dyspnea Embolic stroke
Irregularly irregular rhythm suggests Afib as the most likely diagnosis even before EKG is done A-fib: A fib: most common arrhythmia in the United States
MTBS2CK p.552
MTBS2CK p.552
AtrialArrhythmias
AtrialFibrillation
Atrial Fibrillation and Atrial Flutter Two disorders with nearly identical management Major points of difference are:
Flutter Fl tt is i a regular l rhythm h th vs. fibrillation is irregular Flutter changes to sinus rhythm or deteriorates into fibrillation
Source: Abhay Vakil, MD.
MTBS2CK p.552
MTBS2CK p.553
AtrialFlutter
AtrialArrhythmias/Treatment
Hemodynamically unstable atrial arrhythmias = synchronized cardioversion Synchronization prevents electricity from being delivered during refractory period (ST-T wave) Synchronization prevents change into VT or VF
MTBS2CK p.553
MTBS2CK p.553
20
Chronic Atrial Fibrillation A-fib > 2 days > 7 days risk of clot formation Routine cardioversion is not i di t d indicated Chronic is usually secondary atrial or valvular anatomic change
Chronic Atrial Fibrillation Shocking doesnt correct a dilated left atrium causing A-fib Over 90% will revert to fibrillation Rate control and warfarin is standard of care f A-fib for A fib
Chronic A-fib should be anticoagulated before cardioversion. Unstable, acute disease doesnt need anticoagulation.
MTBS2CK p.553554
MTBS2CK p.553554
Best initial therapy for fibrillation and flutter is to control the rate 1. Goal HR < 100/minute 2. INR between 2-3
1. 1 Slow rate 2. Anticoagulate Rate control drugs do not convert patient into sinus rhythm.
MTBS2CK p.554
Calcium-channel blockers used to control HR with atrial arrhythmias are diltiazem and verapamil
Reliably block AV node Other calcium-channel blockers control BP
No matter how much you might think it better to shock every patient into sinus, it just doesnt work in long run.
MTBS2CK p.554
Warfarin Without anticoagulation 6% a year stroke risk INR 2-3, rate: 2-3% stroke risk Dabigatran and Rivaroxaban Alternatives to warfarin For non-valvular A-Fib No INR monitoring
MTBS2CK p.554
A-fib is caused by anatomic cardiac defects dilating atrium Thats why vast majority revert Acute disease normalizes spontaneously; dont force it Chronic disease reverts into arrhythmia; dont force it either
MTBS2CK p.554
21
Atrial rhythm problems can cause acute PE from loss of atrial kick kick in those with cardiomyopathy.
Lone Atrial Fibrillation Patients with low risk of stroke can use ASA 2-3% per year vs. 1% per year bleeding Scoring S i is i called ll d CHADS score CHADS 2 = warfarin, dabigatran, rivaroxiban
MTBS2CK p.554
MTBS2CK p.554
Definition/Criteria for Low Risk of Stroke from A-fib No cardiomyopathy/CHF/atherosclerosis No HTN Age 75 No diabetes No stroke in past The answer for management of lone atrial fibrillation is: Rate control Aspirin No warfarin or dabigatran
Major bleeding from warfarin is defined as: Intracranial I t i lh hemorrhage h Requires transfusion
MTBS2CK p.554
MTBS2CK p.555
AtrialArrhythmias/Treatment Supraventricular Tachycardia
SVT
Vagal Maneuvers
Carotid Massage Valsalva Dive Reflex Ice immersion
Adenosine
Beta Blockers CCBs Digoxin

22
Wolff-Parkinson-White Syndrome (WPW) WPW is an anatomic abnormality in cardiac conduction pathway Answer most likely diagnosis question by looking for:
SVT alternating with ventricular tachycardia SVT gets worse after diltiazem or digoxin Observing delta wave on EKG Vagal maneuvers slow and convert SVT. They dont convert atrial fibrillation.
MTBS2CK p.556
Most accurate test for WPW is cardiac electrophysiology (EP) studies

MTBS2CK p.556
AtrialArrhythmias
Acute therapy: Procainamide or amiodarone Chronic therapy: Radiofrequency catheter ablation is curative for WPW EP studies tell you where the anatomic defect is Digoxin and calcium-channel blockers are dangerous in WPW
Multifocal Atrial Tachycardia Multifocal atrial tachycardia (MAT) is associated with chronic lung disease such as COPD Treat underlying lung disease Treat MAT as you would A-fib, but avoid beta blockers because of lung disease
MTBS2CK p.556
MTBS2CK p.556
AtrialArrhythmias Woman comes to office for routine evaluation. Shes found to have a pulse of 40 and an otherwise completely normal history and physical examination. What is the most appropriate next step in the management of this patient?
MTBS2CK p.557
a. Atropine You dont know the rhythm y yet y b. Pacemaker Too invasive c. EKG Too invasive d. Electrophysiology studies Can result in ischemia e. Epinephrine f. Isoproterenol Old and no longer used; always wrong g. Nothing; reassurance Without EKG cannot say
MTBS2CK p.557
23
BradycardiaandAVblock
Sinus Bradycardia Isoproterenol is never the right answer to anything Sinus Bradycardia
Asymptomatic Symptomatic
No Treatment
Atropine 1st Pacemaker Long Term
MTBS2CK p.557
MTBS2CK p.558
BradycardiaandAVblock Second-Degree AV block Mobitz I or Wenckebach block: progressively lengthening PR interval results in a dropped beat Mobitz I is most often a sign of normal aging of conduction system. y If there are no symptoms, y p , its managed the same way as sinus bradycardia Dont treat if asymptomatic
First-Degree AV block Use same management as sinus bradycardia

Atropine p and p pacemaker are used for sinus bradycardia only if symptomatic.
MTBS2CK p.558
MTBS2CK p.558
Second-Degree AV block Mobitz II block: far more pathologic than Mobitz I Mobitz II just drops a beat without progressive lengthening of PR interval. Mobitz II progresses or deteriorates into third-degree AV block. Treat it like third-degree AV block. Everyone with Mobitz II block gets a pacemaker even if they are asymptomatic
MTBS2CK p.558
MTBS2CK p.558
24
58-year-old woman is admitted to hospital with an acute MI. On the second hospital day she develops sustained VT even though she is on aspirin, heparin, lisinopril, and metoprolol. What is the most appropriate next step in management?
Which of the following tests would you do for this patient to determine a risk of recurrence?
a. Increase the dose of metoprolol Wont treat ischemia b. Add diltiazem Will not affect rhythm c. Angiography for angioplasty or bypass d. Implantable defibrillator Underlying cause can be fixed e. EP studies Not ectopy, but rather from ischemia
MTBS2CK p.559
For unexplained syncope a. EP studies b. Echocardiography c. MUGA scan (nuclear ventriculography) For perfusion d. Ventilation/perfusion p scan For PE study e. Tilt-table testing For syncope
MTBS2CK p.559
73-year-old man has his third syncopal episode in last 6 months. An EKG done in the field shows VT. His stress test is normal. What is the most appropriate next step in the management of this patient?
a. Metoprolol Not enough g to p prevent death b. Diltiazem Have no affect in VT c. Angiography Normal stress therefore no need for angio d. Implantable defibrillator e. EP studies EKG shows cause so need for EP
46-year-old man has intermittent episodes of palpitations, lightheadedness, and near-syncope. His EKG is normal. The echo shows an EF of 42%. Holter monitor shows several runs of wide complex tachycardia lasting 5-10 seconds. Which of the following is most likely to benefit this patient?
a. Pacemaker placement Dont know underlying cause yet b. Digoxin Does nothing for vent arrhythmias c. Warfarin Low risk for clot d. EP studies e. Swan-Ganz catheter Swan if for diagnosing SHOCK
MTBS2CK p.560
MTBS2CK p.559560
25
PituitaryDisorders Endocrinology
Dr.ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity
Panhypopituitarism DiabetesInsipidus p Acromegaly Hyperprolactinemia
Panhypopituitarism/Etiology
ThePituitaryGland
Compression or damage of the pituitary gland Tumors, cancer, adenomas, cysts, meningiomas, craniopharyngiomas, or lymphoma Trauma and radiation are damaging
MTBS2CK p.107
MTBS2CK p.107
Panhypopituitarism/Etiology
Panhypopituitarism/Presentation
Conditions such as: Hemochromatosis Sarcoidosis Histiocytosis X Infection with fungi fungi, TB TB, or parasites Autoimmune and lymphocytic infiltration damages gland
Prolactin deficiency Men

No symptoms
Women:
Prolactin = In favor of or pro p lactation If deficient, the patient cannot lactate normally after childbirth
MTBS2CK p.107
MTBS2CK p.107
Panhypopituitarism/Presentation Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) deficiency Both genders will have decreased libido and decreased axillary, pubic, and body hair Men
Unable to produce testosterone or sperm Erectile dysfunction and decreased muscle mass
Growth hormone (GH) deficiency Adults

Few symptoms
Children
Dwarfism
Women
Unable to ovulate or menstruate normally and become amenorrheic
Catecholamines, glucagon, and cortisol act as stress hormones
MTBS2CK p.107
MTBS2CK p.108
Panhypopituitarism/DiagnosticTests
Kallman Syndrome Decreased FSH and LH Decreased GnRH Anosmia
Hyponatremia from: Hypothyroidism Glucocorticoid underproduction Potassium levels remain normal

Aldosterone is unaffected and aldosterone excretes potassium
MTBS2CK p.108
MTBS2CK p.108
Panhypopituitarism/DiagnosticTests MRI detects compressing mass lesions on pituitary
Panhypopituitarism/DiagnosticTests Growth Hormone (GH) IGF level Arginine Stimulation: increases GH GHRH stimulation: increases GH ACTH and Cortisol levels High Hi h or normal ll levels l excludes l d panhypopituitarism h it it i Sex Hormones LH, FSH level Testosterone level Thyroid TSH
MTBS2CK p.108
MTBS2CK p.108
Source:JamesG.Smirniotopoulos,MD
Panhypopituitarism/DiagnosticTests Older, Less Useful Tests Metyrapone Inhibits 11-beta hydroxylase and decreases cortisol Normal: ACTH and 11deoxycortisol levels rise I Insulin li stimulation ti l ti Normal: decreased glucose levels raise GH Failure of GH to rise in response to insulin indicates pituitary insufficiency
Panhypopituitarism/Treatment Replace deficient hormones with...

Thyroxine Cortisone Testosterone and estrogen Recombinant human growth hormone Antidiuretic hormone (ADH) and oxytocin (Posterior Pituitary)
Note: No deficiency disease described for oxytocin

Oxytocin helps uterine contraction during delivery, but delivery still occurs even if its absent ADH deficiency also known as central diabetes insipidus
MTBS2CK p.109
MTBS2CK p.109
DiabetesInsipidus/Etiology Decrease in amount of ADH from pituitary (central DI) or its effect on kidney (nephrogenic DI) Central Diabetes Insipidus (CDI) Damage to brain:
Stroke Tumor Trauma Hypoxia Infiltration (sarcoidosis, hemochromatosis) Infection
DiabetesInsipidus/Etiology
Nephrogenic DI (NDI): Chronic pyelonephritis Amyloidosis Myeloma Sickle cell disease Lithium Hypercalcemia or hypokalemia inhibits ADH effect
MTBS2CK p.109
MTBS2CK p.109
DiabetesInsipidus/Presentation Excessive thirst Extremely high-volume urine Volume depletion Severe Hypernatremia Neurological symptoms Confusion, C f i di disorientation, i t ti l lethargy, th and d eventually t ll seizures and coma Only when volume losses are unmatched by fluid intake
DiabetesInsipidus/DiagnosticTests
Urine osmolality: Low Urine sodium: Low Serum osmolality: High Urine volume: Enormous
MTBS2CK p.109
MTBS2CK p.110
DiabetesInsipidus/DiagnosticTests Difference between central and nephrogenic DI is:
DiabetesInsipidus/Treatment
Response to vasopressin
Central DI: Urine volume decrease & urine osmolality increase Nephrogenic DI: No effect of vasopressin use on urine volume or osmolality
MTBS2CK p.110
Central DI: Long-term vasopressin (desmopressin) Nephrogenic DI: 1. Correct the cause (hypokalemia or hypercalcemia) 2. Hydrochlorothiazide, NSAIDs, amiloride
MTBS2CK p.110
DiabetesInsipidus/Evaluation
High-volume urine, plus excessive thirst Volume depletion, plus hypernatremia
DiabetesInsipidus/Evaluation
Vasopressin (Desmopressin) stimulation test
Urine: Volume decrease + osmolality increase Urine: No effect
Serum: Osmolality: Elevated Sodium: Elevated
Urine: Volume: HIGH Osmolality: Decreased Sodium: Decreased
Effect
Diagnosis
Central diabetes insipidus Vasopressin
Nephrogenic diabetes insipidus
Proceed with vasopressin (desmopressin) stimulation test

MTBS2CK p.109
Treatment
Treat underlying cause, hydrochlorothiazide, amiloride, NSAIDs
MTBS2CK p.110
Acromegaly
Acromegaly/Etiology
Soft tissue overgrowth throughout the body
Pituitary adenoma Part of Multiple Endocrine Neoplasias (MEN) Combined with parathyroid and pancreatic disorders (e (e.g., g gastrinoma or insulinoma) Rarely caused by ectopic GH or GHRH production
MTBS2CK p.110
MTBS2CK p.110
Copyright Richard Usatine, M.D. Used with permission.
Acromegaly/Presentation
Increased hat, ring, and shoe size Carpal tunnel syndrome Obstructive sleep apnea from soft tissues enlarging Body odor from sweat gland hypertrophy Teeth widening from jaw growth Deep voice and macroglossia (big tongue)
Acromegaly/DiagnosticTests Colonic polyps Arthralgias from joints growing out of alignment Hypertension for unclear reasons in 50% Cardiomegaly, CHF, and erectile dysfunction from increased prolactin cosecreted with pituitary adenoma Hyperglycemia Glucose intolerance Hyperlipidemia Best initial test... Insulin-like growth factor (IGF) M t accurate Most t t test t... Glucose suppression test Normal: Glucose should suppress growth hormone MRI? Only after the laboratory identification of acromegaly
MTBS2CK p.111
MTBS2CK p.110111
Acromegaly/Treatment 1. Surgery
Transphenoidal resection of pituitary Cures 70%
Hyperprolactinemia/Etiology
Many causes not associated with pituitary adenoma Prolactin increases via: Cosecretion with GH in acromegaly g y Hypothyroidism with pathologically high TRH levels
2. Medications
Cabergoline: Dopamine agonist inhibits GH release Octreotide or lanreotide: Somatostatin inhibits GH release Pegvisomant: GH receptor antagonist
3. Radiotherapy
Only when not responsive to surgery or medications
Hyperprolactinemia/Etiology
Hyperprolactinemia/Presentation
Pregnancy Chest wall stimulation Cutting pituitary stalk Antipsychotic medications, tricyclic antidepressants, p , and SSRIs Methyldopa Metoclopromide Opioids
Women Galactorrhea Amenorrhea Infertility Men Erectile dysfunction Decreased libido Galactorrhea (very rare in men)
MTBS2CK p.111
MTBS2CK p.111
Hyperprolactinemia/DiagnosticTests After the prolactin level is found to be high, perform: Thyroid function tests Pregnancy test BUN/creatinine (kidney disease elevates prolactin) Liver function tests (cirrhosis elevates prolactin) MRI is done after... High prolactin level is confirmed AND Secondary causes like medications are excluded AND Patient is not pregnant
MTBS2CK p.112
Hyperprolactinemia/Treatment
1. Dopamine agonists
Cabergoline is better tolerated than bromocriptine
2 Transphenoidal surgery when NOT 2. responding to medications 3. Radiation is rarely needed

MTBS2CK p.112
Whattolookfor... Hypothyroidism Hyperthyroidism Tachycardia,palpitations, arrhythmia(Afib) Diarrhea(hyperdefecation) Weightloss Anxiety,nervousness, restlessness Hyperreflexia Heatintolerance Fever
ThyroidDisorders
Hypothyroidism Hyperthyroidism ThyroidNodules
Bradycardia Constipation Weightgain Fatigue,lethargy,coma Decreasedreflexes Coldintolerance Hypothermia(hairloss, edema)

MTBS2CK p.113
Hypothyroidism Etiology Most from failure of thyroid gland from burnt-out Hashimoto thyroiditis
Acute phase is rarely perceived
Hypothyroidism Diagnostic tests Best initial test for all thyroid disorders is...
TSH
TSH levels are markedly elevated if gland has failed
Dietary deficiency of iodine Amiodarone

What to look for... Hypothyroidism: Everything is SLOW! Except menstrual flow, which is increased
MTBS2CK p.112
If the TSH level is suppressed, measure...

T4
Treatment Replace thyroxine (synthroid)
MTBS2CK p.113
Hyperthyroidism/Findings
Myxedema
Diagnosis Gravesdisease
Uniquefeature
Eyeproptosis (2040%) Skinfindings(5%) Subacutethyroiditis Tenderthyroid Painlesssilent silent thyroiditis Nontender, Nontender normalP/E Involutedglandisnt Exogenousthyroid palpable hormoneuse HighTSHlevel Pituitaryadenoma
MTBS2CK p.113
MultinodularGoiter
ThyroidBruit
Hyperthyroidism/DiagnosticTests T4 (thyroxine) level Elevated in all forms of hyperthyroidism TSH level Pituitary release of TSH is inhibited in all forms EXCEPT... Pituitary adenomas, will have high TSH level Graves disease (unique features): Eye and skin abnormalities Elevated radioactive iodine uptake TSH receptor antibodies
MTBS2CK p.113114
Hyperthyroidism/Treatment Graves Ophthalmopathy Best initial therapy...

Steroids
For those unresponsive to steroids...

Radiation
What if unresponsive to other therapy...

Decompressive surgery
MTBS2CK p.114
Source: Jonathan Trobe, MD
Hyperthyroidism/Treatment
AcuteHyperthyroidism/ThyroidStorm
Diagnosis Gravesdisease Subacutethyroiditis y Painlesssilent thyroiditis Exogenousthyroid hormoneuse Pituitaryadenoma

MTBS2CK p.114
Treatment Radioactiveiodine Aspirin None Stopuse
Treatment: Propranolol Blocks target organ effect Inhibits peripheral conversion of T4T3 Thiourea drugs Methimazole and propylthiouracil Block hormone production
Surgery
MTBS2CK p.114
AcuteHyperthyroidism/ThyroidStorm
ThyroidNodules
Treatment: Iodinated contrast material Blocks peripheral conversion of T4 to T3 Blocks release of existing hormone Steroids (hydrocortisone) Role in treating hyperthyroidism? Radioactive iodine Ablates gland for permanent cure
MTBS2CK p.114
5% women 1% men 95% benign

Adenoma, colloid nodule, cyst
Thyroid nodules rarely hyperfunctioning
MTBS2CK p.114
ThyroidNodules/DiagnosticTests 46-year-old woman with a small mass on palpation of thyroid. No tenderness and otherwise asymptomatic. What is the most appropriate next step? a. Fine-needle aspiration Done if TFTs are normal b Radionuclide iodine uptake scan Determines etiology b. of hyperfunctionality c. T4 and TSH levels Guides biopsy d. Thyroid ultrasound e. Surgical removal (excisional biopsy)
Biopsy with a fine-needle aspirate if theres normal thyroid function (T4/TSH) Ultrasound or radionuclide scanning not required (tests cannot exclude cancer)
Follicular adenoma when you cant be sure

46-year-old woman with thyroid nodule and normal thyroid function testing has a biopsy showing indeterminate for follicular adenoma. What is the most appropriate next step?
g , determines extent a. Neck CT Doesnt make a diagnosis, a b. Surgical removal (excisional biopsy) c. Ultrasound Cant excluded cancer, still need biopsy d. Calcitonin levels Suggests extent of medullary
CalciumDisorders
Hypercalcemia Hyperparathyroidism Hypocalcemia
carcinoma only
MTBS2CK p.115
Hypercalcemia/Etiology
Hypercalcemia/Etiology
Vitamin D intoxication Sarcoidosis and other granulomatous diseases Thiazide diuretics Hyperthyroidism yp y Metastases to bone and multiple myeloma
Most common cause is...

Primary hyperparathyroidism (PTH) Most cases are asymptomatic Severe, acute symptomatic hypercalcemia a high prevalence of cancer
MTBS2CK p.116
MTBS2CK p.116
Hypercalcemia/Presentation
Hypercalcemia/Treatment
Acute, symptomatic hypercalcemia

Confusion, stupor, lethargy Constipation Bone lesions: Osteoporosis Renal: Nephrolithiasis, Nephrolithiasis DI, DI renal insufficiency Cardiovascular: Short QT syndrome
Acute hypercalcemia, treat with... Saline hydration at high volume Bisphosphonates: pamidronate, zoledronic acid Calcitonin Prednisone: ONLY for sarcoidosis and granulomatous disease
MTBS2CK p.116
MTBS2CK p.116
Hyperparathyroidism
75-year-old man with history of malignancy admitted with lethargy, confusion, and abdominal pain. Found to have a markedly elevated calcium level. After 3L normal saline and pamidronate, his calcium level is still markedly elevated the following day. What is the most appropriate next step in management? a Calcitonin a. Doesnt add to pamidronate b. Zolendronic acid c. Plicamycin Less efficacy than pamidronate. Always wrong d. Gallium Less efficacy than pamidronate. Always wrong e. Dialysis Not needed. Renal failure has low Ca++
Primary hyperparathyroidism: Solitary adenoma (80%85%) Hyperplasia of all 4 glands (15%20%) Parathyroid malignancy (1%)
f. Cinacalcet Inhibits PTH

Hyperparathyroidism
Hyperparathyroidism
Elevation in calcium levels often asymptomatic When symptomatic: Osteoporosis Nephrolithiasis and renal insufficiency Muscle weakness Anorexia, nausea, vomiting, and abdominal pain Peptic ulcer disease (calcium stimulates gastrin)
MTBS2CK p.117
Besides high calcium and PTH levels, you also find: Low phosphate level Short QT on EKG Sometimes an elevated BUN and creatinine Alkaline phosphatase elevated from effect of PTH on bone
MTBS2CK p.117
Hyperparathyroidism/Management
Hyperparathyroidism/Treatment
Bone X-ray is NOT a good test for bone effects of PTH DEXA densitometry is better Preoperative imaging of neck with sonography or nuclear scanning may be helpful in determining the surgical approach
Surgical removal of involved parathyroid glands
MTBS2CK p.117
MTBS2CK p.117 118
10
Hypocalcemia
Hypocalcemia/Presentation Neural hyperexcitability: Chvostek sign (facial nerve hyperexcitability) Carpopedal spasm Perioral numbness Mental irritability Seizures Trousseau sign (tetany)
Low calcium = twitchy, hyperexcitable High calcium = lethargic, slow
Souce: nih.gov
MTBS2CK p.118
MTBS2CK p.118
Hypocalcemia/Diagnosis&Treatment EKG: Prolonged QT May cause arrhythmia

Ventricular tachycardia
AdrenalDisorders
Hypercortisolism Hyperparathyroidism Hypocalcemia
Treatment Replace calcium and vitamin D
MTBS2CK p.118
PituitaryAdrenalAxis
Hypercortisolism Cushing disease Pituitary overproduction of ACTH Cushings syndrome Due to ectopic production of ACTH
C Carcinoid i id ( (most t common i is small ll cell ll carcinoma i of f the lung) Overproduction autonomously in adrenal gland
Prednisone (glucocorticoid use) causes same manifestations of hypercortisolism

Source:nih.gov
MTBS2CK p.119
11
Hypercortisolism/Etiology CauseofHypercortisolism PituitaryACTH (Cushingdisease) Adrenals Ectopic E i ACTH (carcinoid) UnknownsourceofACTH Frequency 70% 15% 10% 5%
Hypercortisolism/Presentation Fat redistribution

Moon face, truncal obesity, buffalo hump, thin extremities, increased abdominal fat
HTN
From increased sodium reabsorption in kidney and increased vascular reactivity
Skin
Striae, easy bruising, decreased wound healing, thinning of skin
Menstrual disorders Erectile dysfunction Polyuria

From hyperglycemia and increased free water clearance
Osteoporosis
MTBS2CK p.119
MTBS2CK p.119
Hypercortisolism/DiagnosticTests Always confirm the source of hypercortisolism with biochemical tests before you perform imaging studies
Hypercortisolism/DiagnosticEvaluation
CC: I feel weak and tired, and I notice hair growth on my face and strange marks on my stomach Low-dose (1mg) dexamethasone suppression test
Decreased = Disease Excluded
10% of population has an abnormality of pituitary on MRI If you start with a scan, you may remove the pituitary when the source is in the adrenals
24-hour urine cortisol Increased
Late-night salivary cortisol Increased
High?
ACTH-dependent Cushings syndrome
Serum ACTH
Low?
ACTH-independent Cushings syndrome
MTBS2CK p.120
MTBS2CK p.119120
Hypercortisolism/DiagnosticEvaluation
ACTH-dependent Cushings syndrome
Pituitary vs. Ectopic ACTH production? High-dose dexamethasone suppression i t test t
ACTH-independent Cushings syndrome

Adrenal Mass? CT Adrenals Increased ACTH & cortisol? Pituitary Mass? Pituitary MRI No mass seen? Petrosal sinus sampling for ACTH
ConfirmatoryLaboratoryFindingsin AdrenalDisorders
Adrenal ACTHlevel Low Pituitary High Ectopic High
Ectopic ACTHsecreting tumor
Chest CT
Petrosalsinus ACTH
Notdone
High g ACTH
LowACTH
Supression of cortisol? Pituitary adenoma (Cushing disease)

MTBS2CK p.120
Highdose Nosuppression dexamethasone
Suppresses Cortisol
Nosuppression
MTBS2CK p.121
12
Hypercortisolism/OtherFindings Cortisol - anti-insulin stress hormone Hyperglycemia Hyperlipidemia Theres some aldosterone-like effect of cortisol Hypokalemia H k l i Metabolic alkalosis Leukocytosis from demargination of WBCs
Hypercortisolism/Treatment
Surgically remove source of hypercortisolism

Transsphenoidal surgery for pituitary sources Laparoscopic removal for adrenal sources
MTBS2CK p.120
MTBS2CK p.121
EvaluationofAdrenalIncidentaloma How far should you go in the evaluation of an unexpected, asymptomatic adrenal lesion found on CT? 1. Metanephrines of blood or urine to exclude pheochromocytoma 2 Renin and aldosterone levels to exclude 2. hyperaldosteronism 3. 1 mg overnight dexamethasone suppression test
Hypoadrenalism(Addisons)/Etiology Addisons disease Chronic hypoadrenalism Etiology

Autoimmune destruction ( (80%) ) Infection (TB) Adrenoleukodystrophy Metastatic cancer to adrenal gland
Adrenal crisis Acute adrenal insufficiency Etiology

Hemorrhage, surgery, hypotension, yp , trauma Suddenly stopping chronic high-dose prednisone
MTBS2CK p.121
MTBS2CK p.121
Hypoadrenalism/Presentation Weakness, fatigue Acute adrenal crisis can also present with Altered mental status profound hypotension, Nausea, vomiting, fever, confusion, and anorexia, hypotension coma Hyperpigmentation from chronic adrenal insufficiency
Hypoadrenalism/DiagnosticTests
Pituitary failure: Hypoglycemia ACTH is low Hyperkalemia Metabolic acidosis Adrenal failure: Hyponatremia ACTH is high High BUN
Eosinophilia is common in hypoadrenalism

MTBS2CK p.121122
CopyrightRichardUsatine,MD Usedwithpermission.
MTBS2CK p.122
13
Hypoadrenalism
Signs & Symptoms Weakness Hypotension Weight Loss Hyperpigmentation
Hypoadrenalism/Treatment
Treatment is more important than testing in acute adrenal crisis Replace p steroids with hydrocortisone y Fludrocortisone
For postural instability A steroid hormone particularly high in mineralocorticoid or aldosterone-like effect
MTBS2CK p.122
Cosyntropin Stimulation Test Plasma cortisol before & after 250 ug cosyntropin IM or IV
Cortisol fails to rise

High ACTH Aldosterone Low too Low ACTH Aldosterone an increase
Primary adrenal insufficiency

MTBS2CK p.121122
Secondary adrenal insufficiency Adrenal atrophy from pituitary insufficiency
PrimaryHyperaldosteronism
Patient brought to ED after sustaining severe abdominal trauma in MVA. On second hospital day, he becomes markedly hypotensive without evidence of bleeding. Theres fever, high eosinophil count, hyperkalemia, hyponatremia, and hypoglycemia. What is the next step?
The autonomous overproduction of aldosterone despite a high pressure with a low renin activity
a. b. c. d. e.
Norepinephrine will constrict CT scan of the adrenals vessels more effectively Draw cortisol level and administer hydrocortisone Treating severe hypotension Cosyntropin stimulation testing more important than finding ACTH level etiology Dexamethasone suppression testing
Solitary adenoma: 80% Bilateral hyperplasia:15-20% Malignant: 1%
MTBS2CK p.122123
MTBS2CK p.123
PrimaryHyperaldosteronism All forms of secondary HTN are more likely in those whose onset is...
< 30 or > 60 years Uncontrolled by 2 antihypertensive medications
PrimaryHyperaldosteronism/DiagnosticTests Best initial test... Plasma aldosterone to plasma renin ratio A low plasma renin with high aldosterone = Primary hyperaldosteronism Most accurate test... Adrenal venous blood sampling high aldosterone! CT Scan? Only after laboratory testing reveals...
Low potassium, low plasma renin, and high aldosterone despite a high-salt diet
MTBS2CK p.123
Has a characteristic finding on the history, physical, or labs Primary hyperaldosteronism = High BP + Low K+
MTBS2CK p.123
14
PrimaryHyperaldosteronism/Treatment Unilateral adenoma Resected by laparoscopy Bilateral hyperplasia Eplerenone or spironolactone Spironolactone causes... Gynecomastia Decreased libido Anti-androgenic
MTBS2CK p.124
Pheochromocytoma Nonmalignant lesion of adrenal medulla Autonomous overproduction of catecholamines despite high BP Pheochromocytoma is the answer when theres: Episodic HTN Headache Sweating Palpitations and tremor
MTBS2CK p.124
Pheochromocytoma/DiagnosticTests Best initial test... Plasma catecholamines Confirmed with... 24-hour urine metanephrines and catecholamines
More accurate than VMA level
Pheochromocytoma/DiagnosticTests Imaging of adrenal glands (CT or MRI) Done only after biochemical testing MIBG scanning Nuclear isotope scan Detects D t t location l ti of f pheochromocytoma h h t that th t originates outside adrenal gland
MTBS2CK p.124
MTBS2CK p.124
Pheochromocytoma/DiagnosticTests
MIBG scan showing unilateral pheochromocytoma
Pheochromocytoma/Treatment
1. 2. 3. 4.
Phenoxybenzamine: (IV alpha blocker) Propranolol Calcium-channel blocker (possible) Laparoscopic removal
Source:LauraNModzelewski
MTBS2CK p.124
15
DiabetesMellitus(DM)
DiabetesMellitus
Presentation Diagnosis Treatment DiabeticKetoacidosis HealthMaintenance Complications
Persistently fastingbloodglucoselevels>125 onatleast2separateoccasions

Type 1 DM
Onset in childhood Insulin dependent from early age Not related to obesity Insulin deficiency
Type 2 DM
Onset in adulthood Directly related to obesity Insulin resistance
MTBS2CK p.124125
DiabetesMellitus/Presentation
DiabetesMellitus/DiagnosticTests
Polyuria, polyphagia, and polydipsia Type 1 DM: thinner than Type 2 diabetics Type 2 DM: more resistant to diabetic ketoacidosis (DKA) Both types: wound healing
2 FBG measurements > 125 mg/dL One glucose level about 200 mg/dL with symptoms Abnormal oral glucose tolerance testing Hemoglobin A1c > 6.5%
MTBS2CK p.125
MTBS2CK p.125
DiabetesMellitus/Treatment
DiabetesMellitus/Treatment Oral Hypoglycemic Medications Best initial drug: metformin Metformin blocks gluconeogenesis Sulfonylureas insulin release from pancreas weight gain Dipeptidyl Peptidase Inhibitors Increase insulin Decrease glucagon Sitagliptin, Saxagliptin, Linagliptin
MTBS2CK p.125
Best initial treatment... Diet, exercise, and weight loss Weight loss controls as much as 25% of cases of type yp 2 DM without medications, , Exercising muscle doesnt need insulin
MTBS2CK p.125
16
Thiazoladinediones (glitazones) Rosiglitazone, Pioglitazone Relatively contraindicated in CHF Increase fluid overload Nateglinide and repaglinide Stimulates insulin release Similar to sulfonylureas No additional therapeutic benefit to sulfonylureas
MTBS2CK p.125126
Incretins (exenatide, liraglutide) Raise insulin Decrease glucagon levels Decrease gastric motility Helps in weight loss
MTBS2CK p.126
DiabetesMellitus/Treatment Alpha-glucosidase inhibitors (acarbose, miglitol) Block glucose absorption in bowel Cause flatus, diarrhea, and abdominal pain Pramlintide Analog A l of f protein t i called ll d amylin li thats th t secreted t d normally with insulin Amylin
decreases gastric emptying decreases glucagon levels decreases appetite
MTBS2CK p.125126
DiabetesMellitus/Treatment Insulin Added if patient isnt controlled with oral hypoglycemic agents Insulin glargine gives steady state of insulin for entire day Dosing isnt isn t tested Glargine provides much more steady blood levels than NPH insulin Combined with short-acting insulin (e.g., lispro, aspart, or glulisine)
MTBS2CK p.126
DiabetesMellitus
DiabetesMellitus/Treatment Pharmacokinetics of insulin formulations

Drug Aspart Glulisine Lispro Regular NPH Lente Ultralente Glargine Type Rapid-acting Onset (hr) 0.20.5 Peak (hr) 0.52 Duration (hr) 34
Short-acting Intermediate Intermediate Long-acting Long-acting
0.51 1.5 1.53 34
23 410 715 915 No peak
68 1624 1624 2228 2436
MTBS2CK p.126
MTBS2CK p.126
17
DiabeticKetoacidosis(DKA) More common with type 1 diabetes Can definitely present in type 2 diabetes Presents with... Hyperventilation Altered mental status Metabolic M t b li acidosis id i with ith i increased d anion i gap Hyperkalemia in blood, but decreased total body potassium because of urinary spillage Increased anion gap on blood testing Serum is positive for ketones
MTBS2CK p.126
DiabeticKetoacidosis/Treatment
Treat with... 1. Large-volume saline and insulin replacement 2. Replace potassium when potassium level approaches normal 3. Correct the underlying y g cause
Noncompliance with medications Infection Any serious illness
MTBS2CK p.127
DiabetesMellitus/HealthMaintenance 57-year-old man admitted to ICU with altered mental status, hyperventilation, and markedly elevated glucose level. Which of the following is the most accurate measure of the severity of his condition? a. Glucose level Can be elevated without DKA If very low, theres risk of death b. Serum bicarbonate Mean very little c. Urine ketones Not all blood ketones are detected d. Blood ketones e. pH level on blood gas Need to know whats
All patients with DM should receive... Pneumococcal vaccine Yearly eye exam to check for proliferative retinopathy, which needs laser therapy Statins to g get LDL < 100 mg/dL g ACEi or ARBs to get BP < 130/80 mmHg ACEi or ARB if urine tests positive for microalbuminuria Foot exam for neuropathy and ulcers
MTBS2CK p.127
responsible for pH level

MTBS2CK p.127
ComplicationsofDiabetes
Gastroparesis Immobility of bowels Bloating, constipation Early satiety, vomiting Abdominal discomfort Treat with metoclopramide or erythromycin
Non-proliferative retinopathy Tighter control of glucose Aspirin doesnt help retinopathy Proliferative retinopathy Neovascularization and vitreous hemorrhages Treated with laser photocoagulation
MTBS2CK p.128
MTBS2CK p.128
18
Neuropathy Decreased sensation in feet Main cause of skin ulcers Leads to osteomyelitis Treatment pain with Pregabalin Gabapentin Tricyclic antidepressants
MTBS2CK p.128
19
Autonomy Ethics
Dr.ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity AdvanceDirectives Minors Brain i Death h
Ethics Every human being of adult years and sound mind has the right to determine what shall be done with his own body; and a surgeon who performs an operation without his patients consent commits an assault, for which he is liable in damagesexcept in cases of emergency where the patient is unconscious and where h it i is necessary t to operate t b before f consent t can be obtained.
Justice Benjamin Cardozo, Schloendorff v. Society of New York Hospital, 211 NY 125, 105 NE 92 (1914)
Ethics
This states the premise underlying half the ethics questions on S2 CK of USMLE: 1. Autonomy 2. Adult 3 Capacity 3. C it t to understand d t d
MTBS2CK p.561
MTBS2CK p.561
Autonomy
Patients have sole right to determine what treatment they shall and shall not accept Autonomy beats Beneficence Beneficence: trying to do good for others Trying y g to help p not as important p as following g wishes Patients have the right to refuse treatments that are good for them if they dont want them.
MTBS2CK p.561
A man has an ugly house you offer to paint free in his favorite color. Everyone in neighborhood agrees the house is ugly & what you offer is clearly superior. He understands everything you are offering, including the clear benefit to him. The man Cost and benefit and the still refuses. common good arent as What do you do? important as the autonomy have to just do a. Honor the mans man s wishes: no paint job individuals what h t they th want t with ith their th i own property. b. Paint his house against his will c. Ask the neighborhood council to consent to the paint job d. Get a psychiatric evaluation on the man e. Get a court order to allow the paint job f. Ask his family for consent to the paint job g. Wait until he is out of town, then paint his house
MTBS2CK p.561562
AdvanceDirectives
Man comes to ED after MVA that causes a ruptured spleen. Hes fully conscious. He understands that hell die without splenectomy, and that hell live if he has the splenectomy. He refuses the repair and blood transfusion. Entire family including brother who is healthcare proxy and document completed only a few weeks ago clearly state, Everything possible should be done, including surgery. What do y you do? a. Honor his current wishes, no surgery b. Wait until he loses consciousness, then perform the surgery You must follow the last known wishes of the c. Psychiatric consult patient, even if they are verbal, and even if they contradict the written proxy. You cannot wait until d. Ethics committee his consciousness is lost, then go against his e. Emergency court order wishes. f. Follow what is written in the documented health-care proxy g. See if there is consensus from the family
MTBS2CK p.562
Tell caregivers parameters of care the patient wanted Agent = person designated by patient to carry out patients wishes Term Agent sometimes used interchangeably with healthcare proxy Healthcare proxy is written document outlining parameters of care Major problem with proxy is details of care often unclear
MTBS2CK p.562
AdvanceDirectives
AdvanceDirectives
Not helpful to just say, No heroic measures To be useful, document must specifically state, No intubation, no CPR, no chemotherapy, no dialysis Can also specifically state wishes about fluid and nutrition If proxy says, No NG tube, no artificial feeding, then its useful Proxy takes effect only when patient has lost capacity to make decisions
MTBS2CK p.561562
Order of Decision Making 1. Patient with capacity supersedes all else 2 Healthcare 2. H lth proxy: an agent t( (person) ) to carry out wishes
MTBS2CK p.563
AdvanceDirectives
AdvanceDirectives
Order of Decision Making 3. Living will

Document outlining patients wishes Stating, I never want dialysis is more valid than a family member or friend saying, From what I know about b t him, hi h he wouldnt ld t want t dialysis, di l i or He H t told ld me he never wants dialysis. Documentation!
Written living will with concrete statements I never want blood transfusion or chemotherapy is valid
Order of Decision Making 4. Persons clearly familiar with the patients wishes
Problem with documentation Difficult for friends to document they knew the patients wishes If case clearly states friend knows and can prove that she knew the patients wishes, then this is the plan of care thats followed
MTBS2CK p.563
MTBS2CK p.563
AdvanceDirectives
AdvanceDirectives
Order of Decision Making 5. Family

General order of decision making
1. 2 2. 3. 4. Spouse Adult children Parents Siblings
Ethics Committee
The answer when: 1. Patient has lost capacity to make decisions 2 Advance directive is missing or unclear 2. Critically important for medical futility E.g. when the patient or proxy asking for tests and treatments that may have no benefit
MTBS2CK p.563
Unlike life, USMLE S2 CK must be clear If family is split, then answer is:
Ethics committee or court order
MTBS2CK p.563
AdvanceDirectives
AdvanceDirectives
Court order is right answer when: Theres no advance directive and 1. Patient has no capacity 2. Family in disagreement
Like a house being g left equally q y to four children who cannot agree what to do with it
Psychiatric Evaluation of Patient The answer when... It is not clear if patient has capacity Question clearly states patient has capacity? Not necessary! Clearly delirious or psychotic? Not necessary!
MTBS2CK p.563
Caregivers want to withdraw care and ethics committee cannot reach a conclusion
MTBS2CK p.563
Minor
Minor
Minors do not have decision-making capacity Cannot consent to or refuse medical treatments Only parents or legal guardian can consent and refuse Exceptions are: Contraception Prenatal care Substance abuse treatment Sexually transmitted diseases (STDs) including HIV/AIDS
MTBS2CK p.564
Abortion States are split on parental notification laws Some require it, some dont Your Y answer is: i Tell the minor patient to notify her parents.
MTBS2CK p.564
BrainDeath
Brain death = death in our legal system If brain dead, you dont need consent to stop therapy such as mechanical ventilation or antibiotics Court order and ethics committee arent correct answers USMLE S2 CK will want you to discuss, educate, explain, and confer before everything else.
MTBS2CK p.564
Consent
DoNotResuscitateOrders PhysicianAssistedSuicide Euthanasia TerminalSedationand LawofDoubleEffect FutileCare OrganandTissueDonation
Consent Only adults can consent to procedures Each procedure needs individual consent Consent implied in emergency Person doing procedure must obtain consent Adverse effects of procedure must be explained to make consent valid Consequences of refusing procedure must be explained to make consent valid Pregnant women can refuse procedures and treatments for their unborn children Telephone consent is valid
MTBS2CK p.564
Consent
Patient signs consent for ovarian biopsy on left side. At surgery you find cancer of right side. What do you do? Wake patient up & obtain consent to remove ovary on right side.
MTBS2CK p.564
Consent Patient needs colonoscopy. Gastroenterologist asks you to obtain consent for procedure. What do you do? The gastroenterologist who will perform the procedure needs to obtain consent. Do you know all complications of the procedure and alternatives? If you dont explain the possibility of perforation because you are unfamiliar with it, the consent isnt valid If patients colon perforates and you didnt explain alternate procedures, the consent isnt valid
MTBS2CK p.564
DoNotResuscitateOrders
DNR orders refer only to withholding CPR They dont refer to withholding any other form of therapy
MTBS2CK p.565
DoNotResuscitateOrders
PhysicianAssistedSuicide
Patient with capacity consents to DNR before losing consciousness. She needs a surgical procedure, but the surgeon refuses because the patient is DNR. What do you do?
Perform the surgery DNR doesnt mean withholding antibiotics, chemotherapy, or surgery DNR means only that, if the patient dies, you wont attempt resuscitation
MTBS2CK p.565
Always a wrong answer!

This includes states in which its legal Ethical requirements for physicians supersede legality Physician Physician-assisted assisted suicide is administered by the patient, but this is still unethical for physicians
Physician ethics come before legal requirements. You cannot do something unethical even if its legal at the moment.
MTBS2CK p.565
Euthanasia
Physician-administered treatment intended to end or shorten patients life
TerminalSedationand LawofDoubleEffect
Always y wrong g
Is it acceptable to administer pain medication even if theres the possibility treatment shortens life? For example, its acceptable to give pain medications to a person with COPD who has metastatic cancer even if the only way to relieve pain is to give enough opiates that breathing may be impaired, causing the patient to die earlier
MTBS2CK p.565
MTBS2CK p.565
TerminalSedationand LawofDoubleEffect
FutileCare
The question is one of intent: If the meds are given with intent to relieve pain, and as an adverse effect they shorten life, its ethical If the primary intent is to shorten life, its unethical
Physician not obligated to render care thats futile even if the family or patient wants it If brain dead & family insists on continued mechanical ventilation ventilation, you are under no obligation to do so You are under no obligation to perform tests and treatments you consider worthless
MTBS2CK p.565
MTBS2CK p.565
OrganandTissueDonation
ConsentforOrganDonation
Payment for ORGANS is unacceptable Payment for RENEWABLE tissues (sperm & eggs) is acceptable
Only organ donor network should ask for consent for organs Ethical conflict of interest for physician to ask for consent for organ donation Organ donor network has fewer refusals than physician Organ donor cards give an indication of patients wishes, but family can refuse organ donation even if patient has organ donor card
MTBS2CK p.566
MTBS2CK p.565
Confidentiality
Physician Responsibilities
Confidentiality Doctor/PatientRelationship GiftsfromIndustry Abuse ImpairedDrivers ExecutionofPrisoners Torture
Patients right to confidentiality can be broken when theres danger to others STDs HIV/AIDS Airborne Ai b communicable i bl diseases di ( (e.g., tuberculosis) Court order demanding information
MTBS2CK p.566
Confidentiality
Right to confidentiality cannot be broken for: Employers Coworkers Government agencies Family Confidentiality is Friends important, but not as
important as protecting others from harm.
MTBS2CK p.566
Patient with HIV/AIDS has repeatedly refused to disclose his HIV status to his sexual partner. The partner accompanies the patient to the office visits and is in the waiting room. The patient insists you not tell the partner. What do you do?
a. b. c. d. Honor the patients wishes is not as important as protecting the health of the partner. Obtain a court order Consult the ethics committee Either the physician or the department of health can notify the partner
The confidentiality of the patient
MTBS2CK p.566
Confidentiality Woman comes to your office with valid identification from a law enforcement/government agency. She requests a copy of your patients medical records. What do you do? Provide health-related protected records to government agencies, including those from law enforcement, f t only l if: if
Valid warrant or subpoena from courts Otherwise violates the constitutional protection against illegal search and seizure of property This violates HIPAA, which protects health information
Confidentiality
HIV-positive healthcare workers do not have to disclose their status to their patients or their employers.
MTBS2CK p.566
MTBS2CK p.566
Doctor/PatientRelationship
GiftsfromIndustry
Physicians arent obligated to accept everyone coming to him or her as a patient You have the right to end the doctor/patient relationship but must give the patient sufficient time to obtain another caregiver Small S ll gifts ift f from patients ti t are acceptable t bl as long as they arent tied to a specific treatment request Romantic or sexual contact between patients and their current physicians is never acceptable
MTBS2CK p.566567
Never acceptable!
Even pens, penlights, pads, and cups are unacceptable Meals in direct association with educational activities arent considered gifts
MTBS2CK p.567
ElderAbuse
DomesticViolenceandSpousalAbuse
You can report elder abuse against the consent of patient Abused older adults may be too weak, fragile, or vulnerable to protect themselves Elder abuse is treated ethically like child abuse
Unlike child abuse, domestic abuse cannot be reported against the patients wishes You can report and intervene only with patients patient s consent
MTBS2CK p.567
MTBS2CK p.567
ImpairedDrivers (SeizureDisordersandDriving)
ExecutionofPrisoners
Least clear area nationally No uniformity of laws between states Answer suggest that the patient find another means of transportation Wrong answers would be:
a. Confiscating car keys and reporting to law enforcement b. Hospitalizing patient c. Refusing to let the patient get in car
MTBS2CK p.567
Never ethical for a physician to participate in executions at any level You cannot ethically formulate a lethal injection or even do so much as pronounce a prisoner dead Even if state law makes execution legal, physicians should never participate at any level
MTBS2CK p.567
Torture
Torture
Physicians are never to participate in torture of prisoners or detainees Even if the question states that youre in the military, your ethical obligation as a physician supersedes your obligation to the military ilit This would include:
a. Refusing orders from military superiors to participate in torture b. Keeping the torture safe so that its not fatal or damaging
MTBS2CK p.567568
Torture is the ethical equivalent of child abuse. Your p participation p is never acceptable; youre obligated only to report it.
MTBS2CK p.568
Esophagus Gastroenterology
NiketSonpal,MD
Achalasia EsophagealCancer EsophagealSpasm Esophagitis RingsandWebs ZenkersDiverticulum Scleroderma MalloryWeissTear BoerhaavesSyndrome
EsophagealDisorders/Definitions
EsophagealDisorders/Presentation Both can lead to weight loss Hence, weight loss cannot be used to answer What is the most likely diagnosis? With the symptoms Weight loss Anemia Heme-positive stool
Dysphagia Difficulty swallowing Odynophagia Pain while swallowing
Endoscopy!
MTBS2CK p.237
MTBS2CK p.237
Achalasia/Diagnosis
Achalasia/Diagnosis
Inability of lower esophageal sphincter (LES) to relax due to a loss of nerve plexus within lower esophagus Etiology unclear Aperistalsis of esophageal body
Look for... Young patient (< 50) Progressive worsening dysphagia to both solids and liquids at the same time No association with alcohol and tobacco use Complain of...
Regurgitation and halitosis
Chagas Disease = recent travel to South America and new onset dysphagia
Achalasia/DiagnosticTests
MarkedDilationoftheEsophagus
Barium esophagram Will show a birds beak
Source:commons.wikimedia.com
Source:NiketSonpal,MD
MTBS2CK p.238
Most accurate test is Manometry
Chest X-ray May show abnormal widening of esophagus, but is neither very sensitive nor very specific
Chest X-ray is never the right answer to diagnose achalasia
MTBS2CK p.238
MTBS2CK p.238
Achalasia/Treatment
Upper endoscopy Shows normal mucosa in achalasia
Cannot exactly be cured All treatment is based on simple mechanical dilation of esophagus
MTBS2CK p.238
MTBS2CK p.238
Achalasia/Treatment
Achalasia/Treatment
Pneumatic dilation
Effective > 80% to 85% of patients Repeat sessions y are necessary
Botulinum toxin injection Will relax LES, but effects wear off in about 3-6 months, requiring reinjection
Site of Botulinum Injection
Freedictionary.com
MTBS2CK p.238
MTBS2CK p.238
Achalasia/Treatment
EsophagealCancer/Diagnosis
Surgical sectioning or myotomy can help to alleviate symptoms Known as Heller M t Myotomy
Look for: Age 50 or older Dysphagia with solids first then progresses to liquids Association with p prolonged g alcohol and tobacco use > 5 years of GERD symptoms
NiketSonpalMD
MTBS2CK p.238
MTBS2CK p.239
EsophagealCancer/DiagnosticTests
EsophagealCancer/DiagnosticTests
Endoscopy is indispensible, since only a biopsy can diagnose cancer NO TISSUE, NO ISSUE
Barium cannot diagnose cancer
CT and MRI scans Only shows extent of tissue PET scan Gives information about other anatomic lesions
MTBS2CK p.239
MTBS2CK p.239
EsophagealCancer/Treatment
EsophagealCancer/Treatment
Surgical resection is always the thing to try No resection (removal) = no cure Chemotherapy and radiation
Stent placement Purely palliative
MTBS2CK p.239
MTBS2CK p.239
EsophagealSpasm/Background
EsophagealSpasm/Diagnosis
Diffuse esophageal spasm (DES) and nutcracker esophagus are clinically indistinguishable Both present
Sudden onset of chest pain Not related to exertion
EKG and stress

Normal
Esophagram best initial test

Normal
Manometry y most accurate test

Abnormal contraction in various section of the esophagus
MTBS2CK p.239
MTBS2CK p.239
EsophagealSpasm/Treatment
EsophagealSpasm/BariumStudy
Treated with: Nitrates

Relax smooth muscle
Calcium-channel blockers No Ca+2= no smooth muscle contraction
MTBS2CK p.240
MTBS2CK p.240
InfectiousEsophagitis/Management
43-year-old man recently diagnosed with AIDS comes to ED with pain on swallowing thats become progressively worse over the last several weeks. Theres no pain when not swallowing. His CD4 count is 43 mm3. The patient isnt currently taking any medications. What is the most appropriate next step in management? Doesnt t diagnose candida a Esophagram Doesn a. b. Upper endoscopy Too invasive c. Oral nystatin swish and swallow Only for oral candida
Dysphagia with HIV CD4 < 100
Yes
Empirically start fluconazole
Yes
Improvement
No
Perform upper endoscopy with biopsy
d. Intravenous amphotericin Too big gun e. Oral fluconazole
Continue therapy and HAART
CMV large ulcerations. Tx: ganciclovir or foscarnet
HSV small ulcerations. Tx: acyclovir
MTBS2CK p.240
InfectiousEsophagitis
RingsandWebs Schatzki ring Schatzki rings and Plummer-Vinson syndrome both cause dysphagia
Source:AaronCho Source:commons.wikimedia.com
MTBS2CK p.241
RingsandWebs Schatzki ring Associated with intermittent dysphagia
RingsandWebs Plummer-Vinson syndrome Triad of: 1. Dysphagia due to Esophageal Webs 2. Iron Deficiency Anemia 3. Glossitis More M proximal i l than th Schatzki S h t ki rings i Diagnosis
Barium esophagram
Treatment
Iron replacement
MTBS2CK p.241
Source:AzmeenaLaila,MD
MTBS2CK p.241
ZenkersDiverticulum Outpocketing of posterior pharyngeal constrictor muscles
ZenkersDiverticulum
Best test for diagnosis is
Esophogram
No medical treatment and surgical intervention is best
StanfordHospitalMedia
MTBS2CK p.241
MTBS2CK p.241
Scleroderma
MalloryWeissSyndrome/Presentation Upper GI bleed secondary to repetitive retching Self-limited Dx: endoscopy
Presentation
Symptoms of reflux Scleroderma or progressive systemic sclerosis
Diagnosis
Manometry
Treatment
PPIs Screening for Barretts esophagus
MTBS2CK p.242
MTBS2CK p.242
MalloryWeissSyndrome/Treatment
BoerhaavesSyndrome
No specific therapy and will resolve spontaneously Severe cases with persistent bleeding are managed with injection of epinephrine or electrocautery to stop bleeding
Esophageal rupture due to prolonged retching

A full thickness tear
Physical exam
Hammens sign crepitus Subcutaneous air = snap crackle and pop
EMERGENCY!
MTBS2CK p.242
Stomach
EpigastricPain GastroesophagealRefluxDisease BarrettsEsophagus Gastritis PepticUlcerDisease NonulcerDyspepsia Gastrinoma DiabeticGastroparesis
44-year-old woman comes to see you because of epigastric pain for several months. She denies nausea, vomiting, weight loss, or blood in her stool. On physical examination you find no abnormalities. What is the most likely diagnosis?
a. b. c. d. e. f. Duodenal ulcer disease No anemia or heme (+) stools Gastric ulcer disease Heme (+) stools Gastritis Need EGD to diagnose Pancreatitis Acute not chronic Non-ulcer dyspepsia Pancreatic cancer No painless jaundice
MTBS2CK p.242243
AbdominalPain/CausesofPainbyLocation
Right Upper Quadrant Cholecystitis Biliary colic Cholangitis Perforated duodenal ulcer Right Lower Quadrant Appendicitis Ovarian torsion Ectopic pregnancy Cecal diverticulitis Left Upper Quadrant Splenic rupture IBS Splenic flexure syndrome
EpigastricPain/MostLikelyDiagnosis Ifthisisinthehistory: Themostlikelydiagnosisis:
Mid-Epigastrium Pancreatitis Aortic dissection Peptic ulcer disease
Left Lower Quadrant Sigmoid volvulus Sigmoid diverticulitis Ovarian torsion Ectopic pregnancy
Painworsewithfood Painbetterwithfood Weightloss Tenderness Badtaste,cough,hoarse Diabetes,bloating Nothing
Gastriculcer Duodenalulcer Cancer,gastriculcer Pancreatitis Gatroesophageal reflux Gastroparesis Nonulcerdyspepsia
MTBS2CK p.243
EpigastricPain/DiagnosticTests Endoscopy Only way to truly understand the etiology of epigastric pain from ulcer disease Only y way y to g give a precise diagnosis
EpigastricPain/Treatment Proton pump inhibitors (PPIs) First line therapy Empiric Minimum 4 weeks H2 blockers Ranitidine, nizatidine, cimetidine, famotidine Not as effective, but will work in about 70% of patients
MTBS2CK p.243
Liquid antacids Roughly the same efficacy as H2 blockers Misoprostol Artificial prostaglandin analogue Used to treat NSAIDinduced gastric damage When PPIs arrived, misoprostol became wrong answer
Wikimedia
MTBS2CK p.243
GastroesophagealRefluxDisease(GERD) Inappropriate relaxation of LES Results in acid contents of stomach coming up into esophagus Patient complains of... Heartburn Metallic taste Cough 42-year-old man comes to office with epigastric pain radiating up under his chest, which becomes worse after lying flat for an hour. He also has a brackish taste in his mouth. What is the most appropriate next step in the management of this patient?
a. Ranitidine Not as effective b. Liquid antacid Not as effective c. Lansoprazole Not the first step must fail 1st d. Endoscopy e. Barium swallow Not an anatomic disease f. 24-hour pH monitoring Too invasive
MTBS2CK p.244
MTBS2CK p.244
GERD/DiagnosticTests Most often diagnosed using patient history When not clear, the most accurate test is...
24-hour pH monitoring
GERD/Treatment
All patients should try lifestyle changes

Lose weight, avoid alcohol, nicotine and certain foods, eat within 3 hours of bedtime Elevate head 6-8 inches
Endoscopy when: Dysphagia or odynophagia Weight loss Anemia or heme-positive stools > 5 years of symptoms to exclude Barretts esophagus
MTBS2CK p.244245
Mild or Intermittent Symptoms May be treated with liquid antacids or H2 blockers Persistent Symptoms or Erosive Esophagitis PPIs for 4-6 weeks
MTBS2CK p.245
GERD/Treatment
BarrettsEsophagus
5% will not respond to PPIs Patients require surgery to tighten LES:
Nissen fundoplication
Stomach wrapped around LES
Due to long-standing GERD Change to columnar metaplasia Typically takes 5 years
Endocinch
Scope used to place a suture around LES
Local heat or radiation of LES

Causes scarring to tighten LES Last resort
MTBS2CK p.245
Diagnosis Biopsy via endoscopy

Only way to assess presence of Barretts esophagus
MTBS2CK p.245
BarrettsEsophagus/Treatment
Gastritis Inflammation or erosion of gastric lining Sometimes called gastropathy

3 levels: mild, moderate and severe With or without hemorrhage
Finding Barrettsalone (metaplasia) Lowgradedysplasia Highgradedysplasia
Management PPIsandrescope every2 3years PPIsandrescope every 612months Ablationwithendoscopy, photodynamictherapy, radiofrequencyablation, orsurgicalremoval
Many causes
Alcohol NSAIDs Helicobacter pylori Portal HTN Stress
Burns, trauma, sepsis, multiorgan failure
MTBS2CK p.246
MTBS2CK p.246
Gastritis/Presentation
Gastritis/Diagnosis
Often with GI bleeding without pain Severe, erosive gastritis can present with epigastric pain Look for NSAIDs or alcoholism in history No unique q p physical y findings g
You cannot answer the most likely diagnosis question from history and physical alone
The most accurate test is... EGD H. py pylori testing g

Treated if associated with gastritis
Capsule endoscopy is not appropriate for upper GI bleeding if endoscopy is one of the choices
MTBS2CK p.246
MTBS2CK p.246
TestingforHelicobacterpylori Test
Whatisgood aboutthistest? Whatisbad aboutthistest?
Gastritis/Treatment
Invasivetest (endoscopy) Lacksspecificity, cantdistinguish current/previous infection Requiresexpensive equipment Requiresstool sample
MTBS2CK p.247
Endoscopic biopsy Serology
Mostaccurateof alltests Inexpensive, excludesinfection ifnegative
Treat with PPIs H2 blockers, sucralfate, and liquid antacids arent effective as PPIs
UreaC13 orC14 Positiveonlyin breathtesting activeinfection,

noninvasive
Sucralfate is an inert substance (aluminum hydroxide complex) that coats the stomach. If sucralfate is presented as a choice, its nearly always the wrong answer.
H.Pylori stoolantigen
MTBS2CK p.246247
Positiveonlyin activeinfection, noninvasive
Gastritis
PepticUlcerDisease(PUD)
Stress ulcer prophylaxis is indicated in: Mechanical ventilation Burns Curlings ulcers Head trauma Cushings ulcers Coagulopathy
PUD refers to both duodenal ulcer and gastric ulcer disease Endoscopy is key to diagnosis and treatment MCCs H. pylori and NSAIDs
Note: Alcohol and tobacco dont cause ulcers. They delay healing of ulcers
MTBS2CK p.247
MTBS2CK p.247248
PepticUlcerDisease
PepticUlcerDisease/Presentation
PUD presents with recurrent episodes of epigastric pain

Abdominal Pain (dull, sore, gnawing) Pain that is improved with eating Pain that is worsened by eating
Duodenal Ulcer
Gastric Ulcer
MTBS2CK p.248
PepticUlcerDisease/Diagnosis
PepticUlcerDisease/Treatment
Upper endoscopy: most accurate test Allows for intervention and biopsy
Ulcer on endoscopy Biopsy positive for H. pylori Bleeding ulcer
PUD responds to PPIs...

But must treat for H. pylori
Duodenal Ulcer Gastric Ulcer
H. pylori in more than 80% to 90% of cases

Antibiotic treatment Clip or epinephrine injection
H. pylori in 50% to 70% of cases
Radiologic Testing
Poor sensitivity and no histology testing
MTBS2CK p.248
Cancer is present in 4% of those with GU but in none of those with DU.

MTBS2CK p.248249
10
56-year-old woman comes to clinic with epigastric pain from endoscopically confirmed duodenal ulcer, which is unresponsive to several weeks of PPI, clarithromycin, and amoxicillin. What is the most appropriate next step?
PCN allergy?
H. pylori Treatment
Biopsy positive for H. Pylori
PPI combined with clarithromycin and amoxicillin
Replace amoxicillin with metronidazole
30-60 day post therapy testing for eradication
a. b. c. d. e. f. g.
Refer for surgery g y Too invasive Switch the PPI to ranitidine PPI is superior to ranitidine Abdominal CT scan CT cant detect H. pylori Capsule endoscopy Cant detect H. pylori Urea breath testing Vagotomy Not necessary and too invasive Add sucralfate Always the wrong answer
MTBS2CK p.243
MTBS2CK p.249
PepticUlcerDisease/Treatment Treatment of Refractory Ulcers If initial therapy doesnt resolve the DU then detecting persistent H. pylori and switching the antibiotics to metronidazole and tetracycline is appropriate or adding bismuth For those with refractory y GU, , a repeat p endoscopy is done to exclude cancer
GastricUlcersvs.DuodenalUlcers
GU is routinely biopsied
Routinely repeating the endoscopy to confirm healing is standard with GU
GU vs. DU
GU is associated with cancer in 4%
GU pain is more often worsened by food
MTBS2CK p.249
MTBS2CK p.250
NonulcerDyspepsia
NonulcerDyspepsia The best initial therapy is with PPIs

NUD < 45-55 years NUD > 45-55 years
Non-ulcer (functional) dyspepsia is epigastric pain that has no identified etiology MCC of epigastric pain in U.S.
Empiric PPI therapy
PPIs and EGD to r/o cancer
Symptoms persist and H. Pylori is present = treat for H. pylori

11
Gastrinoma(ZollingerEllisonSyndrome) Look for patient with ulcers that are: 1. Large > 1 cm 2. Multiple 3. Past 3rd portion of duodenum 4. Presents with: Diarrhea Abdominal pain Anemia Heme-positive stools
MTBS2CK p.251
Gastrinoma/DiagnosticTests
After endoscopy confirms an ulcer, diagnosis made using one of the following three: 1. High gastrin levels after antisecretory therapy (PPIs/H2) 2. High gastrin levels despite a high gastric acid output 3. Persistent high gastrin levels despite injecting secretin (most accurate)
MTBS2CK p.251
Source:NiketSonpalMD
Gastrinoma/DiagnosticTests What is the next best step after diagnosing ZE? Exclude metastatic disease
Somatostatin receptor scintigraphy + Endoscopic ultrasound
Gastrinoma/Treatment
Local disease is removed surgically Metastatic disease requires lifelong PPIs to block acid production
Ultrasound, CT, and MRI of abdomen have poor sensitivity and are never the most accurate test for diagnosing ZE
DiabeticGastroparesis
64-year-old patient with diabetes for 20 years comes to the office with several months of abdominal fullness, intermittent nausea, constipation, and a sense of bloating. On physical examination, a splash is heard over the stomach. What is the next step? a. Abdominal CT scan Can only diagnose static conditions b. Colonoscopy Wrong end! c. Erythromycin d. Upper endoscopy Wouldnt reveal anything e. Nuclear gastric emptying study Most accurate test for
MTBS2CK p.252
Long standing diabetes
Autonomic neuropathy from high glycemic index
+
Resultant dysmotility from an inability to sense stretch in the GI tract
=
Diabetic gastroparesis
MTBS2CK p.252
Nausea, vomiting, and early satiety
diabetic gastroparesis, but rarely used
12
DiabeticGastroparesis
The patients most common complaint is abdominal discomfort with eating large or small meals Nausea & vomiting Bloating & constipation Early satiety
Upper and Lower Symptoms
Colon
GastrointestinalBleeding Diarrhea IrritableBowelSyndrome InflammatoryBowelDisease DiverticularDisorders ColonCancerScreening
Anorexia
Neurologic Symptoms
Endoscopy - large amount of retained food
Succussion splash
Signs elicited by exam
GastrointestinalBleeding
69-year-old woman comes to ED with multiple red/black stools. Past medical history significant for aortic stenosis. Pulse 115/ minute. BP 94/62 mmHg. Examination otherwise normal. What is the next step in management? a. b. c. d. e. f. g. h. Colonoscopy Nasogastric tube placement Upper endoscopy Patient is unstable, Bolus of normal saline Stablized first, THEN CBC diagnose Bolus of 5% dextrose in water Consult gastroenterology D5w doesnt stay intravascular Check for orthostasis
Most common: Ulcer disease
Esophagitis
Upper GI bl di bleeding
Varices
Gastritis Cancer
MTBS2CK p.253
Duodenitis
MTBS2CK p.252253
GastrointestinalBleeding
Most common: Diverticulosis
GastrointestinalBleeding/PhysicalFindings SeverityofBloodLossBasedonHemodynamics PhysicalFinding Orthostasis Pulse>100/minute SystolicBP<100mmHg Percentageofbloodloss 1520% 30% 30%
Polyps
Lower GI bl di bleeding
Hemorrhoids
Remember: orthostasis is defined as...

IBD Cancer
MTBS2CK p.253
UGIB
>10-point rise in pulse when going from supine to sitting or standing up or BP drop of 20 points or more when sitting up
MTBS2CK p.253
13
VaricealBleeding
Vomiting blood +/ black stool
GastrointestinalBleeding/DiagnosticTests
For acute severe bleeding

Replace fluids and check Hct, platelet count, and coagulation tests (PT or INR)
Cirrhosis
Variceal bleeding
Asterixis
For variceal bleeding

Octreotide and urgent endoscopy to control the bleed by banding
Spider angiomata and caput medusa

MTBS2CK p.253 254
Palmar erythema Splenomegaly
MTBS2CK p.254
AdditionalDiagnosticTestsforGIBleeding Test
Nuclearbleedingscan Angiography
GastrointestinalBleeding/Treatment
Indication
Endoscopyunrevealinginamassive acutehemorrhage Specificsiteofbleedingneeds tobeidentifiedpriortosurgeryor yin embolizationofvessel;usedonly massive,nonresponsivebleeding Smallbowelbleedingwhenupperand lowerendoscopydontshowetiology NotusefulinGIbleeding Showsischemiainseverebleeding
Stabilization Treatment
Fluid replacement
1-2 liters an hour
Packed RBCs
Hct < 30 in those who are older or suffer from CAD
Capsuleendoscopy CTorMRIofabdomen EKG
MTBS2CK p.254
MTBS2CK p.255
Stabilization Treatment
Fresh frozen plasma
INR > 1.3
Platelets
< 50,000 when bleeding
Treat Underlying Cause Endoscopy to determine diagnosis and administer treatment (band varices, cauterize ulcers, inject epinephrine into bleeding gastric vessels) IV PPI for upper GI bleeding Surgery to remove site of bleeding if fluids, blood, platelets, and plasma will not control bleed
MTBS2CK p.255
MTBS2CK p.255
14
Diarrhea/Types
Lactose intolerance Carcinoid syndrome
Esophageal and Gastric Varices Octreotide (somatostatin) Banding Transjugular intrahepatic portosystemic shunting h ti (TIPS) Propranolol
Diarrhea
Antibioticassociated diarrhea
Chronic pancreatitis Malabsorption
MTBS2CK p.255
Diarrhea/AntibioticAssociated
Diarrhea/AntibioticAssociated Best initial test is...

Stool C. diff. toxin
Clindamycin associated with highest incidence of antibiotic-associated diarrhea and Clostridium difficile Blood and white cells may be present in stool Presents several days or weeks after start of antibiotics ANY antibiotic can potentially cause diarrhea
Most accurate test is...

C. diff. PCR
Best initial therapy is...

Metronidazole
If theres no response to metronidazole, next step in management is to...

Switch to oral vancomycin or fidaxomicin
IV vancomycin is always wrong for antibiotic-associated diarrhea since it will not pass bowel wall.
MTBS2CK p.255
MTBS2CK p.255 256
Diarrhea/AntibioticAssociated
75-year-old man is admitted to hospital with pneumonia. Several days after start of antibiotics, he has diarrhea. Stool C. diff toxin is positive, and hes started on metronidazole, which leads to resolution of diarrhea over a few days. Two weeks later diarrhea recurs and C. diff toxin is positive again. What is the next step?
a. b. c. d. e. Retreat with metronidazole orally Use vancomycin orally Repeat metronidazole before switching Sigmoidoscopy and treat only if pseudomembranes are found Not necessary Intravenous metronidazole Only if patient cannot take orally Wait for stool culture C. diff. doesnt grow in culture f. Intravenous vancomycin Repeat metronidazole before switching / IV vancomycin does not work
MTBS2CK p.256 Diarrhea after antibiotic Use Yes C. difficile positive? No Consider alternative causes Yes T t with Treat ith metronidazole No Switch to oral vancomycin or fidaxomicin
Improvement?
Yes Continue metronidazole until end of course
15
Diarrhea/Malabsorption All present with steatorrhea: Oily Greasy Stools Floating Foul smelling Causes: Celiac disease Whipples disease Chronic pancreatitis
MTBS2CK p.256
Diarrhea/Malabsorption All forms of fat malabsorption present with deficiency of fat-soluble vitamins (A, D, E, and K) Hence, they can all present with... Deficiency VitaminD VitaminK VitaminB12 Manifestation Hypocalcemia Bleeding,easybruising Anemia,hypersegmented neutrophils,neuropathy
Vitamin B12 needs an intact bowel wall and pancreatic enzymes to be absorbed
MTBS2CK p.256257
Diarrhea/DiagnosticTests Celiac disease Best initial test is...

Anti-tissue transglutaminase
Diarrhea/Malabsorption Whipples Disease Arthralgias Ocular findings Neurologic abnormalities (dementia, seizures) Fever Lymphadenopathy L h d th
Most accurate diagnostic test is...

Small bowel biopsy
Flattening of villi Can exclude lymphoma
Other tests IgA antigliadin antibody Antiendomysial antibody
MTBS2CK p.257
MTBS2CK p.257
Diarrhea/Malabsorption Whipples disease and tropical sprue Most accurate diagnostic test is...
Bowel wall biopsy showing specific organism Treat with ceftriaxone or TMP/SMZ
ChronicPancreatitis/DiagnosticTests Abdominal X-ray 50% to 60% sensitive for calcification of pancreas and very specific when test is abnormal
MTBS2CK p.257
MTBS2CK p.257258
16
ChronicPancreatitis/DiagnosticTests Abdominal CT scan 80% to 90% sensitive for pancreatic calcification
ChronicPancreatitis/DiagnosticTests Secretin stimulation testing Most accurate diagnostic test

Place NG tube; normal pancreas releases large volume of bicarbonate-rich fluids after IV secretin
D-xylose testing Old test to distinguish pancreatitis from bowel wall abnormalities D-xylose normal in pancreatic disorders
MTBS2CK p.257258
MTBS2CK p.257258
Malabsorption/Treatment Disease Chronicpancreatitis Celiacdisease SpecificTreatment Enzymereplacement Avoidglutencontaining foods(wheat,oats,rye, barley) Ceftriaxone,TMP/SMX TMP/SMX,tetracycline
CarcinoidSyndrome Presentation Flushing Wheezing CV murmurs tricuspid regurgitation Diarrhea Best initial diagnostic test is... Urinary 5-hydroxyindoleacetic acid (5-HIAA) test Treatment Octreotide
Whipplesdisease Tropicalsprue
MTBS2CK p.258
MTBS2CK p.258259
LactoseIntolerance Presents like malabsorptive diarrhea, except...

Intermittently No weight loss Normal vitamin levels
IrritableBowelSyndrome(IBS) Pain syndrome with either diarrhea, constipation, or both Pain of IBS is...
Relieved by BM Less at night Relieved by a change in bowel habit (e.g., diarrhea)
Best initial diagnostic test is...

Stool osmolality test
No specific diagnostic test

Diagnosis of exclusion in association with complex of symptoms

Cessation of symptoms after diet change
Best treatment is...

Stop eating milk products and consider exogenous lactase therapy
MTBS2CK p.259
Not associated with...

Weight loss Blood or white cells in stool
MTBS2CK p.259
17
IrritableBowelSyndrome/Treatment
InflammatoryBowelDisease
Fiber in diet Antispasmodic agents

Hyoscyamine Dicyclomine
Tricyclic y antidepressants p
Amitriptyline
Crohns disease (CD) and ulcerative colitis (UC) present with... Diarrhea and abdominal pain Blood in stool anemia Weight g loss Fever
Antimotility agents
Loperamide for diarrhea Lubiprostone (chloride-channel activator)
Increases BM frequency
InflammatoryBowelDisease Extraintestinal manifestations in both CD and UC Arthralgias Uveitis, iritis Skin manifestation (erythema nodosum, pyoderma gangrenosum) Sclerosing cholangitis (more frequent in UC) Risk of cancer associated with CD and UC Both forms of IBD can lead to colon cancer Cancer risk with duration CD involving colon has same cancer risk as UC
MTBS2CK p.259260
InflammatoryBowelDisease ErythemaNodosum PyodermaGangrenosum
Source:commons.wikimedia.org Source:commons.wikimedia.org
InflammatoryBowelDisease/Differences
InflammatoryBowelDisease/DiagnosticTests Most accurate test is...

Endoscopy
Crohnsdisease
Skiplesions Transmuralgranulomas Fistulasandgranulomas Massesandobstruction Perianaldisease
Ulcerativecolitis
Curablebysurgery Entirelymucosal Nofistulas,noabscesses Noobstruction Noperianaldisease
Frequentquestion:Whenshouldscreeningoccur?
Source:commons.wikimedia.org Source:commons.wikimedia.org
Answer:After8to10yearsofcolonicinvolvement, withcolonoscopyevery1to2years.
MTBS2CK p.260
CD thats mainly in small bowel, radiologic tests such as barium studies will detect lesions
MTBS2CK p.260
18
InflammatoryBowelDisease/DiagnosticTests
InflammatoryBowelDisease/Treatment
ANCAandASCAResultsinIBD
Test
Antineutrophilcytoplasmic antibody(ANCA) Antisaccharomyces cerevesiaeantibody(ASCA)
Crohnsdisease Ulcerativecolitis
Negative Positive
Positive
Negative
Acute exacerbations of either CD or UC are treated with steroids Chronic maintenance of remission is with 5ASA derivatives (mesalamine) Asacol for UC Pentasa for CD Perianal CD
Ciprofloxacin and metronidazole
MTBS2CK p.260
MTBS2CK p.260261
InflammatoryBowelDisease/Treatment Azathioprine and 6-mercaptopurine are used to wean patients off steroids Fistulae and severe unresponsive disease Anti-tumor necrosis factor (TNF) agents (infliximab) Surgery only if theres no response to anti-TNF agents NOTE Neither form of IBD is routinely treated with surgery UC can be cured, however, with colectomy In CD, surgery is used exclusively for bowel obstruction as it recurs at surgical site
MTBS2CK p.261
Diverticulosis
Outpocketings of colon Where arteries meet mucosa Vegetarians At risk? Asymptomatic Infection?
MTBS2CK p.261
Diverticulosis
Diverticulitis
Most accurate test is... Colonoscopy Barium studies Fiber Fiber Fiber
Diagnosis LLQ pain and tenderness Fever Leukocytosis Palpable mass sometimes occurs Symptoms such as nausea, constipation, and bleeding can be present, but are nonspecific
MTBS2CK p.261
MTBS2CK p.261
19
Diverticulitis
Diverticulitis
Best initial test is... CT scan of the abdomen 98% accuracy Colonoscopy and barium enema are dangerous g in acute diverticulitis
Increased risk of perforation because infection weakens colonic wall
MTBS2CK p.261
Diverticulitis/Treatment Treatment Antibiotics that cover E. coli and anaerobes that are present in bowel such as...
Ciprofloxacin combined with metronidazole Amoxicillin/clavulanate Ticarcillin/clavulanate Piperacillin/tazobactam
Surgery is for those with...

No response to medical therapy Frequent recurrences of infection Perforation, fistula formation, abscess, strictures, or obstruction
MTBS2CK 261262
Which of the following is the most effective method of screening for colon cancer? a. Colonoscopy b. Sigmoidoscopy All less sensitive c. Fecal occult blood testing (FOBT) than colonoscopy d Barium enema d. e. Virtual colonoscopy with CT scanning Low sensitivity; misses small f. Capsule endoscopy
For small bowel bleeding polyps
MTBS2CK p.262
ColonCancer/FrequencyofScreening
Routine testing Patients should have a colonoscopy every 10 years beginning at age 50 Single g family y member with colon cancer? Begin 10 years earlier than the age at which the family member developed their cancer or age 40, whichever is younger Screen every 10 years if relative > 60 or every 5 years if relative < 60
MTBS2CK p.262
Hereditary nonpolyposis colon cancer syndrome (HNPCC) comprises... 3 family members 2 generations 1p premature ( (< 50) ) Start screening at age 25 with colonoscopy every 1 to 2 years
MTBS2CK p.262
20
Familial adenomatous polyposis (FAP) Presence of thousands of polyps with abnormal genetic test known as adenomatous polyposis coli (APC) test Start screening with sigmoidoscopy at age 12 every year
Previous adenomatous polyp Patient should have colonoscopy...

Every 3 to 5 years
Previous history of colon cancer Patient should have colonoscopy...

1 year after resection Then at 3 years Then every 5 years
MTBS2CK p.263
MTBS2CK p.263
OtherPolyposisSyndromes Peutz-Jeghers syndrome

Multiple hamartomatous polyps, melanotic spots on lips and skin, frequency of breast cancer, gonadal and pancreatic cancer
Pancreas&Liver
Gardner syndrome
Colon cancer associated with: osteomas, desmoid tumors, and other soft tissue tumors
Turcot syndrome
Colon cancer in association with CNS malignancy
Juvenile polyposis
Colon cancer in association with multiple hamartomatous polyps
MTBS2CK p.263
AcutePancreatitis
Drug allergy Most common 1. GB stones 2. ETOH Drug toxicity
AcutePancreatitis/Presentation Acute epigastric pain + tenderness + nausea/vomiting = Pancreatitis Pain intensity is subjective and doesnt correlate with degree of organ damage In severe cases theres hypotension and fever
The pain of pancreatitis goes straight through to the back like a spear stabbed into the abdomen. Cholecystitis pain goes around the side to the back.
MTBS2CK p.264
Ductal obstruction
Pancreatitis
Scorpion sting
Trauma
Hypertriglyceridemia Hypercalcemia
Infection
MTBS2CK p.263264
21
AcutePancreatitis/DiagnosticTests Which of the following is associated with the worst prognosis in pancreatitis? a. Elevated amylase Levels do not correlate with severity b. Elevated lipase c. Intensity of the pain Pain doesnt predict d Low calcium d. e. C-reactive protein (CRP) rising
Elevated with all inflammation Best initial tests are... Amylase and lipase Most specific diagnostic test is CT scan Labs CBC: leukocytosis, drop in Hct over time with rehydration Elevated LDH and AST Hypoxia Hypocalcemia Elevated urinary trypsinogen activation peptide
MTBS2CK p.264265
MTBS2CK p.264
AcutePancreatitis/DiagnosticTests Imaging CT or MRI scan are best

Also detect pseudocysts
AcutePancreatitis/DiagnosticTests
ERCP
Can help determine etiology (stones, stricture, tumor)
Plain X X-ray ray

Sentinel loop of bowel (air-filled piece of small bowel in LUQ) Limited utility
Ultrasound has very poor accuracy

Overlying bowel blocks precise imaging
MTBS2CK p.265
NOTE: Abdominal CT scan is always performed with IV and oral contrast to better define and outline abdominal structures.
AcutePancreatitis/Treatment
AcutePancreatitis/Treatment
NPO (no food) IV hydration Analgesia PPIs pancreatic stimulation from acid entering g duodenum
> 30% necrosis on CT or MRI, add antibiotics (e.g., imipenem) Infected, necrotic pancreatitis should be resected with surgical debridement to prevent ARDS and death Pseudocysts are drained with a needle if they are enlarging or painful
MTBS2CK p.265
MTBS2CK p.265
22
AcutePancreatitis/Complication
LiverDisease
Spider angiomata and palmar erythema Portal hypertension leading to varices
Coagulopathy
Hepatorenal syndrome
Chronic Li Liver Disease
Asterixis and encephalopathy h l th
Hepatopulmonary syndrome
Thrombocytopenia
Hypoalbuminemia & edema and ascites
MTBS2CK p.265
Ascites Paracentesis is performed with... New-onset ascites Abdominal pain and tenderness Fever Low albumin L lb i i in th the ascitic iti fluid? fl id? Portal HTN from cirrhosis is the etiology Serum ascites albumin gradient (SAAG) The difference or gradient of albumin between serum and ascitic fluid
MTBS2CK p.266
Ascites
SAAG:CorrelatingLevelwithSpecificDiseases <1.1g/dL
Infections Cancer Nephroticsyndrome
>1.1g/dL
PortalHTN CHF Hepaticveinthrombosis Constrictivepericarditis
MTBS2CK p.266
SpontaneousBacterialPeritonitis Infection without perforation of bowel Causative organisms

E. coli (most common) Other gram-negative bacilli Pneumococcus Anaerobes (rare)
SpontaneousBacterialPeritonitis Best initial test is... Cell count with > 250 neutrophils Most accurate test is... Fluid culture, but takes too long for results Gram G stain t i is i negative/LDH ti /LDH nonspecific ifi Treatment: cefotaxime or ceftriaxone NOTE: SBP frequently recurs. When the ascites fluid albumin level is quite low, use prophylactic norfloxacin or TMP/SMX.
MTBS2CK p.266
MTBS2CK p.266
23
TreatmentofSpecificFeaturesofCirrhosis
AlcoholicLiverDisease Diagnosis of exclusion No specific therapy Most accurate test is...

Liver biopsy
Feature
Ascitesandedema Coagulopathyand thrombocytopenia Encephalopathy Hypoalbuminemia lb Spiderangiomata andpalmar erythema Varices Hepatorenal syndrome Hepatopulmonary syndrome
Treatment
Spironolactoneandotherdiuretics.Serial pericentesis forlargevolumeascites. FFPand/orplateletsonlyifbleedingoccurs Lactulose,neomycin,orrifaximin f therapy h Nospecific Nospecifictherapy Propranololandbandingviaendoscopy Somatostatin (octreotide),midodrine Nospecifictherapy
Alcohol and drugs causing liver disease give a greater elevation in AST compared to ALT. Viral hepatitis: Higher ALT than AST. Binge drinking: Sudden rise in GGTP.
MTBS2CK p.267
MTBS2CK p.267
PrimaryBiliaryCirrhosis(PBC)
PrimaryBiliaryCirrhosis(PBC) Most unique features of PBC are... Xanthelasma/xanthoma Osteoporosis Most accurate test is... Liver biopsy Most accurate blood test: Antimitochondrial antibody Treatment with... Ursodeoxycholic acid
PBC is most likely diagnosis with... Woman in 40s or 50s Fatigue and itching Normal bilirubin Elevated alkaline phosphatase
MTBS2CK p.267
MTBS2CK p.267268
PrimaryBiliaryCirrhosis(PBC)
PrimarySclerosingCholangitis Pruritus Elevated alkaline phosphatase GGTP Elevated bilirubin level Treatment Cholestyramine Ursodeoxycholic acid
Most accurate test is... ERCP, not liver biopsy Shows beading, narrowing, or strictures in biliary system
MTBS2CK p.268
24
PrimarySclerosingCholangitis
Alpha1AntitrypsinDeficiency Look for... Combination of...
PSC doesnt improve or resolve with resolution of IBD. Even after a colectomy in UC, patient may still progress to needing a liver transplantation.
Liver disease Emphysema (COPD)
Young patient (< 40) Nonsmoker Treatment Replace enzyme exogenously
MTBS2CK p.268
MTBS2CK p.268
Hemochromatosis
Hemochromatosis
Genetic disorder leading to overabsorption of iron in duodenum Mutation: C282y gene Presentation
Patient in their 50s with mild increases in AST and alkaline phosphatase
Erectile dysfunction
Amenorrhea Skin Darkening
Hemochromatosis
Cardiomegaly
Fatigue and joint pain (pseudogout)
Diabetes
MTBS2CK p.268
MTBS2CK p.268269
Hemochromatosis Best initial test is... Iron studies

Increased serum iron and ferritin Decreased iron binding capacity
ChronicHepatitisBandC EKG Conduction defects Echocardiogram Dilated or restrictive cardiomyopathy Best therapy Phlebotomy
Both are associated with... Cirrhosis Liver cancer PAN
Most accurate test is... Liver biopsy

Increased iron
MTBS2CK p.269
MTBS2CK p.269
25
ChronicHepatitisBandC Chronic hepatitis B Surface antigen positive > 6 months Hepatitis B DNA PCR is the best way to determine viral replication activity Liver biopsy for fibrosis Biopsy tracks progress Chronic hepatitis C 80% have chronic infection Never symptomatic when illness contracted Hepatitis C DNA PCR
Determines disease activity
ChronicHepatitisBandC/Treatment Chronic hepatitis B Adefovir Lamivudine Telbivudine Entecavir Tenofovir T f i Interferon Chronic hepatitis C Combination of... Interferon + Ribavirin + Telapavir ( Boceprevir) (or B i)
MTBS2CK p.270
MTBS2CK p.270
HepatitisTreatmentSideEffects Drug AdverseEffects
WilsonDisease/Presentation
Interferon Ribavarin Adefovir Lamivudine Bocepevir Telaprevir

MTBS2CK p.270
Arthralgias,thrombocytopenia, depression,leukopenia Anemia Renaldysfunction None Anemia Rash
Decrease in ceruloplasmin causes buildup of copper Neurological symptoms Psychosis, tremor, dysarthria, ataxia, or seizures Coombs negative hemolytic anemia Renal tubular acidosis or nephrolithiasis
MTBS2CK p.270271
WilsonDisease/Diagnosis
WilsonDisease
Best initial test is... Slit-lamp examination for Kayser-Fleischer rings Most accurate diagnostic g test is... Abnormally increased amount of copper excretion into urine after giving penicillamine
MTBS2CK p.271
MTBS2CK p.271
26
WilsonDisease/Treatment Penicillamine chelates copper and removes it Additional therapies are... Zinc: interferes with intestinal copper absorption Trientine: alternate copper-chelating compound
AutoimmuneHepatitis Look for... Young women Signs of liver inflammation Positive ANA More specific tests: Liver-kidney microsomal antibodies Anti-smooth muscle antibodies
MTBS2CK p.271
Most accurate test: Liver biopsy Treatment Prednisone and/or azathioprine
Decreased ceruloplasmin level is not the most accurate test. This is the most common wrong answer. All plasma proteins can be decreased in those with liver dysfunction and cirrhosis.
MTBS2CK p.271
AutoimmuneHepatitis
NonalcoholicSteatohepatitis Nonalcoholic Fatty Liver Disease Extremely common cause of mildly abnormal liver function tests Disorder is associated with: Obesity Diabetes Hyperlipidemia Corticosteroid use Most accurate test: biopsy Management: weight loss
MTBS2CK p.272
NonalcoholicSteatohepatitis
27
Anemia Hematology
Dr.ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity
Presentation DiagnosticTests y p Symptoms MeanCorpuscularVolume MicrocyticAnemia MacrocyticAnemia NormocyticAnemia Treatment
Anemia Presentation All forms of anemia present with identical symptoms if they have the same hematocrit (Hct) Symptoms based on severity, not etiology What is the most likely diagnosis?
Cannot be answered using symptoms alone
HematocritandSymptoms
Hematocrit
>30 35% 25 30% 20 25% <20 25%
ExpectedSymptoms
None Dyspnea(worseon exertion), ),fatigue g Lightheadedness, angina Syncope,chestpain
Diagnostic Tests Best initial test to evaluate anemia?

Always a complete blood count (CBC)
MTBS2CK p.203
MTBS2CK p.203
Anemia/DiagnosticTests
MeanCorpuscularVolume
Ultimately, cardiac ischemia from anemia proves fatal. Myocytes cant distinguish between: Anemia Hypoxia CAD Carbon monoxide poisoning All of these conditions result in decreased oxygen delivery to tissues
MTBS2CK p.203204
Mean corpuscular volume (MCV)

First clue to knowing etiology
Mean Corpuscular Volume (Normal 80100 fL)
Smaller?
Larger?
Microcytosis
Macrocytosis
MTBS2CK p.204
Microcytosis
Microcytosis Similarities among microcytic anemias Low reticulocyte count Only alpha thalassemia has 3 genes deleted elevated reticulocyte count Microcytic anemias are due to production problems
Nearly synonymous with reticulocyte counts
Causes of low MCV: Iron deficiency Thalassemia Sideroblastic anemia Anemia of chronic disease
MTBS2CK p.204
MTBS2CK p.204
Microcytosis
MacrocyticAnemia/Etiology Causes of high MCV B12 & folate deficiency Alcoholism Sideroblastic anemia Liver disease or hypothyroidism Medications M di ti ( (e.g., zidovudine id di or phenytoin) h t i ) Antimetabolite medications: azathioprine, 6mercaptopurine, hydroxyurea Myelodysplastic syndrome (MDS)
Routine blood smear

Not effective in telling the difference between types of microcytosis
All hypochromic All potentially give target cells
MTBS2CK p.204
MTBS2CK p.204
NormocyticAnemia Acute blood loss & hemolysis rapid drop in Hct (no time for MCV change) Blood loss leads to iron deficiency & microcytosis Hemolysis increases reticulocyte count
Reticulocytes raise the MCV Reticulocytes slightly larger than normal cells
Anemia/Treatment Treatment If severe: give packed RBCs Answering the question At what Hct do I transfuse a patient? depends on the following factors:
1. Symptomatic? Transfuse. 2. Hct very low in elderly person? Heart disease? Transfuse.
MTBS2CK p.204
MTBS2CK p.205
Anemia/Treatment Symptomatic from anemia means: SOB Lightheaded, confused, and sometimes syncope Hypotension and tachycardia Chest pain
BloodProducts Packed Red Blood Cells (PRBCs) Concentrated form of blood
Whole blood - 150 mL plasma = PRBCs

Hct of PRBCs: 70% - 80% Removal of plasma doubles Hct Each unit PRBCs raises Hct by 3 points/unit
Remember: No transfusion if young & asymptomatic
MTBS2CK p.205
MTBS2CK p.205
BloodProducts Fresh Frozen Plasma (FFP) Replaces clotting factors for elevated prothrombin time, aPTT, or INR Most important if actively bleeding FFP used as replacement with plasmapheresis
BloodProducts Cryoprecipitate Used to replace fibrinogen Some utility in disseminated intravascular coagulation (DIC) Provides high amounts of clotting factors in small plasma volume
Whole blood is never correct Whole blood is divided into either PRBCs or FFP
MicrocyticAnemia
Microcytosis = MCV < 80 fL
MicrocyticAnemia
Etiology Presentation DiagnosticTests Treatment
Microcytic,hypochromicanemiaseenonbloodsmear. MTBS2CK p.206

CopyrightJamesVanRhee. Usedwithpermission.
MicrocyticAnemia/Etiology Iron deficiency Blood loss One teaspoon (5 mL/day) blood loss leads to iron deficiency over time Body only needs very tiny amount of iron
1 to 2 mg/day
MicrocyticAnemia/Etiology Chronic disease Initially MCV is normal, then decreases Unclear etiology Any cancer or chronic infection Clear mechanism only in renal failure deficiency of erythropoietin Hemoglobin synthesis will not occur because iron does not move forward Iron is locked in storage or trapped in macrophages or in ferritin
Menstruating women need a little more

2-3 mg/day
Pregnant women need 5-6 mg/day Duodenum absorbs only about 4 mg/day
MTBS2CK p.206
MTBS2CK p.206
MicrocyticAnemia/Etiology Sideroblastic anemia Can be macrocytic when associated with myelodysplasia (MDS) Most common cause: Alcohol effect on marrow Less common causes...
Lead poisoning Isoniazid Vitamin B6 deficiency
MicrocyticAnemia/Etiology Thalassemia Extremely common cause of microcytosis Most with thalassemia trait are asymptomatic
MTBS2CK p.206
MTBS2CK p.206
MicrocyticAnemia/Presentation
MicrocyticAnemia/Presentation
You cant distinguish these anemias based on symptoms Might have a suggestion from history
How to answer What is the most likely diagnosis? for anemia FeatureintheHistory Mostlikelydiagnosis? Bloodloss(GIbleeding) Menstruation Cancerorchronicinfection Rheumatoidarthritis Alcoholic Asymptomatic Irondeficiency Irondeficiency Chronicdisease Chronicdisease Sideroblastic Thalassemia
MTBS2CK p.206
MTBS2CK p.206
MicrocyticAnemia/DiagnosticTests
MicrocyticAnemia/DiagnosticTests
Peripheral smear not useful! All hypochromic All can be associated with target cells
Target cells: most common with thalassemia
MTBS2CK p.207
MTBS2CK p.207
CopyrightJamesVanRhee. Usedwithpermission.
MicrocyticAnemia/IronStudies Unique features and diagnoses of iron studies
MicrocyticAnemia/IronStudies Iron deficiency
UniqueFeature Lowferritin Highiron Normalironstudies
Diagnosis Irondeficiency Sideroblasticanemia Thalassemia
Low ferritin = Iron deficiency

However, one third of patients with iron deficiency will have normal or increased ferritin Ferritin is an acute phase reactant This means any infection or inflammation can raise the ferritin level
MTBS2CK p.207
MTBS2CK p.207
MicrocyticAnemia/IronStudies Both iron deficiency and anemia of chronic disease are associated with low serum iron Iron deficiency: increase in total iron binding capacity (TIBC) TIBC measures unbound sites on transferrin Open sites on transferrin = increased capacity or number of unbound sites
MicrocyticAnemia/IronStudies Chronic disease Serum iron: low in circulation Iron trapped in storage Ferritin (stored iron): elevated or normal Circulating iron: decreased Major M j diff difference i is TIBC i is low l
MTBS2CK p.207
MTBS2CK p.207
MicrocyticAnemia/IronStudies Sideroblastic anemia Only microcytic anemia elevated circulating iron level Thalassemia Genetic disease with normal iron studies
UniqueLaboratoryFeatures Iron deficiency Red cell distribution of width (RDW) increased

Newer cells are more iron deficient Newer cells are smaller in iron deficiency As body runs out of iron, newer cells have less Hb & get p g progressively g y smaller
Elevated platelet count common Single most accurate test is...

Bone marrow biopsy for stainable iron (decreased) Rarely done, but most accurate
MTBS2CK p.207
MTBS2CK p.207
UniqueLaboratoryFeatures Sideroblastic anemia The most accurate test is... Prussian blue staining for ringed sideroblasts Basophilic stippling can occur in any cause of sideroblastic anemia
UniqueLaboratoryFeatures Thalassemia Most accurate test is...
Hb electrophoresis!
MTBS2CK p.207208
MTBS2CK p.208
UniqueLaboratoryFeatures Thalassemia Most accurate test for alpha thalassemia

Genetic studies 3-gene deletion alpha thalassemia
Hb H (beta-4 tetrads) Increased reticulocyte count
ElectrophoresisFindings
Alphathalassemia
Onegenedeleted:normal Twogenesdeleted:mildanemia, normalelectrophoresis Threegenesdeleted:moderate anemiawithHbH(beta4 tetrads),increasedreticulocytes Fourgenesdeleted:gamma4 tetradsorhemoglobinBart;CHF causesdeathinutero
MTBS2CK p.208
Betathalassemia
Inc.HbFandA2 N/A Betathalassemiaintermedia NormalHbF Notransfusiondependence N/A
All thalassemia types have normal RDW
MTBS2CK p.208
MicrocyticAnemia/Treatment Iron deficiency Replace iron with oral ferrous sulfate If insufficient, patients get IM iron Chronic disease Correct underlying disease Only O l end-stage d t renal lf failure il responds d t to erythropoietin Sideroblastic anemia Correct the cause Some respond to vitamin B6 (pyridoxine)
MTBS2CK p.208
MicrocyticAnemia/Treatment Thalassemia Trait not treated Beta thalassemia major (Cooley anemia) Chronic transfusion lifelong Iron I overload l d managed d with ith d deferasirox f i ( (oral li iron chelator) Deferoxamine is parenteral
MTBS2CK p.209
MacrocyticAnemia
Etiology Presentation DiagnosticTests Treatment
73-year-old man in office with fatigue progressively worse over several months. He is short of breath when he walks up one flight of stairs. He drinks 4 vodka martinis a day. He complains of numbness and tingling in his feet. Physical: decreased sensation in feet. Hct: 28% MCV: 114 fL (elevated) What is the next step? 1st is peripheral smear Once hypersegmented neutrophils are seen, a. Vitamin B12 level THEN get B12 & folate levels b. Folate level c. Peripheral blood smear d. Schilling test To see if B12 deficiency is due to pernicious anemia e. Methylmalonic acid level
Confirms diagnosis of B12 deficiency when B12 levels are equivocal
MTBS2CK p.209
MacrocyticAnemia Megaloblastic Hypersegmented neutrophils
MacrocyticAnemia/Etiology Vitamin B12 deficiency is caused by... Pernicious anemia Pancreatic insufficiency Dietary deficiency (vegan/strict vegetarian) Crohns disease damaging terminal ileum Blind loop syndrome (gastrectomy or gastric bypass for weight loss) Diphyllobothrium latum
Many factors raise MCV Only B12 & folate deficiency & antimetabolite medications cause hypersegmentation
Source: Alireza Eghtedar, MD
MTBS2CK p.209210
MTBS2CK p.209
MacrocyticAnemia/Etiology
MacrocyticAnemia/Presentation
Folate deficiency Dietary deficiency (goats milk has no folate and limited iron/B12) Psoriasis & skin loss or turnover Drugs: g p phenytoin, y , sulfa
Alcohol Gives macrocytosis & neurological problems Will not give hypersegmented neutrophils
MTBS2CK p.209
MTBS2CK p.209
MacrocyticAnemia/Presentation B12 deficiency Can give any neurological abnormality Peripheral neuropathy most common Dementia least common Posterior column damage to position & vibratory sensation or subacute subacute combined degeneration degeneration of cord is classic Look for ataxia
MacrocyticAnemia/DiagnosticTests Labs common to both B12 & folate deficiency Megaloblastic anemia Increased LDH & indirect bilirubin levels Decreased reticulocyte count Hypercellular bone marrow Macroovalocytes M l t Increased homocysteine levels Only B12 deficiency is associated with increased methylmalonic acid level
MTBS2CK p.210
MTBS2CK p.210
MacrocyticAnemia/DiagnosticTests B12 & folate deficiency Identical hematologically on blood smear

73-year-old woman with decreased position & vibratory sensation of lower extremities. Hct: 28%, MCV: 114 fL, and hypersegmented neutrophils. B12 level decreased, but near the borderline of normal. What is the next step in management?
a. b. c. d. e. f. Methylmalonic acid level Confirms cause as pernicious Anti-intrinsic factor antibodies anemia after B12 deficiency confirmed Anti-parietal cell antibodies Schillings test Rare test of etiology; premature Folate level Folate doesnt give neurological deficits Homocysteine level Doesnt add anything
Source: Alireza Eghtedar, MD
MTBS2CK p.210
MTBS2CK p.210211
MacrocyticAnemia/DiagnosticTests
MacrocyticAnemia/DiagnosticTests Tested facts about macrocytic anemia B12 & folate deficiency can cause pancytopenia as well as macrocytic anemia Pancreatic enzymes are needed to absorb B12
They free it from carrier (R) protein
Tested facts about macrocytic anemia Schilling test is never the right answer Pernicious anemia is confirmed with antiintrinsic factor and anti-parietal cell antibodies Red cells are destroyed as they leave the marrow, so reticulocyte count is low
Neurological abnormalities will improve as long as they are minor (e.g., peripheral) and short duration
MTBS2CK p.211
MTBS2CK p.211
MacrocyticAnemia/Treatment
Replace what is deficient Folate replacement corrects hematologic problems of B12 deficiency, but not the neurological problems
Which of the following is a complication of B12 or folate replacement? a. Seizures Not associated with treatment b. Hemolysis Cells are produced rapidly, not hemolyzed c Hypokalemia c. High K+ from massive tissue or d. Hyperkalemia cellular breakdown e. Diarrhea
Cause hypokalemia, but not associated with B12 or folate replacement therapy
MTBS2CK p.211
MTBS2CK p.211
HemolyticAnemia All forms lead to: Sudden in Hct Increased LDH, indirect bilirubin & reticulocytes Decreased haptoglobin Slight increase in MCV
Reticulocytes R ti l t > normal l cells ll
HemolyticAnemia Part1
SickleCellDisease HereditarySpherocytosis AutoimmuneHemolysis y
Hyperkalemia
MTBS2CK p.211212
SickleCellDisease Chronic, well-compensated hemolytic anemia Reticulocyte count always high Acute painful vaso-occlusive crisis is caused by... Hypoxia Dehydration Infection I f ti Cold temperatures
SickleCellDisease/Presentation Look for... African American Sudden, severe pain in chest, back & thighs May have fever
Rare for adult to present with acute crisis without clear history of sickle cell disease
MTBS2CK p.212
MTBS2CK p.212
SickleCellDisease/Manifestations Bilirubin gallstones Increased infection from autosplenectomy

Encapsulated organisms
SickleCellDisease/DiagnosticTests Best initial test... - Peripheral smear Most accurate test.. - Hemoglobin electrophoresis Trait (AS disease) does not give sickled cells
Osteomyelitis y
Most commonly from Salmonella
Stroke Enlarged heart with hyperdynamic features and systolic murmur Skin ulcers Avascular necrosis of femoral head
Retinopathy
MTBS2CK p.212
MTBS2CK p.212213
SickleCellDisease/Treatment Which is found on smear in sickle cell disease? a. b. c. d d. e. Basophilic stippling Associated with lead poisoning Howell-Jolly bodies Bite cells Seen with G6PD deficiency Fragmented red cells seen with S hi t Schistocytes t intravascular hemolysis Morulae 1. Oxygen/hydration/analgesia 2. Fever or white cell count higher than usual? Antibiotics given! Ceftriaxone, levofloxacin, or moxifloxacin 3. Folic acid in everyone 4. Pneumococcal vaccine: autosplenectomy 5. Hydroxyurea: prevent recurrences, increases Hb F Dont wait for results of testing! Start antibiotics with fever. No spleen = Overwhelming infection = Death!!
Seen inside neutrophils in Ehrlichia infections
10
SickleCellDisease/Treatment 43-year-old man with sickle cell disease admitted with acute pain crisis. Only med is folic acid. Hct on admission: 34%. On 3rd hospital day, hematocrit drops to 22%. What is the initial test? y count Not best way to gauge severity of a. Reticulocyte b. Peripheral smear hemolysis Causes aplastic crisis which freezes growth of c. Folate level marrow d. Parvovirus B-19 IgM level Most accurate test for parvovirus B-19 is e. Bone marrow PCR for DNA. IVIG is best initial therapy.
Marrow shows giant pronormoblasts, but this isnt better than reticulocyte count at measuring severity of hemolysis
Exchange transfusion for severe vasoocclusive crisis with: Acute chest syndrome Priapism Stroke Visual disturbance from retinal infarction
SickleCellTrait
HereditarySpherocytosis Genetic defect in cytoskeleton of RBCs Leads to abnormal round shape Loss of normal flexibility characteristic of biconcave disc that allows red cells to bend in spleen
Patient is heterozygous for sickle gene (AS) Only manifestation is inability to concentrate urine (isosthenuria) Clinically asymptomatic Normal CBC Normal smear Hematuria sometimes occurs No treatment for sickle cell trait
MTBS2CK p.214
MTBS2CK p.214215
HereditarySpherocytosis/Presentation
HereditarySpherocytosis/Diagnosis
Look for... Recurrent episodes of hemolysis in a young child or newborn Intermittent jaundice Splenomegaly S l l Family history of anemia or hemolysis Bilirubin gallstones
Low MCV Increased mean corpuscular hemoglobin concentration (MCHC) Negative Coombs test
Most acc accurate rate test: test Osmotic fragility fragilit
Cells are placed in slightly hypotonic solution Increased swelling leads to hemolysis
MTBS2CK p.214215
MTBS2CK p.215
11
HereditarySpherocytosis/Treatment
AutoimmuneHemolysis
1. Chronic folic acid replacement supports red cell production 2. Splenectomy stops hemolysis but doesnt eliminate spherocytes
Also known as warm or IgG hemolysis Idiopathic in 50% Clear causes are...
Chronic lymphocytic leukemia (CLL) Lymphoma Systemic lupus erythematosus (SLE) Drugs: penicillin, alpha-methyldopa, rifampin, phenytoin
MTBS2CK p.215
MTBS2CK p.215
AutoimmuneHemolysis/DiagnosticTests
AutoimmuneHemolysis/DiagnosticTests Autoantibodies remove small amounts of red cell membrane and lead to smaller membrane Forces cell to become round Biconcave discs have greater surface than sphere
Most accurate diagnostic test is... Coombs test

Detects IgG on surface of red cells Direct & indirect tests tell basically the same thing Indirect associated with greater amount of antibody
Smear doesnt show fragmented cells because destruction occurs inside spleen or liver, not in blood vessel
AutoimmuneHemolysis/Treatment 1. Glucocorticoids (prednisone) best initial therapy 2. Recurrent episodes: splenectomy 3. Severe, acute hemolysis not responding to prednisone can be controlled with intravenous immunoglobulin g (IVIG) 4. Rituximab when splenectomy doesnt control hemolysis
AutoimmuneHemolysis/Treatment
Alternate treatments to diminish need for steroids: Cyclophosphamide Cyclosporine Azathioprine Mycophenolate mofetil
MTBS2CK p.216
MTBS2CK p.216
12
ColdAgglutininDisease
IgM antibodies against red cells in association with Epstein-Barr virus, Waldenstrm macroglobulinemia, or Mycoplasma pneumoniae Presentation Symptoms in colder parts of body Numbness or mottling of nose, ears, fingers, and toes Symptoms resolve on warming body part
HemolyticAnemia Part2
ColdAgglutininDisease G6PDDeficiency HUSandTTP PNH
Diagnosis
Direct Coombs test positive only for complement Smear normal in most May show spherocytes
MTBS2CK p.216
ColdAgglutininDisease Treatment 1. Stay warm 2. Administer rituximab 3. Cyclophosphamide, cyclosporine, or other immunosuppressive agents stop production of antibody 4. Plasmapheresis in some
ColdAgglutininDisease/Treatment
Cryoglobulins often mixed up with cold agglutinins. Both are IgM and dont respond to steroids. Cryoglobulins are associated with: Hepatitis C Joint pain Glomerulonephritis
Steroids and splenectomy usually dont work

G6PDDeficiency X-linked recessive Inability to generate glutathione reductase and protect red cells from oxidant stress Most common oxidant stress is infection Other causes: dapsone, quinidine, sulfa drugs, primaquine nitrofurantoin primaquine, nitrofurantoin, and fava beans
G6PDDeficiency/Presentation
Look for...
African American or Mediterranean males Sudden anemia & jaundice Normal-sized spleen With infection i f ti or drug d
G6PD deficiency is X-linked recessive, it manifests almost exclusively in males
MTBS2CK p.217
MTBS2CK p.217
13
G6PDDeficiency/Diagnosis Best initial test is... Peripheral smear

Look for Heinz bodies and bite cells
G6PDDeficiency
Treatment Avoid oxidant stress Nothing reverses hemolysis
Most accurate test... G6PD level

1 to 2 months after acute episode of hemolysis
MTBS2CK p.217
MTBS2CK p.218
HUSandTTP Hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are different versions of the same basic disease
HUS Associated with E. coli 0157:H7 More frequent in children TTP Associated with ticlopidine clopidogrel, ticlopidine, clopidogrel cyclosporine, and AIDS Neurological disorders (confusion and seizures) Fever More common in adults
HUSandTTP Both characterized by:
Intravascular hemolysis with fragmented red cells (schistocytes) Thrombocytopenia Renal insufficiency
MTBS2CK p.218
MTBS2CK p.218
HUSandTTP
Diagnosis No one specific test diagnoses either disorder Normal PT/aPTT Negative Coombs test Treatment Severe cases treated with plasmapheresis or plasma exchange
ParoxysmalNocturnalHemoglobinuria
Clonal stem cell defect with increased sensitivity to complement in acidosis Etiology Deficiency of complement regulatory proteins CD 55 and 59, also known as decay accelerating factor (DAF) Gene for phosphatidylinositol glycan class A (PIG (PIG-A) A) is defective overactivation of complement system During sleep, relative hypoventilation leads to pCO2 and acidosis This does nothing to an unaffected person In PNH it leads to hemolysis and thrombosis
MTBS2CK p.218
MTBS2CK p.218
14
Presentation Episodic dark urine with first urination of day from hemoglobin Pancytopenia and iron deficiency anemia
Pancytopenia Most accurate test is...

Decreased CD55 & CD59
Ham test and sucrose hemolysis are never the correct answer
Flow cytometry is another way of saying CD55/CD59 testing
Thrombosis MCC of death

1. Prednisone 2. Allogeneic bone marrow transplant is the only method of cure 3. Eculizumab inactivates C5 in complement pathway and decreases red cell destruction; its a complement inhibitor 4. Folic acid and iron replacement with transfusions as needed
HematologicMalignancies
AplasticAnemia PolycythemiaVera EssentialThrombocytosis Myelofibrosis
MTBS2CK p.219
AplasticAnemia
Pancytopenia of unclear etiology Any infection or cancer can invade marrow causing decreased production or hypoplasia Other causes:
Radiation and toxins (e.g., toluene, insecticides (DDT), and benzene) Drug effect: sulfa, phenytoin, carbamazepine, chloramphenicol, alcohol, chemotherapy SLE PNH Infection: HIV, hepatitis, CMV, EBV B12 and folate deficiency Thyroid-inhibiting medications (e.g., propylthiouracil (PTU) and methimazole)
MTBS2CK p.219
AplasticAnemia
Fatigue of anemia Infections from low white cell counts Bleeding from thrombocytopenia Most accurate test is... is Bone marrow biopsy Aplastic anemia is confirmed by excluding all causes of pancytopenia
MTBS2CK p.219
15
AplasticAnemia/Treatment Treat any underlying cause thats identified THEN... Blood transfusion, antibiotics for infection, and platelets for bleeding Aplastic anemia acts as autoimmune disorder T cells attack patients own marrow Cyclosporine inhibits T cells This brings the marrow back to life!
AplasticAnemia/Treatment True aplastic anemia treated with allogeneic bone marrow transplantation (BMT) if young enough and matched When too old for BMT (> 50) or no matched donor y y g globulin ( (ATG) ) and treatment is anti-thymocyte cyclosporine Tacrolimus is alternative to cyclosporine
MTBS2CK p.219
MTBS2CK p.219220
PolycythemiaVera Unregulated overproduction of all 3 cell lines Red cell overproduction is most prominent Mutation in JAK2 protein which regulates marrow production Red cells grow wildly despite low erythropoietin
PolycythemiaVera Symptoms of hyperviscosity from increased red cell mass such as: Headache, blurred vision, and tinnitus Hypertension Fatigue Splenomegaly Bleeding from engorged blood vessels Thrombosis from hyperviscosity
MTBS2CK p.220
MTBS2CK p.220
PolycythemiaVera
Hematocrit markedly elevated > 60% Platelets and WBC count Erythropoietin Total red cell mass You must exclude hypoxia as cause of erythrocytosis Oxygen levels: normal Vitamin B12 levels are elevated for unclear reasons it s Iron levels because its been used to make red cells
PolycythemiaVera
Most accurate test...

JAK2 mutation (95%)
Increased basophils
All myeloproliferative disorders
Small number converted to AML
MTBS2CK p.220
MTBS2CK p.220
16
EssentialThrombocytosis(ET) Markedly elevated platelet count > 1 million Leads to both thrombosis & bleeding Very difficult to distinguish from an elevated platelet count as a reaction to another stress (e.g., infection, cancer, or iron deficiency)
EssentialThrombocytosis(ET) < 60 & asymptomatic with platelets < 1.5 million Best initial therapy...
Hydroxyurea
Anagrelide with red cell No treatment necessary suppression from hydroxyurea > 60 & thromoboses or platelet count > 1.5 Aspirin for million erythromelalgia (painful, Begin treatment red hands in ET)
MTBS2CK p.221
MTBS2CK p.221
Myelofibrosis
Older persons with pancytopenia Bone marrow shows marked fibrosis Blood production shifts to spleen & liver, which become markedly enlarged Look for teardrop-shaped cells and nucleated red blood cells on smear Thalidomide and lenalidomide: tumor necrosis factor inhibitors that increase bone marrow production Occasional patient < 50-55, allogeneic bone marrow transplantation is attempted
Leukemia
AcuteLeukemia ChronicMyelogenousLeukemia LeukostasisReaction MyelodysplasticSyndrome ChronicLymphocyticLeukemia HairyCellLeukemia
MTBS2CK p.221
AcuteLeukemia/Presentation History of myelodysplasia suggests acute leukemia Signs of pancytopenia (fatigue, infection, bleeding) Even if WBC is normal or increased Infection is common presentation Leukemic cells (blasts) dont function normally
AcuteLeukemia/M3 Most frequently tested acute leukemia is M3, known as acute promyelocytic leukemia (APL) M3 is associated with disseminated intravascular coagulation (DIC)
M3 DIC
No distinct clinical presentation bet between een the 3 subtypes of acute lymphocytic leukemia (ALL)
MTBS2CK p.221
MTBS2CK p.221
17
AcuteLeukemia/Diagnosis Best initial test is... Blood smear

Shows blasts
AcuteLeukemia/Diagnosis Auer rods Eosinophilic inclusions Associated with acute promyelocytic leukemia (M3)
Most accurate test is... Flow cytometry

Distinguishes different subtypes of acute leukemia Detects specific CD subtypes associated with each type of leukemia
Myeloperoxidase Characteristic of acute myelocytic leukemia (AML)
MTBS2CK p.221
MTBS2CK p.221222
AcuteLeukemia/Treatment Both AML & ALL treated initially with chemotherapy to remove blasts from peripheral blood smear Known as inducing remission The question is: proceed to BMT after remission or give more chemotherapy Prognosis poor? go straight to BMT Prognosis good? more chemotherapy
AcuteLeukemia/Treatment
The best indicator of prognosis in acute leukemia is...
Cytogenetics
Assesses specific chromosomal characteristics found in each patient Good cytogenetics = less chance of relapse = more chemotherapy Bad cytogenetics = more chance of relapse = immediate BMT
MTBS2CK p.222
MTBS2CK p.222
1. Add all-trans-retinoic acid (ATRA) to those with M3 (acute promyelocytic leukemia) 1. Add intrathecal chemotherapy such as methotrexate to ALL treatment; prevents relapse of ALL in CNS
Most tested facts for acute leukemia are... M3 (promyelocytic leukemia) gives DIC Add ATRA to M3 Auer rods = AML Add intrathecal methotrexate to ALL
MTBS2CK p.222
MTBS2CK p.222
18
ChronicMyelogenousLeukemia/Presentation Look for... High WBC count: all neutrophils Vague symptoms of fatigue, night sweats, and fever from hypermetabolic syndrome Splenomegaly: early satiety, abdominal fullness, and LUQ pain Pruritus is common after hot baths/showers
Histamine release from basophils
ChronicMyelogenousLeukemia/Diagnosis
Determine if its a reaction to another infection, stress (leukemoid reaction), or leukemia CML may give small numbers of blasts Should be < 5% Basophils increased
MTBS2CK p.223
MTBS2CK p.223
ChronicMyelogenousLeukemia/Diagnosis If leukocyte alkaline phosphatase score (LAP) is a choice, then this is first
Leukemic cells dont have normal amounts of alkaline phosphatase; LAP score low in CML
ChronicMyelogenousLeukemia/Treatment
Imatinib (Gleevec), dasatinib, or nilotinib are the best initial therapy Only BMT cures CML
Never the first therapy
If LAP score is not a choice, or the question is What is the most accurate test? then answer BCR-ABL
Can be done by PCR on peripheral blood
MTBS2CK p.223
MTBS2CK p.223
MyelodysplasticSyndrome(MDS)
54-year-old man with SOB, blurry vision, confusion, and priapism. WBC count 225,000/L. Predominantly neutrophils with about 4% blasts.
a. b. c. d. e. f. g.
What is next step in management of this case?

Leukapheresis In acute leukostasis reaction, BCR ABL testing BCR-ABL i important t t to t remove excessive i Bone marrow biopsy white cells from the blood than Bone marrow transplant to establish a specific Consult hematology/oncology diagnosis, no matter what the etiology Flow cytometry Hydroxyurea Will lower the cell count, but not as rapidly as leukapheresis
Preleukemic disorder in those > 60 Pancytopenia despite hypercellular bone marrow Most never develop AML Infection & bleeding lead to death before leukemia occurs
MTBS2CK p.223224
MTBS2CK p.224
19
MyelodysplasticSyndrome Many present with asymptomatic pancytopenia on routine CBC Symptoms can be... Fatigue & weight loss Infection Bleeding Sometimes splenomegaly No single pathognomonic finding in history or physical examination
MyelodysplasticSyndrome/Diagnosis
CBC: anemia with increased MCV, nucleated red cells, and small number of blasts Marrow: hypercellular Prussian blue stain shows ringed sideroblasts Severity based on percentage of blasts
MTBS2CK p.224
MTBS2CK p.224225
MyelodysplasticSyndrome/Treatment
ChronicLymphocyticLeukemia
CLL is a clonal proliferation of normal, mature-appearing B lymphocytes that function abnormally Occurs over age 50 in 90% affected Most asymptomatic at presentation Most common symptom is fatigue Other symptoms:
Lymphadenopathy (80%) Spleen or liver enlargement (50%) Infection
Transfuse blood products as needed Erythropoietin: about 20% response Lenalidomide for those with 5q deletion Decreases transfusion dependence
No unique physical findings Richter phenomenon: Conversion of CLL into high-grade lymphoma Occurs in 5%
ChronicLymphocyticLeukemia/Diagnosis WBC usually > 20,000/L 80% to 98% lymphocytes Half are hypogammaglobulinemic Anemia & thrombocytopenia occur from marrow infiltration or autoimmune warm IgG antibodies
ChronicLymphocyticLeukemia/Treatment Stage 0 (elevated WBC) & stage I (lymphadenopathy); no treatment Stage II (hepatosplenomegaly), stage III (anemia), and stage IV (thrombocytopenia) treat with fludarabine If choices list fludarabine and rituximab, , this is the best initial therapy for advanced-stage disease (II, III, IV) or any patient who is symptomatic (severe fatigue, painful nodes) PCP prophylaxis is indicated in CLL
Smudge cell: Lab artifact Nucleus crushed by cover slip
MTBS2CK p.225
MTBS2CK p.226
20
ChronicLymphocyticLeukemia/Treatment Refractory cases: cyclophosphamide (more efficacy, but more toxic) Mild cases: chlorambucil Severe infection: IVIG Autoimmune thrombocytopenia or hemolysis: prednisone
HairyCellLeukemia Middle-aged men with:

Pancytopenia Massive splenomegaly Monocytopenia Inaspirable dry tap, despite hypercellularity of marrow
The most accurate test is...

Tartrate resistant acid phosphatase (TRAP) or CD11c
Treat with cladribine
MTBS2CK p.226
MTBS2CK p.226
NonHodgkinLymphoma Proliferation of lymphocytes in nodes and spleen NHL most often widespread at presentation NHL and CLL are extremely similar NHL is solid mass and CLL is liquid or circulating
Lymphoma
NonHodgkinLymphoma HodgkinDisease MultipleMyeloma MGUS WaldenstrmMacroglobulinemia
MTBS2CK p.226
NonHodgkinLymphoma Painless lymphadenopathy May involve pelvic, retroperitoneal, or mesenteric structures Nodes not warm, red, or tender B symptoms:
Fever, Fever weight loss loss, drenching night sweats
NonHodgkinLymphoma Best initial test is...

Excisional biopsy
CBC normal in most cases High LDH correlates with worse severity Staging determines intensity of therapy Typical staging procedures are:
CT scan of chest, abdomen, and pelvis Bone marrow biopsy
Advanced stages in 80% to 90% of cases
MTBS2CK p.227
MTBS2CK p.227
21
NonHodgkinLymphoma Staging Stage I: 1 lymph node group Stage II: 2+ lymph node groups on same side of diaphragm Stage III: both sides of diaphragm Stage IV: widespread disease Most common wrong answer is needle aspiration of node. Aspiration not enough because individual lymphocytes appear normal.
NonHodgkinLymphoma/Treatment Local disease (Stage Ia and IIa): local radiation Advanced disease (Stage III and IV, any B symptoms): combination chemotherapy with CHOP and rituximab (antibody against CD20) C = cyclophosphamide H = adriamycin (doxorubicin or hydroxydaunorubicin) O = vincristine (oncovin) P = prednisone Mucosal Associated Lymphoid Tissue
Lymphoma of stomach is associated with Helicobacter pylori Treat with clarithromycin and amoxicillin
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MTBS2CK p.227
HodgkinDisease Presentation, diagnostic tests, B symptoms, and staging of Hodgkin disease (HD) are same as NHL Hodgkin disease has Reed-Sternberg cells on pathology
Normal lymphocyte ReedSternberg cell
DifferencesbetweenHDandNHL HodgkinDisease
Local,StageI,andStageIIin 8090% Centersaroundcervicalarea gcellson ReedSternberg pathology
NonHodgkinLymphoma
StageIIIandStageIVin8090%
Disseminated gcells NoReedSternberg
Pathologicclassification: Pathologicclassification: Lymphocytepredominanthas Burkitt andimmunoblastic bestprognosis haveworstprognosis Lymphocytedepletedhas worstprognosis

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MTBS2CK p.228
HodgkinDisease/Treatment Stage Ia and IIa: local radiation and Chemo Stage III and IV or anyone with B symptoms: ABVD A = adriamycin (doxorubicin) B = bleomycin Relapses after radiation V = vinblastine therapy are treated with D = dacarbazine chemotherapy. Relapses after chemotherapy are treated with extra high dose chemotherapy and bone marrow transplantation.
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HodgkinDisease/Treatment Complications of Radiation and Chemotherapy Radiation increases the risk of solid tumors such as breast cancer or lung cancer Screening for breast cancer earlier after treatment Radiation increases premature coronary disease The risk of acute leukemia, MDS, and NHL from chemotherapy is about 1% per year
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Which of the following is most useful to determine dosing of chemotherapy in HD? The other choices arent as a. Echocardiogram accurate in determining left b. Bone marrow biopsy ventricular function c. Gender d MUGA or nuclear ventriculogram d. e. Hematocrit f. Symptoms
HodgkinDisease/ AdverseEffectsofChemotherapy
ChemotherapeuticAgent Doxorubicin Vincristine Bleomycin Cyclophosphamide Cisplatin
Toxicity Cardiomyopathy Neuropathy Lungfibrosis Hemorrhagiccystitis Renalandototoxicity
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MTBS2CK p.229
MultipleMyeloma Abnormal proliferation of plasma cells Unregulated production of useless immunoglobulin Usually IgG or IgA Immunoglobulins dont fight infection, but clog up the kidney IgM is a separate disease called Waldenstrm macroglobulinemia
MultipleMyeloma Most common presentation is...

Bone pain from pathologic fractures
Pathologic fracture: bone breaks under normal use Due to osteoclast activating factor (OAF), which attacks the bone causing lytic lesions OAF hypercalcemia Infection common because abnormal plasma cells dont make immunoglobulins effective against infection
MTBS2CK p.229
MTBS2CK p.229
MultipleMyeloma Hyperuricemia: increased turnover of nuclear material of plasma cells Anemia: from infiltration of marrow with plasma cells Renal failure: from immunoglobulins and BenceJones p protein in kidney; y; hypercalcemia yp and hyperuricemia also damage the kidney Renal failure and infection are MCCs of death
MultipleMyeloma First test done is X-ray of affected bone shows lytic lesions Serum protein electrophoresis (SPEP) shows an IgG (60%) or IgA (25%) spike of a single type or clone. One clone = Monoclonal or M spike p Fifteen percent have light chains or Bence-Jones protein only
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MultipleMyeloma Additional abnormalities Hypercalcemia Bence-Jones protein on urine immunoelectrophoresis Beta-2 microglobulin levels correspond to severity of disease Smear with rouleaux Elevated BUN and creatinine Bone marrow biopsy: >10% plasma cells defines myeloma Elevated total protein with normal albumin
MultipleMyeloma
Rouleaux IgG paraprotein sticks to red cells causing them to adhere to each other in a stack or roll
MTBS2CK p.230
MTBS2CK p.230
MultipleMyeloma
69-year-old woman admitted with severe back pain that suddenly worsened--pop felt when she coughs and tenderness over ribs. X-ray: lytic lesions. Calcium is 2 points above normal, Hct 27%, creatinine elevated. UA: trace protein, but 24-hour urine show 5 grams of protein. What do you expect on technetium bone scan? a. Normal b. Lytic lesions at site of fractures c. Increased uptake diffusely d. Decreased uptake Nuclear bone scan shows increased
M-spike on SPEP doesnt mean IgM

Myeloma has a decreased anion gap. IgG is cationic. Increased cationic substances will increase chloride and bicarbonate levels. This decreases the anion gap.
uptake with osteoblastic activity, which is absent in myeloma.
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MTBS2CK p.230
Why the difference between the protein on urinalysis and 24-hour urine?
a. b. c. d. e. False positive 24-hour urine is common in myeloma Calcium in urine creates false negative urinalysis Uric acid creates a false positive 24-hour 24 hour urine Bence-Jones protein isnt detected by dipstick. IgG in urine inactivates urine dipstick Bence-Jones protein is detected by urine immunoelectrophoresis. Urine dipstick detects only albumin.
MTBS2CK p.230
What is the single most accurate test for myeloma? a. Skull X-rays Will show lytic lesions, but not as specific b. Bone marrow biopsy Nothing besides myeloma is associated with > 10% plasma c. 24-hour urine Of those with an M-spike cells on bone marrow biopsy of immunoglobulins, 99% d. SPEP dont have myeloma. e. Urine U i immunoelectrophoresis i l t h i Most IgG spikes are (Bence-Jones protein) from monoclonal
gammopathy of unknown significance that doesnt progress or need treatment.
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MultipleMyeloma/Treatment Best initial therapy is...

Combination of steroids with lenalidomide, bortezomib, or melphalan
MonoclonalGammopathyof UnknownSignificance IgG or IgA spike on SPEP is common in older patients Evaluate with bone marrow biopsy to exclude myeloma Monoclonal gammopathy of unknown significance (MGUS) has small numbers of plasma cells No therapy for MGUS 1% a year transform into myeloma The quantity of immunoglobulin in the spike is main correlate of risk for myeloma: More MGUS = More myeloma
MTBS2CK p.231
Most effective therapy under age 70 is autologous bone marrow transplant with stem cell support
Myeloma therapy is in a state of rapid flux due to numerous advances
MTBS2CK p.231
WaldenstrmMacroglobulinemia Overproduction of IgM Malignant B cells lead to hyperviscosity Presents with... Lethargy Blurry Bl vision i i and d vertigo ti Engorged blood vessels in eye Mucosal bleeding Raynaud phenomenon
WaldenstrmMacroglobulinemia Anemia common IgM spike on SPEP results in hyperviscosity No bone lesions Plasmapheresis is best initial therapy Removes IgM and viscosity L Long-term t treatment t t t with ith chlorambucil hl b il or fludarabine and prednisone Control cells that make abnormal Igs Decrease means of production
MTBS2CK p.231
MTBS2CK p.231
BleedingDisorders First step in evaluation is determining if bleeding is from platelets or clotting factors Platelet Bleeding Superficial Epistaxis, gingival, petechiae, purpura, gums, vaginal bleeding Factor Bleeding Deep Joints and muscles
BleedingDisorders
ITP VonWillebrandDisease Hemophilia FactorXIDeficiency DIC Thrombophilia HeparinInducedThrombocytopenia
Bleeding in brain or GI system can be from either platelet or clotting factor deficiency
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Immune(Idiopathic)ThrombocytopenicPurpura(ITP)
Look for... Isolated thrombocytopenia

Normal Hct Normal N l WBC count t
23-year-old woman comes to ED with increased menstrual bleeding, gum bleeding when she brushes her teeth, and petechiae. Platelet count: 17,000/L (low) What is the next step in therapy? a. Bone marrow biopsy b. Intravenous immunoglobulins c. Prednisone d. Antiplatelet antibodies e. Platelet transfusion
MTBS2CK p.232
Normal-sized spleen
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Prednisone is more important than checking for increased megakaryocytes or antiplatelet antibodies, which is characteristic of ITP.
ITP
ITP/Treatment
Diagnosis of exclusion Occasional tests are:

Antiplatelet antibodies lack specificity, limited benefit Ultrasound or CT scan to exclude hypersplenism Megakaryocytes are elevated in number
Presentation
Nobleeding,count>30,000 Mildbleeding,count<30,000 Severebleeding(GI/CNS), count<10,000 Recurrentepisodes,steroid dependent Splenectomyorsteroidsnot effective
Management
Notreatment Glucocorticoids IVIG,AntiRho(antiD)
Splenectomy Romiplostimoreltrombopag for recurrencesaftersplenectomy Rituximab,azathioprine, cyclosporine,mycophenolate
MTBS2CK p.232
MTBS2CK p.233
ITP
VonWillebrandDisease(VWD) Most common inherited bleeding disorder Von Willebrand factor (VWF) level or function Autosomal dominant Look for bleeding related to platelets (epistaxis, gingival, gums) with normal platelet count Markedly worsened after aspirin aPTT elevated in 50% of patients
Before splenectomy, give vaccination to: Neisseria meningitidis Hemophilus influenzae Pneumococcus
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MTBS2CK p.233
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VonWillebrandDisease(VWD) Diagnosis Bleeding time: increased duration of bleeding VWF (antigen) level may be decreased Ristocetin cofactor assay: detects VWF dysfunction Treatment Initial therapy: DDAVP (desmopressin), which releases subendothelial stores of VWF If no response, use factor VIII replacement or VWF concentrate
MTBS2CK p.233
Hemophilia Look for... Delayed joint or muscle bleeding in male child

Bleeding delayed because primary hemostatic plug is with platelets

Specific assay for factor VIII or IX
Prothrombin time (PT) normal aPTT prolonged
Mixing studies with normal plasma correct aPTT to normal Treat mild cases with DDAVP Severe bleeding treated with replacement of specific factor
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FactorXIDeficiency Most of time, no increase in bleeding with factor XI deficiency With trauma or surgery, theres increased bleeding Look for... Normal PT with p prolonged g aPTT Mixing study: corrects aPTT to normal Treatment Use FFP to stop bleeding
DisseminatedIntravascularCoagulation(DIC) DIC doesnt occur in otherwise healthy people Look for a definite risk such as...
Sepsis Burns Abruptio placenta or amniotic fluid embolus Snake bites Trauma resulting in tissue factor release Cancer
Theres bleeding related to both clotting factor deficiency as well as thrombocytopenia
MTBS2CK p.234
MTBS2CK p.234
DisseminatedIntravascularCoagulation(DIC)
DisseminatedIntravascularCoagulation(DIC)
Diagnostic Tests Elevated PT and aPTT Low platelet count Elevated D-dimer & fibrin split products Decreased fibrinogen level (has been consumed)
Treatment Replace platelets < 50,000/L as well as clotting factors with FFP Heparin has no benefit Cryoprecipitate C i it t may be b effective ff ti to t replace fibrinogen levels if FFP doesnt control bleeding
MTBS2CK p.234
MTBS2CK p.235
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HypercoaguableStates/Thrombophilia
HeparinInducedThrombocytopenia HIT more common with unfractionated heparin

Can still occur with LMW heparin
MCC:
Factor V Leiden mutation
No difference in intensity of anticoagulation Warfarin to INR of 2 2-3 3 for 6 months
Presents 5 to 10 days after start of heparin with a marked drop in platelet count (> 30%) Both venous and arterial thromboses occur
Venous clots more common
HIT rarely leads to bleeding Platelets just precipitate out Diagnostic Tests HIT confirmed with ELISA for platelet factor 4 (PF4) antibodies or serotonin release assay
MTBS2CK p.235
MTBS2CK p.235
HeparinInducedThrombocytopenia Treatment Immediately stop all heparin-containing products Cant just switch unfractionated heparin to LMW heparin Direct thrombin inhibitors
Argatroban, Argatroban lepirudin, lepirudin and bivalirudin
AntiphospholipidSyndromes Two main syndromes - lupus anticoagulant and anticardiolipin antibody Both cause thrombosis Anticardiolipin antibodies associated with multiple spontaneous abortions Antiphospholipid (APL) syndromes specifically cause thrombophilia with abnormal aPTT
After direct thrombin inhibitor is started, use warfarin
MTBS2CK p.235
MTBS2CK p.235
AntiphospholipidSyndromes Best initial test is...

Mixing study
Because its a circulating inhibitor, aPTT remains elevated after mix Most accurate test for lupus anticoagulant is...
Russell viper venom test
Treatment Treat with heparin and warfarin as you would for any cause of DVT or PE APL syndrome may require lifelong anticoagulation
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IntroductiontoAntibiotics InfectiousDiseases
PrinciplesofAnsweringQuestions BetalactamAntibiotics Fluoroquinolones Aminoglycosides Doxycycline Trimethoprim/Sulfamethoxazole Betalactam/BetalactamaseCombinations SpecificOrganismGroupsandTheirTreatments
IntroductiontoAntibiotics
IntroductiontoAntibiotics
Organisms associated with diseases dont change But antibiotics that treat them change M Most t important i t t thing thi Antibiotics associated with each group of organisms
Principles of Answering Infectious Diseases Questions The radiologic test is never the most accurate test Risk factors for an infection aren arent t as important as individual presentation Beta-lactam antibiotics have greater efficacy than other classes
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MTBS2CK p.3
BetalactamAntibiotics
Penicillins
Penicillins, Cephalosporins, Carbapenems, Aztreonam Penicillins Penicillin ( (G, , VK, , benzathine) )

Viridans group streptococci Streptococcus pyogenes Oral anaerobes Syphilis Leptospira
MTBS2CK p.3
Ampicillin and amoxicillin

Cover same organisms as penicillin And E. coli Lyme disease Gram-negative bacilli (few)
MTBS2CK p.3
Penicillins
Penicillins
Answer as Best Initial Therapy for Gram-negative bacteria covered by amoxicillin H. influenzae E. coli Listeria Proteus Salmonella
Otitis media Dental infection and endocarditis prophylaxis Lyme disease limited to rash, joint, or 7th CN involvement UTI in pregnant women Listeria monocytogenes Enterococcal infections
MTBS2CK p.4
MTBS2CK p.3
Penicillins
Penicillinaseresistantpenicillins(PRPs)
Oxacillin, Cloxacillin, Dicloxacillin, and Nafcillin Skin infections: Cellulitis Endocarditis, meningitis, and bacteremia from staphylococci Osteo & Septic arthritis only when proven sensitive Not against Methicillin-Resistant Staphylococcus aureus (MRSA) or Enterococcus
MTBS2CK p.4
Methicillin is never right Causes allergic interstitial nephritis Methicillin sensitive or resistant means oxacillin sensitive or resistant.
MTBS2CK p.4
Penicillins
Piperacillin,Ticarcillin,Azlocillin,Mezlocillin
Piperacillin, Ticarcillin Gram-negative bacilli (e.g., E. coli, Proteus) enterobacteriaciae & pseudomonads Best initial therapy
Cholecystitis & ascending cholangitis Pyelonephritis Bacteremia Hospital-acquired and ventilator-associated pneumonia Neutropenia and fever
MTBS2CK p.4
Also for: streptococci and anaerobes BUT NOT the answer, infection exclusively from these single organisms Use narrower agent Combined with a beta-lactamase inhibitor such as tazobactam or clavulanic acid
MTBS2CK p.4
Cephalosporins Cross-reaction penicillin & cephalosporins is
Cephalosporins
Very small (3% to 5%)

All cephalosporins, in every class, will cover group A, B, and C streptococci, viridans group streptococci, E. coli, Klebsiella, and Proteus mirabilis
If the case describes a rash to penicillin Answer cephalosporins If the case describes anaphylaxis You must use a non-beta-lactam antibiotic
Listeria, MRSA, and Enterococcus are resistant to all forms of cephalosporins.

FirstGeneration
SecondGeneration
Cefazolin, Cephalexin, Cephradrine, Cefadroxyl 1st-gen cephalosporins treat Staphylococci

Methicillin sensitive = oxacillin sensitive = cephalosporin sensitive
Cefotetan, Cefoxitin, Cefaclor, Cefprozil, Cefuroxime, Loracarbef

Cover same organisms as 1st-gen cephalosporins AND Add coverage for anaerobes & more gram-negative bacilli
Streptococci (except Enterococcus) Some gram-negative bacilli such as E. coli, but not Pseudomonas Osteomyelitis, septic arthritis, endocarditis, cellulitis
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MTBS2CK p.5
SecondGeneration Cefotetan, Cefoxitin, Cefaclor, Cefprozil, Cefuroxime, Loracarbef Cefotetan or cefoxitin Best initial therapy for pelvic inflammatory disease (PID) combined with doxycycline Warning Cefotetan and cefoxitin risk of bleeding and give a disulfiram-like reaction with alcohol Cefuroxime, loracarbef, cefprozil, cefaclor Respiratory infections (e.g., bronchitis, otitis media, and sinusitis)
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ThirdGeneration
Ceftriaxone, Cefotaxime, Ceftazidime Ceftriaxone First-line for pneumococcus, including partially insensitive organisms
Meningitis Community-acquired pneumonia (in combination with macrolides) Gonorrhea Lyme involving heart or brain Avoid ceftriaxone in neonates because of impaired biliary metabolism
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ThirdGeneration
FourthGeneration
Cefotaxime
Superior to ceftriaxone in neonates Spontaneous bacterial peritonitis

C ft idi Ceftazidime has h pseudomonal d l coverage
Cefepime Better staphylococcal coverage compared with the 3rd-generation cephalosporins Neutropenia and fever Ventilator-associated pneumonia
Ceftaroline: only cephalosporin to cover MRSA
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MTBS2CK p.5
Carbapenems
Monobactams
Imipenem, Meropenem, Ertapenem, Doripenem Cover gram-negative bacilli, including many thatre resistant Anaerobes Streptococci and staphylococci Neutropenia and fever Ertapenem differs from other carbapenems. Ertapenem does not cover Pseudomonas
MTBS2CK p.6
Aztreonam Only monobactam used
Exclusively
Gram-negative bacilli Including I l di Pseudomonas P d
No cross-reaction with penicillin
MTBS2CK p.6
Fluoroquinolones
Fluoroquinolones
Ciprofloxacin, Gemifloxacin, Levofloxacin, Moxifloxacin
Community-acquired pneumonia, including penicillin-resistant pneumococcus Gram-negative bacilli including most pseudomonads Cipro: NOT for pneumococcus
Ciprofloxacin: Cystitis and pyelonephritis Moxifloxacin: Not for urine/cystitis Diverticulitis and GI infections Combined with metronidazole Don Dont t cover anaerobes except moxifloxacin Moxifloxacin as single agent for diverticulitis without metronidazole
MTBS2CK p.6
MTBS2CK p.6
Fluoroquinolones
Fluoroquinolones
Quinolones cause Bone growth abnormalities in children and pregnant women Tendonitis and achilles tendon rupture Gatifloxacin removed because of glucose abnormalities
Source: Grook Da Oger, commons.wikimedia.org
MTBS2CK p.6
MTBS2CK p.6
Aminoglycosides
Doxycycline
Gentamicin, Tobramycin, Amikacin Gram-negative bacilli (bowel, urine, bacteremia) Synergistic with beta-lactam beta lactam antibiotics for enterococci and staphylococci No effect against anaerobes (need oxygen to work) Nephrotoxic and ototoxic
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Chlamydia Lyme Rash Joint 7th CN palsy MRSA skin
MTBS2CK p.7
Target-shaped rash of Lyme disease or erythema migrans. Source: Nishith Patel.
Doxycycline
Trimethoprim/Sulfamethoxazole
Rickettsia Syphilis: Primary & secondary ONLY if allergic to penicillin Borrelia, Ehrlichia, and Mycoplasma Ad Adverse effects ff t Tooth discoloration (children) Fanconi syndrome (Type II RTA proximal), photosensitivity Esophagitis
MTBS2CK p.7
Cystitis Pneumocystis pneumonia treatment and prophylaxis MRSA of skin and soft tissue (cellulitis) Rash Hemolysis (G6PD deficiency) Marrow suppression (folate antagonist)
Nitrofurantoin has one indication: Cystitis, especially in pregnant women.
MTBS2CK p.7
Betalactam/BetalactamaseCombinations
Amoxicillin/clavulanate Ticarcillin/clavulanate Ampicillin/sulbactam Piperacillin/tazobactam Beta lactamase adds staphylococci effect Beta-lactamase Sensitive Staph only
GramPositiveCocci:Staphylococciand Streptococci
Best initial therapy: Oxacillin, cloxacillin, dicloxacillin, nafcillin First-generation cephalosporins: Cefazolin, cephalexin Fluoroquinolones Macrolides (azithromycin, clarithromycin, erythromycin) are third-line
Less efficacy than oxacillin or cephalosporins Erythromycin more toxic
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MTBS2CK p.7
Oxacillin(Methicillin)ResistantStaph
Anaerobes
Vancomycin Linezolid: Reversible bone marrow toxicity Daptomycin Tigecycline Ceftaroline

Minor MRSA infections of skin are treated with: TMP/SMX Clindamycin Doxycycline
Oral (above diaphragm) Penicillin (G, VK, ampicillin, amoxicillin) Clindamycin Metronidazole (GI) Piperacillin, carbapenems, and 2nd-generation cephalosporins also cover anaerobes
MTBS2CK p.7
MTBS2CK p.8
GramNegativeBacilli(E.coli,Klebsiella, Proteus,Pseudomonas,Enterobacter,Citrobacter)
Bowel (peritonitis, diverticulitis) Urinary tract (pyelonephritis) Cholecystitis or Cholangitis

Quinolones Aminoglycosides Carbapenems Piperacillin, ticarcillin Aztreonam Cephalosporins
MTBS2CK p.8
Man admitted with E. coli bacteremia. Which of the following is the most appropriate therapy?
a. Vancomycin b. Linezolid c. Quinolones, aminoglycosides, carbapenems, piperacillin, ticarcillin, or aztreonam d. Doxycycline They dont cover grame. Clindamycin negative bacilli. f. Oxacillin
MTBS2CK p.8
CentralNervousSystem(CNS)Infections
CentralNervousSystemInfections
Meningitis g Encephalitis
All CNS infections give Fever Headache Vomiting Seizures
MTBS2CK p.9
CluestoAnsweringthe MostLikelyDiagnosisQuestion
Meningitis/Definition
Symptom Stiffneck Photophobia Meningismus Confusion Focalneurological findings

MTBS2CK p.
Diagnosis Meningitis
Infection/inflammation of CNS covering
Encephalitis Abscess
Source: SVG by Mysid, original by SEER Development Team commons.wikimedia.org
Meningitis/Etiology:4bugs95%ofcases Streptococcus pneumonia (60%) Group B streptococci (14%) Haemophilus influenzae (7%) Neisseria meningitidis (15%) Listeria (2%) Staphylococcus with recent neurosurgery
Meningitis/Presentation
Fever Headache Neck stiffness (nuchal rigidity) Photophobia

Patient with Neck stiffness. Source: Sophian, Abraham: Epidemic cerebrospinal meningitis (1913), St. Louis, C.V Mosby , commons.wikimedia.org
S. Pneumoniae Source: CDC/Dr. M.S. Mitchell
MTBS2CK p.9
MTBS2CK p.9
Meningitis/Presentation
WhatistheMostLikelyDiagnosis?
AIDS with <100 CD4 cells/L Stiff Neck Photophobia Adolescent, petechial rash
Acute bacterial (presents in several hours) Focal abnormalities: 30% If confusion occurs, you wont be able to answer What is the most likely diagnosis? without a CT and lumbar puncture (LP) Cryptococcal meningitis: Slow several weeks
None Cryptococcus Camper/hiker Rash R h target-like lik shape Joint pain Facial palsy Tick remembered in 20% Camper/hiker Rash moves from arms/legs t trunk to t k Tick remembered in 60%
Neisseria
Viral
Pulmonary TB in 85%
Lyme disease
Rocky Mountain spotted fever (Rickettsia)
Tuberculosis
Meningitis/DiagnosticTests
CerebrospinalFluidEvaluation
Bacterial Cell count 1000s, Neutrophils Cryptococcus, Tuberculosis Viral Lyme,Rickettsia 10s100s 10s100s 10s100s Lymphocytes Lymphocytes Lymphocytes Possibly elevated Possibly decreased Negative Markedly elevated Maybelow Usually normal Usually normal Negative
Best initial test and Most accurate test Lumbar Puncture
Protein Elevated level Glucose Decreased level Stain Stain: and 5070%; Culture Culture: 90%
MTBS2CK p.10
Negative
MTBS2CK p.10
When Is Head CT the Best Initial Test? If before the LP, there is
Papilledema Seizures Focal neurological abnormalities Confusion
Blurred disc margin
Neuro exam needs patient who understands and follows instructions and answers questions
You cannot do an accurate neurologic exam if the patient is severely confused.

MTBS2CK p.10
Papilledema is a blurred, fuzzy disc margin from increased intracranial pressure. Source: Conrad Fischer, MD
MTBS2CK p.10
BacterialAntigenDetection (LatexAgglutinationTests)
If theres a contraindication to immediate LP, giving antibiotics is best initial step in management
Better B tt to t treat t t and d decrease the accuracy of a test than to risk permanent brain damage.
MTBS2CK p.10
Similar accuracy to Gram stain If positive, theyre extremely specific If negative, could still have infection Not sufficiently sensitive to exclude bacterial meningitis i iti When is a bacterial antigen test indicated? Those receiving antibiotics prior to LP Culture may be falsely negative
MTBS2CK p.11
WhatistheMostAccurateDiagnosticTest?
Tuberculosis Lyme and Rickettsia Cryptococcus Viral
Meningitis/Treatment Bacterial: Ceftriaxone, Vancomycin, and Steroids Base treatment answer on cell count Culture Needs 2 to 3 days Never available when treatment decision is made G Gram stain t i Good if positive False negative: 30% to 50% Protein & Glucose Nonspecific Doesnt allow treatment decision
MTBS2CK p.11
Specific serologic testing, ELISA, western blot, PCR Acid fast stain and culture on 3 high-volume lumbar punctures Centrifuge to concentrate the organisms TB has high CSF protein Uncentrifuged sample of CSF: 10% sensitivity
Diagnosis of exclusion
India ink is 60% to 70% sensitive
Cryptococcal antigen: > 95% sensitive and specific
MTBS2CK p.11
Meningitis/Treatment Steroids (dexamethasone) Lowers mortality only in S. pneumoniae Give when thousands of neutrophils present No culture results for several days
ListeriaMonocytogenes Resistant to cephalosporins Sensitive to penicillins Add Ampicillin to Ceftriaxone and Vancomycin if case describes risk factors for Listeria. Risks
Elderly Neonates Steroid use AIDS or HIV Immunocompromised (includes alcoholism) Pregnant
Thousands of neutrophils on CSF = ceftriaxone, vancomycin, and steroids. Add ampicillin if immunocompromised for Listeria.
MTBS2CK p.11
MTBS2CK p.11
Neisseriameningitidis
Neisseriameningitidis
Respiratory isolation Rifampin or Ciprofloxacin to close contacts Close contacts Major respiratory fluid contact Household contacts Kissing Sharing cigarettes or eating utensils
Routine school and work contacts are not close contacts Healthcare workers qualify only if they
Intubate patient Perform suctioning Or Have contact with respiratory secretions
MTBS2CK p.12
MTBS2CK p.12
Meningitis
Man comes to emergency department with fever, severe headache, neck stiffness, and photophobia. He has weakness in his left arm and leg. Whats the next step in management? a. Ceftriaxone, Vancomycin, and Steroids b. Head CT Focal neurological deficits, initiate therapy c. Ceftriaxone Almost always d. Neurology consultation wrong e. Steroids Not sufficient
Consultation is almost always a wrong answer on USMLE Step 2 CK
What is the most common neurological l i ld deficit fi it of f untreated bacterial meningitis? Eighth cranial nerve deficit or deafness.
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MTBS2CK p.12
Encephalitis Acute onset

Fever, and Confusion
What is the most accurate test of herpes encephalitis? a.Brain biopsy Less accurate than PCR b.PCR of CSF c MRI c.MRI
The radiologic test is never the most acc accurate rate test genital, skin lesions
Many causes
Herpes simplex (most common) ( )
Must do head CT first because of confusion
d.Viral culture of CSF Most accurate test for e.Tzanck prep Best initial test for genital lesion f. Serology for herpes (IgG, IgM) population
Useless, 95% positive
MTBS2CK p.12
MTBS2CK p.13
10
Encephalitis/Treatment
Acyclovir Best initial therapy (Herpes encephalitis) Famciclovir & Valacyclovir IV unavailable Foscarnet Acyclovir-resistant herpes
MTBS2CK p.13
A woman with herpes encephalitis confirmed by PCR gets 4 days of acyclovir. Her creatinine level rises. Whats the most appropriate next step in management? a. Stop acyclovir Important to treat
a Reduce the dose of acyclovir and hydrate a. b. Switch to oral famciclovir or valacyclovir c. Switch to foscarnet
Insufficient for herpes encephalitis > Nephrotoxicity than acyclovir
MTBS2CK p.13
OtitisMedia
HeadandNeckInfections
OtitisMedia Sinusitis Pharyngitis Influenza(TheFlu)
Redness Immobility Bulging Decreased light reflex Pain Decreased hearing Fever
Otitis media. Source: www.sharinginhealth.ca MTBS2CK p.13
OtitisMedia/DiagnosticTests/Treatment
Which of the following is the most sensitive physical finding for otitis media? a. Redness b. Immobility c. Bulging d. Decreased light reflex e. Decreased hearing
Tympanocentesis: Sample of fluid for culture Most accurate diagnostic test Choose tympanocentesis if: Multiple recurrences No response to multiple antibiotics
Theyre less sensitive

MTBS2CK p.1314
Radiologic tests for otitis are always the wrong answer

MTBS2CK p.14
11
OtitisMedia/Treatment
Amoxicillin: Best initial therapy If no response to amoxicillin or it recurs, answer: Amoxicillin/clavulanate Azithromycin A ith i or clarithromycin l ith i Cefuroxime or loracarbef Levofloxacin, gemifloxacin, moxifloxacin Quinolones are relatively contraindicated in children
MTBS2CK p.14
34-year-old woman with facial pain, discolored nasal discharge, bad taste in mouth, fever and facial tenderness. Which of the following is the most accurate diagnostic test? a Sinus biopsy or aspirate a.Sinus Radiologic test never the most b.CT scan accurate test c.X-ray d.Culture of the discharge Always the wrong answer for sinusitis e.Transillumination Doesnt provide precise microbiological diagnosis MTBS2CK p.14
Sinusitis
Culture of nasal discharge is always the wrong answer for sinusitis
34-year-old woman with facial pain, discolored nasal discharge, bad taste in her mouth, and fever. She has facial tenderness. What is the most appropriate next step, action, or management? a. a b. c. d. e. Linezolid doesnt cover Haemophilus CT scan Diagnosis is clear, radiologic testing X-ray unnecessary Amoxicillin and decongestant Erythromycin and decongestant
Poor coverage for S. pneumoniae Excellent for resistant g gram-positive, p
Use Sinus Biopsy or Aspirate Infection frequently recurs No response to different empiric therapies
MTBS2CK p.14
MTBS2CK p.15
Pharyngitis Pain on swallowing Enlarged lymph nodes in neck Exudate in pharynx Fever No cough and no hoarseness
Streptococcal pharyngitis. Source: James Heilman, MD
Pharyngitis/DiagnosticTests Best initial test: Rapid strep test An office/clinic-based test Finds group A beta-hemolytic streptococci in minutes Negative test excludes disease and no antibiotics are needed Positive rapid strep test = positive pharyngeal culture Small vesicles or ulcers: HSV or herpangina Membranous exudates: Diphtheria, Vincent angina, or EBV
MTBS2CK p.15
These features make the likelihood of streptococcal pharyngitis exceed 90%
MTBS2CK p.15
12
Pharyngitis/Treatment
Influenza(TheFlu)
1. Penicillin or amoxicillin is best initial therapy 2. Penicillin allergic:

Cephalexin (reaction only rash)
Clindamycin or macrolide (anaphylaxis)
Streptococcal pharyngitis treated to prevent rheumatic fever
Arthralgias/myalgias Cough Fever Headache Sore throat Nausea, vomiting, or diarrhea, especially in children
Source: Mikael Hggstrm
MTBS2CK p.15
MTBS2CK p.16
Influenza(TheFlu)
Influenza(TheFlu)/Treatment < 48 hours of symptoms: Oseltamivir, zanamivir Neuraminidase inhibitors shorten duration of symptoms Treats both influenza A and B > 48 hours of symptoms: Symptomatic treatment only Analgesics, rest, antipyretics, hydration
The most appropriate next step in management depends on time course from presentation Within 48 hours of onset Perform nasopharyngeal swab or wash Rapidly detects antigen associated with influenza
Oseltamivir and zanamivir dont successfully treat complications of influenza such as pneumonia.
BloodandWBCsinStool
InfectiousDiarrhea
BloodandWBCsinStool NoBloodorWBCsinStool
When you see...in the history the answer is. Poultry Salmonella Campylobacter: MCC associated with Guillain-Barre Syndrome E. coli 0157:H7Hemolytic Uremic Syndrome (HUS) Shigella: 2nd most common association with HUS
MTBS2CK p.16
13
BloodandWBCsinStool
BloodandWBCsinStool The Best initial test is: Blood and/or fecal leukocytes Wont determine specific organism Stool lactoferrin: Greater sensitivity iti it & specificity ifi it than stool leukocytes
Shellfish and cruise ships Vibrio parahaemolyticus: Shellfish, liver & skin disease Vibrio vulnificus: Hemochromatosis blood transfusions Hemochromatosis, Yersinia: High affinity for iron Antibiotics, white and red cells in stool Clostridium difficile
MTBS2CK p.16
WBCs in a stool sample (Methylene Blue Stain). Source: Bobjgalindo
Lactoferrin: Better answer than fecal leukocytes if one of the choices Most accurate test is stool culture
MTBS2CK p.16
No BloodNo WBCsinStool
Viral Giardia:
Camping/hiking and unfiltered fresh water
Treatment
Cryptosporidiosis:
AIDS <100 CD4 cells Test acid fast stain
Mild disease: Oral fluid replacement Severe disease: Fluid replacement and ciprofloxacin
Severe infectious diarrhea means: Hypotension Tachycardia Fever Abdominal pain Bloody diarrhea Metabolic acidosis
MTBS2CK p.17
Bacillus cereus: Vomiting Staphylococcus: Vomiting

Scombroid Most rapid onset Wheezing, flushing, rash Found in fish Treat with antihistamines
MTBS2CK p.1617
DiseaseSpecificTreatment
Organism Treatment
Disease SpecificTreatment Metronidazole, Giardia
Tinidazole Cryptosporidiosis TreatunderlyingAIDS, Ni Nitazoxanide id Fluidsupportasneeded Fluidsupportasneeded
Hepatitis
AcuteHepatitis ChronicHepatitis p
Viral B.cereus, Staphylococcus

MTBS2CK p.17
14
AcuteHepatitis/Definition/Etiology
AcuteHepatitis
Infection or inflammation of liver Majority of acute cases are viral hepatitis A/B Hepatitis C Rarely presents with acute infection Found on blood tests for liver function Evaluation of cirrhosis Hepatitis D Exclusively as coinfection of hepatitis B IDUs
MTBS2CK p.17
Hepatitis E Worst in pregnancy East Asia S Sex, Blood, Bl d M Mom: H Hepatitis titi B B, C C, D Food and water (enteric): Hepatitis A and E You Ate hepatitis A & you Eat hepatitis E
MTBS2CK p.18
AcuteHepatitis/Presentation
AcuteHepatitis/DiagnosticTests
No way to detect specific type from symptoms All forms present with: Jaundice Fever, F weight i ht loss, l and df fatigue ti Dark urine Hepatosplenomegaly Nausea, vomiting, abdominal pain
MTBS2CK p.18
Increased direct bilirubin Increased ratio of alanine aminotransferase (ALT) to aspartate aminotransferase (AST) Increased alkaline phosphatase
Aplastic anemia is a rare complication of acute hepatitis
MTBS2CK p.18
DiseaseSpecificDiagnosticTests
Which correlates with increased mortality?
a. b. c. d d. e.
Bilirubin Prothrombin time ALT AST Alkaline phosphatase
All can be markedly elevated and better fast, except PT
Hepatitis A, C, D, and E: Best initial diagnostic test IgM antibody: Acute infection IgG antibody: Resolution of infection Hepatitis C: Disease activity PCR RNA level = Amount of active viral replication Hepatitis C PCR level = First thing to change PCR drop = Improvement with treatment PCR rises = Treatment failure
MTBS2CK p.18
MTBS2CK p.18
15
SerologicPatterns
Acuteorchronic infection Resolved,old,past infection
SerologicPatterns
Vaccination Windowperiod
Surface antigen eantigen
Positive
Negative
Surface antigen eantigen
Negative
Negative
Positive
Negative PositiveIgG Positive
Negative
Negative PositiveIgM,then IgG Negative
Coreantibody PositiveIgMorIgG Surface antibody Negative
Coreantibody Negative Surface antibody Positive
MTBS2CK p.19
MTBS2CK p.19
Which becomes abnormal first after acquiring hepatitis B infection? a. b. c. d. e. f. Bilirubin Viral replication rises after S Ag e-antigen Surface antigen Measure of bodys Core IgM antibody response to infection ALT Anti-hepatitis B e-antibody Resolution
starting
Which of the following is the most direct correlate with the amount/quantity of active viral replication?
a. b. c. d. e. f.
Bilirubin e-antigen Doesnt tell quantity Surface antigen Core IgM antibody Measure of bodys response to infection ALT Anti-hepatitis B e-antibody
Will appear prior to resolution of all DNA polymerase activity
MTBS2CK p.19
MTBS2CK p.19
Which indicates you cant transmit infection (i.e., active infection has resolved)? a. Bilirubin normalizes b No e-antigen b. e antigen found Normalize long before viral replication stops. No viral replication No serological evidence of disease Will appear prior to resolution of all DNA polymerase activity
Which is the best indication of the need for treatment in chronic disease? b. e-antigen c. Surface antigen a. Bilirubin
c. No surface antigen found d. No core IgM antibody found e. ALT normalizes f. Anti-hepatitis B e-antibody
MTBS2CK p.1920
At least some active disease, it might be on the way to spontaneous resolution and d. Core IgM antibody wouldnt benefit e. ALT Measure of bodys f. Anti-hepatitis B e-antibody response to infection
MTBS2CK p.20
16
Acutehepatitis/Treatment Which of the following is the best indicator that a pregnant woman will transmit infection to her child? At least some active disease, it might a. Bilirubin be on the way to spontaneous b. e-antigen resolution and wouldnt benefit. c. Surface antigen Perinatal transmission: 10% if d. Core IgM antibody positive surface antigen, but eantigen is negative; 90% when e. ALT both positive f. Anti-hepatitis B, e-antibody Hepatitis A and E: Resolve spontaneously over weeks Almost always benign conditions Only acute hepatitis C Hepatitis B: gets medical therapy Ch i i Chronic in 10% No treatment for acute disease Hepatitis C: Use interferon, ribavirin and either telaprevir or boceprevir!!! Treatment decreases likelihood of chronic infection
MTBS2CK p.21
Measure of the bodys response to infection

MTBS2CK p.20
ChronicHepatitis/Treatment Chronic hepatitis B = Surface antigen > 6 months e-antigen = Elevated level of DNA polymerase Treat when BOTH surface and e-antigen are positive Entecavir, or Adefovir, or T Tenofovir, f i or Lamivudine, or Telbivudine, or Interferon (joint & muscle pain, depression, the flu) Interferon is an injection Interferon has most adverse effects
MTBS2CK p.21
ChronicHepatitis/Treatment Adverse effects of interferon: Arthralgia/myalgia Leukopenia & thrombocytopenia Depression & flu-like symptoms
Goal of hepatitis therapy: Reduce DNA polymerase Convert e-antigen to anti-hepatitis e-antibody
MTBS2CK p.21
RoleofLiverBiopsy
ChronicHepatitis
Fibrosis is a strong indication to begin therapy for either hepatitis B or C right away Fibrosis + Active Viral replication will progress to cirrhosis Cirrhosis: Irreversible Who will progress? Old terms chronic active or chronic persistent hepatitis are unhelpful DNA polymerase level is helpful
MTBS2CK p.21
ALT levels arent a good indication of chronic hepatitis activity. You can have significant infection with normal transaminase levels.
MTBS2CK p.21
17
TreatmentofChronicHepatitisC
TreatmentofChronicHepatitisC
Theres no way to determine the duration of infection with hepatitis C, since theres no equivalent of surface antigen test Most patients dont have acute symptoms PCR RNA viral load is elevated, patients If PCR-RNA should be treated with interferon and ribavirin and either boceprevir or telaprevir
Three Drugs! 80% resolution with 3 drugs Interferon AND Ribavirin AND either Telaprevir OR Boceprevir
Ribavirin causes anemia

Urethritis
SexuallyTransmittedDiseases
Urethritis Cervicitis PelvicInflammatoryDisease(PID) Syphilis GenitalWarts(CondylomataAcuminata) Pediculosis(Crabs) Scabies
Look for urethral discharge to answer What is the most likely diagnosis? Both urethritis & cystitis give: Dysuria Frequency Burning Cystitis: No discharge
MTBS2CK p.22
Urethritis/DiagnosticTests Best initial test Men: Urethral swab for Gram stain & WBCs Intracellular gram-negative diplococci = Neisseria gonorrhoeae Urine for nucleic acid amplification test (NAAT) detects gonorrhea and Chlamydia NAAT or DNA probe: Most accurate test Other causes of urethritis: Mycoplasma genitalium Ureaplasma Women: Self-administered vaginal swab
MTBS2CK p.22
Urethritis/Treatment
Combine: One drug for gonorrhea & one for Chlamydia Quinolones arent the best initial therapy because of resistance
Gonorrhea Chlamydia
Cefixime Ceftriaxone
Azithromycin Doxycycline
MTBS2CK p.22
18
Cervicitis
PID/Presentation
Cervical discharge Inflamed strawberry cervix Testing & treatment are identical to previous description for urethritis Except E t self-administered lf d i i t d vaginal i l swab b for NAAT
Lower abdominal tenderness Lower abdominal pain Fever Cervical motion tenderness Leukocytosis
Always to exclude pregnancy first!!
MTBS2CK p.22
MTBS2CK p.2223
PID/DiagnosticTests
LaparoscopyinPID
Cervical swab for: Culture DNA probe or nucleic acid amplification (NAAT) Tests clarify y need for treating gp partner Culture preferred to determine resistance Cervical testing isnt the most accurate test for PID.
MTBS2CK p.23
The most accurate test for PID Only rarely needed Laparoscopy is answer if: Diagnosis is unclear Symptoms persist despite therapy Recurrent episodes for unclear reasons
MTBS2CK p.23
PID/Treatment
Combination of medications for gonorrhea and Chlamydia Inpatient: Cefoxitin or cefotetan combined with doxycycline Outpatient: Ceftriaxone and doxycycline (possibly with metronidazole) Anaphylaxis to penicillin?: Levofloxacin and metronidazole (outpatient) Clindamycin and gentamicin (inpatient)
MTBS2CK p.23
UlcerativeGenitalDisease/ WhatIstheMostLikelyDiagnosis? Often impossible to determine specific diagnostic, visual characteristics Question must have sufficient evidence to g give answer
All genital ulcers can have inguinal adenopathy

MTBS2CK p.23
19
PresentationofSTDs
Historyandphysicalfindings Mostlikelydiagnosis
DiagnosticTests
Diagnosis Syphilis DiagnosticTest Darkfieldmicroscopy(Bestinprimary) VDRLorRPR(75%sensitiveinprimary) FTAorMHATP(confirmatory) Stain&culture(specialmedia)
Painlessulcer Painfululcer
Syphilis Chancroid (Haemophilus ducreyi) Lymphogranuloma venereum Herpessimplex
Chancroid(Haemophilus ducreyi) Lymphogranuloma venereum
Lymphnodestenderand suppurating Vesiclespriortoulcer andpainful

MTBS2CK p.23
Complementfixationtitersinblood Nucleicacidamplificationtestingon swab Tzanckprep:Bestinitialtest Viralculture:Mostaccuratetest
Herpessimplex
MTBS2CK p.24
DiagnosticTests
Treatment
Diagnosis Treatment
If dark-field is positive for spirochetes no further testing for syphilis is necessary necessary.
Syphilis
OnedoseIMbenzathine penicillin Doxycycline,ifpenicillinallergic
Chancroid Azithromycin (singledose) (Haemophilus ducreyi) Lymphogranuloma venereum Herpessimplex Doxycycline Acyclovir,valacyclovir,famciclovir Foscarnet foracyclovirresistant herpes
MTBS2CK p.24
MTBS2CK p.24
Syphilis/Presentation Woman comes to clinic with multiple painful genital vesicles. What is the next step in management? Primary Syphilis Painless genital ulcer with heaped-up indurated edges (it becomes painful if it becomes secondarily infected with bacteria) Painless adenopathy
a. Acyclovir orally y topically p y Worthless b. Acyclovir c. Tzanck prep not necessary

If the presentation is diagnostic testing is Most accurate test, but not necessary, if
RichardUsatine,M.D.Usedwithpermission
d. Viral culture vesicles are clear

infection in the past
e. Serology Cant distinguish genital infection from oral f. PCR

MTBS2CK p.24
PCR encephalitis, not genital
Chancres heal spontaneously even without treatment. Penicillin prevents later stages.
MTBS2CK p.25
20
Syphilis/Presentation
Syphilis/Presentation Tertiary Syphilis Neurosyphilis

Meningovascular (stroke from vasculitis) Tabes dorsalis (loss of position and vibratory sense, incontinence, cranial nerve)
Secondary Syphilis Rash (palms and soles) Alopecia areata Mucous patches Condylomata lata
Tabes Dorsalis . Source: CDC/Susan Lindsley
MTBS2CK p.25
phil.cdc.gov
MTBS2CK p.25
Syphilis/Presentation
SensitivityofDiagnosticTestsbyStage
Test VDRLorRPR FTAABS
Tertiary Syphilis Neurosyphilis

General paresis (memory and personality changes) Argyll Robertson pupil
Primary Secondary Tertiary
75%85% 99% 95%
95% 100% 98%
Aortitis (aortic regurgitation, aortic aneurysm) Gummas (skin and bone lesions)
MTBS2CK p.25
MTBS2CK p.25
Syphilis False positive VDRL/RPR Infection, older age, injection drug use, AIDS, malaria, antiphospholipid syndrome, and endocarditis Titers of VDRL or RPR are reliable at > 1:8 Lower titer is more often falsely positive High titers (> 1:32) are rarely false positive
MTBS2CK p.25
Syphilis/Treatment
Primary & secondary syphilis: Single IM injection of penicillin Oral doxycycline: Penicillin allergy Tertiary syphilis: IV penicillin Desensitize to penicillin if allergic
MTBS2CK p.25
21
Syphilis Jarisch-Herxheimer reaction Fever, headache, myalgias after treatment Give aspirin & antipyretics (itll pass)
GenitalWarts(CondylomataAcuminata)/ Diagnosis
Desensitization the answer for neurosyphilis and pregnant women
Papillomavirus Diagnose based on the visual appearance Wrong answers: Biopsy Serology Stain, smear, or culture
MTBS2CK p.26
Condylomata acuminata (genital warts). Source: Farshad Bagheri, MD.
MTBS2CK p.26
GenitalWarts(CondylomataAcuminata)/ Treatment
Pediculosis(Crabs)
Remove by physical means: Cryotherapy with liquid nitrogen Surgery for large ones Laser Melt with podophyllin or trichloroacetic acid Imiquimod: Apply locally (immunostimulant leads to sloughing off of lesion)
MTBS2CK p.26
Hair-bearing areas (axilla, pubis) Itchy Visible on surface Treat with permethrin; li d lindane i is equal li in efficacy, but more toxic
Pediculosis pubis. Source: commons.wikimedia. Used with permission
MTBS2CK p.26
Scabies Web spaces between fingers and toes or at elbows Around nipples near the genitals Burrows visible (they dig) but smaller than pediculosis Scrape & magnify
Scabies/Treatment
Permethrin Widespread disease: Oral Ivermectin Severe disease needs repeat dosing
Scabies burrow under the skin and must be scraped out to establish a diagnosis. Source: Conrad Fischer, MD.
MTBS2CK p.27
MTBS2CK p.27
22
UrinaryTractInfections(UTI)
UrinaryTractInfections
Cystitis Pyelonephritis y p AcuteProstatitis PerinephricAbscess
Present with dysuria (frequency, urgency, burning), maybe fever Urinalysis shows WBCs E. coli MCC Quinolones Best initial therapy Anatomic defects lead to UTIs:
Stones Strictures Tumor or prostate hypertrophy Diabetes
MTBS2CK p.27
UrinaryTractInfections
Cystitis
Foley catheter is a foreign body Neurogenic bladder is an obstruction

Frequency = Multiple episodes of micturation Polyuria = Increase in volume of urine
Presents with dysuria and: Suprapubic pain/discomfort Mild/absent fever

Men have anatomic abnormalities Women most often dont Best initial test: Urinalysis with > 10 WBCs Most accurate test: Urine culture
MTBS2CK p.27
MTBS2CK p.2728
Cystitis/Treatment
Trimethoprim/sulfamethoxazole (TMP/SMZ) if local resistance is low Ciprofloxacin Cephalexin Nitrofurantoin ( (Pregnant g women) ) All beta-lactam antibiotics are considered safe in pregnancy
36 year old generally healthy woman comes with urinary frequency and burning. UA: > 50 WBC What is the next step in management?
a. b. c. d. e.
TMP/SMZ for 3 days TMP/SMZ for 7 days With anatomic abnormality Urine culture No need of culture Ultrasound of urinary system or imaging when symptoms of cystitis CT scan of urinary system
MTBS2CK p.28
MTBS2CK p.28
are clear & WBCs in urine
23
Pyelonephritis
Pyelonephritis
Dysuria with: Flank or CVA tenderness High fever Occasional abdominal pain UA with high WBCs Imaging studies (CT or sonogram) look for anatomic abnormalities causing infection
MTBS2CK p.28
Treat with: Ampicillin & gentamicin Ciprofloxacin Change based on culture/sensitivity

Any drugs for gram-negative bacilli would be effective for pyelonephritis
MTBS2CK p.28
AcuteProstatitis
PerinephricAbscess
Dysuria with: Perineal pain Tender prostate on examination Diagnostic yield of urine culture greatly increased with p prostate massage g Treat same as you would for pyelonephritis Longer duration TMP/SMZ or ciprofloxacin for 6 to 8 weeks for chronic prostatitis
MTBS2CK p.29
Look for: Pyelonephritis not resolving with appropriate therapy When drug choice & dose are correct failure of infection to resolve is an anatomic problem Do sonogram or CT scan Drainage of fluid collection is mandatory Culture of infected fluid is essential to guide therapy
MTBS2CK p.29
Endocarditis/Definition
Endocarditis
Heart valve infection Leads to fever & murmur Diagnosis: Positive blood cultures Vegetations on echocardiogram
MTBS2CK p.29
24
Endocarditis/Etiology
Endocarditis/Etiology
Rare on normal heart valves (except IDUs) Risk proportional to degree of damage of valves Regurgitant & stenotic lesions have increased risk Prosthetic valves: Highest risk
Can develop on normal valves if: Severe bacteremia Highly pathogenic organisms (Staphylococcus aureus) Dental procedures with blood confer a small risk of endocarditis Surgery of mouth & respiratory tract confers no risk unless severe valve disease is present Artificial valve or cyanotic heart disease Endoscopy confers no risk even with biopsy
MTBS2CK p.29
MTBS2CK p.29
Endocarditis/ WhatIstheMostLikelyDiagnosis?
Endocarditis/Presentation/ WhatIstheMostLikelyDiagnosis?
Osler nodes (raised and painful) Roth spots in eyes Brain (mycotic aneurysm) Kidney (hematuria, glomerulonephritis) Conjunctival petechiae Splenomegaly Septic emboli to lungs
Fever New murmur or change in a murmur Complications of endocarditis

Splinter hemorrhages Janeway lesions (flat and painless)
MTBS2CK p.2930
Source: Splarka http://en.wikipedia.org/wiki/Splinter_hemorrhages
MTBS2CK p.30
Endocarditis/DiagnosticTests
Best initial test Blood culture (95%99% sensitive) If positive do an Echo Transthoracic echo (60% sensitive, but 95% specific) Transesophageal T h l echo h (95% sensitive iti and d specific) EKG rarely shows atrioventricular (AV) block if dissection of conduction system occurs (5% 10%)
A man comes into the ED with fever and a murmur. Blood cultures grow Streptococcus bovis. Transthoracic echocardiography shows vegetation. What is the next step in the management?
a. b b. c. d. e.
Colonoscopy vegetation. Transesophageal echocardiogram Will not show diverticuli CT of the abdomen Repeat the blood cultures No point, already positive Surgical valve replacement Premature
Transthoracic showed
Fever + murmur = endocarditis
MTBS2CK p.30
MTBS2CK p.3031
25
HowtoDiagnose CultureNegativeEndocarditis
Endocarditis/Treatment
1. Oscillating vegetation on echocardiography 2. Three minor criteria: Fever Risk: IDU or prosthetic valve Embolic phenomena
Empiric: Vancomycin and gentamicin When culture results are available Treat based on sensitivities
MTBS2CK p.31
MTBS2CK p.31
Organism Treatment
Organism Treatment
Viridans streptococci Staphylococcus aureus (sensitive) Fungal
Ceftriaxonefor4weeks Oxacillin,nafcillin,or cefazolin Amphotericinandvalve replacement
Staphylococcus epidermidis orresistant Staphylococcus Enterococci
Vancomycin
Ampicillin&gentamicin
MTBS2CK p.31
MTBS2CK p.31
Endocarditis
Endocarditis
Treatment of Resistant Organisms Add aminoglycoside & extend duration of treatment When Is Surgery the Answer? CHF or ruptured valve or chordae tendineae Prosthetic valves Fungal endocarditis Abscess AV block Recurrent emboli while on antibiotics
MTBS2CK p.31
Add rifampin for prosthetic valve endocarditis with Staphylococcus. The single strongest indication for surgery is acute valve rupture and CHF.
MTBS2CK p.3132
26
TreatmentofCultureNegativeEndocarditis
ProphylaxisforEndocarditis
Most common culture negative = Coxiella HACEK: Acronym for organisms difficult to culture causing endocarditis
Haemophilus aphrophilus Haemophilus parainfluenza Actinobacillus Cardiobacterium Eikenella Kingella
Use prophylaxis if theres BOTH: 1. Significant cardiac defect

Prosthetic valve Previous endocarditis Cardiac transplant recipient with valvulopathy Unrepaired cyanotic heart disease
AND! 2. Risk of bacteremia

Dental work with blood Respiratory tract surgery that produces bacteremia
MTBS2CK p.32
Use ceftriaxone for HACEK group

MTBS2CK p.32
Amoxicillin prior to procedure If penicillin allergic use clindamycin, azithromycin, or clarithromycin Procedures and anatomic abnormalities that do not need prophylaxis are: Flexible endoscopy, even with biopsy, ERCP Obstetrical and gynecologic procedures
MTBS2CK p.32
Urology procedures (including prostate biopsy) Mitral valve prolapse, even with murmur Mitral regurgitation, mitral stenosis, aortic regurgitation regurgitation, aortic stenosis stenosis, hypertrophic obstructive cardiomyopathy (HOCM), atrial septal defect (ASD)
MTBS2CK p.32
LymeDisease/Definition
LymeDisease
Arthropod-borne Spirochete: Borrelia burgdorferi What is the most common manifestation? Fever & Rash What is the most common manifestation if untreated? Joint pain Also: Cardiac or neurologic disease
MTBS2CK p.33
27
LymeDisease/Etiology
Transmitted by deer tick (Ixodes scapularis) Tick very small Only 20% patients recall bite
Patients recall being outdoors Hiking or camping Experimental models: Tick must be attached for at least 24 hours in order to transmit organism
Richard Usatine, M.D. Used with permission
MTBS2CK p.33
MTBS2CK p.33
LymeDisease/Presentation
Ixodes tick Northeast states: Connecticut (where the town of Lyme gave the disease its name) Massachusetts New York New Jersey
Rash: Most common manifestation (85% - 90%) Occurs 5-14 days after bite Fever often present
MTBS2CK p.33
cdc.gov
MTBS2CK p.33
Erythema migrans Round, red Pale center Target or bulls-eye
Joint pain 60% without treatment Oligoarthritis = few joints Joint fluid: ~ 25,000 WBCs/L Similar number to gout, pseudogout and many infections i f ti
The knee is the most commonly affected joint in Lyme disease.
Target-shaped rash of Lyme disease or erythema migrans. Source: Nishith Patel.
MTBS2CK p.3334
MTBS2CK p.33
28
Neurological manifestations 10% 15% CNS or peripheral Meningitis, encephalitis, or CN palsy

Bells palsy or 7th CN is most common neurological manifestation of Lyme disease.
Cardiac: 4% - 10% Any part of myocardium or pericardium Myocarditis or ventricular arrhythmia
Transient AV block is the most common cardiac manifestation in Lyme disease.
MTBS2CK p.33
MTBS2CK p.33
LymeDisease/DiagnosticTests
LymeDisease/Treatment
Manifestation Treatment
Typical rash doesnt need serologic testing to start treatment Serologic testing for Lyme is essential for: Joint Neurologic g Cardiac manifestations Most 7th CN palsy, arthralgia & AV block are not caused by Lyme Testing is with IgM, IgG, ELISA, Western blot, and PCR testing
MTBS2CK p.34
Asymptomatictickbite
Notreatment routinely Doxycycline Amoxicillin Doxycycline Amoxicillin IVceftriaxone
Rash
Joint,7th CNpalsy
Cardiacandneurologic manifestationsotherthan7th CN palsy

MTBS2CK p.34
AsymptomaticTickBite
Bites without symptoms rarely need treatment Who DOES need treatment? Single dose of doxycycline Within 72 hours of tick bite when:
Ixodes scapularis clearly identified as tick Tick attached for > 24-48 hours Engorged nymph-stage tick Endemic area
MTBS2CK p.34
HIV/AIDS
29
HIV/AIDS/Definition
A retrovirus infecting CD4 (T-helper) cells CD4 cells drop from normal (600-1000) at a rate of 50 to 100/year untreated 5 and 10 years before clinical manifestations Not HIV itself that leads to death Low CD4 leads to illness
MTBS2CK p.35
HIVlifecycle
Source: nih.gov
HIV/AIDS/Etiology
Transmitted by: IDU Sex, particularly men who have sex with men Transfusion (extremely rare since 1985) Perinatal Needle stick or blood-contaminated sharp instrument injury Kissing is not proven to transmit HIV.
MTBS2CK p.35
RiskofTransmissionofHIV WithoutProphylacticTreatment
Modeof transmission Vaginaltransmission Percentageofriskwitheachevent 1:30001:10,000forinsertiveintercourse 1:1000forreceptiveintercourse 1:1000forreceptivefellatiowithejaculation Unclearforinsertivefellatioorcunnilingus 1:300 1:100forreceptiveanalintercourse 25%30%perinataltransmissionwithout medication
Oralsex
Needlestickinjury Analsex Mothertochild

MTBS2CK p.35
HIV/AIDS/Presentation
HIV/AIDS/DiagnosticTests
Infections when CD4 drops < 50/L PCP < 200/L CD4 > 200/L (few infections occur) Infections > 200/L are:
Varicella zoster (shingles) Herpes simplex TB Oral and vaginal candidiasis Bacterial pneumonia
Best initial test: ELISA test Confirmed with Western blot Infected infants: Diagnose with PCR or viral culture ELISA testing is unreliable in infants Maternal HIV antibodies are present for up to 6 months after delivery
MTBS2CK p.35
MTBS2CK p.36
30
ViralLoadTesting(PCRRNAlevel)
ViralLoadTesting(PCRRNAlevel)
Measures response to therapy Decreasing levels good Detect treatment failure Rising levels bad Diagnoses HIV in babies
The goal of therapy is to drive down viral load Undetectable levels (< 50/L): CD4 will rise CD4 rises = Opportunistic infections stop Life expectancy when viral load is undetectable by PCR-RNA is equal in duration to HIV-negative person
MTBS2CK p.36
MTBS2CK p.36
ViralResistanceTesting(Genotyping)
HIV/AIDS/Treatment
Perform prior to initiating antiretroviral medications Decreases likelihood of starting medication to which patients virus is resistant Resistance testing: Evaluates treatment failure Guides choice of medications Select 3 drugs from 2 different classes to which patients virus is susceptible
MTBS2CK p.36
For HIV: Treatment is initiated when: CD4 < 500/L or Viral load is very high (>100,000/L) or Opportunistic infection occurs
MTBS2CK p.36
HIV/AIDS/Treatment
ChoiceofInitialAntiretroviralMedication Initial drug regimen:
Treatment failure first manifests with rising PCRRNA viral load
Emtricitabine, Tenofovir, and Efavirenz

USMLE Step 2 CK doesnt doesn t test dosing
MTBS2CK p.36
MTBS2CK p.36
31
ChoiceofInitialAntiretroviralMedication
AntiretroviralFirstlineMedicationsbyClass
Nucleosideand Non nucleotidereverse nucleoside transcriptase RTIs inhibitors(RTIs) Zidovudine Didanosine Stavudine Lamivudine Emtricitabine Abacavir Tenofovir Efavirenz Etravirine Nevirapine Proteaseinhibitors
Treatment failure: Rising viral load CD4 count decreases or fails to rise CD4 changes are slower than changes in viral load Alternate Drug Regimens If emtricitabine/tenofovir/efavirenz cannot be used because of resistance alternate regimens are based on combination of 3 drugs from at least 2 different classes
MTBS2CK p.37
Ritonavir Saquinavir Nelfinavir Amprenavir Fosamprenavir
Lopinavir Atazanavir Indinavir Tipranavir Darunavir
MTBS2CK p.37
AdditionalClassesofSecondlineAgents Used with drug resistance to multiple classes of first-line agents Entry inhibitors:
Enfuvirtide Maraviroc
PostexposureProphylaxis
Integrase inhibitor:
Raltegravir
All significant needle stick injuries Sexual exposures Bites Give 4 weeks of combination therapy Urine & stool arent an indication for postexposure prophylaxis (PEP)
USMLE Step 2 CK wont require you to know details of efficacy differences between classes.
PostexposureProphylaxis
AdverseEffectsofHIVMedications
Drug Zidovudine Adverseeffect Anemia Peripheralneuropathyandpancreatitis Hypersensitivity,StevensJohnson Reaction Hyperlipidemia,hyperglycemia Nephrolithiasis Renalinsufficiency
Postexposure prophylaxis isnt routinely indicated for needle stick injury if HIV status of needle is unknown
Stavudine anddidanosine Abacavir
Proteaseinhibitors Indinavir Tenofovir

32
PreventionofPerinatalTransmission
PreventionofPerinatalTransmission
Pregnant Patients If already on antiretroviral medications Continue same treatment If pregnant and not already on medications di ti Start combination antiretrovirals Only Efavirenz is NOT used in pregnancy
MTBS2CK p.38
After Delivery for Mother CD4 > 500 and she doesnt need them Stop after delivery CD4 < 500 or viral load high Continue after delivery Baby Zidovudine during delivery (intrapartum) AND For 6 weeks after to help prevent transmission
MTBS2CK p.38
IndicationsforAntiretrovirals DuringPregnancy
Condition Action
CesareanDeliveryforHIVPositiveMothers
Patientonantiretroviralsat Continuesamemedications, thetimeofpregnancy exceptswitchefavirenzto proteaseinhibitor Notonantiretrovirals, CD4loworviralloadhigh Initiateantiretrovirals immediately.Continueafter delivery Antiretroviralsimmediately, stoptheminmotherafter birth
Viral load >1000 L: Perform Cesarean delivery Everyone: Intrapartum zidovudine Fully controlled HIV (viral load undetectable) gives <1% transmission.
Notonantiretrovirals, CD4high andviralloadlow

MTBS2CK p.38
MTBS2CK p.39
33
Nephrology
EmmaHolliday, Holliday MD ResidentPhysician RadiationOncology UniversityofTexasMDAndersonCancerCenter
DiagnosticTests inNephrology
Urinalysis WhiteBloodCells Hematuria Cytoscopy Casts
Urinalysis Measures:
Protein WBCs or leukocyte esterase RBCs Specific gravity and pH Nitrites
Dipstickvs.Urinalysis Both give some quantitative values Dipstick described as direct (e.g., 300 mg protein) or scale number: 0, 1+, 2+, 3+, or 4+ Microscopic urinalysis reports number of cells/highpowered field
Pyuria with positive nitrites = UTI
Dont worry about the precise scale Every USMLE Step 2 CK test comes with a range of normal values attached to assess severity
MTBS2CK p.299
MTBS2CK p.299
Urinalysis/Protein Renal tubules secrete slight amounts of TammHorsfall protein

Should be < 30 to 50 mg/24 hours
Urinalysis/Protein 2 - 10% of population has transient proteinuria Benign reasons for proteinuria:
Orthostatic proteinura or physical exertion
If symptoms of proteinuria - best initial test? Urinalysis/Dipstick
Greater amounts of protein associated with either tubular disease or glomerular disease Very large amounts of protein excreted with glomerular disease 1+ proteinuria ~ 1g/day 2+ proteinura ~ 2g/day 3+ proteinuria ~ 3g/day 4+ proteinuria ~ 4g/day
MTBS2CK p.300
If positive, order urine protein to creatinine ratio or 24 hour urine collection Most accurate for determining etiology?
MTBS2CK p.300
Renal biopsy
Urinalysis/Proteinuria Limitations of dipstick for proteinuria: Only detects albumin Cant detect Bence Jones protein
Present in multiple myeloma Best test for Bence Jones proteinuria is UPEP (urine protein electrophoresis)
Urinalysis/Microalbuminuria
Microalbuminuria
Tiny amounts of protein too small to detect on UA
An important screening test in diabetic patients

Should be performed yearly
Cant detect very low amounts of protein
Long-term microalbuminuria
Leads to worsening renal function in diabetic patient and should be treated
Pyuria Diabetic patient is evaluated, UA shows no protein. Microalbuminuria is detected (level between 50 - 300 mg/24 hours). Whats the next best step in management? a. Enalapril b Kidney biopsy Extreme! We know the etiology already b. c. Hydralazine Less effective & with more adverse effects d. Renal consultation NEVER consult on Step 2 e. Low-protein diet Bad for glycemic control f. Repeat UA annually and treat when trace protein is Starting early will delay disease progression detected
MTBS2CK p.301
White blood cells in urine:

Inflammation Infection Allergic interstitial nephritis
Neutrophils cant be distinguished from eosinophils on UA Neutrophils indicate infection (UTI or urethritis) Eosinophils indicate allergic or acute interstitial nephritis (NOT NSAID-induced renal disease) Wright and Hansel stains detect eosinophils in the urine.
MTBS2CK p.301
Hematuria Etiology: Stones Coagulopathy Infection (cystitis, pyelonephritis) Cancer Cancer C T Treatments t t (cyclophosphamide) ( l h h id ) Trauma Glomerulonephritis False positive = hemoglobinuria or myoglobinuria Dysmorphic RBCs = glomerulonephritis
Woman is admitted with trauma and dark urine. The dipstick is markedly positive for blood. What is the best initial test? a. Microscopic examination of urine Overkill - best test to look for bladder mass b. Cystoscopy Best test for hydronephrosis c Renal ultrasound c. d. Renal/bladder CT scan Most accurate test for stones e. Abdominal X-ray Best test for ileus or to detect free air f. Intravenous pyelogram Never the right answer - slow
test uses nephrotoxic contrast
WhenIsCystoscopytheAnswer?
Casts Microscopic collections of material clogging up the tubules and being excreted in urine Type of cast Red cell White cell Eosinophil Hyaline Broad, waxy Granular, muddybrown
MTBS2CK p.302303
When theres hematuria without infection or prior trauma and:

The renal ultrasound or CT doesnt show etiology Bladder sonography shows mass for possible biopsy
Cystoscopy is the most accurate test of the bladder.
MTBS2CK p.302
Association Glomerulonephritis Pyelonephritis Acute interstitial nephritis Dehydration Chronic renal disease Acute tubular necrosis (are dead tubular casts)
AcuteKidneyInjury
Acute kidney injury (AKI)
AcuteKidneyInjury
AcuteTubularNecrosis Hepatorenal p Syndrome y Atheroemboli Acute(Allergic)InterstitialNephritis AnalgesicNephropathy
Decrease in creatinine clearance Results in sudden rise in BUN and creatinine
The definition is not based on specific values of BUN and creatinine Categories:
Prerenal azotemia (decreased perfusion) Postrenal azotemia (obstruction) Intrinsic renal disease (ischemia and toxins)
MTBS2CK p.303
Acute Kidney Injury

Prerenal Intrinsic Renal

AcuteKidneyInjury/Presentation
Post Renal
BPH/Prostate cancer Ureteral stone Cervical cancer Urethral stone Neurogenic bladder Retroperitoneal fibrosis (chemo or XRT)
AKI usually = asymptomatic rise in BUN and creatinine; when symptomatic:

Nausea and vomiting Fatigue/malaise Weakness SOB, edema (fluid overload)
ATN Hypotension - Toxins - Sepsis NSAIDs - Anaphylaxis AG, ampho Cis, Cis cyclosporine - Bleeding - Prolonged ischemia - Dehydration AIN Hypovolemia - PCN, sulfa Rhabdo/hemoglobinuria - Diuretics Contrast - Burns Crystals - Pancreatitis Bence-Jones proteins Post-strep infection - pump fxn - Low albumin - Cirrhosis MTBS2CK p.303304 artery stenosis Renal
Very severe disease presents with:

Confusion Arrhythmia from hyperkalemia and acidosis Sharp, pleuritic chest pain from pericarditis
MTBS2CK p.304305
AcuteKidneyInjury/DiagnosticTests
The best initial test is...

BUN and creatinine
What is the best initial imaging test?

Renal sonogram because it isnt invasive and doesnt need contrast
Nonfunctional kidneys creatinine rises ~ 1 point/day (1 mg/dL) If the BUN:creatinine BUN creatinine ratio is > 20 20:1 1 the etiology is either prerenal or postrenal damage Intrinsic renal disease ratio closer to 10:1
MTBS2CK p.305
Kidney biopsy is rarely the right answer for AKI
MTBS2CK p.305
AcuteKidneyInjury/DiagnosticTests When cause is unclear next best diagnostic step is:

Urinalysis Urine sodium (UNa) Fractional excretion of sodium (FENa) or urea (FEUrea) Urine osmolality
AcuteKidneyInjury/DiagnosticTests Urine Sodium and Fractional Excretion of Sodium Normal kidney:

blood pressure aldosterone aldosterone sodium reabsorption sodium in the urine (< 20)
Damaged kidney (e.g., ATN):

Kidneys cant reabsorb Na appropriately (> 20) Prerenal azotemia: low UNa (below 20) = low FENa (less than 1%) You can answer all the questions on USMLE Step 2 CK without knowing the mathematical formula for FENa.
If all of these are choices always go with urinalysis first
MTBS2CK p.306
MTBS2CK p.306
Urine Osmolality Normal kidney:

intravascular volume ADH ADH water reabsorption at collecting duct urine osmolarity
20-year-old African-American man has screening test for sickle cell. Hes found to be heterozygous (trait or AS) for sickle cell. Sickle cell trait rarely What is the best advice for him?experience pain crises
Damaged kidney (e.g., ATN):

Kidneys cant concentrate urine appropriately - will see Osm similar to blood (~300mOsm)
MTBS2CK p.306
a. b. c. d. e.
Nothing needed until he has a painful crisis y Avoid dehydration Hydroxyurea Only if > 4 pain crises per year. Folic acid supplementation Indicated if hemolysis Pneumococcal vaccination present (high RBC
Indicated if functionally asplenic turnover)
MTBS2CK p.307
ClassificationofAcuteRenalFailure
Test Prerenal azotemia Acutetubular necrosis
AcuteTubularNecrosis/Definition
BUN:Creatinine UrineSodium(UNa) F ti Fractional lexcretion ti ofsodium(FENa) Urineosmolality (UOsm)
>20:1 <20mEq/L <1%
<20:1 >20mEq/L >1%
Injury to kidneys from ischemia and/or toxins result in sloughing of tubular cells into urine Proteinuria isnt significant since protein, not tubules, spill into urine when glomeruli are damaged
>500 mOsm/kg
<300 mOsm/kg
Acute renal failure and a toxin in history are your clues to What is the most likely diagnosis? question for ATN
MTBS2CK p.307
MTBS2CK p.307
Patient presents with fever and acute LLQ abdominal pain. Blood cultures grow E. coli and Candida albicans. Patient started on vancomycin, metronidazole, gentamicin, and amphotericin. CT scan reveals diverticulitis. After 36 hours, her creatinine rises dramatically. Which of the following is most likely the cause of her renal insufficiency? a. Vancomycin Need 5-10 days exposure b. Gentamicin Need 5-10 days exposure c. Contrast media d. Metronidazole Hepatically excreted e. Amphotericin Need 5-10 days exposure
74-year-old blind man admitted with obstructive uropathy and chest pain. History of hypertension and diabetes. Creatinine drops from 10 mg/dL to 1.2 mg/dL 3 days after catheter placement. The stress test shows reversible ischemia. This is still What is the most appropriate management? considered
MTBS2CK p.308
MTBS2CK p.308
a. Coronary artery calcium score on CT scan experimental a b. One to two liters of normal saline hydration prior and during angiography Evidence not as strong c. N-acetylcysteine prior to angiography d. Mannitol during angiography Doesnt help e. Furosemide during angiography Loop diuretics are dangero worsen it f. Intravenous sodium bicarbonate before and during angiography Evidence not as strong
ExtraDifficultQuestion A patient with mild renal insufficiency undergoes angiography and develops 2 mg/dL rise in creatinine from ATN despite the use of saline hydration before and after procedure. What do you expect to find on laboratory testing?
a. b. c. d. Urine sodium FENa Urine specific gravity 8 (low) >1% 1.035 (high) 58 (high) >1% 1.005 (low) 5 (very low) <1% 1.040 (very high) 45 (high) >1% 1.005 (low) Spasm of afferent arteriole leads to reabsorption of Na (and thus water) very concentrated urine ( specific gravity)
ExtraDifficultQuestion
A patient with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later creatinine rises. What is the most likely cause?
a. b b. c. d. e.
Cisplatin Takes 5-10 days Hyperuricemia Can cause renal insufficiency Bence-Jones proteinuria but would not get worse with treatment Hypercalcemia Hyperoxaluria Oxalate crystals can be present in
urine in cases of bowel resection
MTBS2CK p.309
MTBS2CK p.309
ExtraDifficultQuestion
ExtraDifficultQuestion Suicidal patient ingests an unknown substance and develops renal failure 3 days later. Her calcium level is low and urinalysis shows an abnormality. What did she take?
What wouldve prevented this event? Allopurinol, hydration, and rasburicase Given prior to chemotherapy to prevent renal failure from tumor lysis syndrome
a. b. c. d. e. f.
Aspirin Doesnt affect Ca levels or cause crystals p Hepatotoxic p Acetaminophen Ethylene glycol Constrict afferent arteriole ATN and Ibuprofen papillary necrosis Opiates Can cause FSGS, but not AKI Methanol Affects retinal inflammation not AKI
MTBS2CK p.309
MTBS2CK p.310
AcuteTubularNecrosis/Toxins
AcuteTubularNecrosis
3 things increase risk of toxic/insult ATN: Hypoperfusion of kidney Underlying renal insufficiency Hypertension Diabetes Older age We lose 1% of renal function every year past age of 40.
MTBS2CK p.310
Summary of Causes: Slow onset (5 - 10 days) Drug-related injury

Aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir, cyclosporine Dose dependent
Mag risk for aminoglycoside and cisplatin
Immediate toxicity (24 48 hrs) Contrast media

Best prevented with saline hydration N-acetylcysteine and sodium bicarbonate arent consistently proven as beneficial
MTBS2CK p.310
AcuteTubularNecrosis
Rhabdomyolysis
Summary of Causes: Hemoglobin and myoglobin Hyperuricemia Ethylene Glycol Multiple Myeloma NSAIDs
Etiology?
Trauma, prolonged immobility, snake bites, seizures, and crush injuries
The best initial test?

UA (dipstick AND microscopic analysis)
Characteristic findings?
Blood is positive on dipstick but NO RBCs are seen on microscopic exam
MTBS2CK p.311
MTBS2CK p.310
Rhabdomyolysis
Rhabdomyolysis
Most specific lab test?

Urine myoglobin
Abnormal lab findings?

Creatine phosphokinase (CPK) Hyperkalemia H k l i Hyperuricemia Hyperphosphatemia Hypocalcemia
MTBS2CK p.311
Treat with: Saline hydration Mannitol Bicarbonate

Dont treat hypocalcemia in rhabdomyolysis if asymptomatic. In recovery, the calcium will come back out of muscles.
MTBS2CK p.311
AcuteTubularNecrosis/Treatment A man comes to the ED after a triathlon followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and urine is dark. IV fluids are started. What is the next best step in management?
No therapy proven to benefit ATN Patients should be managed with

Hydration, if theyre volume depleted and correction of electrolyte abnormalities
a. b. c. d. e.
CPK level Would suggest gg rhabdo as cause, , but not life threatening complications. EKG Potassium replacement Would be fatal Urine dipstick Same reason as A Urine myoglobin Same reason as A
Diuretics increase urine output, but dont change overall outcome More urine output with diuretics doesnt mean renal failure is reversing.
MTBS2CK p.312
MTBS2CK p.311312
AcuteTubularNecrosis/Treatment
AcuteTubularNecrosis/Treatment
Answering treatment questions for ATN is based on recognizing the most common wrong answers:
Low-dose dopamine Diuretics Mannitol Steroids
All these are ineffective in reversing ATN Correct underlying cause

MTBS2CK p.312
When Is Dialysis the Answer? Dialysis is initiated if theres: Fluid overload Encephalopathy Pericarditis Metabolic acidosis A- acidosis E- electrolytes Hyperkalemia
I- intoxications O- overload of volume U-uremia
MTBS2CK p.312
AcuteTubularNecrosis/Rhabdomyolysis Patient develops ATN from gentamicin. Shes vigorously hydrated and treated with high doses of diuretic, low-dose dopamine, and calcium acetate as a phosphate binder. Urine output increases, but she still progresses to end-stage renal failure. She also becomes deaf. What caused her hearing loss?
a. b. c. d. e. Hydrochlorothiazide No otoxicity Dopamine No ototoxicity Furosemide Chlorthalidone No ototoxicity Calcium acetate No ototoxicity
HepatorenalSyndrome
Renal failure developing secondary to liver disease Kidneys normal Look for:
Severe liver disease (cirrhosis) New-onset renal failure with no other explanation Very low urine sodium (> 10 15 mEq/dL) FeNa < 1% Elevated BUN:creatinine ratio (> 20:1)
Treat with:
Albumin, midodrine, octreotide
MTBS2CK p.313
MTBS2CK p.313
Atheroemboli/Etiology
Atheroemboli/Etiology Livedo reticularis
Can occur during catheter procedures:

Cardiac catheterization, angiogram
Emboli can go to:

Kidney, leading to AKI Eye Cutaneous vessles livedo reticularis Peripheral pulses are normal in atheroemboli atheroemboli. Theyre too small to occlude vessels such as the radial or brachial artery.
Lab findings:
Eosinophilia/Eosinophiluria, compliment, ESR
Most accurate test:

Biopsy cholesterol crystals
Source: Farshad Bagheri, MD MTBS2CK p.313314 MTBS2CK p.314
Acute(Allergic)InterstitialNephritis Antibodies and eosinophils attack cells lining tubules Reaction to drugs (70%), infection, and autoimmune disorders
Penicillins and cephalosporins Sulfa drugs (including diuretics like furosemide and thiazides which are sulfa derivatives) thiazides, Phenytoin The medications that cause AIN Rifampin are the same as those that cause: Quinolones Drug allergy and rash Allopurinol Stevens-Johnson syndrome PPI Toxic epidermal necrolysis
Hemolysis
MTBS2CK p.314315
Acute(Allergic)InterstitialNephritis Presentation: What Is the Most Likely Diagnosis? Look for acute renal failure (rising BUN and creatinine) with: Fever (80%) Rash (50%) Arthralgias Eosinophilia and eosinophiluria (80%) BUN/Cr ratio < 20:1 WBC and RBC in urine What is the most accurate test? Wright/Hansel stain to identify eosinophiluria
MTBS2CK p.315316
Acute(Allergic)InterstitialNephritis
AnalgesicNephropathy
Treatment AIN usually resolves spontaneously with stopping drugs or controlling infection Severe disease is managed with dialysis, which may be temporary When creatinine continues to rise after stopping the drug, giving glucocorticoids (prednisone, hydrocortisone, methylprednisolone) is the answer
Analgesic nephropathy presents with: ATN from direct toxicity to tubules AIN Membranous glomerulonephritis Papillary necrosis
MTBS2CK p.316
MTBS2CK p.316
AnalgesicNephropathy
PapillaryNecrosis
Presentation Vascular insufficiency of kidney from inhibiting prostaglandins

Prostaglandins dilate the afferent arteriole NSAIDs constrict the afferent arteriole and decrease renal perfusion p Asymptomatic in healthy patients When patients are older and have underlying renal insufficiency from diabetes and/or hypertension, NSAIDs can tip them over into clinically apparent renal insufficiency due to direct toxicity to tubules
MTBS2CK p.316
Sloughing off renal papillae Etiology NSAIDs or sudden vascular insufficiency

Death of cells in papillae and their dropping off the internal structure of kidney
Occurs with underlying kidney damage:

Sickle Cell DM Urinary obstruction Chronic pyelonephritis
MTBS2CK p.316
PapillaryNecrosis
Clinical presentation:
Fever, hematuria, and sudden onset flank pain Looks like pyelonephritis
DifferencesbetweenPyelonephritis andPapillaryNecrosis Pyelonephritis Onset Symptoms Urineculture CTscan Treatment Fewdays Dysuria Positive Diffuse swollenkidney Antibiotics,suchas ampicillin/gentamicin orfluoroquinolones Papillarynecrosis Fewhours Necroticmaterial inurine Negative Bumpy contour ofkidneyinterior Notreatment
Best initial test:

UA
Most accurate test:

CT scan
Treatment:
No specific therapy
TubularDisease
GlomerularDiseases
Chronic Immune mediated All nephrotic Need biopsy Often steroids, cyclophosphamide, mycophenolate
GlomerularDiseases
Goodpasture Syndrome IgANephropathy Postinfectious Glomerulonephritis Alport Syndrome Polyarteritis Nodosa LupusNephritis Amyloidosis Nephrotic Syndrome
Acute Caused by toxins Not nephrotic No biopsy No steroids or immunosuppressives
MTBS2CK p.318
GlomerularDiseases/DiagnosticTests
Goodpasture Syndrome
All forms of glomerulonephritis have: UA with hematuria Dysmorphic red cells (deformed as they squeeze through an abnormal glomerulus) Red cell casts Urine sodium and FENa are low Proteinuria The amount of
proteinuria is the main difference between glomerulonephritis and nephrotic syndrome.
MTBS2CK p.318
Lung + kidney involvement No upper respiratory tract involvement Diagnosis Best initial test:
Antiglomerular basement membrane antibodies Kidney biopsy in
Most accurate test: Lung or kidney biopsy
Goodpasture syndrome shows linear deposits.
MTBS2CK p.319
Diagnosis Anemia from hemoptysis CXR abnormal, but not diagnostic Treatment Plasmapheresis Steroids Cyclophosphamide
Commons.wikimedia. Used with permission
MTBS2CK p.319
MTBS2CK p.319
10
IgAnephropathy(Bergerdisease)
PostinfectiousGlomerulonephritis
MCC of acute glomerulonephritis in U.S. Presentation: Gross hematuria 1 to 2 days after an upper respiratory tract infection IgA levels in 50% Most accurate test = kidney y biopsy p y No treatment: will resolve, progress to ESRD Steroids and ACE-inhibitors may help severe proteinuria
MTBS2CK p.319320
Most common infection is Streptococcus Follows throat infection or skin infection (impetigo) by 1 to 3 weeks Presentation
Cola-colored urine Edema (periorbital) HTN Oliguria
MTBS2CK p.320
Postinfectious Glomerulonephritis
Diagnostic Tests 1st - UA glomerulonephritis 2nd - Antistreptolysin O (ASO) titers and anti-DNAse antibody titers Most M t accurate t - Biopsy Bi
Commons.wikimedia, James Heilman, MD. Used with permission
MTBS2CK p.320
Treatment Management of strep infection does not reverse glomerulonephritis Use supportive therapies such as: Antibiotics A tibi ti Diuretics to control fluid overload
<5% of those with PSGN will progress.
MTBS2CK p.320
Commons.wikimedia. Used with permission
MTBS2CK p.320
11
AlportSyndrome
Polyarteritis Nodosa
Congenital defect of collagen Results in glomerular disease combined with:

Sensorineural hearing loss Visual disturbance from loss of collagen fibers that hold lens of eye in place
Definition Systemic vasculitis of small and medium-sized arteries Spares lungs Associated A i t d with ith hepatitis h titi B
PAN is nonspecific. Theres no single finding that allows you to answer the most likely diagnosis question.
MTBS2CK p.321
Theres no specific therapy to reverse this defect of type IV collagen

MTBS2CK p.320
PolyarteritisNodosa/Presentation The most common organ systems involved are: GI

Abdominal pain, bleeding, nausea, and vomiting occur
PolyarteritisNodosa/DiagnosticTests Blood tests will show: Anemia and leukocytosis ESR and C-reactive protein ANCA: Not present in most cases ANA and rheumatoid factor: Sometimes present in low titer Angiography Renal, mesenteric, or hepatic artery showing aneurysmal dilation Biopsy Most accurate if at symptomatic site
MTBS2CK p.321
Neuro
Peripheral neuropathy or mononeuritis mononeuritis multiplex. multiplex.
Skin
Petechiae, purpura, ulcers, livedo reticularis
Cardiac
Stroke or MI, particularly in young person
MTBS2CK p.321
Polyarteritis Nodosa
LupusNephritis SLE can give any degree of renal involvement Normal Mild, asymptomatic proteinuria Membranous glomerulonephritis Glomerulosclerosis scars kidneys without inflammation leading to ESRD requiring dialysis Diagnosis Biopsy (tells severity) Treatment Steroids, cyclophosphamide, mycophenolyate
MTBS2CK p.322
Treatment Prednisone and cyclophosphamide mortality Treat hepatitis B when its found
MTBS2CK p.321322
12
Amyloidosis
Amyloidosis
Amyloid is an abnormal protein produced in association with: Myeloma Chronic inflammatory diseases Rheumatoid arthritis Inflammatory bowel disease Chronic infections Amyloid, HIV
nephropathy, polycystic kidneys, and diabetes give large kidneys on sonogram and CT scan.
MTBS2CK p.322
Most accurate test = biopsy Apple-green birefringence with Congo red staining Best treatment = control underlying disease 2nd line Treatment = melphalan and prednisone
MTBS2CK p.322
Amyloidosis
NephroticSyndrome/Definition Measure of the severity of proteinuria in association with any form of glomerular disease
> 3.5 g/24 hrs
Liver can no longer increase the production of albumin to compensate for urinary losses Massive proteinuria leads to:
Edema (periorbital) Hyperlipidemia Thrombosis:
From urinary loss of natural anticoagulants protein C, protein S, and antithrombin
MTBS2CK p.322
Katsumi M. Miyai, MD, PhD. Regents of the University of California. Used with permission
MTBS2CK p.322
Nephrotic Syndrome/Etiology
NephroticSyndrome/DiagnosticTests
MCC = diabetes and hypertension Any of the glomerular diseases just described Other associations are: Cancer (solid organ): membranous Children: minimal change disease Injection drug use and AIDS: focal-segmental NSAIDs: minimal change disease and membranous SLE: Any of them
Best initial test = urinalysis Next best test = albumin/creatinine ratio or 24-hour urine protein collection Most accurate test = biopsy:
Focal-segmental Focal segmental Membranous Membranoproliferative Minimal change Mesangial
MTBS2CK p.323
MTBS2CK p.323
13
NephroticSyndrome/DiagnosticTests
NephroticSyndrome/Treatment
By definition, nephrotic syndrome is: Hyperproteinuria (> 3.5 g/24 hours) Hypoproteinemia Hyperlipidemia Edema
Treatment Best 1st therapy = glucocorticoids 2nd line = cyclophosphamide ACE inhibitors or ARBs to control proteinuria Edema managed with salt restriction and diuretics Hyperlipidemia is managed with statins as you would any form of hyperlipidemia
MTBS2CK p.324
MTBS2CK p.324
EndStageRenalDisease/Definition
EndStageRenalDisease
Etiology Presentation Manifestations Treatment KidneyTransplantation
Not defined as a particular BUN or creatinine Loss of renal function symptoms and laboratory abnormalities known as uremia Uremia is defined as the presence of:
Metabolic acidosis Fluid overload Encephalopathy Hyperkalemia Pericarditis
Peritoneal dialysis and hemodialysis are equally effective at removing wastes from the body.
Acute indications for dialysis

MTBS2CK p.324325
Manifestations of Renal Failure Anemia: Normocytic, normochromic

Loss of EPO
Manifestations of Renal Failure (contd) Bleeding:

No degranulation cant aggregate
Hypocalcemia: Cant absorb Ca from GI tract

25-hydroxy-vitamin D 1,25-dihydroxy-vitamin D
Infection:
No degranulation cant fight infection
Osteodystophy: Demineralized bones, soft/weak

Secondary hyperparathyroidism
Accelerated atherosclerosis:
Abnormal WBCs cannot clear lipid accumulation from arteries
Hyperphosphatemia: Cant excrete

PTH release of PO4 from bones
Pruritus:
Unclear reasoning; urea accumulating in skin causes itching
MTBS2CK p.325
Hypermagnesemia: Cant excrete

MTBS2CK p.325
14
TreatmentofESRDManifestations Manifestation
Anemia Hypocalcemia Bleeding Pruritus Hyperphosphatemia Hypermagnesemia Atherosclerosis Endocrinopathy
Manifestations of Renal Failure (contd) Endocrinopathy:

Women are anovulatory Men have testosterone erectile dysfunction Hyperinsulinemia and insulin resistance
Either hyper- or hypoglycemic
Treatment
Erythropoietinreplacementand ironsupplementation ReplacevitaminDandcalcium DDAVPincreasesplateletfunction Dialysisandultravioletlight Oralbinders,seeHyperphos Rx RestrictionofhighMgfoods,laxatives, andantacids Dialysis Dialysis,estrogen&testosterone replacement
MTBS2CK p.325
MTBS2CK p.325
Treatment of Hyperphosphatemia Medications: Calcium acetate Calcium carbonate Use sevelamer and Sevelamer lanthanum when calcium level is high. Lanthanum
Never use aluminum containing phosphate binders. Aluminum causes dementia.
MTBS2CK p.326
Kidney Transplantation Only 50% of ESRD patients will be suitable for transplantation The donor doesnt have to be alive or related although these are both better related,
HLA-identical, related donor kidneys last 24 years on average.
MTBS2CK p.326
SurvivalbyMethod
1year 3years 5years
Thromboticthromobocytopenicpurpura andHemolyticSyndrome
Living,relateddonor Deceaseddonor Dialysisalone Diabeticsondialysis

MTBS2CK p.326
95% 90% Variable Variable
88% 78% Variable Variable
72% 58% 3040% 20%
Different variants, same disease TTP is associated with HIV, cancer, and drugs (e.g., cyclosporine, ticlopidine, and clopidogrel) HUS is MC in children and the most frequently tested association is E. coli 0157:H7 and Shigella
MTBS2CK p.326
15
Both TTP and HUS are associated with:

Intravascular hemolysis Renal insufficiency Thrombocytopenia
TTP also l is i associated i d with: ih

Neurological symptoms Fever
The hemolysis is visible on smear with schistocytes, helmet cells, and fragmented red cells
Thromboticthromobocytopenicpurpuraand HemolyticSyndrome Most cases of HUS from E. coli will resolve spontaneously Plasmapheresis is generally urgent in TTP Severe HUS also needs urgent plasmapheresis If plasmapheresis is not one of the choices choices, use infusions of fresh frozen plasma (FFP) Steroids dont help Platelet transfusion is never the correct choice for TTP or HUS
MTBS2CK p.327
CysticDisease
SimpleversusComplexCysts Polycystic y y Kidney yDisease
Benign(Simple)vs.Malignant(Complex)Cysts SimpleCyst Echogenicity Walls Demarcation Transmission Echofree Smooth,thin Sharp Goodthrough toback ComplexCysts Mixedechogenicity Irregular,thick Lowerdensity onbackwall Debrisincyst
PolycysticKidneyDisease
Polycystic kidney disease (PCKD) presents with: Pain Hematuria Stones No therapy exists to Infection prevent or reverse cysts of any type. HTN
MTBS2CK p.326
MTBS2CK p.328
16
What is the MCC of death from PCKD?

a. b. c. d d. e. Intracerebral hemorrhage aneurysms Stones Can occur but do not lead to death Infection Pyelo is more common but rarely fatal potential. Doesn Doesnt t progress Malignancy No malignant potential Renal failure to RCC
Only 10-15% have cerebral
Sodium&Potassium Disorders
Hypernatremia Hyponatremia Hyperkalemia Hypokalemia
MTBS2CK p.328
Hypernatremia/Etiology
Hypernatremia/Etiology
Loss of free water Examples are:

Sweating Burns Fever F Pneumonia (insensible losses from hyperventilation) Diarrhea Diuretics
MTBS2CK p.328
Diabetes Insipidus (DI) High urinary volume water loss Insufficient or ineffective ADH Symptoms
Confusion Disorientation Lethargy Seizures
Sodium disorders cause CNS problems
If uncorrected, severe hypernatremia causes coma and irreversible brain damage

MTBS2CK p.328
DiabetesInsipidus(DI)
CentralDI NephrogenicDI
Hypernatremia/DiagnosticTests
Definition
LossofADH production CNSdisorders: Stroke Tumor Trauma Hypoxia Infection
LossofADH effect Lithium Demeclocycline Chronickidney disease Hypokalemia Hypercalcemia
Etiology
To distinguish DI from other causes of hypernatremia look for: Increased urine volume Decreased urine osmolality Decreased D d urine i sodium di
Increased urine volume despite dehydration and hyperosmolality of blood suggests DI
MTBS2CK p.329
MTBS2CK p.328329
17
DiagnosingDI
Best initial test? Continued high volume dilute urine
CentralDIvs.NephrogenicDI
Water deprivation test
urine volume osmolality
CDI
NDI
Polyuriaandnocturia Urineosmolalityandsodium Positivewaterdeprivationtest
Yes Low Yes Yes Low
Yes Low Yes No High
Diabetes Insipidus
Next best test?
Psychogenic Polydipsia
ADH administration test

urine volume osmolality Continued high volume dilute urine
Central DI
MTBS2CK p.329
Nephrogenic DI
**Most accurate test = ADH level NDI CDI
ResponsetoADH ADHlevel
MTBS2CK p.329
Hypernatremia/Treatment
Hypernatremia/Treatment
Fluid loss:
Correct underlying cause of fluid loss
CDI:
Replace ADH (vasopressin also known as DDAVP)
NDI:
Correct potassium and calcium Stop lithium or demeclocycline Give hydrochlorothiazide or NSAIDs for those still having NDI despite these interventions
MTBS2CK p.330
Complications of Therapy Cerebral edema: sodium levels brought down too rapidly Cerebral edema presents with worsening confusion and seizures
MTBS2CK p.330
Hyponatremia/Etiology
Hyponatremia/Etiology Intravascular volume depletion CHF, nephrotic syndrome, cirrhosis
Hypervolemia MCC of hyponatremia with hypervolemic state are:

CHF Nephrotic syndrome Cirrhosis
Increased ADH levels Stimulated by baroreceptors in atria and carotids
Free water reabsorption Sodium concentration drops

18
Hypovolemia Sweating Burns Fever Pneumonia Diarrhea Diuretics
Addisons disease Loss of adrenal function loss of aldosterone Aldosterone causes Na+ reabsorption If the body y loses aldosterone, , it loses Na+
MTBS2CK p.330
MTBS2CK p.331
Hyponatremia/Presentation
Euvolemic Hyponatremia MCCs:

Pseudohyponatremia (hyperglycemia) Psychogenic polydipsia Hypothyroidism H th idi Syndrome of inappropriate ADH (SIADH) release
Hyponatremia presents entirely with CNS symptoms: Confusion Lethargy Disorientation Seizures Symptoms of hyponatremia Coma
are dependent on how fast it occurs.
MTBS2CK p.331
MTBS2CK p.331
Hyponatremia/DiagnosticTests
ResponsetoHyponatremia
Normallevels SIADH
SIADH High urine osmolality High urine sodium Low uric acid level and BUN Most accurate test is a high ADH level
Urine osmolality Urine sodium
Low (<100mOsm/kg) Low(<20mEq/L)
High
High(>40mEq/L)
MTBS2CK p.332
MTBS2CK p.332
19
Hyponatremia/Treatment
ClinicalManifestationsofHyponatremiabySeverity Degreeof hyponatremia Specific manifestation Management
Mild hyponatremia
Nosymptoms
Restrictfluids
The treatment answer isnt based on sodium level; ; its based on the symptoms.
Moderate
Minimalconfusion
Salineandloop diuretics Hypertonicsaline, conivaptan, tolvaptan
Severe
Lethargy,seizures, coma
MTBS2CK p.332
MTBS2CK p.332
Hyponatremia/Treatment
CentralPontineMyelinolysis
Complications of Treatment Goal: increase in Na is 0.5 to 1 mEq/hour (12 to 24 mEq/day) If the sodium level is brought up to normal too rapidly central pontine myelinolysis (osmotic demyelinization occurs)
MTBS2CK p.332
MTBS2CK p.332
Hyperkalemia
Hyperkalemia/Etiology
K > 5mEq/L
Typically defined as [K+] > 5mEq/L

Pseudohyperkalemia
Severe hyperkalemia can stop the heart in seconds if the level is high enough.
Decreased Excretion
Increased Release from Tissues
Hemolysis Leukocytosis Thrombocytosis

Repeat the blood sample
Renal failure Acute or chronic Low aldosterone state ACE inhibitors/ARBs RTA IV Drugs Addison disease
Cell lysis Low insulin Acidosis Drugs Beta blockers Digoxin Heparin
MTBS2CK p.332
MTBS2CK p.333
20
Hyperkalemia/Presentation
Hyperkalemia/DiagnosticTests
Potassium disorders interfere with muscle contraction and cardiac conductance Look for:
Weakness Paralysis when severe Ileus (paralyzes gut muscles) Cardiac rhythm disorders
If hyperkalemia is suspected Most urgent test:

EKG
The EKG in severe hyperkalemia shows:

Peaked T waves Wide QRS PR interval prolongation
Hyperkalemia does not cause seizures.

Hyperkalemia/Treatment
K > 5mEq/L
Hyperkalemia/Treatment When theres hyperkalemia and an abnormal EKG, the most appropriate next step is clearly calcium chloride or gluconate.
No
Kayexalate Loop diuretics
Pseudohyperkalemia?
Yes
No treatment needed
EKG Changes?
Calcium chloride or calcium gluconate Insulin and glucose, inhaled beta agonist Give bicarbonate if acidosis is the cause Consider hemodialysis
Sodium = CNS symptoms Hyperkalemia = muscular and cardiac symptoms
MTBS2CK p.334
MTBS2CK p.334
Hypokalemia/Etiology
K < 3.5 mEq/L
Hypokalemia/Presentation
Decreased Intake
Shift into cells
Renal Losses
GI Losses
Very Rare Kidney can adjust excretion
Alkalosis Insulin agonists (stimulate Na/K ATPase pump)
aldosterone Conns Volume Cushings Bartters Licorice Hypomagnesemia RTA I and II
Hypokalemia leads to problems with muscular contraction and cardiac conduction Potassium is essential for proper neuromuscular contraction Hypokalemia presents with:
Weakness Paralysis Loss of reflexes
MTBS2CK p.335
Vomiting Diarrhea Laxatives
Muscular abnormalities may be so severe as to cause rhabdomyolysis.
MTBS2CK p.334335
21
Hypokalemia/Presentation
Hypokalemia/Treatment
EKG findings U waves are the most characteristic finding of hypokalemia Other findings are ventricular ectopy (PVCs), flattened T waves, and ST depression
No maximum rate of oral potassium replacement

GI tract cannot absorb potassium faster than the kidneys can excrete it
IV potassium replacement, however, can cause a fatal arrhythmia if its it s done too fast
You must allow time for potassium to equilibrate into cells
Hypokalemia does not cause seizures.
IV potassium replacement must be very slow.

MTBS2CK p.335
MTBS2CK p.335
Patient is admitted with vomiting and diarrhea from gastroenteritis. His volume status is corrected with IV fluids and diarrhea resolves. His pH is 7.40 and serum bicarbonate has normalized. Despite vigorous oral and IV replacement, his potassium level fails to rise. What should you do?
Woman with ESRD and G6PD deficiency skips dialysis for a few weeks. She experiences a crush injury during a MVA. She is taking dapsone and has recently eaten fava beans. What is the most urgent step?
a. b. c. d. e.
Consult nephrology Dont consult except for procedures! Magnesium level Parathyroid hormone level Mg needed for PTH release Intracellular pH level Not MCC 24-hour urine potassium level Doesnt tell you
underlying cause or change tx
a. b b. c. d. e. f. g. h.
Initiate dialysis Must look for EKG changes 1st EKG Bicarbonate administration Take 15-20min to work Insulin administration Kayexalate Take hours to work Urine dipstick Doesnt address life threatening CPK levels complications Urine myoglobin
MTBS2CK p.335336
MTBS2CK p.336
Nonaniongapmetabolicacidosis(NAGMA)
AcidBaseDisturbances
RenalTubularAcidosis UrineAnionGap p MetabolicAcidosis MetabolicAlkalosis RespiratoryAcidosisandAlkalosis
The anion gap is: Na+ - (Cl- + HCO3- ) Normal anion gap is 6 12 The difference in + & is due to negative charges g on albumin Elevated gaps means increased acids (negatively changed) present
MTBS2CK p.336
22
Nonaniongapmetabolicacidosis
RenalTubularAcidosis(RTA)
What causes NAGMA?

RTA Diarrhea
Distal RTA (Type I) Pathology in distal tubule Inability to generate enough bicarbonate
Inadequate bicarb acid cannot be excreted p pH of urine is high, g ,p pH of blood is low
Why is the gap normal in these?

They y have elevated Cl ( (hyperchloremic yp metabolic acidosis)
The anion gap increases from ingested substances (e.g., ethylene glycol or methanol), or organic acids (e.g., lactate) that are anionic and drives chloride levels down
MTBS2CK p.336337
Caused by factors damaging distal tubule

Amphotericin SLE or Sjgren syndrome
MTBS2CK p.337
RenalTubularAcidosis
DistalRTA(TypeI)/DiagnosticTests
Distal RTA (Type I) Symptoms to look out for?

Calcium oxalate kidney stones Due to alkaline urine
Best initial test

Urine pH (> 5.5)
Most accurate test

Infuse ammonium chloride (acid) Normal person excretes acid urine pH decreases Distal RTA cannot excrete acid urine pH remains high
Distal RTA calcifies kidney parenchyma (nephrocalcinosis)
No acid into the tubule makes the urine basic
Treatment
Replace HCO3
MTBS2CK p.337
MTBS2CK p.337
RenalTubularAcidosis
RTATypeII/DiagnosticTests
Proximal RTA (Type II) Pathology in proximal tubule Inability to absorb filtered bicarb Caused by factors damaging proximal tubule:
Amyloidosis Myeloma Fanconi syndrome Acetazolamide Heavy metals
MTBS2CK p.337
Proximal RTA (Type II) Urine pH: Low (< 5.5)

Because distal tubule absorbs bicarb normally If you give bicarb: urine pH increases
Osteomalacia
Chronic metabolic acidosis leaches calcium out of the bones and become soft
MTBS2CK p.337
23
RTATypeII/Treatment
RTATypeIV/Definition/DiagnosticTests
Treatment: MASSIVE doses of bicarbonate

Because proximal tubule doesnt absorb it normally
Thiazide diuretics
Cause volume depletion bicarb reabsorption
Both proximal and distal RTA are hypokalemic. Potassium is lost in the urine.
Hyporeninemic, Hypoaldosteronism (Type IV RTA) Pathology in distal nephron Problem is decreased amount or effect of aldosterone
Loss of Na+, retention of K+ and H+
Caused by diabetes Best test High urine Na even after Na-restricted diet Hyperkalemia
MTBS2CK p.338
MTBS2CK p.338
RTATypeIV/Treatment
TypesofRenalTubularAcidosis(RTA)
Proximal(TypeII) Distal(TypeI) UrinepH Variable High>5.5 Low TypeIV <5.5 High
Treatment: Fludrocortisone
To promote Na+ reabsorption, K+ and H+ secretion
Fludrocortisone is the steroid with the highest mineralocorticoid or aldosterone-like effect.
MTBS2CK p.338
Bloodpotassium Low level Nephrolithiasis Diagnostictest No Administer bicarbonate Thiazides
Yes
No
Administeracid Urinesalt loss Bicarbonate Fludrocortisone
Treatment
MTBS2CK p.338
UrineAnionGap/Definition
MetabolicAcidosis
NAGMA UAG Positive RTA Negative Diarrhea
Normal anion gap (612):

RTA and diarrhea
Elevated anion gap (>12):

The anion gap is increased if there are unmeasured anions driving bicarbonate level down
Respiratory alkalosis from hyperventilation compensates for all forms of metabolic acidosis.
MTBS2CK p.339
24
CausesofMetabolicAcidosiswith anIncreasedAnionGap
Cause Lactate Hypotensionor hypoperfusion DKA,starvation Ethyleneglycol overdose Test Bloodlactate level Acetonelevel CrystalsonUA Treatment Correct hypoperfusion Insulin&fluids Fomepizole, dialysis Formic acid
CausesofMetabolicAcidosiswith anIncreasedAnionGap
Cause Methanol overdose Renalfailure Test Inflamedretina Treatment Fomepizole, dialysis
Ketoacids Oxalicacid
Uremia Salicylates
BUN,creatinine Dialysis Alkalinizeurine
Aspirinoverdose Aspirinlevel
MTBS2CK p.339
MTBS2CK p.339
MetabolicAcidosis Arterial Blood Gas in Metabolic Acidosis The arterial blood gas (ABG) in metabolic acidosis will always have:
Decreased pH < 7.4 Decreased pCO2 indicating respiratory alkalosis as compensation p Decreased bicarbonate
You cannot determine the etiology of metabolic acidosis from the ABG. Metabolic problems always show compensation.
MTBS2CK p.339
MetabolicAlkalosis Key laboratory finding? Elevated serum bicarbonate level Respiratory compensation? Decreased respiratory rate CO2 retention respiratory acidosis Etiology GI loss: vomiting or nasogastric suction aldosterone: primary, Cushing, ACTH, volume contraction, licorice Diuretics Milk-alkali syndrome Hypokalemia
MTBS2CK p.339340
MetabolicAlkalosis/Etiology
RespiratoryAcidosisandAlkalosis
Arterial Blood Gas in Metabolic Alkalosis The ABG in metabolic alkalosis will always have:
Increased pH > 7.40 Increased pCO2 (compensatory respiratory acidosis) Increased bicarbonate
Metabolic derangements kill patients with cardiac arrhythmia. They also alter potassium levels.
MTBS2CK p.340
Minute ventilation is a more precise measure of respiratory status than respiratory rate Minute ventilation = RR x TV
Hyperventilation may occur with a tiny tidal volume.This does not increase minute ventilation.
MTBS2CK p.340
25
CausesofRespiratoryAcidosisandAlkalosis
Respiratoryalkalosis DecreasedpCO2 Increasedminuteventilation Metabolicacidosisas Compensation Anemia Anxiety Pain Fever Interstitiallungdisease Pulmonaryemboli
MTBS2CK p.340
Respiratoryacidosis IncreasedpCO2 Decreasedminuteventilation Metabolicalkalosisas Compensation COPD/emphysema Drowning Opiateoverdose 1antitrypsindeficiency Kyphoscoliosis Sleepapnea/morbidobesity
Nephrolithiasis
Etiology Treatment LongtermManagement MetabolicAcidosisandStoneFormation
Nephrolithiasis/Pearls
Most common stone?

Calcium oxalate
Forms more frequently in?

Alkaline urine
46-year-old man comes to the ED with excruciating left flank pain radiating to groin. He has some blood in urine. What is the next step?
Most M t common risk i kf factor? t ?

Overexcretion of calcium in urine
a. b. c. d. e.
Ketorolac X-ray Sonography Provide pain relief before diagnostic tests Urinalysis Serum calcium level
MTBS2CK p.340
MTBS2CK p.341
Nephrolithiasis/Treatment What is the most accurate diagnostic test for nephrolithiasis?

a. b. c. d. e. CT scan X-ray 10-20% false negative. Misses uric acid stones Sonography Less accurate Urinalysis y ay s show o hematuria, e a u a, not o spec specific c to o cause May Intravenous pyelogram Requires contrast, takes hours
The best initial therapy for acute renal colic is with: Analgesics Hydration Imaging I i CT noncontrast t t
Cystine stones are managed with surgical removal, alkalinizing urine.
Uric acid stones are not detectable on X-ray, but visualized on CT.
26
Nephrolithiasis/Treatment
Etiology of the stone determined with: Stone analysis Serum calcium, sodium, uric acid, PTH, magnesium, and phosphate levels 24-hour 24 h urine i f for volume, l calcium, l i oxalate, citrate, cystine, pH, uric acid, phosphate, and magnesium
Fat malabsorption increases stone formation.
MTBS2CK p.341
Woman with her first episode of renal colic has a 1.8 cm stone in the left renal pelvis. No obstruction. Normal BUN and creatinine. What is the next step in management?
a. a b. c. d. e.
Wait for it to pass; hydrate and observe If < 5mm Lithotripsy Surgical removal If > 2cm Hydrochlorothiazide Decreases calcium in urine Stent placement Only releives hydronephrosis
MTBS2CK p.342
Nephrolithiasis
50% with kidney stones will recur over the next 5 years
UTI gives struvite stones (magnesium/ammonium/pho sphate). Remove them surgically.
A man with a calcium oxalate stone is managed with lithotripsy. Stone is destroyed and passes. Urinary calcium level is increased. Besides increasing hydration, which is most likely to benefit this patient?
a. b. c. d. e.
Calcium restriction Can rate of oxalate stones Hydrochlorothiazide Furosemide Increases urinary calcium Stent placement Only relieves obstruction Increased dietary oxalate Can rate of oxalate stones
MTBS2CK p.342
MTBS2CK p.342
Nephrolithiasis
UrinaryIncontinence
Stressincontinence Urgeincontinence
Metabolic acidosis removes calcium from bones and increases stone formation In addition, metabolic acidosis decreases citrate levels
Citrate binds calcium, making it unavailable for stone formation
Symptoms
Olderwomanwith painlessleakagewith coughing,laughing,or liftingheavyobjects Havepatientstand andcough;observe forleakage
Suddenpaininbladder followedimmediatelyby theoverwhelmingurge tourinate Pressuremeasurement inhalffullbladder; manometry
Test
MTBS2CK p.342
MTBS2CK p.343
27
UrinaryIncontinence
Stressincontinence Urgeincontinence
Treatment
1. Kegel exercises 2. Localestrogen cream
3. Surgical tighteningof urethra

MTBS2CK p.343
1. Bladdertraining exercises 2. Localanticholinergic therapy 1. Oxybutynin y y 2. Tolterodine 3. Solifenacin 4. Dariferancin 3. Surgicaltighteningof urethra
Hypertension
Definition Etiology gy Presentation DiagnosticTests Treatment HypertensiveCrisis
Hypertension/Definition
Hypertension/Etiology Most common etiology? (95%)

Essential hypertension
Systolic pressure > 140 mmHg Diastolic pressure > 90 mmHg Special population with lower threshold?
Diabetics
Common secondary causes?

Renal artery stenosis Glomerulonephritis Coarctation of aorta Acromegaly Pheochromocytoma Hyperaldosteronism Cushing syndrome or any cause of hypercortisolism including therapeutic use of glucocorticoids Congenital adrenal hyperplasia
MTBS2CK p.343344
Definition of hypertension? > 130/80
MTBS2CK p.343
Hypertension/Presentation
Typically asymptomatic Symptoms of end organ damage:

Coronary artery disease Cerebrovascular disease CHF Visual disturbance Renal insufficiency Peripheral artery disease
MTBS2CK p.344
Presentation of Secondary Hypertension Renal artery stenosis:

Bruit is auscultated at flank and is continuous throughout systole and diastole
Glomerulonephritis p Coarctation of aorta:

Upper extremity > lower extremity BP
MTBS2CK p.344
28
Hypertension/DiagnosticTests
Acromegaly Pheochromocytoma: Episodic hypertension with flushing Hyperaldosteronism: Weakness from hypokalemia
Other tests to perform in hypertensive patients EKG Urinalysis Glucose Gl measurements t to t exclude l d concomitant diabetes Cholesterol screening
MTBS2CK p.344
MTBS2CK p.344
Hypertension/Treatment
Hypertension/DrugTherapy
Best initial therapy? Lifestyle modifications:

Weight loss (*most effective*) Sodium restriction Dietary modification Exercise Tobacco cessation
Lifestyle modifications are tried for 3 to 6 months before medications are started.
MTBS2CK p.344345
Best first drug? (all-comers)

Hydrochlorothiazide
If BP > 160/100?
Defines Stage 2 HTN Start 2 medications immediately
MTBS2CK p.345
Hypertension
Hypertension
If diuretics dont control BP, the most appropriate next step in management is:
ACE inhibitor Angiotensin receptor blocker (ARB) Beta blocker (BB) Calcium-channel blocker (CCB)
Medications for refractory hypertension: Central-acting alpha agonists

Alpha methyldopa, clonidine
Peripheral-acting alpha antagonists

Prazosin, terazosin, doxazosin
Direct-acting vasodilators
Hydralazine, minoxidil
MTBS2CK p.345
MTBS2CK p.345
29
Hypertension/CompellingIndications
Ifthisisinthehistory Thisisthebestinitialtherapy
HypertensiveCrisis
Coronaryarterydisease Diabetesmellitus Benignprostatic hypertrophy Depressionandasthma Hyperthyroidism Osteoporosis

MTBS2CK p.345
BB,ACE,ARB ACE,ARB Alphablockers
Defined as HTN with SYMPTOMS Confusion Blurry vision Dyspnea Chest Ch t pain i
AvoidBBs BBfirst Thiazides

MTBS2CK p.345346
HypertensiveCrisis
The best initial therapy? Labetolol or nitroprusside 2nd line agents? Enalapril CCBs:
Diltiazem Verapamil
Esmolol
MTBS2CK p.346
30
Stroke Neurology
ConradFischer,MD
AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity
Definition Etiology Presentation DiagnosticTests Treatment
Stroke/Definition
Stroke/Etiology
Sudden onset neurological deficit Death of brain tissue 3rd most common cause of death in the USA Risk Ri k f factors t
Hypertension Diabetes Hyperlipidemia Tobacco
MTBS2CK p.273
Bleeding (15%) Blockage of flow (85%)

Thrombosis Embolus Heart H t
Atrial fibrillation Valvular heart disease DVT via Patent foramen ovale
Carotid stenosis
MTBS2CK p.273
Stroke/Presentation
Stroke/Presentation
Middle cerebral artery (MCA) >90% of all strokes Weakness or sensory loss
Opposite (contralateral) side from stroke
Contralateral homonymous hemianopsia Eyes look toward the side of lesion Aphasia If stroke on same side as speech center On left in 90%
MTBS2CK p.273
MTBS2CK p.273
Stroke/Presentation
Stroke/DiagnosticTests
Anterior cerebral artery (ACA)

Personality/cognitive defects (e.g., confusion) Urinary incontinence Leg > arm weakness
Posterior cerebral artery y (PCA) ( ) Loss of consciousness

Ipsilateral (same side) sensory loss of face, 9th, and 10th CNs Contralateral sensory loss of limbs Limb ataxia
MTBS2CK p.274
Best initial test for stroke is... CT scan of the head With or without contrast?... Without contrast Most accurate test for stroke is... MRI
MTBS2CK p.274
Stroke/DiagnosticTests
Stroke/Treatment Nonhemorrhagic Best initial therapy when LESS than 3 hours since onset...
Thrombolytics
CT Done first Excludes hemorrhage Prior to treatment
More than 3 hours since onset...

Aspirin
If the patient is already on aspirin...

ADD dipyridamole OR SWITCH to clopidogrel
Source:MohammadMaruf,MD
MTBS2CK p.274
MTBS2CK p.274 275
Stroke/Treatment
Stroke/EvaluationofCauses&Treatment
Hemorrhagic Best initial treatment... Nothing
Echocardiogram Damaged valves? Surgical replacement Thrombi? Heparin followed by warfarin to INR of 2-3
MTBS2CK p.275
MTBS2CK p.275
Electrocardiogram Atrial fibrillation or atrial flutter Warfarin as long as arrhythmia persists

noPwave Afib Pwave NSR
Source:JHeuser Source:KjetilLenes
Holter monitor
Detect arrhythmias If initial EKG is normal: Do Holter monitor Detect atrial arrhythmias G t sensitivity Greater iti it than th EKG
Holter monitor
MTBS2CK p.275
Source:Macro987
Stroke
Patient presents with: Sudden onset unilateral weakness Facial droop +/- Speech deficits
Carotid duplex ultrasound Carotid stenosis is a frequent cause of emboli Surgery? Symptomatic S t ti and d >70% 70% stenosis t i Endarterectomy superior to carotid angioplasty
Best Initial Test: Head CT without contrast
No acute process
Acute hemorrhage
Likely ischemic stroke

MTBS2CK p.275
Likely hemorrhagic stroke
Stroke
Likely ischemic stroke
Stroke
Likely hemorrhagic stroke Symptoms last < 24 hours, then resolve
< 3 hours from onset of symptoms
> 3 hours from onset of symptoms
Treatment: Consider TPA, if no hx of bleeding
Treatment: Aspirin ADD dipyridamole or switch to clopidogrel if already on aspirin
Transient ischemic attack
Treatment: Control blood pressure Optimal systolic BP is between 140-160 mmHg If > 170 mmHg, mmHg use nicardipine, nicardipine enalaprilat, enalaprilat or labetalol Reverse anticoagulation If patient is on warfarin fresh frozen plasma, vitamin K If patient is on heparin protamine sulfate
MTBS2CK p.274 275
Perform further studies to asses etiology
Stroke
Goals!
Diabetes
Hemoglobin A1C <7%
Headache
Types Physical y Examination DiagnosticTests Treatment Trigeminal&PostherpeticNeuralgia
Hypertension
BP <140/90 mmHg
LDL
<100 mg/dL if carotid stenosis is the cause
Tobacco smoking
Must stop!
MTBS2CK p.276
Headache
Headache/TensionHeadache Constant pressure Mild to moderate pain, mainly bilateral Lasts 4-6 hours Physical exam Nothing! Diagnostic tests None (all normal) Treatment NSAIDs and other analgesics
MTBS2CK p.276
Types Tension Migraine Cluster Giant cell (temporal) arteritis Pseudotumor cerebri
MTBS2CK p.276
Headache/Migraine
Visual disturbance Photophobia aura May be related to: Food/menses Precipitated by emotions Ph i l exam Physical Rare cases: aphasia, numbness, dysarthria, weakness Diagnostic tests All normal Scan head the first time, then stop
MTBS2CK p.276
Headache/Migraine
Treatment Abortive
Triptans or ergotamine
Prophylactic (preventive)
> 3 migraines/month Propranolol
Other preventive medications: Calcium-channel blockers Tricyclic antidepressants SSRIs Botulinum toxin injections
MTBS2CK p.277
Headache/ClusterHeadache Symptoms
Frequent, short duration, high intensity
Headache/ClusterHeadache Treatment Abortive Triptans Ergotamine 100% oxygen Preventive Verapamil Lithium Prednisone
MTBS2CK p.277
Men 10X MORE than women!!! Physical examination

Red, tearing g eye y with rhinorrhea Horner syndrome occasionally
Diagnostic tests
Scan head first time No need for subsequent imaging with recurrences
MTBS2CK p.276
Headache/GiantCell(Temporal)Arteritis Symptoms
Visual disturbance, jaw claudication Muscle pain, fatigue, and weakness
Headache
Headache
Episodic pain Unilateral periorbital intense pain Lacrimation Eye-reddening Nasal stuffiness Lid ptosis +/- Aura, photophobia Related to food/emotions/menses Rare: aphasia, numbness, dysarthria
Physical exam
Visual loss, temporal area tenderness
Bilateral band-like pressure Lasts 4-6 hours Normal P/E
Diagnostic tests
Elevated ESR Most accurate test? Biopsy!
Tension Headache H d h
Treatment NSAIDs Acetaminophen
Migraine
Treatment Avoid triggers NSAIDs 5-HT1 agonists 3 attacks/month Prophylaxis Propranolol Sodium valproate
Cluster Headache
Acute Treatment Sumitriptan Octreotide Oxygen Prophylaxis Verapamil Prednisone Sodium valproate
Treatment
Prednisone
MTBS2CK p.276 MTBS2CK p.389.4
Headache/PseudotumorCerebri
CranialNerve6Palsy
Associated with Obesity Oral contraceptives Vitamin A toxicity Mimics brain tumor: nausea & vomiting Physical exam Papilledema Diplopia: 6th CN (abducens) palsy
MTBS2CK p.276
Diagnostic tests CT or MRI Normal Done to exclude intracranial mass Lumbar puncture Increased pressure CSF Normal
MTBS2CK p.277
Treatment Acetazolamide +/- furosemide Weight loss Steroids Repeated lumbar puncture Ventriculoperitoneal shunt
MTBS2CK p.277
Headache/TrigeminalNeuralgia Idiopathic 5th CN Severe, overwhelming knife-like facial pain Precipitated by Chewing Touching the face Pronouncing words in which the tongue strikes the back of front teeth No specific diagnostic test
MTBS2CK p.278
Headache/TrigeminalNeuralgia
Treatment Carbamazepine or oxcarbazepine Baclofen Lamotrigine Surgical decompression when failing medications
MTBS2CK p.278
Headache/PostherpeticNeuralgia
Headache/PostherpeticNeuralgia
Residual pain following resolution of herpes zoster (shingles) vesicular lesions Shingles Shi l i is a painful i f l dermatomal rash that occurs in 15% with prior varicella zoster (chickenpox) infection
MTBS2CK p.278
Shinglesrashcausedbyherpeszostervirus.Source:NIAID
Acute Treatment: Acyclovir, famciclovir, or valacyclovir reduce the incidence of pain Steroids do not help
MTBS2CK p.278
Headache/PostherpeticNeuralgia Treatment
Tricyclic antidepressants (amitriptyline) Gabapentin or pregabalin Carbamazepine Phenytoin Topical capsaicin Antiepileptic medications
Have some beneficial effect in neuropathic pain (e.g., postherpetic neuralgia or peripheral neuropathy)
PreventionofHerpesZoster(Shingles)
Zoster vaccine Everyone > 60 High dose varicella vaccine Decreases reactivation of varicella into zoster t
None work in > 50% to 70%

ClassificationofSeizures
Seizures
Classification DiagnosticTests Treatment Management
Partial Absence (petit mal) Generalized (tonic-clonic) Status S a us epilepticus ep ep cus
MTBS2CK p.279
PartialSeizures
AbsenceSeizures
Focal to one part of the body

Limited to arm or leg
Partial seizures can be: Simple

Intact consciousness
Complex
Loss of consciousness
Also referred to as petit mal Consciousness briefly impaired Patient often remains upright and often appears normal or stares into space Absence Ab seizures i occur more often ft i in children
MTBS2CK p.279
MTBS2CK p.280
GeneralizedSeizures
GeneralizedSeizures/Causes
Also referred to as tonic-clonic Generalized seizure Varying phases Muscular rigidity (tonic) Followed by jerking of muscles for several minutes (clonic)
Hyponatremia or hypernatremia Hypoxia Hypoglycemia Any CNS infection Encephalitis, meningitis, abscess Any CNS anatomic abnormality Trauma, stroke, tumor
MTBS2CK p.280
MTBS2CK p.278
GeneralizedSeizures/Causes
Seizures/DiagnosticTests
Hypocalcemia Uremia (elevated creatinine) Hepatic failure Withdrawal Alcohol, barbiturate, and benzodiazepine Cocaine toxicity Hypomagnesemia (rare)
MTBS2CK p.278
Electroencephalogram (EEG) The right answer after the other tests are done If CT or MRI are normal No N point i ti in EEG if th there i is a clear l metabolic, toxic, or anatomic defect causing the seizure
MTBS2CK p.279
Delerium,Stupor,andComa Altered consciousness Unresponsiveness to stimuli From metabolic, toxic, and CNS infections Also called Confusion Difficulty Diffi lt with ith arousal l Obtundation When severe enough, a seizure occurs Confusion is to coma and seizure, as angina is to myocardial infarction
MTBS2CK p.279
TreatmentofStatusEpilepticus
The only seizure treatment that is clear Best initial therapy... Benzodiazepine Lorazepam Diazepam intravenously
MTBS2CK p.279
TreatmentofStatusEpilepticus If seizure persists... Phenytoin or fosphenytoin Fosphenytoin = phenytoin efficacy Fosphenytoin has fewer adverse effects Ph Phenytoin t i Hypotension and AV block Fosphenytoin No BP or cardiac effect Can be given more rapidly
MTBS2CK p.279
1. Benzodiazepines did NOT work 2. Fosphenytoin did NOT work 3. Use phenobarbital
MTBS2CK p.279
What if barbiturates do NOT work?

1. Neuromuscular blocking agents allow intubation: Succinylcholine Vecuronium Pancuronium
2. General anesthesia
Midazolam or propofol Place on ventilator before propofol, which can stop breathing
MTBS2CK p.278
To summarize... 1. Benzodiazepine 2. Fosphenytoin 3. Phenobarbital 4. General anesthesia
MTBS2CK p.280
EpilepsyTreatment/Indications
ChoiceofAntiepilepticDrugs Status epilepticus treatment is clear Epilepsy long-term treatment is not clear No medication is clearly superior to the others Phenytoin, valproic acid, and carbamazepine all have nearly equal efficacy Gabapentin, Gabapentin topiramate, topiramate lamotrigine, lamotrigine oxcarbazepine, or levetiracetam Ethosuximide is the best therapy for absence seizures You cannot be asked to choose between them based on efficacy
MTBS2CK p.280
Antiepileptic drugs Not long term for single seizure When should you start after a single seizure? Presentation P t ti in i status t t epilepticus il ti Abnormal EEG Family history of seizures
MTBS2CK p.280
ChoiceofAntiepilepticDrugs
DiscontinuanceofAntiepilepticMedication
If not controlled with single agent, an alternate medication should be tried If still not controlled, add a second drug If multiple medications do not work: Surgery!
Wait until seizure-free for 2 years Sleep deprivation EEG: The best way to detect possibility of recurrence Elicits abnormal activity with more sensitivity This is NOT a 100% sensitive test!
MTBS2CK p.281
MTBS2CK p.280
38-year-old man evaluated for seizures achieves partial control with second medication. He drives to work daily. What do you do about his ability to drive?
a. Confiscate his license Rules vary state to state Cannot b. Allow him to drive if he is seizure-free for 1 year prevent c. Allow him to drive as long as his seizure history is noted t d on hi his li license Rules vary state to state d. Recommend that he find an alternate means of transportation e. Do not let him leave the office unless he is picked up by someone; no further driving Cannot incarcerate f. Allow him to drive as long as he is accompanied Being accompanied does not prevent seizures
Subarachnoid Hemorrhage
Definition/Etiology DiagnosticTests Treatment
MTBS2CK p.281
10
SubarachnoidHemorrhage
CircleofWillis
Rupture of aneurysm Usually in Circle of Willis (anterior) Aneurysms found in 2% of autopsies Majority never rupture Cause of rupture not clear
SubarachnoidHemorrhage/Diagnosis
What is the most likely diagnosis? Look for...

Sudden onset of severe headache with meningeal irritation (stiff neck, photophobia) and fever!
How does SAH differs from meningitis? Very sudden in onset Loss of consciousness
Loss of consciousness in 50% Sudden increase in intracranial pressure Focal neurological complications occur in 30%
MTBS2CK p.281
MTBS2CK p.281
SubarachnoidHemorrhage/Diagnosis Best initial test is... CT without contrast (95% sensitive) Most accurate test is... Lumbar puncture showing blood
LP necessary only for 5% with falsely negative CT CSF in SAH has both increased WBCs and RBCs WBC can mimic meningitis Ratio of WBCs to RBCs will be normal in SAH
Source:SabaAnsari,MD
MTBS2CK p.282
MTBS2CK p.282
11
WBC count > normal 1:500?

Suspect meningitis
Xanthochromia
Yellow CSF From breakdown red cells in CSF
EKG
May show large or inverted T waves Suggestive of myocardial ischemia Cerebral T waves From excessive sympathetic activity
MTBS2CK p.282
Angiography Determines site of aneurysm Guides lesion repair MRA Diagnosis based on... CT and sometimes LP Only angiography can tell location
MTBS2CK p.282
SubarachnoidHemorrhage/Treatment
Nothing reverses hemorrhage Nimodipine (calcium-channel blocker) prevents subsequent ischemic stroke
MTBS2CK p.282
MTBS2CK p.283
Embolization (coiling) Catheter clogs up site of bleeding Prevents repeated hemorrhage Interventional neuroradiologist places platinum wire p Embolization superior to surgical clipping for survival and complications
Ventriculoperitoneal shunt SAH associated with hydrocephalus Shunt only if hydrocephalus develops
MTBS2CK p.283
MTBS2CK p.283
12
Seizure prophylaxis Phenytoin is not routine If the question asks Which of the following is most likely to decrease mortality? ... mortality?
Phenytoin is not the answer
Consultation is only right when you want to do a procedure that isnt given as a choice.
MTBS2CK p.283
MTBS2CK p.284
A woman in the ED with a severe headache one day prior to admission. Temp 103F, nuchal rigidity & photophobia. Head CT is normal. LP CSF WBCs: 1,250 RBCs: 50,000 Whats the next step?
SpineDisorders
AnteriorSpinalArteryInfarction SubacuteCombinedDegenerationoftheCord SpinalTrauma BrownSquardSyndrome Syringomyelia
Angiography g g p y For location of SAH, this is not SAH 50 000 RBC should 50,000 h ld only l Ceftriaxone and vancomycin give 50-100 WBCs Nimodipine Prevent SAH stroke 1,250 WBCs is infection Embolization Permanent SAH fix Surgical clipping Worse alternative to embolization Useless for blood Repeat CT scan with contrast Neurosurgical consultation Dont consult unless you REALLY want a procedure MTBS2CK p.283 not listed a. b. c. d. e. f. g.
AnteriorSpinalArteryInfarction
Loss of all function except posterior column Position and vibratory sensation intact Flaccid paralysis below the level of infarction Loss of deep tendon reflexes (DTRs) at level of infarction Evolves into spastic paraplegia several weeks later Loss of pain and temperature Extensor plantar response
SubacuteCombinedDegeneration oftheCord
B12 deficiency or neurosyphilis Position & vibratory sensation lost Everything else intact
No specific therapy
MTBS2CK p.284
MTBS2CK p.284
13
SpinalTrauma Acute limb weakness and/or sensory disturbance Below level of injury Severity in proportion to degree of injury Sphincter p function impaired p Loss of DTRs at level of injury Followed by hyperreflexia below level of trauma Treat with glucocorticoids
MTBS2CK p.284
BrownSquardSyndrome Unilateral hemisection of spinal cord Due to injury Knife cutting half the cord On physical exam...
Ipsilateral Motor Position Vibration Contralateral Pain Temperature
No treatment
MTBS2CK p.284
Syringomyelia Fluid-filled, dilated central canal of spinal cord Widening bubble or cavitation damages neural fibers passing near center of spine Caused by tumor or severe trauma to spine
Syringomyelia What is the most likely diagnosis? Look for: Loss of pain & temperature bilaterally Across the upper back and both arms Look for the phrase capelike capelike distribution distribution Loss of reflexes Muscle atrophy
MTBS2CK p.285
MTBS2CK p.285
Syringomyelia The most accurate test is... MRI The best treatment is... Surgical Removal of tumor Drain cavity
Source:MohammadMaruf,MD.
CNSAbscess&Disease
Brainabscess Neurocutaneousdiseases
MTBS2CK p.285
14
BrainAbscess/Definition&Etiology Collection of infected material in brain parenchyma Acts as space-occupying lesion Spreads from contiguous infection Starts in sinuses, , mastoid air cells, , or otitis media Any bacteremia
Pneumonia and endocarditis cause bacteremia, which can lead to a brain abscess
BrainAbscess/Presentation
Headache, nausea, vomiting, fever, seizures, and focal neurological findings No way to distinguish brain abscess from cancer without a biopsy Cancer gives fever fever, too
MTBS2CK p.285
MTBS2CK p.286
BrainAbscess/DiagnosticTests
Best initial test is... Head CT or MRI Most accurate test is... Brain biopsy
BrainAbscess/DiagnosticTests
Scan shows a ring or contrast-enhancing lesion Surrounding edema Mass effect Cancer and infection are indistinguishable based on imaging study alone
Source:NishithPatel Source:NishithPatel
MTBS2CK p.286
MTBS2CK p.286
BrainAbscess/Microbiology
Biopsy is essential Only biopsy distinguishes abscess from cancer Only way to know sensitivity of organism Abscesses can be... Staphylococci, streptococci, Gram-negative bacilli, and anaerobes Frequently mixed (polymicrobial) Treat for... 6 to 8 weeks intravenously Followed by 2 to 3 more months orally
MTBS2CK p.286
BrainAbscess/Treatment
Empiric therapy Penicillin + metronidazole + ceftriaxone (or cefepime) Vancomycin (alternative to penicillin) Use vancomycin if theres been recent neurosurgery
MTBS2CK p.287
15
NeurocutaneousDiseases
TuberousSclerosis
Neurological abnormalities
Seizures, slowly progressive mental deterioration
Tuberous sclerosis Neurofibromatosis (von Recklinghausen Disease) Sturge-Weber Syndrome
Skin
Adenoma sebaceum (reddened facial nodules) Shagreen patches (leathery plaques on trunk) Ash leaf (hypopigmented) patches

MTBS2CK p.287
Retinal lesions Cardiac rhabdomyomas No specific treatment Control seizures

MTBS2CK p.287
Neurofibromatosis (vonRecklinghausenDisease)
Neurofibromas: soft, flesh-colored lesions attached to peripheral nerves 8th CN tumors Cutaneous hyperpigmented lesions (caf au lait spots) Meningioma and gliomas
Source:MohammadMaruf,MD.
Neurofibromatosis (vonRecklinghausenDisease)
No specific treatment Lesions affecting 8th CN may require surgical decompression to preserve hearing
MTBS2CK p.287
MTBS2CK p.287
SturgeWeberSyndrome Port-wine stain of face Seizures CNS

Homonymous hemianopsia Hemiparesis Mental subnormality
MovementDisorders Part1
EssentialTremor Parkinsonism RestlessLegSyndrome Huntington Disease TouretteDisorder MultipleSclerosis
Skull X-ray
Calcification of angiomas
No treatment Control seizures

MTBS2CK p.288
16
EssentialTremor
Occurs at both rest and intention (i.e., reaching for things) Tremor greatest in hands, but can affect head Affects some manual skills
Handwriting or use of computer keyboard
EssentialTremor
Caffeine makes it worse Treat with propranolol
Tremor at rest and exertion improved with a drink of alcohol is key to diagnosis
MTBS2CK p.288
Parkinsonism/Definition Loss of substantia nigra Decrease in dopamine Movement disorder Tremor and gait disturbance
Parkinsonism/Etiology Head trauma from boxing Use of antipsychotic medications

Thorazine
Encephalitis Reserpine Metoclopromide
No test for parkinsonism Diagnosis is entirely on clinical presentation
MTBS2CK p.288
MTBS2CK p.288
Parkinsonism/Presentation
Look for 50-60 (or older) with... Tremor Muscular rigidity Bradykinesia (slow movements) Shuffling gait with unsteadiness on turning Tendency T d to t fall f ll Cogwheel rigidity (slowing of movement on passive flexion or extension of extremity) Facial expression limited (hypomimia) Writing is small (micrographia)
MTBS2CK p.289
PillRollingTremor
17
ParkinsonFacies
Parkinsonism/Presentation Postural instability or orthostatic hypotension Inability of pulse and BP to reset Lightheadedness when getting up from seated position
The most frequent Parkinsonism question is: Treatment

Know the drugs!
MTBS2CK p.289
Parkinsonism/Treatment Mild disease Anticholinergic medications relieve tremor and rigidity Benztropine and trihexyphenidyl Adverse effects Dry mouth Worsening prostate hypertrophy Constipation More frequent in older patients
MTBS2CK p.289
Parkinsonism/Treatment Mild disease Amantadine Increases release of dopamine from substantia nigra Definitely y the answer in older patients p ( (> 60) ) intolerant of anticholinergic medications
MTBS2CK p.289
Parkinsonism/Treatment Severe disease Inability to care for themselves, orthostatic Dopamine agonists Pramipexole Ropinirole Bromocriptine and cabergoline are older agents Infrequent use because of adverse effects
Parkinsonism/Treatment Severe disease Levodopa/carbidopa Single most effective medication Associated with on/off phenomena Episodes of insufficient dopamine (off) ( off ) characterized by bradykinesia The on effect is too much dopamine resulting in dyskinesia
MTBS2CK p.289
MTBS2CK p.289
18
Parkinsonism/Treatment Severe disease COMT inhibitors (tolcapone, entacapone) Extends duration of levodopa/carbidopa Blocks metabolism of dopamine Used only with levodopa/carbidopa Use when there are on/off phenomena to even out dopamine level When response to therapy is inadequate
Parkinsonism/Treatment
Severe disease MAO inhibitors (rasagiline, selegiline)
As single agent or an adjunct to levodopa/carbidopa Block metabolism of dopamine
Deep brain stimulation

Electrical stimulation Highly effective in some patients
MTBS2CK p.289
MTBS2CK p.289
Spasticity
70-year-old man with extremely severe parkinsonism comes to ED with psychosis and confusion developing at home. Hes maintained on levodopa/carbidopa, ropinirole, and tolcapone. Whats the most appropriate next step in management?
a. b. c. d. e.
Stop levodopa/carbidopa Severe Parkinsonism Start clozapine Stop ropinirole Dont stop meds severe parkinsonism Stop tolcapone Dont stop meds severe parkinsonism Start haloperidol More adverse effects than clozapine
Dont Don t stop meds!
Painful, contracted muscles From damage to CNS Often associated with MS No single treatment always effective Baclofen and tizanadine (central-acting alpha agonist) may work
MTBS2CK p.290
MTBS2CK p.290
RestlessLegsSyndrome
HuntingtonDisease(HD)
Uncomfortable sensation in legs Creepy and crawly at night Bed partner who is being kicked at night Discomfort worsened by caffeine Relieved by moving legs Treat with dopamine agonists (e.g., pramipexole)
Hereditary disease CAG trinucleotide repeat sequences on chromosome 4
MTBS2CK p.290
MTBS2CK p.291
19
HuntingtonDisease/Presentation What is the most likely diagnosis? HD is the answer when you see... Choreaform movement disorder (dyskinesia) Dementia Behavior changes Irritability, moodiness, antisocial behavior Onset between 30 - 50 Often with family history of HD
HuntingtonDisease
Diagnosis Symptom triad Movement Memory Mood
Genetic testing >99% accurate
MTBS2CK p.291
MTBS2CK p.291
HuntingtonDisease
TouretteDisorder Idiopathic disorder Vocal tics, grunts, and coprolalia Motor tics (sniffing, blinking, frowning) Obsessive-compulsive behavior No specific diagnostic test Treat with neuroleptics e.g. Fluphenazine, clonazepam, pimozide ADHD drugs Methylphenidate
MTBS2CK p.291
Treatment No treatment can reverse HD Dyskinesia treated with tetrabenazine Psychosis treated with haloperidol or quetiapine ti i
MTBS2CK p.291
MultipleSclerosis
MultipleSclerosis/Presentation
What is the most likely diagnosis? Look for: Multiple neurological deficits of CNS Affects any aspect of CNS Most common presentation:
Blurry vision Visual disturbance from optic neuritis
Idiopathic disorder Exclusively CNS (brain and spinal cord) More common in white women living in colder climates
MTBS2CK p.291
MTBS2CK p.291
NEUR_02_19
20
MultipleSclerosis/Presentation
After optic neuritis, the most common abnormalities are motor and sensory Other findings
Fatigue Spasticity and hyperreflexia Cerebellar deficits
MultipleSclerosis/DiagnosticTests
MRI: Best initial AND Most accurate test
Least common findings Cognitive defects Dementia Sexual dysfunction

Source:SabaAnsari,MD
MTBS2CK p.292
MTBS2CK p.292
MultipleSclerosis/DiagnosticTests
Lumbar puncture: CSF Mild elevation in protein < 50 - 100 WBCs
Oligoclonal bands: Found in 85% of MS Oligoclonal bands: Not specific to MS
MultipleSclerosis/Treatment
The best initial therapy for acute exacerbations of MS... High-dose steroids
Oligoclonal bands are the answer in 3% - 5% with equivocal (nondiagnostic) MRI
MTBS2CK p.292
MTBS2CK p.292
MultipleSclerosis/Treatment Drugs that prevent relapse and progression Glatiramer (copolymer1) Beta-interferon Natalizumab Mitoxantrone Fingolimod Dalfampridine Azathioprine and cyclophosphamide (rarely used)
MTBS2CK p.292
MultipleSclerosis/Treatment A new MS treatment is started. MRI shows new, multiple white matter hypodense lesions. What is it? Progressive g multifocal leukoencephalopathy (PML) What is the cause? Natalizumab
MTBS2CK p.293
21
AmyotrophicLateralSclerosis(ALS)
MovementDisorders Part2
AmyotrophicLateralSclerosis CharcotMarieTooth Disease PeripheralNeuropathy FacialNervePalsy GuillainBarrSyndrome MyastheniaGravis
Exclusively a loss of upper and lower motor neurons
Idiopathic
MTBS2CK p.293
AmyotrophicLateralSclerosis(ALS)
What is the most likely diagnosis? Look for... Weakness starting in 20s to 40s Combination of upper and lower motor neuron loss Initial presentation... Difficulty Diffi lt chewing h i and d swallowing ll i Decrease in gag reflex Pooling of saliva in pharynx and weak cough Frequent episodes of aspiration Death in patients within 3 to 5 years after diagnosis Most commonly due to respiratory failure
MTBS2CK p.293
PresentationofAmyotrophicLateralSclerosis UpperMotorNeurons LowerMotorNeurons
Weakness Weakness Spasticity Wasting Hyperreflexia Fasciculations Extensorplantarresponses
MTBS2CK p.293
KineticTremor
Fasciculations
22
AmyotrophicLateralSclerosis/DiagnosticTests
AmyotrophicLateralSclerosis/Treatment
Riluzole Reduces glutamate buildup in neurons Delays progression Baclofen Treats spasticity CPAP and d BiPAP Help respiratory difficulties secondary to muscle weakness Tracheostomy Maintenance on ventilator necessary when disease advances
MTBS2CK p.293
Electromyography
Loss of neural innervation in multiple muscle groups CPK levels
MTBS2CK p.293
CharcotMarieToothDisease
Genetic disorder Lose both motor and sensory innervation
Distal weakness & sensory loss Wasting in legs Decreased DTRs Tremor
PeripheralNeuropathy
MCC: Diabetes mellitus Other causes: uremia, alcoholism, and paraproteinemias (e.g., MGUS) Best initial therapy
Pregabalin, gabapentin
Foot deformity with high arch common (pes cavus) Legs look like inverted champagne bottles Most accurate test: Electromyography No treatment
MTBS2CK p.294
Tricyclic antidepressants Most seizure medications effective in some people

Phenytoin Carbamazepine Lamotrigine
MTBS2CK p.294
SpecificPeripheralNerveNeuropathies
Nerve Ulnarnerve Precipitatingevent Biker,pressureonpalmsof hands,medialelbowtrauma Presentation Wastingof hypothenar eminence, 4th/5th digitpain p Wristdrop
SpecificPeripheralNerveNeuropathies
Nerve Tibial nerve Peroneal nerve Precipitatingevent Worsenswithwalking Presentation Pain/numbnessin ankle&soleoffoot Weakfootwith decreased dorsiflexionand eversion Thenar eminince, pain/numbness in1st 3fingers
Radialnerve
pp arm, Pressureoninner/upper useofcrutches,Saturdaynight palsy (fallingasleeponarm) Obesity,pregnancy,sittingwith crossedlegs
Highboots,pressureonthe backofknee
Lateral cutaneousn. ofthethigh

MTBS2CK p.294
Pain/numbness ofouteraspect ofthigh
Median nerve
Typists,carpenters, workingwithhands
MTBS2CK p.294
23
Facial(SeventhCranial)NervePalsy
Paralysis of entire side of face Stroke paralyzes only lower half of face Upper half of face innervate from both cerebral hemispheres Difficulty closing eye If they can wrinkle forehead on affected side worry about stroke
Also known as Bells palsy Mostly idiopathic Some identified causes

Lyme, sarcoidosis, herpes zoster, and tumors
Look for statement the face feels stiff or pulled to one side
MTBS2CK p.294
Cannot wrinkle forehead = Bell's palsy!
MTBS2CK p.295
Facial(SeventhCranial)NervePalsy Hyperacusis Sounds are extra loud 7th CN supplies stapedius muscle Acts as a shock absorber on ossicles of middle ear Taste disturbance 7th CN supplies sensation of taste to anterior two-thirds of tongue
MTBS2CK p.295
The most accurate test is... Electromyography and nerve conduction studies But...no test is usually done
MTBS2CK p.295
The best initial therapy is... Prednisone But...

60% of patients have full recovery even without treatment
38-year-old with pain near his ear followed by weakness of one side of his face. Both upper and lower parts of face are weak. Sensation is intact. What is the most common complication?
Acyclovir does not help
a. b. c. d. e. f.
Corneal ulceration Aspiration pneumonia Gag reflex and cough are normal Sinusitis Nasal discharge & face pain Otitis media Ear pain, decreased hearing Deafness Sounds are actually extra loud Dental caries Cavities do not paralyze your face!
MTBS2CK p.278
MTBS2CK p.295
24
GuillainBarrSyndrome
Acute inflammatory polyneuropathy Autoimmune damage of multiple peripheral nerves
What is the most likely diagnosis? Look for: Weakness of legs that ascends from feet Moves toward chest Loss of DTRs Some S have h mild ild sensory di disturbance t b Respiratory muscle weakness
No CNS involvement
Circulating antibody attacks myelin sheaths of peripheral nerves Associated with Campylobacter jejuni
GBS hits diaphragm!

Autonomic dysfunction with hypotension, HTN, or tachycardia can occur
CSF = increased protein + normal cell count Most specific diagnostic test Nerve conduction studies/electromyography
Decrease in propagation of electrical impulses along nerves
GuillainBarrSyndrome Tests of respiratory muscle involvement Inspiration is the active part of breathing and the patient loses the strength to inhale
Decrease in FVC Decrease in peak inspiratory pressure
PFTs tell who might die from GBS
MTBS2CK p.296
MTBS2CK p.296
Treatment Intravenous immunoglobulin (IVIG) or plasmapheresis are equal in efficacy
Woman comes with bilateral leg weakness over last few days. No knee jerk or ankle jerk reflexes. Weakness started in feet and progressed up to calves and thighs. Which of the following is the most urgent step?
Prednisone is a wrong answer for GBS, doesnt help Combining IVIG and plasmapheresis is incorrect
MTBS2CK p.296
a. b. c. d. e.
Pulmonary function testing Arterial blood gas Dont wait for inc CO2 on ABG Nerve conduction study Most accurate, but not next Lumbar puncture For Dx, not severity assessment Peak flow meter Assesses expiratory flow
MTBS2CK p.296
25
MyastheniaGravis
MyastheniaGravis/Presentation
What is the most likely diagnosis? Look for...
Double vision and difficulty chewing Weakness of limb muscles worse at end of the day Ptosis Weakness with sustained activity Normal pupillary responses
Muscular weakness from antibodies against acetylcholine receptors at the NMJ
Extraocular muscles & mastication (masseter) are often the only 2 muscular activities universally done by people (e.g., watching TV and eating)
MTBS2CK p.297
MTBS2CK p.297
MyastheniaGravis/DiagnosticTests Best initial test is... Acetylcholine receptor antibodies (80% 90% sensitive) Better answer than edrophonium testing Edrophonium
Short-acting inhibitor of acetylcholinesterase Temporary bump up in acetylcholine levels Associated with a clear improvement in motor function that lasts for a few minutes
MyastheniaGravis/DiagnosticTests
Most accurate test is... Electromyography
Shows decreased strength with repetitive stimulation
Questions often ask What What imaging test should be done? Answer... Chest something!
Chest X-ray, CT, or MRI are done to look for thymoma or thymic hyperplasia
MTBS2CK p.297
MTBS2CK p.297
MyastheniaGravis/Treatment
MyastheniaGravis/Treatment If meds dont control disease, the most appropriate next step in management is... Thymectomy if < 60 If > 60 prednisone is used Azothioprine, p , cyclophosphamide, y p p , or mycophenolate are used in order to get patient off steroids
Best initial treatment is... Neostigmine or pyridostigmine Longer acting versions of edrophonium
MTBS2CK p.297
MTBS2CK p.298
26
MyastheniaGravis/Treatment
Acute myasthenic crisis Severe, overwhelming disease Profound weakness Respiratory involvement Treated with IVIG or plasmapheresis
MTBS2CK p.298
27
Obstetricsand Gynecology
JasonM.Franasiak,MD ChiefResidentPhysician Obstetrics&Gynecology UniversityofNorthCarolina
Pregnancy
Definitions SignsandDiagnosisofPregnancy Ph i l i Ch Physiologic Changesi inP Pregnancy
Pregnancy Pregnancy Symptoms

Amenorrhea Breast tenderness Nausea and vomiting Fatigue
27-year-old woman with nausea and vomiting for 2 weeks. Symptoms worsen in the morning, but occur at any time during the day. She has a decrease in appetite. Her last menstrual period (LMP) was 6 weeks ago. Physical examination is unremarkable. Which is the best next step?
The surge in estrogen, progesterone, and betahuman chorionic gonadotropin (beta-HCG) leads to many symptoms of pregnancy
p for anemia, , but a. Complete p blood count Helpful not next step b. Beta-HCG c. HIDA scan Not initial work-up for nausea/vomitting d. Comprehensive metabolic panel Important, but must diagnose cause e. Urinalysis Important, but must diagnose cause
MTBS2CK p.441
MTBS2CK p.441
Definitions
DatingMethods Developmental age (DA): Days since fertilization Gestational age (GA): Days/weeks since the LMP
Fetus Infant
Embryo
On average, 2 weeks longer than DA
Ngele rule: Estimate day of delivery

Take the first day of LMP, subtract 3 months then add 7 days
1 year
Bi th Birth 8 weeks gestation Fertilization
Example: LMP = 7 / 1 / 2010 -3 +7 EDD = 4 / 8 / 2011
MTBS2CK p.441
MTBS2CK p.442
TrimesterBreakdown
1st Trimester Fertilization 12 weeks DA 14 weeks GA
FIRST screening Fetal heart tones with doppler
TermLengths
2nd Trimester 24 weeks DA 26 weeks GA 3rd Trimester Delivery
Frequent visits Monitoring for labor
Previable Fertilization
Preterm
Term
Postterm 42 weeks GA
Genetic triple or quad screen Fetal movement at 16-20 weeks GA Anatomic ultrasound at 18-20 weeks GA
24 weeks GA
37 weeks GA
MTBS2CK p.442
MTBS2CK p.442
Gravidity/Parity
G6P2124
Gravity Number of Pregnancies Parity Full-term birth Living Children Abortions
20-year-old woman presents to the office because she believes shes pregnant. Her sexual partner usually wears a condom, but didnt 2 weeks ago. She is now 4 weeks late for her menstruation. Which of the following is a first sign of pregnancy?
Preterm birth
F-PAL = Full-term (F); Preterm (P); Abortions (A); Living Children (L)
MTBS2CK p.442443
a. Quickening b. Goodell sign c. Ladin sign d. Linea nigra e. Chloasma
Not felt until second trimester Seen at 6 weeks gestation Seen in second trimester Seen at 16 weeks gestation
MTBS2CK p.443
SignsofPregnancy
Sign Goodellsign Ladinsign Chadwicksign Telangiectasias/ palmarerythema Chloasma Lineanigra PhysicalFinding Softeningofcervix Softeningofuterine midline Bluediscolorationof vaginaandcervix Smallbloodvessels/ reddeningofpalms Hyperpigmentationof theface,worsewithsun Hyperpigmentation downabdomenmidline TimefromConception 46weeks 6weeks 68weeks 1st trimester 16weeks 2nd trimester
DiagnosticEvaluation Beta-hCG Urine and serum testing all highly sensitive Produced by cytotrophoblast or syncytiotrophoblast in placenta First trimester Doubling every 48 hours for first 4 weeks Urine pregnancy tests are positive 4 weeks following the first day of LMP Peak levels at 10 weeks gestation Levels drop in 2nd trimester
MTBS2CK p.444
MTBS2CK p.444
DiagnosticEvaluation
PhysiologicChangesinPregnancy Cardiovascular changes Cardiac output increases 30-50% Lower blood pressure
Decreased afterload Increased blood volume
Step2KeyPoints
Ultrasound confirms intrauterine pregnancy At 5 weeks, or a beta-HCG of 1500 IU/L, a gestational sac should be seen on ultrasound
Gestational Sac
Yolk Sac Image: X.Compagnion , commons.wikimedia.org
MTBS2CK p.444
MTBS2CK p.444
PhysiologicChangesinPregnancy
PhysiologicChangesinPregnancy
Gastrointestinal changes Morning sickness

Caused by increase in estrogen, progesterone, and HCG made by placenta
GenitourinaryandRenalChanges
Increase in the size of kidney and ureters
Increased risk of pyelonephritis Increased incidence of stress urinary incontinence
Physiologic hydronephrosis in pregnancy
Gastroesophageal reflux
Lower L esophageal h l sphincter hi t h has d decreased dt tone Displacement of stomach by uterus
Constipation
Motility in large intestine decreased
Increase in GFR
Decrease in BUN/creatinine
Image: Nevit Dilmen, WikiCommons
MTBS2CK p.445
MTBS2CK p.445
PhysiologicChangesinPregnancy Hematology Changes Increased...

RBCs Plasma Coagulation factors
PhysiologicChangesinPregnancy Hematology Changes Hypercoagulable state

Fibrinogen (Factor I) increases 50% along with fibrin split products (Factors VII, VIII, IX, X) Protein C and S (inhibitors of coagulation) decrease No increase in PT, , PTT, , or INR Recall: Virchow triad
Hypercoagulation
Anemia
Plasma volume > RBCs
Endothelial Damage
Stasis
PrenatalCare/FirstTrimester Visits every 4 to 6 weeks Between 11 and 14 weeks

Ultrasound confirms gestational age and check for nuchal translucency
PrenatalCare
FirstTrimester SecondTrimester ThirdTrimester OtherScreeningTests
A thickened or enlarged nuchal translucency is an indication of Down syndrome.
MTBS2CK p.445
Image: Dr. Wolfgang Moroder WikiCommons
PrenatalCare/SecondTrimester 17-year-old woman presents for routine prenatal checkup at 12 weeks. Which of the following is the most accurate method to establish gestational age? Genetic Screening: Risk of chromosomal anomalies 15-20 weeks gestation Triple screen
Maternal serum alpha-fetoprotein (MSAFP) beta-HCG Estriol
a. Ultrasound b. Beta-HCG c. Pelvic exam d. Fundal height e. LMP
Levels vary y widely y May change with multiple gestations May change with multiple gestations May be unreliable
Quad screen
Inhibin A added to triple screen
Banana Sign
MTBS2CK p.445446
MTBS2CK p.446
PrenatalCare/SecondTrimester Increased MSAFP may indicate dating error, neural tube defect, or abdominal wall defect
Banana Sign
PrenatalCare/SecondTrimester Landmarks in 2nd trimester: Auscultation of fetal heart rate 16 to 20 weeks: Quickening Fetal movement first detected by mother Multiparous M lti may experience i earlier li Anatomic ultrasound
18 to 20 weeks
Ultrasound at 16 weeks showing banana sign created by compression of cerebellum in posterior fossa due to neural tube defect.
Image: Dr. W. Moroder, WikiCommons
MTBS2CK p.446
MTBS2CK p.446
PrenatalCare/ThirdTrimester Visits are every 2 to 3 weeks until 36 weeks Weekly visits after 36 weeks Braxton-Hicks Contractions
Oft Often occur during d i 3rd trimester ti t Sporadic and dont cause cervical dilation If they become regular, the cervix should be checked to rule out preterm labor before 37 weeks
ThirdTrimesterTesting Week
27
Test
Completeblood count
Action
Ifhemoglobin<11, replaceironorally *withstoolsoftener Ifglucose>140atone hour performoral hour, glucosechallengetest Treatifpositive
2428 Glucosechallenge
36
Cervicalculturesfor Chlamydia andgonorrhea Prophylacticantibiotics Rectovaginal culturefor duringlabor groupBStreptococcus
MTBS2CK p.446
MTBS2CK p.446
PrenatalCare/ThirdTrimester Glucose challenge test: Fasting or nonfasting ingestion of 50 g of glucose and serum glucose check 1 hour later
PrenatalCare/OtherScreeningTests Chorionic Villus Sampling Done at 10 to 13 weeks Obtains fetal karyotype Catheter into intrauterine cavity to aspirate chorionic villi from placenta
Glucose challenge test: Fasting serum glucose, ingestion of 100 g of glucose Serum glucose checks at 1, 2, and 3 hours Elevated glucose during any two of these tests is abnormal
Image: National Human Genome Research Institute, WikiCommons
PrenatalCare/OtherScreeningTests
PrenatalCare/OtherScreeningTests
Amniocentesis Done after 15-20 weeks Obtains fetal karyotype Needle placed transabdominally into amniotic i ti sac and d withdraw ithd amniotic i ti fluid
Percutaneous umbilical blood sample In cases of Rh isoimmunization and when a fetal CBC is needed Needle placed transabdominally into uterus to get blood from umbilical cord
MTBS2CK p.447
MTBS2CK p.447
EctopicPregnancy
RiskFactors Presentation Diagnosis Management
29-year-old woman with history of chlamydia and abnormal vaginal bleeding presents with left lower quadrant abdominal pain for the past eight hours. Her LMP was 6 weeks ago. Her temperature is 99F, heart rate is 100 bpm, blood pressure is 130/80 mmHg, and respiratory rate is 13 breaths/minute. Which of the following is the most likely diagnosis? a. Ectopic pregnancy b. Menstrual cramps Altered menstrual pattern present c. Diverticulitis Does not cause vaginal bleeding d. Ovarian torsion e. Ovarian cyst
MTBS2CK p.447448
EctopicPregnancy Pregnancy implants outside the uterus Most commonly occurs in ampulla of fallopian tube
EctopicPregnancy/RiskFactors Risk Factors Previous ectopic pregnancies (strongest risk factor) Pelvic inflammatory disease (PID) Intrauterine devices (IUD)
70-80%
Source: Kaplan Lecture Notes
Source: Nevit Dilmen, wikimedia commons
MTBS2CK p.448
MTBS2CK p.448
Source: Gloecknerd, wikimedia commons
EctopicPregnancy
EctopicPregnancy
Presentation
Period of amenorrhea Unilateral lower abdominal or pelvic pain Vaginal bleeding If ruptured ruptured, can be hypotensive with peritoneal irritation
Differential diagnosis Abortion Acute appendicitis Adnexal torsion Corpus luteum cyst rupture
Diverticulitis Endometriosis Gastroenteritis PID UTI
MTBS2CK p.448
EctopicPregnancy
EctopicPregnancy/TransvaginalUltrasound
Diagnostic Tests Beta-hCG

Confirms pregnancy
Uterus Bladder
Ultrasound
Locates implantation p site
Laparoscopy:
Invasive test and treatment to visualize and remove the ectopic pregnancy
Ectopic pregnancy
MTBS2CK p.448
Image: Courtesy of Jason Franasiak, MD
EctopicPregnancy/Treatment
Ectopic Confirmed Ruptured Medical Treatment Stable Unstable IV fluids, blood products, dopamine Surgical Treatment Not Ruptured
EctopicPregnancy/MedicalTreatment
Baseline labs: CBC LFTs Kidney function -hCG Methotrexate given, -hCG checked 4 & 7 days later
< 15% drop in -hCG
> 15% drop in -hCG
2nd dose of methotrexate, -hCG checked day 4 & 7 > 15% drop in -hCG Surgical treatment
Surgery (Laparoscopy)
Persistently high -hCG
Observe for side effects, no other Rx necessary
MTBS2CK p.448
MTBS2CK p.449
EctopicPregnancy Exclusion Criteria for Methotrexate

Hemodynamically unstable patients Signs of impending or ongoing ectopic mass rupture Clinically important abnormalities in baseline hematologic, renal, or hepatic laboratory values Immunodeficiency, active pulmonary disease, or peptic ulcer disease Hypersensitivity to Methotrexate Coexistent viable intrauterine pregnancy Breastfeeding Unwilling or unable to be compliant with post-therapeutic monitoring Do not have timely access to a medical institution
MTBS2CK p.449
EctopicPregnancy/SurgicalTreatment
Surgical Treatment Salpingostomy Salpingectomy ostomy = cut ectomy = remove
Images: Courtesy of Jason Franasiak, MD
MTBS2CK p.449450
EctopicPregnancy Mothers who are Rh negative should receive anti-D Rh immunoglobulin (RhoGAM) to prevent hemolytic disease
Abortion
MTBS2CK p.450
Abortion
20-year-old woman presents to ED for vaginal bleeding and lower abdominal pain for one day. She states that shes 15 weeks pregnant. T 99.0F, HR 100 bpm, BP 110/75 mmHg, and RR 12/min. Pelvic exam, blood present in vault. Ultrasound shows intrauterine bleeding, products of conception, and dilated cervix. Which is the most likely diagnosis?
A pregnancy that ends < 20 weeks gestation or fetus weighs 500g 80% of spontaneous abortions occur prior to 12 weeks gestation
a. Complete abortion b. Incomplete abortion c. Inevitable abortion d. Threatened abortion e. Septic abortion
We are going to review the definitions in this section
MTBS2CK p.450
MTBS2CK p.450
Abortion Maternal factors that increase risk of abortion Maternal age Anatomic abnormalities
Abortion
MTBS2CK p.450
Source: Ed Uthman, MD., commons.wikimedia.org
Source: RadsWiki, commons.wikimedia.org
Abortion
Abortion
Maternal factors that increase risk of abortion

5 6 3 2

1. 2. 3. 4. 5. 6. Dye injector Cervix Uterus Adhesions Right Tube Left Tube
Maternal Age Anatomic abnormalities Infections Immunological factors (e.g. Anti-phospholipid syndrome or SLE) Endocrinological factors Malnutrition Trauma
MTBS2CK p.450
Source: Floranerolia, commons.wikimedia.org
Abortion/Presentation
Abortion/DiagnosticTests
Signs/Symptoms Cramping abdominal pain Vaginal bleeding Hypotension Tachycardia
CBC Blood type and Rh screen Pelvic ultrasound
You cannot answer the most likely diagnosis question about abortion without an ultrasound
MTBS2CK p.451
MTBS2CK p.450
Abortion/Types
Complete Incomplete Inevitable Threatened Missed Septic
Abortion
No products of conception Follow up in office
Products of conception intact, but intrauterine bleeding present and dilation of cervix D&C/Medical
Death of fetus, but all products of conception present in the uterus D&C/M di l D&C/Medical Infection of uterus and surrounding areas D&C and IV Antibiotics (levofloxacin & metronidazole)
Mothers whore Rh negative should also receive anti-D Rh immunoglobulin at this time
Some products of conception Dilation & Curettage (D&C) / Medical

MTBS2CK p.451
Products of conception intact, intrauterine bleeding, No dilation of cervix Bed rest, pelvic rest
MTBS2CK p.451
MultipleGestations/Presentation
MultipleGestations
Signs/Symptoms Exponential growth of uterus Rapid weight gain by mother Elevated beta-HCG and Maternal S Serum Al Alpha-Fetoprotein h F t t i (MSAFP) Fertility drugs increase multiple gestations
MTBS2CK p.451
MultipleGestations/DiagnosticTests Ultrasound visualizes fetus Monozygotic 1eggand Identicaltwins 1sperm Samegender thatsplits Samephysicalcharacteristics Samebloodtype Fingerprintsdiffer Dizygotic 2eggsand Fraternaltwins 2sperm Differentorsamesex Theyresembleeachother Asanysiblingswould
MultipleGestations
MTBS2CK p.452
Source:Trlkly , commons.wikimedia.org
MultipleGestations/DiagnosticTests
MultipleGestations
For monozygotic twins, amnionicity and chorionicity depend on timing of cleavage
10
MultipleGestations
MultipleGestations
Complications
Spontaneous abortion of one fetus Premature labor and delivery Placenta previa Anemia
Source: Kevin Dufendach, commons.wikimedia.org
MTBS2CK p.452
PretermLabor
28-year-old woman 28th week of pregnancy with severe lower back pain. The pain is cyclical and is increasing in intensity. On physical examination she seems to be in pain. T 98.9F, HR 104 bpm, BP 135/80 mmHg, RR 15/min. Cervix is 3 cm dilated. Which of the following is the most likely diagnosis?
a. Premature rupture of membranes Membranes intact b. Preterm labor c. Cervical incompetence Presents with contractions d. Preterm contractions Cervical dilation present
MTBS2CK p.452
PretermLabor
PretermLabor/RiskFactors
Preterm births occur < 37 weeks gestation

Spontaneous: preterm labor Indicated: maternal or fetal
Preterm labor
Activation of hypothalamic-pituitary-adrenal yp p y (HPA) axis Decidual hemorrhage Inflammation Uterine distension
Premature rupture of membranes Multiple gestation Previous history of preterm labor Placental abruption Maternal factors
Uterine anatomical abnormalities Infections
MTBS2CK p.452453
11
MTBS2CK p.453
Source: RadsWiki, commons.wikimedia.org
MTBS2CK p.453
Source: Ed Uthman, , commons.wikimedia.org
PretermLabor/Presentation
PretermLabor/Evaluation
Contractions
Cervical change
Initial evaluation Gestational age Fetal weight Presenting fetal part
Occurring between 20 and 37 weeks gestation
MTBS2CK p.453
MTS2CK p.453
PretermLabor/Evaluation Indications for delivery

Maternal severe HTN Maternal cardiac disease Maternal cervical dilation > 4 cm Maternal hemorrhage (abruptio placenta, DIC) Fetal death Chorioamnionitis Preterm rupture of membranes (34 weeks) Fetal distress Intrauterine growth restriction with reverse diastolic flow
PretermLabor
Preterm labor Stop delivery if Delivery if EGA 24-33 wks EGA 34-37 wks EFW 600-2,500 600-2 500 g EFW > 2,500 2 500 g Betamethasone & Tocolytics
MTS2CK p.453
When any of these is present, answer delivery

MTS2CK p.453
12
PretermLabor/Corticosteroids Corticosteroids Betamethasone or dexamethasone Effects of betamethasone begin within 24 hours and peak at 48 hours Goal Decrease risk of RDS and neonatal mortality
PretermLabor/Tocolytics
Goal Delay preterm labor Allows time for steroids to work Transport to specialist unit Agents Magnesium sulfate
Corticosteriods increase surfactant and thus mature fetal lungs

MTS2CK p.453 MTS2CK p.454
PretermLabor
Magnesium toxicity leads to respiratory depression & cardiac arrest, check deep tendon reflexes often!
Goal Decrease contractions Given to allow time for steroids to work Agents Magnesium sulfate Calcium-channel blockers -adrenergic agents Prostaglandin synthetase inhibitors
MTS2CK p.454
Toxicity: Give calcium gluconate
MTS2CK p.454
PrematureRuptureof Membranes
Ductus Arteriosus
13
PrematureRuptureofMembranes(PROM)
PrematureRuptureofMembranes
The rupture of chorioamniotic membrane before onset of labor
Diagnosis Sterile speculum examination

Fluid pools in posterior fornix Fluid turns nitrazine paper blue When dry, fluid has ferning pattern
Source: Elizabeth August, MD
MTS2CK p.454
MTS2CK p.454
PrematureRuptureofMembranes
PrematureRuptureofMembranes/Treatment
Before 32 weeks gestation
Corticosteroids Antibiotics
PROM can lead to Preterm labor Cord prolapse Placental ace a ab abruption up o Chorioamnionitis
PROM = Do fewer exams!
MTS2CK p.454455
>37 weeks gestation, unknown GBS, > 18 hours rupture

Penicillin administered for prophylaxis
34-37 34 37 weeks gestation, unknown GBS

Initiate Penicillin
Known GBS negative

NO Antibiotics
<34 weeks gestation, unknown GBS

Erythromycin and Penicillin initiated
MTS2CK p.455
ThirdTrimesterBleeding
DDx
Vulva (trauma, varicose veins) Vagina (lacerations) Cervix (polyp, cervicitis, carcinoma) Ut i Uterine Uterine rupture Placenta previa Vasa previa Placental abruption
14
ThirdTrimesterBleeding/Previa
Placenta previa Abnormal implantation of placenta over internal cevical os Risk Ri k F Factors t
Previous uterine scar Multiple gestations Previous placenta previa
MTS2CK p.456
24-year-old woman in her 32nd week of pregnancy presents to ED. She woke up in bed in a pool of blood. Denies contractions or pain. HR 105 bpm, BP 110/70 mmHg. Which is the next step?
a. Digital vaginal exam knowing placental location b. Transabdominal ultrasound c. Immediate vaginal delivery Gather information first d. Immediate cesarean delivery e. Transvaginal ultrasound Abdominal US is safer
Never do digital exam w/o
MTS2CK p.455
Digital vaginal exam contraindicated in third trimester vaginal bleeding Can cause Separation between placenta and uterus Severe hemorrhage
Source: Jason Franasiak, MD
MTS2CK p.455
ThirdTrimesterBleeding/PreviaTypes
Partial Complete Marginal Fetal vessel present over cervical os Vasa Previa Lowlying Placenta
Presentation PAINLESS vaginal bleeding Usually presents > 28 weeks Diagnosis Transabdominal ultrasound
Placenta location
Partial covering of the internal cervical os, but covers more than th the marginal Complete covering of the internal cervical os
MTS2CK p.456
Marginal covering of the internal cervical os
Placenta thats implanted in lower segments of uterus but not covering internal cervical os
MTS2CK p.456
15
ThirdTrimesterBleeding/PreviaTypes Full moon Half moon Crescent moon
ThirdTrimesterBleeding/PreviaTypes
Umbilical cord Placenta Fetal vessels Internal os

Source: Sigrid de Rooij, comons.wikimedia.org
MTS2CK p.456
MTS2CK p.457
ThirdTrimesterBleeding/Treatment
ThirdTrimesterBleeding/Accreta
Treatment of placenta previa Strict pelvic rest Type and screen, CBC Fetal considerations Delivery by C-section
Labor Severe hemorrhage Fetal distress
MTS2CK p.457
Placental invasion (based on depth) Accreta Increta Percreta
MTS2CK p.457458
ThirdTrimesterBleeding/Accreta
Placental invasion (based on depth) Accreta Increta Percreta Risk Factors Placenta previa Prior uterine scars
16
ThirdTrimesterBleeding/Abruption Placental abruption Abnormal, premature separation of placenta from uterus Effects Complete Partial
Life-threatening g bleeding Premature delivery Uterine tetany DIC And Hypovolemic shock
MTS2CK p.458
PlacentalAbruption
Minor bleed No clinical signs/symptoms
PlacentalAbruption/Etiology
PlacentalAbruption/Presentation
Risk factors Maternal HTN (chronic, preeclampsia, eclampsia) Prior placental abruption Tobacco T b and/or d/ cocaine i use Trauma
Clinical presentation Vaginal bleeding Severe abdominal PAIN (uterine tenderness) Contractions C t ti Possible fetal distress
MTS2CK p.458
MTS2CK p.458
PlacentalAbruption/Presentation
Late Decelerations
PlacentalAbruption/DiagnosticTests
Diagnosis Transabdominal ultrasound Clinical scenario
Placenta previa = painLESS vaginal bleeding

Placental abruption = painFUL vaginal bleeding

MTS2CK p.459
17
PlacentalAbruption/DiagnosticTests
PlacentalAbruption
Type Concealed Description Bloodwithinuterine cavity Placentamorelikely tobecompletely detached Complications Seriouscomplications: DIC Uterinetetany Fetalhypoxia Fetaldeath Sheehansyndrome (postpartum hypopituitarism)
External
Source: Nevit Dilman commons.wikimedia.org
Blooddrainsthrough Usuallysmallerwithminimal complications cervix Placentamorelikely tobepartially detached
MTS2CK p.459
PlacentalAbruption/Treatment
PlacentalAbruption/Treatment
Delivery plan Cesarean delivery

Uncontrollable hemorrhage Fetal distress
Mothers who are Rh negative should also receive anti-D Rh immunoglobulin at this time
Vaginal delivery
Placental separation is limited Fetal heart tracing is assuring Fetal death prior to presentation
MTS2CK p.459
MTBS2CK p.451
UterineRupture Spontaneous complete transection of uterus from endometrium to serosa Usually occurs during labor
UterineRupture
Life threatening to mother and baby Life-threatening
Immediate delivery!
MTS2CK p.459
18
UterineRupture/RiskFactors Risk factors Previous C-section

Classical: higher risk of uterine rupture Low transverse
UterineRupture
Trauma Uterine myomectomy Uterine overdistention

Polyhydramnios Multiple gestations
Types of cesarean scars. Source: Elizabeth August, MD.
Placenta percreta
UterineRupture/Presentation
UterineRupture/Treatment Treatment Emergent laparotomy and delivery Repair of uterus or hysterectomy Future management Early delivery via C C-section section Uterine rupture requires immediate laparotomy and delivery of the fetus
Clinical presentation: Extreme abdominal pain Abnormal bump in abdomen Lack of uterine contractions Regression of fetus
MTS2CK p.460
MTS2CK p.461
RhIncompatibility
Rh incompatibility
RhIncompatability
Mother RhD negative Baby RhD positive Leads to isoimmunization Rh isoimmunization Fetal RBCs cross placenta Maternal antibodies to RhD antigen are made
MTS2CK p.461
19
RhIncompatibility Clinical significance 1st pregnancy: mild anemia/hyperbilirubinemia 2nd pregnancy: maternal antibodies attack the second Rh positive baby
RhIncompatibility Hemolytic Disease of Newborn Fetal anemia Extramedullary production of fetal RBCs
Hemolysis heme and bilirubin levels

Neurotoxicity from hyperbilirubinemia High output cardiac failure Hydrops fetalis
Leads to hemolysis of fetal RBCs Hemolytic disease of newborn
MTS2CK p.461
MTS2CK p.461
RhIncompatibility Rh Antibody Screening Rh Negative Antibody titer Sensitized Further Monitoring

MTS2CK p.461
RhIncompatibility
Rh Positive No further screening
Antibody screen: if mother is Rh or Rh+ Antibody titer: how many maternal antibodies to Rh+ blood
Unsensitized
Repeat at 28 weeks and give Rhogam as indicated
MTS2CK p.461
RhIncompatibility
RhIncompatibility
Rhogam indications for Rh unsensitized patients 28 weeks gestation Delivery Procedures (amniocentesis) ( ) Bleeding (abortion, abruption) Unsensitized = no anti-Rh antibodies present
Antibody Screen Positive Antibody titer Titer 1:4 Sensitized Titer 1:16 consider treatment algorithm l ith
MTS2CK p.461462
MTS2CK p.462
20
RhIncompatibility
Antibody titer 1:16
RhIncompatibility
Antibody titer 1:16 Fetus is Rh Antigen Positive Middle Cerebral Artery Dopplers
Determine paternal Rhesus type
Homozygote Positive Treatment algorithm
Heterozygote or unsure paternity
Homozygote g Negative
Peak MCA Velocity is >1 5 MOM >1.5 (Multiples of median)
No Treatment Fetal genotyping performed on samples of chorionic villi, amniocytes or fetal blood Cordocentesis with transfusion if fetal Hct is <30%
MTS2CK p.462.3
MTS2CK p.462
RhIncompatibility
RhIncompatibility
Source: Jason Franasiak, M.D. Source: Jason Franasiak, M.D.
RhIncompatibility
Antibody titer 1:16 No MCA Doppler Capability
Amniocentesis for fetal cells to be evaluated under spectrophotometer (evaluated bilirubin) Indeterminate Affected Transfusion zone Fetus probably is anemic Do percutaneous umbilical blood sample (fetal hematocrit) Fetal Hct is <30% Perform an intrauterine transfusion
MTS2CK p.462.3
Hypertension
Repeat amniocentesis 2-3 weeks
Repeat amniocentesis 1-2 weeks
21
Hypertension/Chronic
29-year-old woman G2P1 in her 30th week of pregnancy presents for routine prenatal visit. Her wedding ring is getting too tight. BP 150/100 mmHg, HR 92 bpm, RR 12, T 99F. Urine 1+ protein. LFTs: normal. Which is the most likely diagnosis? a. Chronic hypertension b. Gestational hypertension No proteinuria c. HELLP syndrome No laboratory abnormalities d. Preeclampsia e. Eclampsia Pre-eclampsia + seizures
Chronic HTN BP 140/90 mmHg before 20 weeks gestation Treatment

Labetalol, nifedipine, or methyldopa ACE inhibitors and ARBs cause fetal malformations Dont use during pregnancy
MTS2CK p.463
MTS2CK p.463
Hypertension/Gestational
Gestational HTN BP 140/90 mmHg after 20 weeks gestation No proteinuria Treatment T t t Labetalol, nifedipine, or methyldopa
Only during pregnancy
Hypertension/Preeclampsia Mildpreeclampsia Severepreeclampsia Hypertension Proteinuria >140/90 Dipstick1+to 2+;24hour urine>300mg Hands,feet,face No No No >160/110 Dipstick3+;24hour urine>5g Generalized Yes Yes Yes
Edema Mental lstatus changes Visionchanges Impairedliver function
MTS2CK p.463
MTS2CK p.463
Hypertension/Preeclampsia
Mild BP > 140/90 mmHg Proteinuria 1+ to 2 + At term Induce I d delivery Preterm 1. Betamethasone a. Mature fetus lungs 2. Magnesium sulfate a. Seizure prophylaxis 1. Prevent Eclampsia p a. Magnesium sulfate 2. Control BP a. Hydralazine 3. Delivery a. Preterm b. Term Preeclampsia Severe BP > 160/110 Proteinuria 3+ to 4+
Preeclampsia Risk Factors Nulliparity Multiple gestation Advanced maternal age Chronic HTN Renal disease History of preeclampsia
MTS2CK p.463
MTS2CK p.464
22
Hypertension/Eclampsia
The only definitive treatment in preeclampsia is delivery
Eclampsia Tonic-clonic seizures occurring in patient with preeclampsia Treatment Stabilize St bili mother th
Seizure control: magnesium BP control: hydralazine and labetalol
Deliver baby
Hypertension HELLP
HELLP Syndrome Hemolysis, Elevated Liver enzymes, Low Platelets Treatment Stabilize mother
BP control: hydralazine and labetalol
GestationalDiabetes
Deliver baby
MTS2CK p.464
PregestationalDiabetes
28-year-old woman in her 27th week of gestation presents for routine prenatal visit. No complaints. T 99F, BP 120/80 mmHg, HR 87 bpm. The patient is given 50 mg of glucose. An hour later, blood glucose 145 mg/dL. Which is the best next step? a. Treat with insulin The 1h GTT is a screening test b. Treat with sulfonylurea c. Do a fasting blood glucose level A 3h GTT is needed d. Perform oral glucose tolerance test
Pregestational diabetes Diabetes before pregnancy Either Type 1 or Type 2 DM
MTS2CK p.464465
MTS2CK p.465
23
Maternal Complications Preeclampsia Spontaneous abortion Increased rate of infection Increased postpartum hemorrhage
Fetal Complications Congenital anomalies Macrosomia

Shoulder dystocia
Preterm P t labor l b
MTS2CK p.465
MTS2CK p.465
PregestationalDiabetes/Evaluation
PregestationalDiabetes DMtype Type1 Type2 Routeofadministration Insulinpump Subcutaneousinsulin Insulintype NPH NPH,lispro
Additional prenatal testing EKG 24-hour urine for baseline renal function HbA1C Ophthalmological exam
Oral Medications Metformin and glyburide
MTS2CK p.465
MTS2CK p.465
PregestationalDiabetes/FetalTesting Age (weeks) 32-36 >36 37 38-39

Weekly nonstress test (NST) and ultrasound NST: fetal well-being Ultrasound: fetal size Lecithin/sphingomyelin ratio (L/S ratio) L/S ratio: assess fetal lung maturity test (if mat mature re delivery) deli er )
GestationalDiabetes/Complications Gestational diabetes (GDM) Glucose intolerance identified during pregnancy Complications Preterm birth Fetal F t l macrosomia i Birth injuries from fetal macrosomia Neonatal hypoglycemia Development of overt Type 2 DM postpartum
Twice-weekly testing; one NST and one biophysical prole (BPP) NST: fetal well-being BPP: amount of amniotic uid and fetal well- being
MTS2CK p.466
Continue testing, IOL at 39 weeks
MTS2CK p.466
24
GestationalDiabetes/Complications
GestationalDiabetes/Evaluation
Erbs Palsy
Diagnosis Routine screening between 24 and 28 weeks GA 1-hour glucose tolerance test
Positive Positi e if > 140 mg/dL
3-hour glucose tolerance test

Klumpkes Palsy
MTS2CK p.466
GestationalDiabetes
Glucose load test Non-fasting ingestion of 50g glucose followed by No serum measurement one hour later < 140 mg/dL NO gestational diabetes > 140 mg/dL Oral glucose tolerance test Fasting ingestion of 100 mg of glucose followed by serum glucose measurements at 1, 2, and 3 hours after ingestion Elevation of serum glucose at 1, 2, or 3 hours Gestational diabetes
MTS2CK p.467
Diabetes/Treatment Treatment Diabetic diet and exercise (walking) Medical management

Insulin Oral hypoglycemics
All glucose levels are normal
No further test
Dont tell pregnant patients to lose weight. Its the most common wrong answer. Once patients are put on insulin they should follow fetal testing schedule starting at 32 weeks.
MTS2CK p.467
Diabetes/Treatment
Gestational diabetes needs formal 2-hour GTT postpartum to screen Type 2 DM
FetalGrowthAbnormalities
IntrauterineGrowthRestriction Macrosomia
MTS2CK p.467
25
IntrauterineGrowthRestriction Fetuses with intrauterine growth restriction (IUGR) weigh in bottom 10% for gestational age TypesofIUGR Type Symmetric Characteristic Braininproportionwithrestofbody Occurs<20weeksgestation
IntrauterineGrowthRestriction/Etiology
Chromosomal abnormalities Neural tube defects Infections (viral, protozoans) Multiple gestations Maternal disease
HTN or renal disease Malnutrition Substance abuse Hemoglobinopathies
Asymmetric Brainweightisntdecreased Abdomenissmallerthanhead Occurs>20weeks

MTS2CK p.467468
MTS2CK p.468
IntrauterineGrowthRestriction Physical examination Fundal height = gestational age in weeks Example: a patients fundal height at 28 weeks should be 28 cm
IntrauterineGrowthRestriction
Diagnosis Ultrasound done to confirm gestational age and fetal weight

MTS2CK p.468
Source: Jason Franasiak, M.D.
26
Complications Premature labor Stillbirth Fetal hypoxia Lower IQ Seizures Mental retardation
Treatment/Prevention Quit smoking Prevent maternal infection with immunizations Determine D t i optimal ti l d delivery li ti time
MTS2CK p.468
MTS2CK p.468
Macrosomia/RiskFactors
Macrosomia/DiagnosticTests
Macrosomia Estimated birth weight > 4500 g Risk factors Maternal M t l diabetes di b t or obesity b it Advanced maternal age Post term pregnancy Fetal genetic syndromes
MTS2CK p.468
Physical examination
Fundal height = gestational age in weeks Example: a patients fundal height at 28 weeks should be 28 cm
Macrosomia
Fundal height 3 cm greater than GA
MTS2CK p.469
Macrosomia/DiagnosticTests
Physical Examination Fundal height 3 cm than GA Ultrasound Ultrasound confirms the estimated weight by Femur length Abdominal circumference Head circumference and biparietal diameter
MTS2CK p.469
27
Macrosomia
ShoulderDystocia/ClavicleFracture
Complications Shoulder dystocia Birth injuries Low Apgar scores Hypoglycemia
MTS2CK p.469
Source: Nevit Dilman, commons.wikimedia.org
GestationalDiabetes/Complications
Macrosomia
Treatment Induction of labor

Erbs Palsy
Lungs mature EFW < 4500 grams
Cesarean deli delivery er

EFW > 5000 grams
Klumpkes Palsy
MTS2CK p.469
28
NonstressTest Allows for evaluation of fetal well-being in utero
LaborandDelivery
FetalTesting ElectronicFetalMonitoring g PhysiologicChangesBeforeLabor InductionofLabor
MTS2CK p.469
NonstressTest
BiophysicalProfile
Biophysical profile (BPP) Test NST g FetalBreathing FetalMovement Tone AmnioticFluid

Score 0or2 0or2 0or2 0or2 0or2
MTS2CK p.469
MTS2CK p.470
ElectronicFetalMonitoring
MTS2CK p.470
MTS2CK p.470
29
Type Early decelerations Variable decelerations Description Decreaseinheartratethat occurswithcontractions Decreaseinheartrateand returntobaselinewith no relationshiptocontractions Decreaseinheartrateafter contractionstarted.No returntobaselineuntil contractionends Cause Head compression Umbilicalcord compression
Late decelerations (mostserious anddangerous)
Fetalhypoxia
MTS2CK p.470
MTS2CK p.471
PhysiologicalChangesBeforeLabor
Labor&Delivery Stages of Labor

Stage 1 Onset of labor full dilation of cervix Primipara: 618 h p 210 h Multipara: Latent phase Onset of labor 4 cm dilation Primipara: 67 h Multipara: 45 h Stage 2 Full dilation of cervix delivery of neonate Primipara: p 2h Multipara: 1 h Active phase 4 cm dilation full dilation Primipara: 1.2 cm/h (minimum) Multipara: 1.5 cm/h (minimum) Stage 3 Delivery of neonate delivery of placenta 30 min
Early Changes Lightening Braxton-Hicks contractions Bloody show
MTS2CK p.471
MTS2CK p.471
30
Labor&Delivery
Labor&Delivery
Monitoring (Stage 1) Maternal BP and pulse Electronic fetal monitor: fetal HR and uterine contractions Examine E i cervix i ( (every 2 h hours) )
Cervical dilation Cervical effacement Fetal station
MTS2CK p.471
NOT effaced NO dilation
Fully effaced 1 cm dilated
5 cm dilation
Source: Fred the Oyster, commons.sikimedia.org
Fully dilated at 10 cm
Labor&Delivery
Labor&Delivery
Stage 2 Cervix fully dilated to delivery

Internal vs. External Fetal Monitoring
MTS2CK p.472
Stages of fetal head descent. Source: Elizabeth August, MD.
Labor&Delivery Internal vs. External Fetal Monitoring
Labor&Delivery Internal vs. External Fetal Monitoring
Source: Jason Franasiak, MD Source: Jason Franasiak, MD Source: Jason Franasiak, MD
31
Labor&Delivery
Labor&Delivery
Stage 2 Cervix fully dilated to delivery

Internal vs. External Fetal Monitoring Rupture of amniotic membranes Spontaneous or artificial Meconium
Stage 2: Cervix is fully dilated to delivery Cardinal Movements of Labor

1. 2. 3 3. 4. 5. 6. 7. Engagement Descent Flexion Internal Rotation Extension External Rotation Expulsion
MTS2CK p.472473
Labor&Delivery Stage 3 From delivery of neonate to placenta Immediately after delivery Repair lacerations of vagina Signs of placental separation include: Fresh bleeding from vagina Umbilical cord lengthening Uterine fundus rising Uterus becoming firm
MTS2CK p.473
OperativeDelivery
Operative Vaginal Delivery Forceps Vacuum C-section
OperativeDelivery
InductionofLabor/Medications
Induction of labor Initiating labor via medical means Medications PGE2 used for cervical ripening Oxytocin
Types of cesarean scars. Source: Elizabeth August, MD.
MTS2CK p.460
MTS2CK p.473
32
InductionofLabor/Medications
Mechanical means Amniotomy Foley Balloon

Inspect for a prolapsed umbilical cord after puncturing amniotic sac
ComplicationsofLabor andDelivery
ProlongedLatentStage ProtractedCervicalDilation ArrestDisorders Malpresentation ShoulderDystocia PostpartumHemorrhage
MTS2CK p.473
ProlongedLatentStage
22-year-old primipara in 39th week of pregnancy, with intense abdominal pain thats intermittent. Gush of fluid felt 3 hours ago. Cervix 3 cm dilated, 50% effaced, and fetus head is felt at 2 station. The next 3 hours she progresses, her cervix is 5 cm dilated, 60% effaced, and fetal head at 1 station. Six hours after presentation, her cervix is 5 cm dilated and 60% effaced, fetal head at 0 station. Which is the most likely diagnosis? a. Prolonged latent stage Cervix has not dilated b. Protracted cervical dilation Cervix has not dilated c. Arrest of descent Fetal head has descended d. Arrest of cervical dilation
Prolonged latent stage Latent phase 20 hours for primipara Latent phase 14 hours for multipara Etiology Sedation Unfavorable cervix Uterine dysfunction with irregular/weak contractions
MTS2CK p.474
MTS2CK p.474
ProlongedLatentStage
ProtractedCervicalDilation Stage 1 of labor < 1.2 cm/hour in primipara < 1.5 cm/hour in multipara Etiology: 3 Ps Power: strength and frequency of contractions Passenger: size and position of fetus Passage: size of pelvis
Treatment of Prolonged Latent Phase Rest Hydration

Most will convert to spontaneous delivery in 6 to 12 hours
MTS2CK p.474
MTS2CK p.474475
33
ProtractedCervicalDilation
ArrestDisorders/Types
Treatment of protracted cervical dilation Power

Pitocin Amniotomy
Arrest of Cervical Dilation No cervical dilation for 2 hours Arrest of Fetal Descent No fetal descent for 1 hour
Passenger/Pelvis
C-section
MTS2CK p.475
MTS2CK p.475
ArrestDisorders/Etiology
Etiology Cephalopelvic disproportion

Cesarean delivery
Excessive sedation/anesthesia
Rest or reversal
Malposition
Time Operative delivery (forceps) Cesarean delivery
25-year-old woman in 35th week of gestation presents for routine prenatal checkup. T 98F, BP 130/90, HR 87, and RR 12. Her abdomen is gravid. A hard circular surface is felt in proximal part of the uterus. Which is the next step? a. External cephalic version Perform ultrasound first b. Ultrasound c. CT scan Ultrasound is used to determine position d. X-ray
MTS2CK p.475
MTS2CK p.475
Malpresentation/Presentation
Presenting Part Part of fetal body thats closest to vaginal canal and will be engaged when labor starts Cephalic
Head
Diagnosis Physical Examination

Leopold maneuvers Vaginal exam
Ultrasound Ultraso nd Should always confirm suspected diagnosis on physical examination with ultrasound
MTS2CK p.476.
Malpresentation
Foot or buttock
MTS2CK p.476
34
TypesofBreechPresentation
Type
Description
Frankbreech Fetushipsareflexedwithextended kneesbilaterally Complete b breech h Footling breech Fetushipsandkneesareflexed bil bilaterally ll Fetusfeetarefirst oneleg(singlefootling) or bothlegs(doublefootling)
MTS2CK p.476
Source: Elizabeth August, MD.
MTS2CK p.476
MTS2CK p.477
MTS2CK p.477
Malpresentation/Treatment
ShoulderDystocia
Treatment External cephalic version C-section
Shoulder dystocia Entrapment of anterior shoulder behind pubic symphisis after delivery of fetal head
MTS2CK p.477
MTS2CK p.477
35
ShoulderDystocia
ShoulderDystocia/RiskFactors
Risk Factors Maternal diabetes Maternal obesity Post-term pregnancy History of prior shoulder dystocia Any factor that indicates fetus is too big or the pelvis is too small is a risk factor for shoulder dystocia
MTS2CK p.478
MTS2CK p.478
ShoulderDystocia/Treatment
Treatment 1. McRoberts Maneuver
McRoberts maneuver. Source: Elizabeth August, MD.
MTS2CK p.478479
MTS2CK p.478
PostpartumHemorrhage/Etiology
Treatment
1. McRoberts maneuver 2. Rubin maneuver 3. Woods maneuver 4. Delivery of posterior arm 5. Deliberate fracture of fetal clavicle 6. Zavanelli maneuver
Postpartum hemorrhage More than 500 mL after delivery Early vs. late postpartum bleeding Etiology gy a = without Uterine atony tony = contractions Laceration Retained products of conception Coagulopathy
MTS2CK p.479
MTS2CK p.478
36
PostpartumHemorrhage/RiskFactors
Risk factors for atony Anesthesia Uterine overdistention Prolonged/rapid labor Augmented labor Uterine leiomyoma Preeclampsia with magnesium therapy
PostpartumHemorrhage/Treatment Evaluation/Treatment
Examination of perineum, vagina, and cervix Bimanual examination of uterus (+/- compression/massage) Administer uterotonics (oxytocin, methylergonovine maleate, 15 methyl-PGF2alpha/Hemabate, misoprostol) Operative management
Uterine artery y embolization D&C Bakri balloon placement
Collapsed silicone ballon inserted in uterus, later filled with fluid
B-Lynch stitch Uterine artery ligation Hysterectomy

MTS2CK p.479
MTS2CK p.479
PostpartumHemorrhage/Treatment B-Lynch Suture Uterine Artery Ligation
PostpartumHemorrhage/Treatment
Evaluation/Treatment Examination of perineum, vagina, and cervix Bimanual examination of uterus Administer uterotonics Operative management Blood products
PRBCs, FFP, Cryoprecipitate
Source: Niels Olson, commons.wikimedia.org Modified: Jason Franasiak, MD
PostpartumHemorrhage/Treatment Product PackedRBCs Contents Effect
RBCs,WBCs,plasma Hct3% Hgb1g/dL Solubleplasma proteins p fibrinogen10 mg/dL g/ fibrinogen10 mg/dL 5000 10,000/mm3 per unit
TheUterus
PremenstrualSyndrome Menopause AUB/DUB Contraception
FFP
Cryoprecipitate FactorsVIIIandXIII, fibrinogen, fibronectin,vWF Platelets Platelets,RBCs, WBCs,plasma
37
PMS/PMDD
PMS/PMDD
Premenstrual syndrome (PMS) Physical, mood-related, and behavioral changes
Over 200 symptoms attributed to PMS Common symptoms

Headache Breast B t tenderness t d (mastodynia) ( t d i ) Pelvic pain, bloating Irritability, lack of energy
Premenstrual Dysphoric Disorder (PMDD) Severe form of PMS
MTBS2CK p.481
MTBS2CK p.481
PMS/PMDD
PMS/PMDD
Diagnostic criteria Present for 2 consecutive cycles Symptom-free in first part of cycle Symptoms present in second half of cycle Dysfunction in social or economic performance
Treatment of PMS/PMDD Lifestyle

Limit caffeine, alcohol, cigarettes, and chocolate Aerobic exercise Increase calcium and magnesium
Pharmacologic
NSAIDs Severe: SSRIs
MTBS2CK p.481
MTBS2CK p.481
Menopause
Menopause
Menopause Permanent cessation of menses Due to permanent cessation of estrogen production Median M di age of f onset: t 51
Physiology Early
The oocytes produce less estrogen and progesterone t LH and FSH start to rise Shortening of menstrual cycles
Late
Changes in sex hormones Testosterone Androstenedione Estrone Estradiol
MTBS2CK p.482
38
Menopause
Menopause
Symptoms Menstrual irregularity Sweats and hot flashes Mood changes Dyspareunia (pain during sexual intercourse) Women are symptomatic for an average of 12 months, but some experience symptoms for years
MTBS2CK p.482
Physical Examination Decrease in breast size Vaginal/cervical atrophy Uterovaginal prolapse Atrophic vaginitis: vaginal epithelium is estrogen dependent. The absence of estrogen causes thinning, presents as itching, burning, and/or dyspareunia.
MTBS2CK p.482
Menopause/Osteoporosis
Menopause Hormone replacement therapy (HRT) Estrogen +/- progesterone Contraindications

Estrogen-dependent carcinoma History of PE or DVT
HRT associated with endometrial hyperplasia, can lead to endometrial carcinoma
Vertebral body fractures. Source: Dr Robert CARLIER, CHU Raymond Poincar, Garches, France, commons.wikimedia.org
MTBS2CK p.482
AbnormalUterineBleeding
Menorrhagia
Heavy, prolonged menstrual bleeding Gushing of blood Clots may be seen Endometrial hyperplasia Uterine fibroids Dysfunctional uterine bleeding Intrauterine device Light menstrual flow May only have spotting Obstruction (hymen, cervical stenosis) OCPs
Metrorrhagia
Intermenstrual bleeding Endometrial polyps Endometrial/cervical cancer Exogenous estrogen administration d i i t ti Menometrorrhagia Oligomenorrhea Menstrual cycles > 35 days long Pregnancy Menopause Significant weight loss (anorexia) Tumor T secreting ti estrogen t Postcoital bleeding
Hypomenorrhea
Irregular bleeding Time intervals Duration u at o Amount of bleeding
Endometrial polyps Endometrial/cervical cancer Exogenous estrogen administration Malignant tumors
Bleeding after intercourse Cervical cancer Cervical polyps Atrophic vaginitis
MTBS2CK p.482483
MTBS2CK p.483
39
AbnormalUterineBleeding Uterine fibroid
Postcoital bleeding is cervical cancer until proven otherwise
Any patient > 35 with abnormal bleeding should undergo endometrial biopsy to rule out endometrial carcinoma
Source: James Heilman, MD, commons.wikimedia.org
MTBS2CK p.482483
AbnormalUterineBleeding Normal squamous cells HPV infects cells causing mild dysplasia
Anovulatory Uterine Bleeding Estrogen produced No progesterone

No ovulation no corpus luteum no progesterone Prevents withdrawal bleeding
Source: Ed Uthman MD, commons.wikimedia.org
DysfunctionalUterineBleeding
Diagnosis/Evaluation CBC Pregnancy test PT/PTT Pelvic ultrasound Endometrial biopsy Pap smear Thyroid studies Prolactin levels
Dysfunctional uterine bleeding (DUB)

Unexplained abnormal bleeding
Theres no specific test for DUB Diagnosis by exclusion

MTBS2CK p.483
40
Treatment of DUB Oral contraceptive pills (OCP) Cyclic progesterone Acute hemorrhage D&C IV estrogen
Long-term Endometrial ablation Hysterectomy
MTBS2CK p.484
Source: Hic et nunc, commons.wikimedia.org
Contraception/FemaleCondoms
Advantages Offer some protection against HIV and STDs Under female control Disadvantages Not as effective as other methods They are larger and bulkier than male condoms
MTBS2CK p.484
Contraception/FemaleCondoms
Contraception/VaginalDiaphragm
Source: : ka Grzywacz, commos.wikimedia.org
Source: Axefan2, commons.wikimedia.org
MTBS2CK p.484
MTBS2CK p.484
41
Contraception/CervicalCap
Contraception/VaginalDiaphragm
Advantages Under female control Disadvantages Need to be fitted properly Requires advance preparation Improper placement or dislodging reduces efficacy
Source: Dake, commons.wikimedia.org
Source: Ceridwen, commons.wikimedia.org
MTBS2CK p.484
Contraception/OralContraceptivePills
Hormones Combination of both estrogen and progestin Progestin only Use 21 days of active pill 7 days placebo Menses occurs during 7 days of placebo pills
Source; Matthew Bowden, commons.wikimedia.org
MTBS2CK p.484
MTBS2CK p.484
Contraception/VaginalRing
Advantages Effective with perfect use Reduces rates of ovarian and endometrial cancer Easily y reversible Disadvantages User dependent Risk of thromboembolism
MTBS2CK p.484
A flexible vaginal ring inserted in vagina

Releases both estrogen and progesterone Remains in place for 3 weeks
The vaginal aginal ring has similar side effects and efficacy to OCPs
MTBS2CK p.485
42
Contraception/TransdermalPatch
Contraception/TransdermalPatch
Transdermal patch
Combination of estrogen and progesterone Placed on skin for 7 days
Patches shouldnt sho ldnt be placed on breast Side effects and efficacy = OCPs
Source : Keitei, commons.wikimedia.org
MTBS2CK p.485
MTBS2CK p.485
Contraception/Injectable
Contraception/Implantable
Depo-Medroxyprogesterone Acetate (DMPA)

IM injection Every 3 months
Implant contraceptive system Releases progestin daily Inhibits ovulation and thickens cervical mucus
Contraception/IntrauterineDevice
Intrauterine device (IUD)

Copper device Levonorgestrel device
Most commonly used worldwide Most effective aside from sterilization
Source: Gloecknerd, commons.wikimedia.org
MTBS2CK p.485
MTBS2CK p.485
43
Contraception/Sterilization
Tubal Ligation/Occlusion Vasectomy
Source: Nevit Dilmen ,commons.wikimedia.org
MTBS2CK p.485
VulvaandVagina/LabialFusion Fusion Occurs when excess androgens are present

Exogenous Endogenous
VulvaandVagina
MCC of labial fusion is 21-B hydroxylase deficiency Treatment Conservative Reconstructive surgery
MTBS2CK p.485
VulvaandVagina/EpithelialAbnormalities
Abnormality Lichen sclerosus Agegroup affected Anyage Ifpostmenopausal, increasedconcern forcancer Description White,thinskin fromlabiato perianalarea, parchment Treatment Topical steroids
VulvaandVagina/BartholinGlandCyst
Bartholin Glands Location: lateral sides of vulva Function: secrete mucus Bartholin Gland Cyst/Abscess y Presents with pain, tenderness, and dyspareunia Edema and inflammation with deep fluctuant mass
MTBS2CK p.486
q Any yage; g p patients Squamous Patientswith cell whovehadchronic chronicirritation hyperplasiavulvarpruritus develophyper keratosis(raised whitelesion) Lichen planus 30s60s
Sitzbathsor lubricants (relieve pruritus)
Pruritic,polygonal, Topical papularand steroids Purple
MTBS2CK p.486
44
VulvaandVagina/BartholinGlandCyst
Clitoris Labia Minora Urethra Skenes glands g Vagina Bartholins glands
VulvaandVagina/BartholinGlandCyst Bartholin Abscess Simple incision and drainage (I&D) Word catheter placement 4-6 weeks duration Small rubber catheter, inflatable balloon tip is inserted into cyst incision, incision after the contents of the cyst have been drained Recurrence: marsupialization or excision During I&D, fluid released should be cultured for STDs (e.g., Neisseria gonorrhea and Chlamydia trachomatis)
MTBS2CK p.486
Source: Nicholasolan, commons.wikimedia.org
Vaginitis/RiskFactors 19-year-old woman with vaginal pruritus and discharge for one week. Discharge is green and profuse. Shes had multiple sexual partners in past 2 months. LMP 2 weeks ago. Wet mount: motile flagellates. Which is the most likely diagnosis? a. Chlamydia Dx w/ culture or DNA probe b. Bacterial vaginosis Clue cells on wet mount c. Neisseria gonorrhoeae d. Candidiasis Hyphae on wet mount e. Trichomonas vaginalis
Vaginitis: spectrum of conditions Risk factors

Antibiotic use (Lactobacillus normally keeps vaginal pH < 4 4.5) 5) Diabetes Overgrowth of normal flora
MTBS2CK p.486487
MTBS2CK p.487
TypesofVaginitis
Bacterial vaginosis Candidiasis Trichomonas (most common nonviral STD)
Vaginitis
Gardnerella Vaginal discharge with fishy odor; gray white Saline prep: clue cells Metronidazole or clindamycin
Candida albicans White, cheesy vaginal discharge Potassium hydroxide (KOH): pseudohyphae; vaginal culture is most specific Miconazole or clotrimazole, econazole, or nystatin
Trichomonas vaginalis Profuse, green, frothy vaginal discharge Saline prep: motile flagellates Treat both patient and partner with metronidazole
Trichomonas: partners need to be treated
MTBS2CK p.487
MTBS2CK p.487
45
Vaginitis/Gardnerella
Vaginitis/Candidaalbicans
Clue cells. Source: Per Grinsted, commos.wikimedia.org
Source: Nephron, commons.wikimedia.org
Vaginitis/Trichomonasvaginalis
Vulva/MalignantDisorders
Paget Disease Intraepithelial neoplasia Most common in postmenopausal Caucasians Presentation Vulvar soreness and pruritus Appears as a red lesion with superficial white coating
Trichomonas. Source: cdc.gov Trichomonas. Source: Alex Brollo, commons.wikimedia.org
MTBS2CK p.487
Large cells with clear cytoplasm in epidermis
Biopsy is needed for definitive diagnosis Treatment Wide local excision or vulvectomy 2 cm margin is optimal
Source: Nephron, commons.wikimedia.org
MTBS2CK p.487
46
Vulva/MalignantDisorders Squamous Cell Carcinoma Most common type of vulvar cancer Presentation Pruritus, bloody vaginal discharge, and postmenopausal bleeding Exam: ranges from a small ulcerated lesion to large cauliflower-like lesion A biopsy is essential for diagnosis
StagingofSquamousCellCarcinoma
Stage 0 I II III IV IVa
Findings Carcinomainsitu Limitedtovaginalwall<2cm Limitedtovulvaorperineum>2cm Tumorspreadingtolowerurethraoranus, unilateral il llymph l hnodes d present Tumorinvasionintobladder,rectum,or bilaterallymphnodes Distantmetastasis
MTBS2CK p.488
MTBS2CK p.488
Treatment Unilateral: modified radical vulvectomy Bilateral: radical vulvectomy Lymph nodes thatre involved must undergo lymphadenectomy
UterineAbnormalities
MTBS2CK p.488
UterineAbnormalities/Adenomyosis Adenomyosis Invasion of endometrial glands into myometrium Typically between ages of 35 and 50 Risk factors Endometriosis Uterine fibroids Presentation Dysmenorrhea and menorrhagia
MTBS2CK p.488
UterineAbnormalities/Adenomyosis
Diagnosis Clinical diagnosis Physical examination

Uterus is large, globular, boggy
MRI Treatment Hysterectomy - only definitive treatment
MTBS2CK p.488
47
UterineAbnormalities/Endometriosis Endometriosis Endometrial tissue outside of endometrial cavity Most common sites are ovary and pelvic peritoneum Endometriosis occurs in women of reproductive age More common if first-degree relative has endometriosis
UterineAbnormalities/Endometriosis
Presentation Cyclical pelvic pain Abnormal bleeding Infertility
Physical examination Nodular uterus Adnexal mass
Dysmenorrhea and dyspareunia are common in endometriosis
MTBS2CK p.488
MTBS2CK p.488489
UterineAbnormalities/Endometriosis
UterineAbnormalities/Treatment
Mild disease NSAIDs Combined OCPs Severe disease Danazole Leuprolide acetate (leupron) Surgery
Source: Julie M. Hastings, Asgerally T. Fazleabas, commons.wikimedia.org
MTBS2CK p.489490
MTBS2CK p.489
48
UterineAbnormalities/Treatment
OvarianAbnormalities
PolycysticOvarianSyndrome/Symptoms
PolycysticOvarianSyndrome/Diagnosis
Presentation Amenorrhea or irregular menses Hirsutism and obesity Acne Insulin resistance MCC of androgen excess and hirsutism
MTBS2CK p.489
Diagnostic test Pelvic ultrasound Elevated free testosterone LH to FSH ratio > 3:1
MTBS2CK p.489490
Uterus
Ovary
Source: Schomyny, commons.wikimedia.org
49
PolycysticOvarianSyndrome/Treatment
Treatment Weight loss OCPs Spironolactone (hirsutism) Metformin (insulin resistance) Clomiphene (infertility)
MTBS2CK p.490
50
Oncology
EmmaHolliday, Holliday MD ResidentPhysician RadiationOncology UniversityofTexasMDAndersonCancerCenter
BreastCancer
Presentation Diagnosis g GeneticTests Treatment
BreastCancer/Presentation
BreastCancer/Presentation Painless lump Skin changes Nipple retraction Nipple discharge
Most often found by patient Found in asymptomatic women

- On screening mammography - By palpation of a mass Hard immobile Hard, immobile, fixed to the chest wall
Source:http://www.4woman.gov/faq/cancerillustrations-with-t.gif
MTBS2CK p.347
MTBS2CK p.347
BreastCancer/DiagnosticTests Biopsy is the best initial test Different methods are: Fine needle aspiration (FNA)
Best initial biopsy
BreastCancer/DiagnosticTests
Mammography Screen the general population starting at age 50
Core needle biopsy

Tells receptor status
Open surgical biopsy

Most accurate test
MTBS2CK p.347
MTBS2CK p.347
WhenIsUltrasoundtheAnswer? A woman finds a hard, nontender breast mass on self-examination. There is no alteration of the mass with menstruation. She is scheduled to undergo a FNA biopsy. Which of the following is most likely to benefit the patient?
a. Mammography b. BRCA testing c. Ultrasound d. Bone scan e. PET scan
MTBS2CK p.348
Clinically indeterminate mass lesions. It tells cysts versus solid lesions Answer ultrasound if the lesion: Is painful Varies in size or pain with menstruation
Confirms an extra risk of cancer Tells cystic vs solid To exclude bone metastases
To look for metastatic disease

MTBS2CK p.348
WhenIsPETScantheAnswer? Determines content of abnormal lymph nodes that are not easily accessible to biopsy. Cancer increases uptake on PET scan.
WhenIsPETScantheAnswer? For example: 80-year-old woman with biopsy-proven breast cancer has no nodes with cancer in the axilla. The primary lesion is small and the woman may not need adjuvant j chemotherapy. py Chest CT shows an abnormal hilar lymph node.
How do you tell the content of an abnormal, inaccessible lesion without biopsy? Try PET scan.
MTBS2CK p.348
MTBS2CK p.348
WhenIsBRCATestingtheAnswer? BRCA associated with increased risk of breast cancer, particularly within families BRCA associated with ovarian cancer What is not clear is what to do when BRCA is positive BRCA not shown to add mortality benefit positive.
WhenIsSentinelLymphNodeBiopsy theAnswer? When you want to know how likely it is that the breast cancer has spread
The precise utility of MRI for breast cancer is not yet clear.
Source:http://www.cancer.gov/ncicancerbulletin/022211/page2
MTBS2CK p.348
MTBS2CK p.349
WhenAreEstrogenandProgesterone ReceptorsTested? Estrogen receptor (ER) and progesterone receptor (PR) testing is routine for all patients Hormone manipulation therapy is done if either test is positive
BreastCancer/Treatment Surgery Options Lumpectomy Modified Radical Mastectomy Radical Mastectomy
Radical mastectomy is always the wrong answer Lumpectomy + Radiation is JUST AS GOOD as modified radical mastectomy
HormonalManipulation All ER or PR positive patients should receive:

Tamoxifen Raloxifene Aromatase inhibitors (anastrazole, letrozole, exemestane) If all are among the answer choices, aromatase inhibitors are the answer to the most likely to benefit the patient question
BreastCancer/Treatment Know the differences in side effects:
Tamoxifen rarely gives endometrial cancer and clots (tamoxifen is a selective ER modifier). ) Aromatase inhibitors give osteoporosis (aromatase inhibitors inhibit estrogen effect everywhere, even the good effects, like on bone density).
MTBS2CK p.349
MTBS2CK p.349
WhenIsTrastuzumab theAnswer? All breast cancers should be tested for HER 2/neu. This is an abnormal estrogen receptor Those who are positive should receive antiHER 2/neu antibodies known as trastuzumab Trastuzumab decreases the risk of recurrent disease
WhenIsChemotherapy theAnswer?
Neoadjuvant means therapy given BEFORE the definitive treatment. Goal is to decrease cancer burden Adjuvant means an additional therapy to clean up presumed microscopic cancer cells too small in amount to be detected
MTBS2CK p.350
MTBS2CK p.350
WhenIsAdjuvantChemotherapy theAnswer? Adjuvant chemotherapy is the answer when: Lesions >1 cm Positive axillary lymph nodes found Use tamoxifen when multiple first-degree relatives have breast cancer. It lowers the risk of breast cancer.
BreastCancer/Treatment
We do not know what to do about BRCA when it is positive.
All of these definitely lower mortality: Mammography ER/PR testing, then tamoxifen/raloxifene Aromatase inhibitors Adjuvant chemotherapy Lumpectomy and radiation Modified radical mastectomy Trastuzumab (anti-Her 2/neu) Prophylaxis with tamoxifen
MTBS2CK p.350
MTBS2CK p.350
ProstateCancer/Presentation
ProstateCancer
Presentation Treatment Screening
Obstructive symptoms Palpable mass Elevated or rising PSA
Source:http://www.cancer.gov/cancertopics/pdq/treatment/prostate/Patient/page2
MTBS2CK p.350
ProstateCancer
ProstateCancer/Treatment
Biopsy is the best initial test and the most accurate test.
Prostatectomy Radiation therapy Brachytherapy Hormonal therapy Watchful waiting
Half of men above age 80 have prostate cancer on autopsy.

MTBS2CK p.350
Source:http://kidney.niddk.nih.gov/kudiseases/pubs/i magingut/
MTBS2CK p.350351
ProstateCancer/Treatment
GleasonGrading Gleason Score = Tumor Grade High Gleason grade suggests greater g benefit of surgical removal of the prostate
Source:http://www.training.seer.cancer.gov/prostate/abstract-codestage/morphology.html
Prostatectomy has slight benefit over radiation in terms of survival Most common complications of prostatectomy are:
Erectile dysfunction Urinary incontinence
Get it out before it metastasizes if the Gleason grade is high

HormonalManipulationinProstateCancer
ManagementThatIsDefinitely NotBeneficialinProstateCancer These answers are ALWAYS wrong: Screening imaging study like ultrasound Lumpectomy Chemotherapy Hormonal manipulation to prevent recurrences
Flutamide
Competitive inhibitor of testosterone & DHT
Leuprolide, goserelin
GNRH agonists: downregulates LH & FSH
Ketoconazole K t l
Suppresses testosterone
Orchiectomy
Stops endogenous production
MTBS2CK p.351
MTBS2CK p.351
ProstateSpecificAntigen(PSA) PSA is controversial: No mortality benefit with PSA PSA is not to be routinely offered Normal PSA does not exclude prostate cancer High PSA doesnt always mean prostate cancer
ProstateSpecificAntigen(PSA)
If question specifically says, The patient is requesting PSA to screen for cancer, then the answer is do the test
The higher the PSA, the greater the risk of cancer. PSA corresponds to the volume of cancer.
ElevatedPSAAlgorithm Elevated PSA Palpable mass Biopsy p y the mass No palpable mass Transrectal ultrasound
LungCancer
Mass seen Biopsy the mass
No mass seen Multiple blind biopsies
MTBS2CK p.351
LungCancer
Surgery
Who can get surgery? Size of the tumor alone does not determine whether or not it can be resected
Large tumors can be resected with
Demonstration of suffficient residual lung volume by PFTs It is solitary and surrounding tissue is healthy
Small tumors cannot be resected if PFTs indicate poor lung function

MTBS2CK p.352
Source:http://www.cancer.gov/cancertopics/pdq/treatment/non- Source:http://www.cancer.gov/cancertopics/pdq/treatment/non small-cell-lung/Patient/page4 -small-cell-lung/Patient/page4
Source:http://www.cancer.gov/cancertopics/pdq/treatment/n on-small-cell-lung/Patient/page4
LungCancer
Surgery is not possible in these cases: Bilateral disease Malignant pleural effusion Heart, carina, aorta, or vena cava is involved Small cell cancer is considered unresectable in 95% of cases because it is metastatic or spread outside one lung
OvarianCancer
Screening Diagnosis g Treatment
MTBS2CK p.352
OvarianCancer
OvarianCancer/Diagnosis
No screening test for ovarian cancer Presentation:

Woman >50 years old Increasing abdominal girth
No history of liver disease
The initial test is an ultrasound or CT scan
Weight loss, fatigue

Source:http://www.cancer.gov/cancertopics/pdq/treatment/ovaria nepithelial/Patient/page1 Source: James Heilman, MD, http://en.wikipedia.org/wiki/File:POvarianCA.png
MTBS2CK p.352
MTBS2CK p.352
OvarianCancer/Diagnosis
OvarianCancer/Treatment
Most accurate test is biopsy
The only cancer in which removing large amounts of locally metastatic disease benefits patient Remove all visible tumor and pelvic organs and give chemotherapy
Source: http://en.wikipedia.org/wiki/File:Ovarian_carcinoma.JPG
MTBS2CK p.352
MTBS2CK p.352
TesticularCancer/Presentation Young men: 20-40 years old Painless lump in the scrotum
Next best step?
Transillumination Scrotal Ultrasound
TesticularCancer
Presentation Diagnosis g Treatment
Differential ee a d diagnosis? ag os s
Epididymitis Hematocele Varicocele
MTBS2CK p.352
TesticularCancer/Diagnosis
TesticularCancer/Diagnosis Seminoma Non-seminoma

Yolk sac or Endodermal sinus
AFP
Diagnostic Testing Remove the whole testicle with inguinal orchiectomy Do not cut the scrotum, which hi h can spread d th the disease Needle biopsy of the testicle is always a wrong answer
Has NORMAL AFP Can have elevated bHCG LDH correlated with disease burden
Embryonal
AFP and bHCG
Choriocarcinoma
AFP and bHCG
Teratoma
AFP and bHCG
MTBS2CK p.352
Source:Ed Uthman, MD. http://en.wikipedia.org/wiki/File:Seminoma_of_the_Testis.jpg
TesticularCancer/Staging
TesticularCancer/Treatment
Staging is performed with:

CT scan of the abdomen, pelvis, and chest Lymphatic channels in the retroperitoneum spread testicular cancer into the chest
1st- orchiectomy 2nd- radiation 3rd- chemotherapy Testicular cancer is one of the only malignancies in which chemotherapy can cure widely metastatic disease, including spread into the brain
MTBS2CK p.353
http://emedicine.medscape.com/article/437966-clinical#a0218
MTBS2CK p.353
PreventionofInvasiveCervicalCancer Human papillomavirus (HPV) vaccine is given to all women between ages 11 and 26 Pap smear is performed starting at age 21 Every y3y years, , with cytology, until 30 years old After age 30, every 5 years, if HPV testing added Stop at age 65 with adequate screening history and low risk
MTBS2CK p.353
CervicalCancer
Prevention/earlydetection ClinicalPresentation Treatment
Source:http://www.cdc.gov/cancer/dcpc/prevention/vaccination.htm
Source: Nephron, http://en.wikipedia.org/wiki/File:Adenocarcinoma_on_pap_test_1.jpg
DetectionofCervicalCancer Atypical squamous cells of undetermined significance (ASCUS)

HPV testing
If positive colposcopy and biopsy If negative repeat Pap in 6 mo
DetectionofCervicalCancer
Low-grade g and high-grade g g dysplasia y p

Colposcopy and biopsy
Pap smear does not lower mortality as much as mammography or colonoscopy.
MTBS2CK p.353
MTBS2CK p.353
CervicalCancer/Presentation Asymptomatic
Detected on Pap
CervicalCancer Symptomatic
Abnormal vaginal bleeding Post coital bleeding Abnormal discharge Pelvic p pain or fullness Dysuria
The management of early cervical cancer = hysterectomy
Source: Hic et nunc, http://en.wikipedia.org/wiki/File:Scheme_hysterectomy-en.svg
Ophthalmology Ophthalmology
ConradFischer,MD AssociateProfessorofMedicine TouroCollegeofMedicine NewYorkCity Conjunctivitis TheRedEye(OphthalmologicEmergencies) Cataracts DiabeticRetinopathy RetinalArtery&VeinOcclusion RetinalDetachment MaculaDegeneration
ComparisonofViralandBacterial Conjunctivitis Viralconjunctivitis Bacterialconjunctivitis Bilateral Waterydischarge Easilytransmissible Normalvision Itchy Preauricular adenopathy Nospecifictherapy Unilateral Purulent,thickdischarge Poorlytransmissible Normalvision Notitchy Noadenopathy Topicalantibiotics
Conjunctivitis Viral conjunctivitis Bacterial conjunctivitis
David C Cogan Ophthalmic Pathology Collection
Source: phil.cdc.gov
MTBS2CK p.497
Conjunctivitis
EtiologiesofTheRedEye
Conjunctivitis
Presentation
Uveitis Autoimmune diseases Photophobia
Glaucoma Pain Fixed midpoint pupil Tonometry Acetazolamide Mannitol Pilocarpine Laser trabeculoplasty
Abrasion Trauma Feels like sand in eyes Fluorescein stain No specific therapy Patch not clearly beneficial
The must know subjects in ophthalmology are: The red eye (emergencies) Diabetic retinopathy Artery and vein occlusion Retinal detachment
Discharge
Eyefindings
Normal pupils
Most accuratetest
Clinical diagnosis
Bestinitial therapy
Slit lamp examination
Topical antibiotics
Topical steroids
Glaucoma/ChronicGlaucoma
Most often asymptomatic Diagnosed by screening Confirmation with tonometry Elevated intraocular pressure
Glaucoma/ChronicGlaucoma Treattodecreaseproductionofaqueoushumoror increasedrainage Prostaglandin analogues Topical carbonic Latanaprost anhydrase Travoprost inhibitors
Bimatoprost
Topical p beta blockers

Timolol Carteolol Metipranolol Betaxolol Or Levobunolol
Dorzolamide Brinzolamide
Alpha-2 agonists
Apraclonidine
Pilocarpine Laser
MTBS2CK p.498
MTBS2CK p.498
Glaucoma/AcuteAngleClosureGlaucoma
Conjunctival vessels dilated at corneal edge
Look for Sudden onset Extremely painful, red eye hard to palpation Walking into dark room precipitates pain because of p pupillary p y dilation Pupil doesnt react to light because its stuck Cup-to-disc ratio > 0.3
Hazy cornea
Author:Jonathan Trobe, M.D. Source: commons.wikimedia.org
MTBS2CK p.498
HerpesKeratitis
Diagnosis Confirmed with tonometry Treatment IV acetazolamide IV mannitol (osmotically draws of fluid out) Pilocarpine & beta blockers constrict pupil & enhance drainage Laser iridotomy
MTBS2CK p.498
Infection of cornea Eye is red, swollen, and painful, but dont use steroids Steroids markedly increase production of virus
Fluorescein stain confirms dendritic pattern
MTBS2CK p.499
HerpesKeratitis
Cataracts
Treatment Oral acyclovir, famciclovir, or valacyclovir Topical trifluridine or idoxuridine
Beware of steroid use for herpes keratitis Steroids worsen condition
No medical therapy for cataracts Surgically remove lens & replace with new intraocular lens New lens may automatically have bifocal capability Early cataracts are diagnosed with an ophthalmoscope or slit-lamp exam Advanced cataracts visible on exam
MTBS2CK p.499
MTBS2CK p.499
Cataracts
DiabeticRetinopathy Annual screening exams INDISPENSIBLE!!!! Detects retinopathy before visual loss occurs Nonproliferative or background retinopathy is managed by controlling glucose level Most accurate test is
Fluorescein angiography
Proliferative: treated with laser photocoagulation Vascular endothelial growth factor inhibitors (VEGF) injected in some patients to control neovascularization
nih.gov
MTBS2CK p.499
DiabeticRetinopathy Vitrectomy may be necessary to remove a vitreal hemorrhage obstructing vision
RetinalArteryandVeinOcclusion Both present with Sudden onset monocular visual loss Cant make diagnosis without retinal examination No conclusive therapy for either condition
MTBS2CK p.499
New blood vessel formation obscures vision. Source: Conrad Fischer, MD.
MTBS2CK p.500
RetinalArteryOcclusion
RetinalVeinOcclusion
Retinal artery occlusion presents with sudden loss of vision and a pale retina and dark macula. Source: Conrad Fischer, MD.
Retinal vein occlusion leads to extravasation of blood into the retina. Source: Conrad Fischer, MD.
MTBS2CK p.500
MTBS2CK p.500
RetinalArteryandVeinOcclusion Treatment of artery occlusion attempted with... 100% oxygen Acetazolamide to intraocular pressure Thrombolytics
RetinalDetachment
Macula Mac la is described as cherry redin artery occlusion because the rest of retina is pale
MTBS2CK p.500
Caused by Trauma Extreme myopia (changes shape of eye) Diabetic retinopathy Anything that pulls on retina can detach it Presents with Sudden onset of painless, unilateral loss of vision Described as curtain coming down
MTBS2CK p.501
RetinalDetachment Reattachment by mechanical methods Surgery, laser, cryotherapy Injection of expansile gas pushes retina back up against globe of eye
MacularDegeneration MCC of blindness in older persons in U.S. Idiopathic Atrophic (dry) type and neovascular (wet) type Far more common in older patients Bilateral N Normal l external t l appearance of f eye Central vision lost
MTBS2CK p.501
Sudden painless loss of vision like a courtain coming down. Source: Conrad Fischer, MD.
MTBS2CK p.501
MacularDegeneration Neovascular disease More rapid More severe New vessels grow between retina and underlying Bruchs membrane Neovascular or wet type causes 90% of permanent blindness from macular degeneration Atrophic macular degeneration has no proven effective therapy
MTBS2CK p.501
MacularDegeneration
MTBS2CK p.502
Macular degeneration can be diagnosed only by visualization of the retina. Source: Conrad Fischer, MD.
MacularDegeneration
Best initial therapy for neovascular disease VEGF inhibitors

Ranibizumab or bevacizumab
Injected directly into vitreous chamber every few weeks Over 90% stop progression 1/3 improve vision
MTBS2CK p.502
Pediatrics
RyanClose,MDMPH ResidentPhysician InternalMedicinePediatrics HospitaloftheUniversityofPennsylvania
RoutineManagement oftheNewborn
PhysicalExam ApgarScore EyeCare RoutineScreeningandPrevention
PhysicalExam
ApgarScore
Adults Newborns Physical exams start with vital signs...

HeartRate(HR) RespiratoryRate (RR) SystolicBlood Pressure(SBP) DiastolicBlood Pressure(DBP)
MTBS2CK p.403
60100BPM 1224BrPM
120160BPM 4060BrPM
Important part of physical exam Translates physical exam into a score

Used for management decisions
Provides both short- and long-term prognostic indicators
120mmHg
65mmHg
80mmHg
50mmHg
MTBS2CK p.404
ApgarScore
ApgarScore 0points
Appearance Skincolor Pulse Rate
Scores calculated at 1 minute and 5 minutes Score at 1 minute Represents conditions during labor and delivery Indicates need for resuscitation Score at 5 minutes Represents effectiveness of resuscitation efforts Prognostic of survival
MTBS2CK p.404
1point
2points
Pinkallover >100bpm S Sneeze, cough, h loudcry Active movement Strong
Blueallover Pinktorso/blue extremities <60bpm or 60100bpm asystole
Grimace G i N response Grimace/ No Gi / Reflex&irritability feeblecry Activity Muscletone Respiration Breathing

MTBS2CK p.404
None Absent
Someflexion Weak,irregular
ApgarScore
A 28-year-old G1PO woman delivers a 3.9 kg male infant whose Apgar scores are 9 and 10 at 1 and 5 minutes, respectively. The delivery was uncomplicated, and both mother and child are in no acute distress. Whats the most appropriate first step upon delivery of this patient? a. Intubate the child No signs of respiratory distress / high Apgar score b. Send cord blood for arterial blood gas (ABG) Patient is stable c. Suction the mouth and nose d. Nasogastric tube (NGT) placement No need for decompression e. Give prophylactic antibiotics No evidence of infection or sepsis
What we are not told: - Is this child term, or pre-term? - Vital signs ?
Low Apgar score isnt predictive of cerebral palsy
Knowing differences in management if Apgar score is low
MTBS2CK p.404
MTBS2CK p.403
Prevention/EyeCare A 3.9 kg male infant whose Apgar scores were 9 and 10 at 1 and 5 minutes, respectively, presents five days after delivery because of red eyes. The delivery was without any complications. What is the most likely diagnosis at day 5 of life? a. Chemical irritation b. Neisseria gonorrhoeae c. Chlamydia trachomatis d. Group-B Streptococci e. Herpes simplex
- Erythromycin ointment - Tetracycline ointment - Silver nitrate drops
Prevention/EyeCare
Chemical Irritation Due to silver nitrate Developing countries Not an allergy
Neisseria gonorrhea Gram Gramnegative diplococci

Prevent with ointments
Chlamydia trachomatis Not effectively prevented by prophylaxis ointments Treat with oral erythromycin
Herpes Simplex Treat with systemic acyclovir and topical vidarabine
Treat with ceftriaxone
MTBS2CK p.404405
Prevention/EyeCare A 3.9 kg male infant whose Apgar scores were 9 and 10 at 1 and 5 minutes, respectively, presents five days after delivery because of red eyes. The delivery was without any complications. What is the most likely diagnosis at day 5 of life? a. Chemical irritation b. Neisseria gonorrhoeae c. Chlamydia trachomatis d. Group-B Streptococci e. Herpes simplex
Prevention&Screening/VitaminKDeficiency Vitamin K deficient bleeding = hemorrhagic disease of newborn Neonate colon lacks normal bacterial flora that produces vitamin K Vitamin K is responsible for clotting factors II, VII, IX, , and X as well as proteins p C and S
Vit K
Inactive Clotting Factors Active Clotting Factors
Treatment: one IM injection of vitamin K

Oral doses will not work
MTBS2CK p.405
Prevention&Screening/VitaminKDeficiency
Intrinsic Pathway
XIIa XI IX VIII XIa IXa VIIIa Xa V Va IIa Thrombin Fibrin Fibrinogen X TF VIIa II VII
Prevention&Screening/Testing Newborns should be screened for: Phenylketonuria (PKU) Congenital adrenal hyperplasia (CAH) Biotinidase Beta-thalassemia Galactosemia G l t i Hypothyroidism Homocysteinuria G6PD deficiency Hearing test
MTBS2CK p.405 406
Extrinsic Pathway
TransientConditionsoftheNewborn
The Big Transient Three
MedicalConditions oftheNewborn
Transientconditions Polycythemia Tachypnea Hyperbilirubinemia Deliveryassociatedinjuries Newborninfections
Polycythemia
Tachypnea
Hyperbilirubinemia
MTBS2CK p.406407
TransientPolycythemiaoftheNewborn
TransientPolycythemiaoftheNewborn
Polycythemia
Increased RBCs
Epo!
Transient Polycythemia
Primary vs. Secondary

Primary: Normal or low EPO levels Secondary: High EPO levels
Source:JamesVanRhee
Benign Most often related to cord clamping

Hypoxia EPO!
Polycythemia of the Newborn

Can be very harmful
Hyperviscosity, decreased perfusion, thromboses LGA, SGA, and IDM
TransientTachypneaoftheNewborn(TTN)
TransientTachypneaoftheNewborn(TTN)
Tachypnea
60 BrPM (40 60 is normal)
TTN or Respiratory Distress Syndrome II (RDS II)
Benign condition 1% to 2% of newborns

Causes
Excess remaining lung fluid Pulmonary immaturity Surfactant deficiency/insufficiency
The Takeaway: Benign condition Term infants Delivered via C-section Oxygen, antibiotics, and watch closely Watch for
Sepsis
Management
Oxygen and antibiotics Work-Up: CBC and chest radiograph
MTBS2CK p.406407
MTBS2CK p.406407
TransientHyperbilirubinemia Hyperbilirubinemia Production > Elimination increased TSB

From increased production, decreased elimination, or both
TransientHyperbilirubinemia
Any hyperbilirubinemia < 24 hr of life Evaluation Any conjugated hyperbilirubinemia Evaluation
Indirect = Unconjugated bilirubin Direct = Conjugated bilirubin

(Total Bili) (Direct Bili) = Indirect Bili
Transient Hyperbilirubinemia
Benign and very common (~60% newborns) Peaks at 2-3 days of life Increased production of unconjugated bilirubin
TransientConditionsoftheNewborn
DeliveryAssociatedInjuries Types of injuries Subconjunctival hemorrhage Skull fracture Scalp injuries Brachial palsies Clavicular Cl i l fracture f t Facial nerve palsy
Microhemorrhages Benign Caput succedaneum Cephalohematoma
The Big Transient Three

Polycythemia
Tachypnea
Brief paralysis of facial nerve
Hyperbilirubinemia
BrachialPlexusInjuries General Macrosomic infants (e.g., IDM) Shoulder dystocia Duchenne-Erb Paralysis 90% of brachial palsies C5 C6 Waiters tip Cannot abduct or externally rotate Klumpke Paralysis C7 T1 Claw hand +/- Horner syndrome
MTBS2CK p.407408
BrachialPlexusInjuries
ClavicularFracture
PhysicalExam Physical exams start with vital signs...

Heart Rate (HR) Respiration Rate (RR) Systolic Blood Pressure (SBP) Diastolic Blood Pressure (DBP)
Most common newborn fracture Usually result of:

Shoulder dystocia
Age Group
Best diagnostic tool:

Radiograph g p
Adult Newborns 60-100 BPM 16-24 BrPM 120-160 BPM 40-60 BrPM
120 mmHg 65 mmHg
80 mmHg 50 mmHg
Most appropriate management:

Immobilize
MTBS2CK p.408
NeonatalSepsis
Early Late
ToRCHInfections
Type Presentation Diagnostictests Treatment
Initial:IgM Mostaccurate:PCR Initial:VDRL/RPR Mostaccurate:FTA ABS/DarkField Elevatedmaternal rubellaIgM with clinicalpicture Initial:Urine/saliva viraltiters Most accurate:PCR Initial:Tzanck smear Most accurate:PCR Chorioretinitis,hydrocephalus, Toxo plasmosis ringenhancing lesion
Pyrimethamine andsulfadiazine Penicillin IV
Syphilis
GBS E. Coli Listeria IVF Cultures Antibiotics Ampicillin Gentamicin Cefotaxime*
MTBS2CK p.433 Staphylococci
Rashonpalms/soles,snuffles, frontalbossing,Hutchinson 8th n.palsy,saddlenose PDA,cataracts,deafness, hepatosplenomegaly, lowplts, elevatedbilirubins Periventricularcalcifications, microcephaly,chorioretinitis, hearingloss Week1:ShockandDIC Week2:Vesicular skinlesions Week3:Encephalitis
E. Coli GBS
Rubella CMV
Supportive
Ganciclovir
Ampicillin Gentamicin Cefotaxime*
Herpes
Acyclovirand supportivecare
MTBS2CK p.434
AmnioticFluidAbnormalities
CommonAbnormalities oftheNewborn
AmnioticFluidAbnormalities AbdominalAbnormalities GenitourinaryAbnormalities
Amniotic Fluid 80% from mother 20% from infant Problems Polyhydramnios (too much) Oligohydramnios (too little)
MTBS2CK p.408
AmnioticFluidAbnormalities Polyhydramnios Too much fluid Overproduction / Decreased resorption CNS malformations
AmnioticFluidAbnormalities Polyhydramnios GI malformations

Esophageal atresia
MTBS2CK p.408
MTBS2CK p.408
AmnioticFluidAbnormalities Oligohydramnios Too little fluid (Low AFI) Under production Causes
Post-term pregnancies Renal agenesis and renal failure
AbdominalAbnormalities A premature infant born at 28 weeks in respiratory distress with grunting, nasal flaring, and use of accessory muscles. Bowel sounds heard upon auscultation of the back and chest X-ray shows air fluid levels in the chest. Which of the following is the most likely diagnosis? a. Hydrocele b. Gastroschisis c. Diaphragmatic Hernia d. Hiatal Hernia e. Omphalocele
MTBS2CK p.409
Cord Compression ACE-inhibitors Potters syndrome

MTBS2CK p.408
AbdominalAbnormalities
AbdominalAbnormalities Which of the following is the most likely diagnosis? a. b. c. d d. e.

Urological issue not respiratory issue Hydrocele Abdominal wall defect Gastroschisis Diaphragmatic Hernia M More common i in GERD seen in i adults d lt Hi t l H Hiatal Hernia i Omphalocele Abdominal wall defect
Source: Niket Sonpal, MD
MTBS2CK p.409
MTBS2CK p.409
AbdominalAbnormalities Diaphragmatic Hernia Congenital defect in diaphragm Two types: Bochdalek and Morgagni
LEFT side most common
AbdominalAbnormalities Omphalocele
Midline wall defect With sac covering Associations
Imperforateanus Congenitalheartdefects(50%) Conjoinedtwins Trisomy 18(Edwards syndrome) BeckwithWiedemann syndrome
Gastroschisis
Lateral wall defect No sac covering Atresias Surgery is necessary
Key findings:
Respiratory distress Scaphoid abdomen Bowel sounds in chest Abnormal chest radiograph
First step in management

Intubation
MTBS2CK p.409
Surgery is necessary
MTBS2CK p.410
AbdominalAbnormalities
AbdominalAbnormalities/Tumors Wilms Tumor Most common primary renal malignancy in peds Presents with
An elevated AFP in abdominal wall defects The MCC of elevated AFP is incorrect dating
Asymptomatic flank mass Hematuria Hypertension and aniridia
Umbilical hernias: Similar to omphaloceles
First step in evaluation: Abdominal ultrasound MC diagnostic test: Computed tomography Relationships with syndromes
WAGR, Denys-Drash, Beckwith-Wiedemann
Treatment: Surgery + chemotherapy + radiation

AbdominalAbnormalities/Tumors Neuroblastoma Very common among children Often involves adrenal gland Presents with
Painful abdominal mass Neurological findings
Opso(myo)clonus
GenitourinaryAbnormalities
Diarrhea
Diagnostic keys
Urine catecholamines and their metabolites
Vanillyl Mandelic Acid (VMA) Homovanillic acid (HVA)
MTBS2CK p.411
Hydrocele Painless, benign, fluid-filled Cryptorchidism Undescended testis, increased cancer risk Surgical correction after 6 months Hypospadias Ventral surface opening, surgery Epispadias Dorsal surface opening, surgery
MTBS2CK p.411
CyanoticHeartDefects
Tetralogy of Fallot Transposition of the Great Vessels Hypoplastic Left Heart Syndrome Truncus Arteriosus Total Anomalous Pulmonary Venous Return
TetralogyofFallot
TetralogyofFallot
The most common cyanotic heart defect in children Four aspects p Pulmonary stenosis VSD Overriding aorta Right ventricular hypertrophy
MTBS2CK p.412
TetralogyofFallot/Signs&Symptoms Cyanosis Lips and extremities Squatting Increases systemic pressure Shunts blood to pulmonary circulation Holosystolic H l t li murmur VSD There are 3 holosystolic murmurs Mitral regurgitation (MR) Tricuspid regurgitation (TR) Ventricular septal defect (VSD)
MTBS2CK p.412413
TetralogyofFallot
TetralogyofFallot
TranspositionoftheGreatVessels
Two separate circulations Right heart/systemic circulation Left heart/pulmonary circulation Defect dependent Patent ductus arteriosus (PDA) VSD Atrial septal defect (ASD)
Most common cyanotic lesion of neonates
MTBS2CK p.413
Treatment Prostaglandin E1 Surgery
MTBS2CK p.413
HypoplasticLeftHeartSyndrome
HypoplasticLeftHeartSyndrome
Syndrome Absent pulses Right ventricular heave Mild cyanosis/gray
MTBS2CK p.414
TruncusArteriosus
TruncusArteriosus
One Great Vessel The less common heart defect (2%) NOT dependent on PDA Mild cyanosis Big problem: Pulmonary hypertension Treat with Surgery!
MTBS2CK p.414
TotalAnomalousPulmonaryVenousReturn
TAPVR 2
Sign/Symptoms TAPVRwith obstruction Earlyinlifewith respiratory distressand severecyanosis Presentslater Age12years withheart failure Tests CXRshows pulmonary edema Echoistestof choice Treatment Surgery
Abnormal pulmonary venous return Pulmonary veins Right atrium PFO dependent Right heart overload Two types: With obstruction Without obstruction
TAPVRwithout obstruction
S Surgery CXRshows snowman sign Echoistestof choice
MTBS2CK p.414415
MTBS2CK p.415
10
R LShunt TOF TGV Hypoplastic LH Truncus Art TAPVR PDAdep VSD Surgery
AcyanoticHeartDefects
AcyanoticHeartDefects
Heartmurmurinachild
3-year old female brought in because her parents say she wont eat anymore. Upon physical examination, a loud pansystolic murmur is appreciated. The child appears small for her age, but her records dont show any maternal or delivery complications.
Which of the following is the most likely finding on EKG?
VSD ASD PDA Coarctation of the aorta
a. b. c. d. e.
Right ventricular hypertrophy RBBB ST-segment elevation QT-prolongation P-wave inversion
MTBS2CK p.415
VentricularSeptalDefect
VSD,Murmurs,andAuscultation
There are 3 holosystolic murmurs... MR TR VSD

VSD
VSD is the most common congenital heart defect

MTBS2CK p.415
11
VentricularSeptalDefect Pathophysiology
Left-to-Right shunt (opposite of cyanotic defects) Pulmonary hypertension
VentricularSeptalDefect
Presentation
Dyspnea with distress Loud pulmonic S2 High-pitched holosystolic murmur
Tests
CXR: Findings are not diagnostically helpful Best initial test is an echocardiogram Most diagnostic (definitive) test is a cardiac catheterization
MTBS2CK p.416
Heartmurmurinachild
VSD
a. b. c. d. e.
Right ventricular hypertrophy RBBB ST-segment elevation QT-prolongation P-wave inversion
MTBS2CK p.415
VSD &Eisenmenger Syndrome

a. b. c. d. e.
Right ventricular hypertrophy RBBB ASD or ischemic disease ST-segment elevation Myocardial infarction Electrolyte disturbances QT-prolongation P-wave inversion Atrial arrhythmias
MTBS2CK p.415
12
AtrialSeptalDefect Types of ASDs

Primum, secundum, and sinus venosus 2xs common in men
AtrialSeptalDefect
Usually asymptomatic Fixed wide-splitting S2 vs. Physiologic splitting Tests

Best initial test is an echocardiogram (bubble study) Most diagnostic test is a cardiac catheterization
Prognosis
Most close without intervention
MTBS2CK p.416417
AtrialSeptalDefect Without closure

Atrial enlargement Dysrhythmias Embolic Risk
PatentDuctusArteriosus Failure of closure after 12 hours Left-to-Right shunt Presentation

Machinery-like murmur Wide pulse pressures Bounding pulses
Treatment
Surgical
Tests
Best initial test is an echocardiogram Most diagnostic test is a cardiac catheterization
Treatment
NSAIDS (indomethacin)
MTBS2CK p.417
PatentDuctusArteriosus
PatentDuctusArteriosus
13
CoarctationoftheAorta Congenital narrowing of aorta

Usually after cephalic branches
CoarctationoftheAorta
Turners Syndrome Presentation

Differential blood pressure
Between upper and lower body Hypertension
CHF and respiratory distress
Tests
Best initial tests are an echo or CXR Most diagnostic test is a cardiac catheterization
MTBS2CK p.418419
Volvulus What is it? How is it managed?

Decompression of gut + IVF Surgery Malrotation of gut
Gastroenterology Part2
Volvulus&Intussusception MeckelsDiverticulum Diarrhea&Gastroenteritis
What causes it?

Non-rotation during development
If decompensating...
Proceed immediately y to OR Get antibiotics on board
How does it present?

90% within first year of life Bilious vomiting Colicky abdominal pain
MTBS2CK p.424425
Intussusception Telescoping bowel Presentation

Colicky abdominal pain Bilious vomiting Currant-jelly stool Sausage-like Sausage-like mass
This triad is commonly used on S2!
Intussusception Testing and Treatment

Best initial test: Ultrasound Air contrast/barium enema
Diagnostic and therapeutic
First steps in management:

IVF and correction of electrolytes NG tube for decompression
Signs of peritonitis/perforation Su Surgery ge y Recurrence ~10%
Source: Brad L. Kocher
MTBS2CK p.425426
MTBS2CK p.426
Source: Boma O. Afiesimama
14
BiliousVomiting
Bilious Vomiting
Duodenal Atresia Volvulus Intussusception
MeckelsDiverticulum Rule of 2s
2% prevalence 2 years old 2 ft proximal to ileocecal valve 2 inches long 2 types of ectopic tissue Males 2x more affected 2% symptomatic
Within 1st day Initial test: AXR Double
Within 1st year Initial test: AXR
Within 1st year Initial test: US Doughnut First Step: IVF! Treatment Air Enema
bubble
First Step IVF! Treament Surgery
MTBS2CK p.424 426
First Step IVF! Treament Surgery
Painless rectal bleeding

Katsumi M. Miyai, M.D., Ph.D., Regents of the University of California. Used with permission.
MTBS2CK p.426427
DiarrheaandGastroenteritis
Infectious Diarrhea
The most important questions to ask: Is this chronic or acute? Infectious or not? Bloody or not? How sick is the child?
Viral
Parasites
Fungal
Bacterial
Giardia Cryptosporidia
Candida spp Histoplasma
Salmonella Shigella C difficile C. E. Coli Campylobacter Yersinia
MTBS2CK p.427
Infectious Diarrhea
Viral
Rotavirus
Most M tcommon Winter Symptoms: Fever,emesis NOblood <7days Viralprodrome Vaccine
Adenovirus
Endemic E d i Yearround Symptoms: Fever,emesis NOblood >7days Viralprodrome
Small,round
Norwalk N lk EPIdemic Symptoms: Explosive Cramping,pain Shortlived 12days
Management Hydration is key Almost always the answer Antibiotics for suspected bacterial i f ti infection WBC or blood in stool NEVER use antidiarrheal meds in these patients
MTBS2CK p.428
15
LargeforGestationalAge/Macrosomia
A 10.5-pound infant is born to a mother with Type I diabetes. Upon examination of newborn, he is shaking, and a holosystolic murmur is heard over precordium. The babys right arm is adducted and internally rotated. His lab findings show an elevated bilirubin. Which of the following is the most appropriate next step in management?
Endocrinology
InfantsofDiabeticMothers Congenital g AdrenalHyperplasia yp p (CAH) ( ) VitaminDDeficiencies
a. b. c. d. e.
IV insulin Blood sugar level Serum calcium levels Serum TSH CT head and neck
MTBS2CK p.429
InfantsofDiabeticMothers(IDM)
InfantsofDiabeticMothers(IDM)
Maternal Hyperglycemia
Fetal / Infant Hyperglycemia
Infant Hyperinsulinemia
Four primary issues... Macrosomia Hypoglycemia Electrolyte abnormalities Jaundice
MTBS2CK p.430
MTBS2CK p.430
IDM/Macrosomia Macrosomia = weight 4500 g Large for gestational age (LGA) = top 90th percentile Causes in IDM Oversupply of AAs, glucose, etc. Insulin is a growth factor Consequences C Trauma Risk of C-section Treatment None Prevention!
MTBS2CK p.430
IDM/Hypoglycemia
Maternal Hyperglycemia
Infant Hyperglycemia
Infant Hyperinsulinemia
Birth
MTBS2CK p.430
16
IDM/Hypoglycemia Direct consequence of maternal hyperglycemia Hypertrophied pancreatic beta-cells Insulin overproduction Hyperresponsive After birth: No N changes h i in i insulin li production/activity d ti / ti it Consequences Severe hypoglycemia Seizures Treatment Monitoring + Glucose
MTBS2CK p.430
IDM/Electroyteabnormalities Hypocalcemia Hypomagnesemia / Hyperphosphotemia Twitching and Tremulousness Cardiac arrhythmias Calcium and Magnesium levels linked Always Al check h kb both th Correct together
MTBS2CK p.430
IDM/Jaundice One-third of IDMs will develop jaundice Unconjugated/Indirect hyperbilirubinemia Overproduction of bilirubin Resolving hematomas Polycythemia Treatment T t t Phototherapy
A 10.5-pound infant is born to a mother with Type I diabetes. Upon examination of newborn, he is shaking, and a holosystolic murmur is heard over precordium. The babys right arm is adducted and internally rotated. His lab findings show an elevated bilirubin. Which of the following is the most appropriate next step in management?
a. b. c. d. e.
IV insulin Blood sugar level Serum calcium levels Serum TSH CT head and neck
IDMs have hyperinsulinemia
Check, but not most immed. Good test, but not relevant No concern trauma or bleed
MTBS2CK p.430
MTBS2CK p.429
IDM/Other Other abnormalities Small left colon syndrome Respiratory distress syndrome (RDS) Cardiac abnormalities
CongenitalAdrenalHyperplasia(CAH)
Cholesterol
Pregnenolone
17-OHg Pregnenolone
17-OHProgesterone
Deoxycortisol
Cortisol
DHEA Androstenediol
Androstenedione Testosterone
Estrone Estradiol
17-hydroxylase deficiency 21-hydroxylase deficiency

MTBS2CK p.430
11-hydroxylase deficiency
17
CAH:17HydroxylaseDeficiency
Cholesterol
Aldosterone
CongenitalAdrenalHyperplasia
17hydroxylasedef 21hyroxylasedef 11hydroxylasedef
Cortisol
Aldosterone Cortisol Sexhormones HYPERtensive
SexDevelopment p
Testosterone Estradiol
Girls:nml atbirth Boys:pseudo hermaphroditism
Classic S2CK: teenage girl presents with delayed puberty and incidentally found to have elevated BP
Electrolytes
Hypokalemia
MTBS2CK p.430
MTBS2CK p.430
21HydroxylaseDeficiency
Cholesterol
Aldosterone
Cortisol
Aldosterone Cortisol Sexhormones HYPOtensive

Saltwasting Shock
SexDevelopment p
SexDevelopment
Girls:virilized Boys:nml atbirth
Electrolytes
Hypokalemia
Electrolytes
Hyponatremia Hypochloremia Hyperkalemia
11HydroxylaseDeficiency
Cholesterol
11-DOC Aldosterone
Cortisol
Aldosterone Cortisol Sexhormones HYPOtensive

Saltwasting Shock
SexDevelopment p
Aldosterone Cortisol Sexhormones 11DOC HYPERtensive

SexDevelopment
SexDevelopment
Electrolytes
Hypokalemia
Electrolytes
Hyponatremia Hypochloremia Hyperkalemia
Fewelectrolytes abnormalities
MTBS2CK p.430
MTBS2CK p.430
18
Cholesterol
Pregnenolone
Rickets Disorder of children Soft and weak bones fractures Vitamin D, calcium, and phosphate Children are particularly susceptible Rapidly growing bones Breast B t milk ilk d deficiency fi i i in vitamin it i D Prophylaxis with vitamin D supplements
17-OHg Pregnenolone
17-OHProgesterone
Deoxycortisol
Cortisol
DHEA Androstenediol
Androstenedione Testosterone
Estrone Estradiol
17-hydroxylase deficiency 21-hydroxylase deficiency
Rickets
BoneMetabolism/Simplified
Vitamin D PTH
Calcium
Phosphate
BoneMetabolism/Simplified
Vitamin D PTH
Rickets
Calcium
Phosphate
Source:PaulMMichaud
MTBS2CK p.432
19
Rickets Disorder of children Soft and weak bones fractures Vitamin D, calcium, and phosphate Children are particularly susceptible Rapidly growing bones Breast B t milk ilk d deficiency fi i i in vitamin it i D Prophylaxis with vitamin D supplements Treat with vitamin D and calcium supplements
Pulmonary
Croup Epiglottitis pg WhoopingCough Asthma
MTBS2CK p.431
Croup
2-year-old brought in by daycare provider for severe cough, fever, and runny nose. The childs cough sounds like a bark and shes in obvious respiratory distress. Upon physical examination, the child refuses to lie flat. A chest X-ray shows a positive steeple sign. What is the most appropriate next step in management?
Anatomyofupperairwaydisease
a. b. c. d. e.
Intubate Racemic epinephrine Empiric antibiotics Acetaminophen CT-scan of neck
Not necessary in croup Not first step in improving airway Not first step in improving airway Not first step in improving airway
Croup
MTBS2CK p.435
commons.wikimedia.org. Used with permission
Croup
Laryngotracheitis or Laryngotracheobronchitis Infection of upper airway Subglottic space Viral Parainfluenza or RSV Presentation Triad: barking cough, coryza, and stridor Respiratory distress: accessory muscle use CXR: Steeple sign
MTBS2CK p.435
Epiglottitis
Treatment Moderate severity: Steroids Severe: Racemic epinephrine and steroids
Think bacterial causes: (1) older kids or (2) those unresponsive to racemic epinephrine
4-year-old child brought in by daycare provider because hes extremely irritable and refuses to eat. He refuses to lean back, speaks in muffled words, looks extremely ill, and is drooling. Chest radiograph shows a positive thumb-print sign. What is the most appropriate next step in management?
The MOST common cause of stridor in children
a. b. c. d. e.
Intubate Racemic epinephrine Empiric antibiotics Acetaminophen CT-scan of the neck
Only for croup Good not most immeidate Fever is not a concern Further imaging not warranted
MTBS2CK p.436
20
Anatomyofupperairwaydisease
Epiglottitis
Upper-airway infection and emergency MCC: Bacterial Non-vaccinated: H. influenzae type-B Vaccinated: Streptococcus species and nontypeable H. influenzae Presentation Fever, F drooling, d li respiratory i t di distress t NO coryza, NO prodrome, NO cough Management Transfer to O.R. INTUBATE Start empiric antibiotics: ceftriaxone or cefuroxime No imaging required
commons.wikimedia.org. Used with permission
Epiglottitis
Croup
MTBS2CK p.436
Epiglottitis
Pertussis
Bordetella pertussis Whooping Cough Gram-negative, non-invasive Causes ciliary paralysis Three Stages:
Source: MS-4 USU
MTBS2CK p.437
Pertussis/Stages
~ 14 days 14 30 days ~ 14 days
Pertussis
Bordetella pertussis Whooping Cough Gram-negative, noninvasive Causes ciliary paralysis Three Stages: Catarrhal Stage: 14 days Runny R nose, congestion, ti URI S Symptoms t Most contagious time period Paroxysmal Stage: 14-30 days Severe coughing, posttussive emesis Convalescent Stage: 14 days Resolution of symptoms
MTBS2CK p.437
Catarrhal Rhinorrhea, congestion, cold sxs sx s cold Most contagious time period Only time abx helpful to patient
MTBS2CK p.437
Paroxysmal Severe coughing Post-tussive emesis Usually no fever Low requirement for admission Abx prescribed to reduce transmissibility
Convalescent Prolonged resolution of symptoms Coughing fits remain less respiratory distress
21
Pertussis
Diagnosis This is a clinical diagnosis CXR is helpful PCR useful where available Management Patient: P ti t Primarily Pi il supportive ti Catarrhal stage azithromycin/erythromycin Everybody gets treated Close contacts: Macrolides The community: Vaccination campaigns
MTBS2CK p.437
ViralInfectionsofChildhood
Virus
Varicella
Presentation
Multiplehighlypruritic vesicularrash;startsonface; fever/malaise Cough,Coryza,and Conjunctivitis;Koplik spots FeverandURIsymptoms; l slapped dcheeks h k rash h
Diagnostictests Treatment
Initial:Tzanck smear Mostaccurate: culture
Supportive
Rubeola (Measles) Fifths d disease
Initial:Clinical Supportive Mostaccurate:IgM
Clinicaldiagnosis
Supportive
Roseola Mumps
FeverandURIprogressing Clinicaldiagnosis todiffuserash

Feverprecedesclassic parotidglandswellingwith possibleorchitis
Supportive Supportive
Clinicaldiagnosis
MTBS2CK p.434
Asthma
The most common chronic disease in children Pathophysiology Reversible obstruction Hyperresponsiveness Inflammation Remodeling Diagnosis Decreased FEV1 and No single available test FEV1/FVC ratio! Clinical Pulmonary Function Tests (PFTs) Bronchoprovocation CXR
MTBS2CK p.129130
Asthma
Treatment Avoidance of triggers Short-acting 2-agonists (SABA) Inhaled corticosteroids (ICS) Long-acting 2-agonists (LABA) Leukotriene L k ti antagonists t i t (modifiers) ( difi ) (LTRA)
MTBS2CK p.131132
Asthma/Treatment
SABA as needed
ADD Low-dose ICS
ADD LABA, LTRA or LTRA, move to mediumdose ICS
High-dose ICS and LABA
High-dose ICS and LABA and Oral steroids
Severity of Symptoms
MTBS2CK p.131132
22
ChildhoodDisorders Psychiatry
SamAsgarian,MD/MBA Classof2012 TulaneUniversity
MentalRetardation PervasiveDevelopmentalDisorders AttentionDeficitHyperactivityDisorder TouretteDisorder
MentalRetardation To determine the level of retardation patients must exhibit deficits in both Intellectual functioning
Cognitive abilities
TypesofMentalRetardation
Mild
IQ range
5055 to 70
Moderate
IQ range
3040 to 5055
Level of functioning
6th grade level Can work and live independently Needs help in difficult or stressful situations
2nd grade level May work with supervision and support Needs help in mildly stressful situations
Social adaptive functioning

Perform daily activities
More frequent in boys Highest incidence being in school-age children
MTBS2CK p.503
MTBS2CK p.503
TypesofMentalRetardation
MentalRetardation/Treatment
Severe
IQ range
2025 to 3540
Profound
IQ range
< 20
Little or no speech, y limited abilities to very manage self care
Needs continuous p care and supervision
Treatment Genetic counseling, prenatal care, and safe environments for expectant mothers If due to medical condition (e.g., PKU) treat disorder Special education to improve level of functioning Behavioral therapy to reduce negative behaviors
MTBS2CK p.503
MTBS2CK p.503504
PervasiveDevelopmentalDisorders/Definition Characterized by Social, behavioral, and language problems

Occurs before age 3
AutisticDisorder
Incidence: boys > girls Lacks peer relationships, poor eye contact, and social smile Absent or bizarre speech Repetitive behaviors
Stacking Injurious behavior to self or others
Childhood Developmental Disorders Autistic disorder Rett disorder Childhood disintegrative disorder Asperger disorder
~18 mo boy with autism, obsessively stacking cans Source: Andwhatsnext , commons.wikimedia.org
MTBS2CK p.504
MTBS2CK p.504
AutisticTreatment Improve ability to develop relationships, attend school, and achieve independent living May benefit from behavioral modification programs If aggressive, use antipsychotic medications
Rettdisorder Greater incidence in girls Progressive encephalopathy Microcephaly Hand-wringing Loss of speech Ataxia At i Psychomotor retardation Treatment Symptomatic Behavior therapy for self-injurious behavior Physiotherapy for muscular dysfunction
MTBS2CK p.504
MTBS2CK p.504
ChildhoodDisintegrativeDisorder
ChildhoodDisintegrativeDisorder/Treatment
Greater incidence in boys Normal development for 2 years, followed by marked functional regression in
Loss of language Social interaction Motor function Bladder function
Improve ability to develop relationships, attend school, and achieve independent living May benefit from behavioral modification programs If aggressive, use antipsychotic medications
Repetitive/stereotyped behaviors
MTBS2CK p.504
MTBS2CK p.504
AspergerDisorder Greater incidence in boys Social and behavioral problems No language or intellectual deficits Preoccupied with rules
Often display intense interests. Source: Poindexter Propellerhead at the English language, commons.wikimedia.org
Gabriel is a healthy 2-year-old boy whose parents have taken him to the pediatrician. His problems started at 18 months of age, when he did not speak much. He does not have much attachment to his parents and seems aggressive toward other children. What is the most likely diagnosis?
a. Deafness
Ruled out Impaired judgment,
b. Schizophrenia, childhood onset behavior, and reality
Treatment Improve relationships with others

MTBS2CK p.504
c. Rett disorder speech, ataxia, and psychomotor d. Autism

retardation
Progressive encephalopathy, loss of
e. Learning decit No evidence of learning deficit

MTBS2CK p.504505
AttentionDeficitHyperactivityDisorder Characterized by Inattention Short attention span Or Hyperactivity that interferes with daily functioning in school, home, or work Must be present for > 6 months and usually appears before age 7 The symptoms may persist into adulthood
MTBS2CK p.505
ADHD Symptomsmustbepresentinatleast2areas,suchas: School Home

Interrupt others Fidget in chairs Run or climb excessively y Unable to engage in leisure activities Talk excessively Unable to pay attention Make careless mistakes in schoolwork Do not follow through with instructions Difficulties organizing tasks Easily distracted
Source: cdc.gov
MTBS2CK p.505
Treatment First-line: methylphenidate and dextroamphetamine

Side effects: insomnia, decreased appetite, and headache
DisruptiveBehavioralDisorders
Second-line: atomoxetine (norepinephrine reuptake inhibitor)
Oppositional Defiant Disorder Epidemiology Usually noted by age 8 Boys > girls before puberty
But equal incidence after puberty
On the USMLE Step 2 CK, atomoxetine is usually chosen over the first-line treatment, given the side effect proles of those treatments
MTBS2CK p.505
MTBS2CK p.506
DisruptiveBehavioralDisorders/ OppositionalDefiantDisorder
Features
DisruptiveBehavioralDisorders/ OppositionalDefiantDisorder
Argues often Loses temper Easily annoyed Blames others for their mistakes Tends to have problems with authority figures
Justifies behavior as response to others actions
Treatment Teach parents appropriate child management skills and how to lessen oppositional iti lb behavior h i
Source: Chris Willia, commons.wikimedia.org
MTBS2CK p.506
MTBS2CK p.506
DisruptiveBehavioralDisorders
Conduct Disorder Epidemiology Seen more frequently in

Boys whose parents have antisocial personality disorder and alcohol dependence
DisruptiveBehavioralDisorders/ ConductDisorder
Features Persistent behavior where rules are broken Behaviors include aggression toward others:
Bullying Cruelty to animals Fighting Or Using weapons
Source: Diego Grez, commons.wikimedia.org
Vandalize and destroy property; set fires Steal items from others or lie to obtain goods from others Violate rules (truancy, running away from home, breaking curfew)
DisruptiveBehavioralDisorders/ ConductDisorder
Treatment Behavioral intervention using rewards for prosocial and nonaggressive behavior If aggressive
Antipsychotic medications have been used
A 10-year-old boy is seen by the school counselor after teachers complained of his behavior. He frequently becomes angry toward others and loses his temper. His parents report that he refuses to comply with house rules, stays up past his bedtime, and frequently talks back to them. What is the most likely diagnosis? a. Conduct disorder Breaks rules of society or commits crimes b. Tourette disorder Multiple tics
c. Adjustment disorder Maladaptive reaction to identifiable stressor d. Oppositional Deant Disorder e. Learning disorder, not otherwise specied Needs evidence of a learning problem
MTBS2CK p.506
MTBS2CK p.506
TouretteDisorder
TouretteDisorder/Treatment
Characterized by onset of multiple tics

Lasting > 1 yr Occurs before age 18
Seen more frequently in

Boys Begins at age 7
Motor tics most commonly involve

Facial and neck muscles (e.g., head shaking and blinking)
Dopamine p antagonists g
Antipsychotic medications (e.g., risperidone)
The vocal tics include

Grunting, coughing, and throat clearing
MTBS2CK p.506
MTBS2CK p.507
MoodDisorders Psychiatry
SamAsgarian,MD/MBA Classof2012 TulaneUniversity
MajorDepression BipolarDisorder Dysthymia Cyclothymia AtypicalDepression SeasonalAffectiveDisorder Bereavement(Grief)
MajorDepression Mood disorders present with at least a 2-week course of symptoms thats a change from the previous level of functioning
MajorDepression Symptoms Depressed mood or anhedonia (absence of pleasure) And 4 others including
Depressed mood most of day Weight changes Sleep changes Psychomotor disturbances
MTBS2CK p.507
Fatigue Poor concentration Thoughts of death and worthlessness
Vincent van Gogh's 1890 painting Sorrowing old man ('At Eternity's Gate') Source: The Yorck Project, commons.wikimedia.org
MTBS2CK p.507
MajorDepression/DiagnosisandTreatment Diagnosis Rule out medical causes

Most common (hypothyroidism)
MajorDepression/Treatment
SSRIs Effective and relatively mild side effects Less toxic in overdose than other antidepressants If some improvement, but not full response Increase dose of SSRI Psychotherapy (e.g., cognitive therapy) proven to be effective Goal of cognitive therapy is Reduce depression by teaching patients to identify negative cognitions and develop positive ways of thinking
Most common neurological associations are

Parkinson disease and dementia
First-line treatment: SSRIs Fluoxetine Paroxetine Sertraline Citalopram Escitalopram

MTBS2CK p.507
MTBS2CK p.507
MajorDepression
ExceptionstoSSRIUse
Varietyofdepression SpecificalternativetoSSRIs Usedesvenlafaxine Approvedforboth depression&neuropathy Bupropionhasfewer sexual lside id effects ff and dless l weightgainthanSSRIs Alsousedasadjunct treatmentforSSRI inducedsexualsideeffects
SSRIs should NOT be taken with MAO inhibitors as they will cause a dramatic increase in serotonin.
Patientwithdepressionand neuropathicpain
USMLE Step 2 CK wont give you 2 SSRIs from which to choose
Patientwithdepressionwho isf i fearful f lof fweight i h gain i or sexualsideeffects
MTBS2CK p.507508
MTBS2CK p.507
MajorDepression
45-year-old woman was seen by her PCP due to complaints of depressed mood, lack of pleasure, sleep problems, decreased appetite and weight, decreased energy, and problems with concentration. She states that these symptoms started when she was fired from her job about 4 weeks ago, and that since then, she has been unable to function. What is the most indicated treatment at this time? a. Alprazolam Anxiolytic b. Paroxetine c. Bupropion Not 1st line d. Venlafaxine When initial therapy doesnt e. Trazodone work, or depression more f. Electroconvulsive therapy severe and associated with psychotic features
Choices on USMLE may include an SSRI and another antidepressant medication Pick the cleanest: SSRI
MTBS2CK p.508
MTBS2CK p.508
BipolarDisorder
BipolarDisorder
Mood disorder Patient experiences

Manic symptoms that last at least 1 week Cause significant distress in level of functioning
Manicsymptoms
Elevated mood Increased self-esteem Distractibility Pressured speech Decreased need for sleep Increase in goaldirected activity Racing thoughts Excessive involvement pleasurable in p activities
MTBS2CK p.508
MTBS2CK p.508
BipolarDisorder
BipolarDisorder The difference between mania and hypomania Severity of symptoms Level of functioning Duration Mania M i
> 1 week Affect functioning Warrant hospitalization
Typically starts with depression Diagnosis Exclude drug use Cocaine/amphetamine Obtain history and urine drug screen
Hypomania H i
< 1week Dont severely affect functioning Dont warrant hospitalization
MTBS2CK p.508
MTBS2CK p.508
TypesofBipolarDisorders
BipolardisordertypeI BipolardisordertypeII Maniaanddepression Hypomaniaanddepression 21-year-old college student was taken to the university clinic after she was noted to be acting bizarrely in class. She is talking fast and reported that she has not slept for over 4 days. She appears to be giggling and not paying attention in class. Her roommate reported that she has been drinking alcohol excessively over the last few days and has had many sexual contacts with unknown men. Wh t is What i th the most t lik likely l di diagnosis? i ? a. Alcohol-induced mood disorder No history of alcoholism
b. c. d. e.
MTBS2CK p.509
Bipolar disorder type I Bipolar disorder type II Hypomania Major depression with psychosis Thoughts of death, preoccupation with Cyclothymia Hypomanic worthlessness, episodes and psychomotor mild depression MTBS2CK p.509 retardation, psychosis
BipolarDisorder/Treatment You must distinguish whether Acute mania 1st line

Lithium Valproic acid Atypical antipsychotics
BipolarDisorder
If kidneys are compromised, dont use lithium
Bipolar depression
Severe symptoms, consider
Lithium Lamotrigine
Lithi Lithium i is th the correct t answer t to most t bipolar questions
Atypical antipsychotics
Shorter onset of action
Dysthymia
33-year-old man was taken to emergency room by police after neighbors complained about his behavior. His family informed the doctor hes been diagnosed with bipolar disorder and was recently started on lithium. While in the emergency room, he became combative and punched a nurse on the mouth. What is the next step in the management of this patient? a. Obtain lithium level Symptoms are acute b. Admit to psychiatric unit > important to treat c. Refer to psychiatry Never refer 1st line is an antipsychotic d. Add valproic acid e. Olanzapine
Characterized by Depressed mood that lasts most of the day and is present almost continuously Symptoms must be present for: > 2 years Treatment
Antidepressant medications and psychotherapy
MTBS2CK p.510
MTBS2CK p.509510
Cyclothymia
AtypicalDepression
Characterized by Hypomanic episodes and mild depression Symptoms must be present for: > 2 years Treatment
Lithium, valproic acid, or carbamazepine Psychotherapy
Characterized by
Reverse vegetative changes Increased sleep Increased weight Increased appetite Mood tends to be worse in evenings and patients may complain of extremities feeling heavy
MTBS2CK p.510
MTBS2CK p.510
AtypicalDepression/Treatment
SeasonalAffectiveDisorder Characterized by Seasonal changes in mood during fall and winter Symptoms
Weight gain Increased sleep Lethargy
SSRIs or MAOIs SSRIs have better side-effect profile If MAOIs and SSRIs are in the same question, choose SSRIs because of sideeffect profile Usually MAOIs are answer on Step 2 for atypical depression
Treat with
Phototherapy and bupropion
MTBS2CK p.510
MTBS2CK p.510
PostpartumDisorders
Disorder Onset Symptoms Mothersfeelings towardbaby Treatment Postpartumbluesorbabyblues Immediatelyafterbirthupto2weeks Sadness,labilemood,tearfulness Nonegativefeelings Supportive,usuallyselflimited
PostpartumDisorders
Disorder Onset Symptoms Mothersfeelings towardbaby Treatment Postpartumdepression Within13monthsafterbirth Depressedmood,weightchanges,sleep disturbances,andexcessiveanxiety Mayhavenegativefeelingstowardbaby Antidepressantmedications
MTBS2CK p.511
MTBS2CK p.511
PostpartumDisorders
Disorder Onset Symptoms Postpartumpsychosis Within23weeksafterbirth Depression,delusions,andthoughts ofharm Mothersfeelingstowardbaby Mayhavethoughtsofharmingbaby Treatment Antipsychoticmedication,lithium, andpossiblyantidepressants
Bereavement(Grief)
Bereavement Majordepression (greaterseveritythanbereavement)
Beginsafterdeathof lovedone Feelingsof Sadness Worrying y g Irritability Sleepdifficulties Poorconcentration Tearfulness <6months,butcango onlonger
MTBS2CK p.511
Thoughtsofdeath Morbidpreoccupationwith worthlessness Markedpsychomotor retardation Psychosis Prolongedfunctional impairment >2monthsandadversely affectfunctioning
MTBS2CK p.511
Bereavement(Grief) Treatment
Supportive psychotherapy
A 65-year-old man brought to office by daughter. He has been hopeless and helpless since his wife died 3 months ago. Daughter is worried about his isolative behavior and lack of appetite. He lost over 30 pounds. He doesnt seem interested in getting better and believes he should have died with his wife. What is the most likely diagnosis? a. Bereavement Severe symptoms just to be bereavement b. Dysthymia Depressed mood, lasts most of the day and continuously c. Major depression Anxiety, depression or d. Adjustment disorder disturbances of conduct
Medical therapy is wrong answer
Source: Bundesarchiv, Bild 146-1996-036-01 / Unknown / CC-BY-SA, commons.wikimedia.org
e. Bipolar disorder
Mood disorder with manic symptoms, at least 1 week
Antidepressants,MoodStabilizers, ElectroconvulsiveTherapy
Typeofmedication Adverseeffects
Tricyclic antidepressants
Amitriptyline Nortriptyline Imipramine
Hypotension Drymouth Constipation Confusion Arrhythmias Sexualsideeffects Weightgain GIdisturbances
Monoamine oxidaseinhibitors
- Phenelzine - Isocarboxazid - Tranylcypromine
Monitordiet,giventhat foodrichintyraminewill producehypertension

Safe foods include white wine and processed cheese Unsafe foods include red wine, aged cheese, and chocolate
MTBS2CK p.512
MTBS2CK p.512
Source: Vincent van Gogh, Still life with bottle, two glasses, cheese and bread. commons.wikimedia.org
Serotoninselective Headaches reuptakeinhibitors Weightchanges - Fluoxetine Sexualsideeffects - Paroxetine GIdisturbances

Sertraline Citalopram Escitalopram Fluvoxamine
Serotoninnorepinephrine reuptakeinhibitors - Venlafaxine - Duloxetine - Desvenlafaxine
Hypertension Blurryvision Weightchanges Sexualsideeffects GIdisturbances
MTBS2CK p.512
MTBS2CK p.512
10
Others
Bupropion Trazodone Mirtazapine
Bupropion:seizures Trazodone:priapism Mirtazapine:weightgain andsedation
Lithium
Tremors,weightgain,GI disturbance,nephrotoxic, teratogenic,leukocytosis, diabetesinsipidus Severetoxicitygives confusion,ataxia,lethargy, andabnormalreflexes
MTBS2CK p.512
MTBS2CK p.512
Typeofmedication Lamotrigine Electroconvulsive therapy Adverseeffects StevensJohnsonsyndrome Headaches,transientmemoryloss
Valproicacid
Tremors,weightgain,GI disturbances,alopecia, teratogenic,hepatotoxic Mustmonitorlevels;toxicity causes

Hyponatremia Coma Death
MTBS2CK p.512
MTBS2CK p.512
SerotoninSyndrome
What is the single most effective treatment for depression? a. Electroconvulsive therapy b. Fluoxetine Equally efficacious, but the SSRIs c. Venlafaxine are used more frequently due to side-effect profiles d. Imipramine
Potentially life-threatening From use of SSRIs, often with interactions between drugs, overdose, or recreational use of drugs that are serotonergic in origin Symptoms Cognitive effects
Agitation, confusion, hallucinations, hypomania
e. Phenelzine
MTBS2CK p.513
MTBS2CK p.513
11
SerotoninSyndrome Autonomic effects

Sweating, hyperthermia, tachycardia, nausea, diarrhea, shivering
PsychoticDisorders
Schizophrenia DelusionalDisorder
Somatic effects
Tremors, myoclonus
Treatment Stop SSRI medication Symptomatic treatment of fever, diarrhea, hypertension Cyproheptadine (serotonin antagonist)
MTBS2CK p.513
ClassificationofPsychoticDisorders
BriefPsychoticDisorder
Duration of symptoms > 1 day, but < 1 month Symptoms Delusions Hallucinations Disorganized speech Grossly disorganized Catatonic behavior Treatment Antipsychotic medication
SchizophreniformDisorders
Duration of symptoms > 1 month, but < 6 months Symptoms Delusions Hallucinations Disorganized speech Grossly disorganized Catatonic behavior
MTBS2CK p.513
Negative symptoms
Flat affect Poor grooming Social withdrawal
Treatment Antipsychotic medication
MTBS2CK p.513
PsychoticDisorders Duration of symptoms distinguishes brief psychosis, schizophreniform, and schizophrenia If no time is mentioned, always choose schizophrenia as the correct answer to the What is the most likely y diagnosis? g question q
Schizophrenia
Duration of symptoms > 6 months Symptoms Delusions Hallucinations Disorganized speech Grossly disorganized Catatonic behavior Negative symptoms
MTBS2CK p.513
Severely affects level of functioning Treatment Antipsychotic medication
MTBS2CK p.514
12
Schizophrenia/Definition
Schizophrenia/Definition
Thought disorder: impairs judgment, behavior, and ability to interpret reality At least 6 months and must affect functioning Incidence: men = women
Affects men at young age
Urine drug screen

Cocaine Amphetamine
A schizophrenic patient at the Glore Psychiatric Museum made this piece of cloth and it gives us a peek into her mind. Source: Cometstarmoon, commons.wikimedia.org
MTBS2CK p.514
TypesofSchizophrenia/Diagnosticcriteria Paranoid Delusions or hallucinations, mostly persecutory or grandiose type Most common type of schizophrenia Later age of onset Catatonic Psychomotor disturbances from retardation to excitation
Stupor, rigidity, excitement, or posturing
TypesofSchizophrenia/Diagnosticcriteria
Disorganized Marked regression to disinhibited behavior with little contact with reality Typically appear disheveled and have bizarre emotional responses Worst prognosis and earliest age of onset
Mutism is common
MTBS2CK p.514
MTBS2CK p.514
TypesofSchizophrenia/Diagnosticcriteria Residual Lack of positive symptoms

Hallucinations Delusion
Schizophrenia/Treatment
Hospitalize: acutely psychotic Ensure patient safety, administer atypical antipsychotic such as
Risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, or paliperidone
Presence of negative symptoms

Flat affect Poor grooming Social withdrawal
In emergency situation where intramuscular medication is needed consider

Olanzapine or ziprazidone Haloperidol may be used, but has more side effects
MTBS2CK p.514515
Undifferentiated Characterized by not meeting criteria for other types

MTBS2CK p.514
13
If noncompliant with medication

Long-acting antipsychotic
Risperidone: first-line
Haloperidol may be used, more side effects
Clozapine Use when NO response to a trial of typical

or atypical antipsychotics
Never used as first-line
Know the differences in the side effect profiles of the atypical antipsychotics Its common to have 2 appear on the test; you need to pick the best based on side effects
MTBS2CK p.515
MTBS2CK p.515
AdverseEffectsof AtypicalAntipsychoticMedications
Olanzapine Greater incidence of diabetes and weight gain; avoid in diabetic & obese Risperidone Greater incidence of movement disorders Quetiapine Less incidence of movement disorders
22-year-old woman with schizophrenia. Shes 30 pounds overweight and suffers from type 2 DM. She is concerned about her medications and asks for advice. Which of the following would be most indicated in this patient?
Ziprasidone Increased risk of prolongation of QT interval; avoid in conduction defects

MTBS2CK p.515
Clozapine High risk of agranulocytosis; monitor CBC on regular basis; never used as firstline treatment given sideeffect profile
a. b. c. d. e.
Aripiprazole Olanzapine Highest risk of metabolic abnormalities Quetiapine Have medium risk Clozapine Risperidone
MTBS2CK p.515
ManagementofAdverseEffectsof AtypicalAntipsychoticMedications
Onset of symptoms Acute dystonia Hours to days Symptoms Muscle spasms
Torticollis Laryngeal spasms Occulogyric crisis

Acutedystonia
Treatment
Benztropine Trihexyphenidyl Diphenhydramine
Muscle spasms
Akathisia
Weeks
Generalized restlessness Pacing Rocking Inability to relax
Reduce dose Beta blockers Switch to atypical

MTBS2CK p.516
14
ManagementofAdverseEffectsof AtypicalAntipsychoticMedications
Onset of symptoms Symptoms Abnormal involuntary movements of
Head Limb Trunk Perioral, most common Muscular rigidity Fever Autonomic changes Agitation Obtundation
Treatment
Tardive dyskinesia
Rare before 6 months
Switch to atypical antipsychotic Clozapine has least risk
Neuroleptic malignant syndrome
Not time limited
Dantrolene or bromocriptine
23-year-old man recently diagnosed with schizophrenia is started on haloperidol. Within a few hours he develops muscle stiffness. His eyes roll upward and he cannot move them down. What is the most likely diagnosis? a Tardive dyskinesia 6 mo. involuntary, perioral movements a. No time, muscular b. Neuroleptic malignant syndrome rigidity, fever Weeks. Generalized restlessness, c. Akathisia pacing, rocking, inability to relax d. Serotonin syndrome SSRIs e. Acute dystonic reaction
MTBS2CK p.516
MTBS2CK p.516
DelusionalDisorder Characterized by Non-bizarre delusions for > 1 month and NO impairment in level of functioning The p patient may y believe the country is about to be invaded, but he or she still obeys the law, goes to work, and pays bills
DelusionalDisorder
Hallucinations arent present Treatment

Atypical antipsychotic: first-line therapy Psychotherapy to help promote reality testing
MTBS2CK p.516
MTBS2CK p.516
PanicDisorder/Definition Is the experience of intense anxiety along with feelings of dread and doom
AnxietyDisorders
PanicDisorder Phobias
MTBS2CK p.517
15
PanicDisorder/Definition
PanicDisorder/Definition
Thisisaccompaniedbyatleast4symptoms ofautonomichyperactivitysuchas
Diaphoresis Trembling Chest pain Fear of dying Chills Palpitations SOB Nausea Dizziness Dissociative symptoms Paresthesias
Last < 30 minutes and may be accompanied by agoraphobia

Fear of places where escape is felt to be difficult
Typically in women, can occur at any time, and usually has no specific stressor R/O thyroid disease, hypoglycemia, and cardiac disease
MTBS2CK p.517
MTBS2CK p.517
PanicDisorder/Treatment SSRIs, typically

Fluoxetine, paroxetine, and sertraline are indicated for this disorder
Which is the first-line treatment for panic disorder?
Along with SSRIs, patients may benefit from benzodiazepines (e.g., alprazolam)
Begin g with both Then taper the benzodiazepine (potential abuse)
Behavioral and individual therapy

Helpful But Not sufficient as only treatment
MTBS2CK p.517
a. b. c c. d. e.
Alprazolam Panic attack Buspirone Generalized anxiety Sertraline Imipramine Major depression, enuresis Fluvoxamine Not 1st-line
MTBS2CK p.517
PhobiasDefinition
TypesofPhobias
Fear of an object or situation and the need to avoid it
Specific phobia
Fear of an object (e.g., animals, heights, or cars)
Social phobia Fear of a situation

Public restrooms Eating in public Public speaking
May be learned, involves 2 main types
Situations where something potentially embarrassing may happen

Source: Kilarin, commons.wikimedia.org
Source: Alex.Ramek, commons.wikimedia.org
MTBS2CK p.517518
MTBS2CK p.518
16
Phobias/DiagnosisandTreatment
Phobias/Treatment Relaxation techniques such as

Breathing Or Guided imagery
Beta blockers (e (e.g., g atenolol or propanolol) are used for performance anxiety such as stage fright. They are given 30 minutes to 1 hour before performance.
Diagnosis History of
Anxiety symptoms in specific situations Or When in contact with feared objects
Treatment Behavioral modification techniques such as

Systematic desensitization:
Expose individuals to their feared objects moving from least most anxiety-provoking
MTBS2CK p.518
MTBS2CK p.518
40-year-old man referred to psychiatrist because he is too shy. He has problems going to parties, feels anxious about getting close to others, and stays at home in fear that others would laugh at him. When confronted by others, he develops severe anxiety as well as hyperventilation and increased sweating. Which is the most likely diagnosis?
ObsessiveCompulsive Disorder
a. Panic disorder autonomic hyperactivity symptoms b. Social anxiety Chronic worrying about things c. Generalized anxiety disorder that dont merit concern d. Specific phobia Fear of an object e. Acute stress disorder Stressor, 2 days to 1 month, relive
the event
MTBS2CK p.518
Intense anxiety, dread and doom, 4
ObsessiveCompulsiveDisorder(OCD)/ Definition
DifferencebetweenObsessionsand Compulsions
Obsessions alone Or, most commonly Combination of obsessions and compulsions l i Typically affect the individuals level of functioning
MTBS2CK p.518
Obsessions
Thoughts that are intrusive, senseless, and distressing, thus increasing anxiety Includes fear of contamination
Compulsions
Rituals such as counting and checking done to neutralize thoughts Time consuming and tends to lower anxiety
Source: Lars Klintwall Malmqvist, commons.wikimedia.org
MTBS2CK p.519
17
OCD/DiagnosisandTreatment
Diagnosis More frequent in young patients Incidence: men = women OCD can coexist with Tourette disorder Treatment SSRIs: treatment of choice Most common, first-line: fluoxetine, paroxetine, sertraline, citalopram, or fluvoxamine Main behavioral therapy used Exposure and response prevention
PosttraumaticStressDisorder andAcuteStressDisorder
MTBS2CK p.519
PosttraumaticStressDisorder(PTSD)and AcuteStressDisorder/Definition In both, individuals have Usually overwhelming been exposed to a (e.g., war, rape, stressor to which they hurricanes, or react with fear and earthquakes)
helplessness Patients continually relive li the h event and d avoid anything that reminds them of event
PTSDandAcuteStressDisorder/Definition
Affect the patients level of functioning Other symptoms Increased startle response Hypervigilance Sleep disturbances Anger outbursts Concentration difficulties
Source: Department of Defense visual information (DVIC) Author: US Army, Office of War Information (OWI)
MTBS2CK p.519
MTBS2CK p.519
DifferencebetweenPTSDand AcuteStressDisorder
PTSDandAcuteStressDisorder/Diagnosis
PTSD Symptoms last for > 1 month
Acutestressdisorder Symptoms last for > 2 days and a maximum of 1 month th They occur within 1 month of traumatic event
Main feature
Determine the time period when traumatic events occurred in relationship to symptoms
Rule out
Depression and substance abuse Both worsen diagnosis
MTBS2CK p.519
MTBS2CK p.519520
18
PTSDandAcuteStressDisorder/Treatment
First-line treatment
Paroxetine and sertraline
Relaxation techniques and hypnosis, proven helpful Psychotherapy after traumatic events will allow
Development of coping techniques and acceptance of event
35-year-old woman with palpitations, dizziness, and increased sweating for 8 months. Has visited numerous physicians, none have been helpful. Her husband is concerned because she cannot relax and worries about everything. She worries about her parents health even though they are healthy. She worries about her finances, although her husband assures her theyre financially secure. Wh t is What i th the most t lik likely l di diagnosis? i ? a. Generalized anxiety disorder b. Phobias Fear of an object or a situation Intense anxiety, dread and doom, 4 autonomic c. Panic disorder hyperactivity symptoms d. Adjustment disorder Maladaptive reaction to a stressor e. Social anxiety Anxiety to social interactions, situations
MTBS2CK p.520
MTBS2CK p.520
GeneralizedAnxietyDisorder/Definition Excessive anxiety and worry about most things, lasting > 6 months Typically, anxiety is out of proportion to event Accompanied by
Fatigue Concentration difficulties Sleep problems Muscle tension Restlessness
GeneralizedAnxietyDisorder
Usually women, who complain of feeling anxious as long as they can remember
MTBS2CK p.520
GeneralizedAnxietyDisorder/Treatment
SSRIs
Fluoxetine, paroxetine, sertraline, or citalopram
AntianxietyMedicationsand TheirAdverseEffects
Antianxietymedication
Benzodiazepines Diazepam Lorazepam Clonazepam Alprazolam Oxazepam Chlordiazepoxide Temazepam Flurazepam Buspirone
Adverseeffects
Sedation Confusion Memory deficits Respiratory depression And Addiction potential
Venlafaxine and buspirone have also been used Psychotherapy and behavioral therapy
Beneficial Not considered first-line
Headaches Nausea Dizziness
MTBS2CK p.520
MTBS2CK p.521
19
AntianxietyMedicationsand TheirSpecificIndications
AntianxietyMedicationsand TheirSpecificIndications
Lorazepam Used frequently in emergency situations because it can be given intramuscularly Clonazepam May be used if addiction is a concern concern, longer half-life Chlordiazepoxide, oxazepam Used frequently in treatment of alcohol withdrawal
MTBS2CK p.521
Alprazolam Used frequently in panic disorder Flurazepam, temazepam, Flurazepam temazepam triazolam Approved as hypnotics (rarely used)
MTBS2CK p.521
GeneralizedAnxietyDisorder
Flumazenil is a benzodiazepine antagonist used only when The overdose is acute And: Youre certain that theres no chronic dependence
SubstanceRelatedDisorders
Flumazenil can cause seizures in benzodiazepinedependent patients. It causes acute withdrawal: tremor or seizures similar to delirium tremens (alcohol withdrawal).
MTBS2CK p.521
SpecificSubstanceAbuse/Definition Intoxication Reversible experience - substance leads to either psychological or physiological changes Withdrawal Cessation or reduction of a substance leading to either psychological or physiological changes
SubstanceRelatedDisorders/Definition
Abuse Maladaptive pattern - substances that leads to

Engaging in hazardous situations Legal problems Inability to fulfill obligations Continued use despite adverse consequences
MTBS2CK p.521
MTBS2CK p.521
20
SubstanceRelatedDisorders/Definition Dependence Maladaptive pattern, substances leads to

Tolerance
IntoxicationandWithdrawal/Alcohol
Alcohol Intoxication
Signs & Symptoms
Withdrawal
Source: GeographBot, commons.wikimedia.org
Withdrawal when trying to cut down Patients spend a great deal of time engaging in drug use Continued use despite adverse consequences
Source: Carlos t . commons.wikimedia.org
Talkative Sullen Gregarious Moody Disinhibited
Tremors Hallucinations Seizures Delirium tremens
Treatment
Mechanical ventilation, if severe

MTBS2CK p.522
MTBS2CK p.521
Benzodiazepines Thiamine Multivitamins Folic acid
IntoxicationandWithdrawal/ Amphetamines&Cocaine
Intoxication Amphetamines & Cocaine Withdrawal
Signs & Symptoms Signs & Symptoms
IntoxicationandWithdrawal/Cannabis
Cannabis Intoxication
Signs & Symptoms
Withdrawal
Signs & Symptoms
Euphoria Hypervigilance Autonomic hyperactivity Weight loss Pupillary dilatation Perceptual disturbances
Treatment
Anxiety Tremulousness Headache Increased Appetite Depression Risk of suicide

Treatment
Impaired motor coordination Slowed sense of time Social withdrawal Increased appetite Conjunctival injection
Treatment
None
Treatment
Source: JonRichfield, commons.wikimedia.org
None
Antipsychotics and/or benzodiazepines and/or antihypertensives

MTBS2CK p.522
Bupropion and/or bromocriptine
None
MTBS2CK p.522
IntoxicationandWithdrawal/Hallucinogens
Hallucinogens Intoxication
Signs & Symptoms
IntoxicationandWithdrawal/Inhalants Hallucinogens Intoxication

Signs & Symptoms
Withdrawal
Signs & Symptoms
Withdrawal
Signs & Symptoms
Ideas of reference Perceptual disturbances Impaired judgment Tremors Incoordination Dissociative symptoms
Treatment
None
Treatment
Source: Ksd5 Ksd5, commons commons.wikimedia.org wikimedia org
None
Belligerence Apathy Aggression Impaired judgment Stupor Coma

Treatment
None
Treatment
None
Antipsychotics and/or benzodiazepines and/or talking down

MTBS2CK p.522
Antipsychotics
MTBS2CK p.522
21
IntoxicationandWithdrawal/Opiates
Opiates Intoxication
Signs & Symptoms
IntoxicationandWithdrawal/ Phencyclidine(PCP)
Intoxication
Signs & Symptoms
Withdrawal
Signs & Symptoms
PCP
Apathy Dysphoria Pupillary constriction Drowsiness Slurred speech Coma Death

Treatment
Fever Chills Lacrimation Abdominal cramps Muscle spasms Diarrhea

Treatment
Source: Eleassar, commons.wikimedia.org
Belligerence Psychomotor agitation Violence Nystagmus HTN Seizures

Treatment
Withdrawal
Signs & Symptoms
Source: Jara172, commons.wikimedia.org
None
Treatment
Naloxone
MTBS2CK p.522
Clonidine Methadone Or Buprenorphine
Antipsychotics and/or benzodiazepines and/ or talking down

MTBS2CK p.522
None
IntoxicationandWithdrawal/AnabolicSteroids
Anabolic Steroids Intoxication
Signs & Symptoms
SubstanceRelatedDisorders/Treatment
If you suspect someone is an alcoholic, do CAGE test. Two positive responses to four questions are considered a positive test and indicate that further assessment is warranted.
Withdrawal
Signs & Symptoms
Irritability Aggression Mania Psychosis

Treatment
Depression Headaches Anxiety Increased concern over bodys physical state

Treatment
Source: Cristian navas roman roman, commons.wikimedia.org
Antipsychotics
C - Have you ever felt you should cut down on your drinking? A - Have people annoyed you by criticizing your drinking? G - Have you ever felt bad or guilty about your drinking? E - Eye opener: Have you ever had a drink first thing in the morning to steady your nerves or to get rid of a hangover?
SSRIs
SubstanceRelatedDisorders/Treatment
Detoxification
Usually 5-10 days Mostly in hospital settings to assure safe detoxification 65-year-old engineer suffered femur fracture and some cuts and bruises after being involved in an MVA. Hes admitted to the medicine floor and started on oxycodone. The day after admission, he appears confused with observable tremors in both extremities. He becomes concerned about bugs on the walls in his room and asks for your help. What is the most likely explanation for his symptoms? a. Brain concussion Typically after injury b. Alcohol withdrawal c. Oxycodone intoxication Constipation, miosis
behavior >1 day but <1 month, delusions,
Rehabilitation
Usually 28 days or more with a focus on relapse prevention techniques
Alcoholics Anonymous Narcotics Anonymous Pharmacologic treatments often include:

Disulfram (acetaldehyde dehydrogenase inhibitor) Naltrexone (opioid receptor antagonist) Acamprosate
MTBS2CK p.523
d. Brief psychotic disorder hallucinations, disorganized speech & e. Schizophrenia >6 months, delusions, hallucinations, disorganized
MTBS2CK p.523
speech & behavior
22
SomatoformDisorders Characterized by
Physical symptoms with no medical explanation
SomatoformDisorder, FactitiousDisorder,and Malingering
Symptoms severe enough to adversely affect level of functioning More frequent in young women Usually has psychological component, which the patient is unaware Treatment of choice: psychotherapy
Source of symptoms is psychological
MTBS2CK p.523
TypesofSomatoformDisorders/ Diagnosticcriteria Somatization disorder Hypochondriasis Patients must have at Patients believe that least they have some specific disease 4 Pain despite constant 2 GI reassurance 1 Se Sexual al
And 1 Pseudoneurological symptom
TypesofSomatoformDisorders/ Diagnosticcriteria
Conversion Affects voluntary motor or sensory functions, indicative of a medical condition Usually caused by psychological factors Associated with la belle indifference
Unconcerned about impairment
MTBS2CK p.524
MTBS2CK p.524
TypesofSomatoformDisorders/ Diagnosticcriteria Body Dysmorphic Disorder Patients believe that some part of the body is abnormal, defective, or misshapen
Pain Disorder Main complaint: presence of pain And must have Psychological f t factors associated i t d with pain
35-year-old married mother of 3 has frequent complaints of dizziness, nausea, diarrhea, vomiting, pain during intercourse, paresthesias, leg pain, stomach pain, food intolerance, and headaches. She has tried numerous medications, but none have been beneficial. Neurological examination: normal. What is the next step in the management of this patient? a. Lorazepam Anxiety disorder b. Sertraline Fibromyalgia & depression c. Individual psychotherapy d. Lithium Bipolar disorder e. Risperidone Psychosis
MTBS2CK p.524
Source: elovedfreak, commons.wikimedia.org
MTBS2CK p.524
23
FactitiousDisorder
FactitiousDisorder Inflict life-threatening injuries on themselves Behavior may be compulsive at times Formerly known as Mnchausen syndrome Factitious disorder by proxy, caretaker fakes signs and symptoms in another person
Usually a child child, in order to assume the sick role by proxy as the caregiver
Individual fakes an illness to get attention and emotional support in patient role Either psychological or physical illness Psychological symptoms
Hallucinations, delusions, depression, and bizarre behavior
Physical symptoms
Abdominal pain, fever, nausea, vomiting, or hematomas
MTBS2CK p.524
MTBS2CK p.525
FactitiousDisorder Typically, women with a history of being employed in healthcare Men more often have physical symptoms Patients ultimate goal: admission to hospital Always exclude any medical disorder with similar symptoms
MTBS2CK p.525
FactitiousDisorder/Treatment
No specific therapy has been proven to be effective When a child is involved in factitious disorder by proxy
Contact child protective services to ensure childs safety
Factitious disorder cannot be diagnosed without first ruling out medical illness
MTBS2CK p.525
Malingering Characterized by Conscious production of signs and symptoms for an obvious gain, such as
Avoiding work Evading criminal prosecution Or Achieving financial gain
Malingering/Diagnosis
Diagnosis More frequently in prisoners and military personnel Typically diagnosed when theres a discrepancy between
Patients complaints And Actual physical or laboratory findings
Not a mental illness
MTBS2CK p.525
MTBS2CK p.525
24
Malingering
If medical evaluation reveals malingering Confront patient with the outcome
AdjustmentDisorder
A lack of cooperation from patients is characteristic of malingering
MTBS2CK p.525
AdjustmentDisorder
Characterized by Maladaptive reaction to an identifiable stressor
Loss of job Divorce Or Failure in school
AdjustmentDisorder/Treatment
Symptoms
Anxiety Depression Disturbances of conduct
Severe enough to cause impairment in functioning
Treatment of choice Psychotherapy Both individual and group therapy have been used effectively
Usually occur within 3 months of stressor and must remit within 6 months of removal of stressor
PersonalityDisorders
Characterized by Personality patterns that are:
Pervasive Inflexible Maladaptive
Cl t A Cluster Cl t B Cluster Cl t C Cluster
PersonalityDisorders
Paranoid Schizoid Schizotypal
Histrionic Antisocial Borderline Narcissistic
Avoidant Dependent Obsessive compulsive
MTBS2CK p.525526
25
TypesofPersonalityDisorders
Paranoid Schizoid Schizotypal
Histrionic
Suspicious Mistrustful Secretive Isolated A d And Questioning loyalty of family & friends
Choice of solitary activities Lack of close friends Emotional E i l coldness No desire for or enjoyment of close relationships
Ideas of reference Magical thinking Odd thinking thi ki Eccentric behavior Increased social anxiety Brief psychotic episodes
MTBS2CK p.526
Must be center of attention Inappropriate sexual behavior Self-dramatization Use physical appearance to draw attention to self
MTBS2CK p.526
Antisocial Failure to conform to social rules Deceitful Lack of remorse Impulsive I l i Aggressive towards others Irresponsible Must be 18+ Borderline Unstable relationships Impulsive Recurrent suicidal behaviors Chronic Ch i f feelings li of emptiness Inappropriate anger Dissociative symptoms when severely stressed Brief psychotic episodes Narcissistic Grandiose sense of self Belief that they are special Lack empathy Sense S of f entitlement Require excessive admiration
Avoidant Dependent Obsessive compulsive Preoccupied with details Rigid y Orderly Perfectionists Excessively devoted to work Inflexible
Unwilling to get involved with people Views self as socially inept Reluctant to take risks Feelings of inadequacy
MTBS2CK p.526
Difficulty making day-to-day decisions Unable to assume responsibility Unable to express disagreement Fear of being alone Seeks relationship as source of care
MTBS2CK p.526
PersonalityDisorders/Treatment
Individual psychotherapy Medications if mood or anxiety symptoms are present
Which of the following personality disorders has been associated with positive psychotic symptoms? a. Borderline & Schizotypal b Histrionic b. Not c. Schizoid associated d. Paranoid e. Antisocial
MTBS2CK p.526
MTBS2CK p.527
26
EatingDisorders
AnorexiaNervosa BulimiaNervosa EatingDisorderNot OtherwiseSpecified
15-year-old girl brought to clinic by her mother, who found her vomiting in the bathroom. She vomits daily after each meal and exercises excessively. She has numerous calluses on her hands as well as cavities. She is 55 and weighs 90 pounds. What is her most likely diagnosis? a. Bulimia nervosa Frequent binge eating, normal weight, obesity history Neither b. Anorexia nervosa anorexia c. Eating disorder not otherwise specified nor bulimia d. Obesity Increased weight e. Atypical depression Increased apetite & weight
MTBS2CK p.527
AnorexiaNervosa
Characterized by
Failure to maintain a normal body weight Fear and preoccupation of gaining weight Body image disturbance
AnorexiaNervosa/Diagnosis
Lose weight by
Strict caloric control Excessive exercise Purging
Laxative & diuretic
Source: http://www.womenshealth.gov/bodyimage/eating-disorders/
And Fasting F ti
Bradycardia Lanugo hair And Edema EKG changes

Potassium deficiency y
Unrealistic self-evaluation as overweight Amenorrhea is common from low body weight Deny their emaciated condition Great concern with appearance and frequently examine and weigh themselves
MTBS2CK p.527
More frequently, teenage girls 14 -18 years of age Severe weight loss Hypotension
Arrhythmia MCC of death
MTBS2CK p.527
AnorexiaNervosa/Treatment
BulimiaNervosa
Characterized by
Hospitalization to prevent
Dehydration Starvation Electrolyte imbalances Death
Frequent binge eating in a discrete amount of time Lack of control of overeating episodes
Accompanied by compensatory behavior to prevent weight gain

Purging
Laxatives & diuretics
Psychotherapy Behavioral therapy SSRIs

To promote weight gain
Source: girlshealth.gov
Fasting And Excessive exercise
Self-evaluation influenced by body shape and weight
MTBS2CK p.528
MTBS2CK p.528
27
BulimiaNervosa Diagnosis More frequently women and later in adolescence than anorexia nervosa Most normal weight, but history of obesity Treatment Doesnt require hospitalization, unless
Severe electrolyte abnormality
EatingDisorderNotOtherwiseSpecified
Doesnt meet criteria for either anorexia nervosa or bulimia nervosa Examples
Criteria for anorexia present in girls, but menstruation is normal Anorexic patient with normal weight Use of compensatory behavior after eating normal amounts of food
Psychotherapy SSRIs
MTBS2CK p.528
MTBS2CK p.528
Narcolepsy Characterized by
Excessive daytime sleepiness And Abnormalities of REM sleep
SleepDisorders
Narcolepsy Insomnia
Most frequently begins in young adulthood Sleep studies are usually indicated in diagnosis
MTBS2CK p.528
Source:http://www.cdc.gov/sleep/
Narcolepsy
No curative therapy Forced daytime naps Modafinil

To maintain alertness
Psychiatric&PhysicalSymptoms ofNarcolepsy(SleepDisorder)
Sleep attacks Specific feature of narcolepsy Cataplexy Episodic irresistible sleepiness And Feeling refreshed upon awakening Sudden muscle tone loss: pathognomonic And May be precipitated by loud noise or emotions Sleep paralysis
Hypnogogic and hypnopompic hallucinations
MTBS2CK p.528529
MTBS2CK p.529
Hallucinations occur as patient is going to sleep and waking up
Awake but unable to move Typically upon awakening
28
Insomnia Characterized by
Inability to initiate or maintain sleep
Insomnia Sleep hygiene techniques

Going to bed and waking up at the same time Avoiding caffeinated beverages And Avoiding daytime naps
May be due to anxiety and depression g to affect Severe enough level of functioning Typically women who complain of feeling tired or have increased appetite and yawning
MTBS2CK p.529
Source: nih.gov
Behavioral modification techniques include

Using the bed only for sleeping (not for reading, watching TV, or eating)
Medical therapy
Zolpidem, eszopiclone, or zaleplon
MTBS2CK p.529
TerminologyofHumanSexuality Sexual identity Based on a persons secondary sexual characteristics Gender identity Based on a persons sense of maleness or femaleness, established by age 3 Gender role Based on external patterns of behavior that reflect inner sense of gender identity Sexual orientation Based on persons choice of love object; may be heterosexual, homosexual, bisexual, or asexual
HumanSexuality
MTBS2CK p.529
HumanSexuality Masturbation Normal precursor of object-related sexual behavior All men and women masturbate Problematic if it interferes with daily functioning Homosexuality H lit Not considered a mental illness unless it is egodystonic (person not happy with sexual orientation) May be considered normal experimentation in teenagers
TypesofSexualDysfunction
Impotence Persistent or recurrent inability to attain or maintain an erection until completion of sexual se ua act
Treatment
Premature ejaculation Ejaculation before penetration or just after penetration, usually due to anxiety
Treatment
R/O medical causes or medication Psychotherapy, couples sexual therapy
Psychotherapy, behavioral modification techniques (stop and go, squeeze), SSRI medication
MTBS2CK p.530
MTBS2CK p.530
29
TypesofSexualDysfunction
Dyspareunia Pain associated with sexual intercourse, not diagnosed if due to medical condition
Treatment
Paraphilias
Vaginismus Prolonged and painful contraction or spasm of the vagina Usually severe enough to prevent intercourse
Treatment
Group of disorders that are recurrent, sexually arousing, and seen more frequently in men Usually focus on humiliation, nonconsenting partners, or use of nonliving objects Must occur
> 6 months and cause distress Affect level of functioning
Psychotherapy
Psychotherapy Dilator therapy
Dont diagnose if experimentation
MTBS2CK p.530
MTBS2CK p.530
TypesofParaphilias Exhibitionism Recurrent urge to expose oneself to strangers Pedophilia Recurrent urges or arousal toward prepubescent children Masochism Recurrent urge or behavior involving the act of humiliation
TypesofParaphilias
Sadism
Recurrent urge or behavior involving acts in which physical or psychological suffering of victim is exciting
Transvestic fetishism
Fetishism Recurrent use of nonliving objects to achieve sexual pleasure
MTBS2CK p.531
Recurrent urge or behavior involving cross dressing for sexual gratification; usually in heterosexual males
MTBS2CK p.531
TypesofParaphilias Frotteurism Rubbing ones pelvis or erect penis against a nonconsenting person for sexual gratification
Paraphilias/Treatment
Individual psychotherapy Behavioral modification techniques

Aversive conditioning
Antiandrogens or SSRIs to reduce sexual drive
MTBS2CK p.531
Source: Dschwen, commons.wikimedia.org
MTBS2CK p.531
30
GenderIdentityDisorder Characterized by
Persistent discomfort and sense of inappropriateness regarding the patients assigned sex
GenderIdentityDisorder Patients will take hormones when older to deepen voice, if female, or soften voice, if male Women may bind their breasts and men may hide their penis and testicles Its seen more frequently in young men Treatment Sexual reassignment surgery if approved Individual psychotherapy
Diagnosis Wearing g opposite pp g genders clothes Using toys assigned to opposite sex Play with opposite-sex children when young And Feeling unhappy about ones own sexual assignment
MTBS2CK p.531
MTBS2CK p.531
Suicide Recent suicide attempt Complaints of suicidal thoughts Admission of suicidal thoughts Demonstration of suicidal behaviors
Buying weapons Giving away possessions Writing a will
MTBS2CK p.532
Source: samhsa.gov
Suicide
Source: samhsa.gov
Suicide Risk Factors Men Older adults Social isolation Presence of psychiatric illness/drug abuse Perceived hopelessness Previous attempts Treatment Hospitalize patient Take all threats seriously
MTBS2CK p.532
31
Asthma/Definition Asthma or reactive airway disease Abnormal bronchoconstriction of airways Characterized by Reversible airway obstruction secondary to bronchial smooth muscle hyperactivity Airway inflammation, mucus plugging, and smooth muscle hypertrophy
Can lead to chronic, irreversible airway obstruction
Asthma
StephenBagley,MD ResidentPhysician InternalMedicine HospitaloftheUniversityofPennsylvania
MTBS2CK p.129
Asthma/Etiology
Asthma/Etiology Causes acute exacerbations of symptoms Allergens such as pollen, dust mites, cockroaches, and cat dander Infection Changes in weather (especially cold air) Exercise Catamenial (related to menstrual cycle) Aspirin, NSAIDs, beta blockers, tobacco smoke Gastroesophageal reflux disease (GERD)
Extremely common Etiology unknown Associated with atopic disorders and obesity Asthma prevalence, incidence, and hospitalization rates are increasing
MTBS2CK p.129
MTBS2CK p.129
Asthma/Presentation Most often presents with

Wheezing Acute onset of SOB Cough And Chest tightness
Asthma/Presentation
Whichofthefollowingismostlikelytobefound inanasthmaticpatient?
Symptoms worse at night Nasal polyps Eczema or atopic physical y dermatitis on p examination Increased length of expiratory phase of respiration
I/E ratio decreases (normal is 1:2)
MTBS2CK p.129130
Increased sputum production common Fever is often not present Remember all that wheezes is not asthma!
MTBS2CK p.129
Increased use of accessory respiratory muscles (e.g., intercostals) Hyperresonance to percussion, pulsus paradoxus
Asthma/Presentation
Asthma/DiagnosticTests
The answer to the best initial test question in asthma is based on the severity of presentation
The best initial test in an acute exacerbation Arterial blood gas (ABG) or peak expiratory flow (PEF)
ABG if mild, mild early earl e exacerbation: acerbation mild hypoxia, respiratory alkalosis ABG if severe, late exacerbation: severe hypoxia, respiratory acidosis
MTBS2CK p.130
MTBS2CK p.130
Chest X-ray
Most often normal in asthma, but may show hyperinflation Useful for excluding other disease processes
Pneumonia, CHF, pneumothorax
Most accurate diagnostic test is pulmonary function testing (PFTs) You must understand lung volumes!
MTBS2CK p.130
MTBS2CK p.130
Asthma/DiagnosticTests PFTs in asthma show OBSTRUCTION: FEV1 and FVC with a FEV1/FVC ratio HYPERINFLATION: total lung capacity (TLC) AIR TRAPPING: in residual volume REVERSIBILITY: in FEV1 > 12% with use of albuterol BRONCHIAL HYPERRESONIVENESS: FEV1 > 20% with use of methacholine
MTBS2CK p.131
15-year-old boy with occasional SOB every few weeks. Currently feels well. No medications and denies any other medical problems. Pulse is 70 and RR is 12. Chest examination is normal. Which is the single most accurate diagnostic test at this time? Acute exacerbation a. Peak expiratory flow Less likely in asymptomatic b. Increase in FEV1 with albuterol Asymptomatic c. Diffusion capacity of carbon monoxide d. > 20% decrease in FEV1 with use of methacholine e. Increased alveolar-arterial oxygen difference Asymptomatic (A-a gradient) f. Increase in FVC with albuterol Less likely in asymptomatic g. Flow-volume loop on spirometry Best for fixed obstructions h. Chest CT scan Shows nothing or hyperinflation i. Increased pCO2 on ABG Acute exacerbation
MTBS2CK p.130
Acetylcholine and histamine provoke bronchoconstriction and increase in bronchial secretions Methacholine is artificial form of acetylcholine used in diagnostic testing
MTBS2CK p.131
Asthma/Treatment
Additional testing options include CBC may show an increased eosinophil count Skin testing to identify specific allergens that provoke bronchoconstriction Increased IgE levels suggest allergic etiology
Also seen in allergic bronchopulmonary aspergillosis
Chronic management Stepwise fashion of progressively adding more types of treatment if no response
MTBS2CK p.131
MTBS2CK p.131
Asthma/ChronicManagement
Step 1 Step 2 Step 3 Step 4
Asthma/Treatment
Moderate persistent: daily, or > 1 night/week Add a longg beta acting agonist (LABA) to a SABA & ICS Severe persistent: continual, frequent Increase d dose of f ICS to maximum in addition to LABA & SABA
Mild intermittent: < 2 days/week < 2 nights/ month Inhaled shortacting ti beta b t agonist SABA Albuterol Levalbuterol
Mild persistent: > 2 days/week > 2 nights/month
Adverse effects of inhaled steroids are dysphonia and oral candidiasis Alternate long-term control agents include
C Cromolyn l and d nedocromil: d il i inhibit hibit mast t cell ll mediator di t release useful for exercise Theophylline: phosphodiesterase inhibitor increasing cAMP levels (cardio- and neurotoxicity) Leukotriene modifiers: montelukast, zafirlukast, or zileuton best with atopic patients
MTBS2CK p.131
Add a long-term control agent: Low-dose inhaled corticosteroids (ICS) for daily use Beclomethasone Budesonide Flunisolide Fluticasone Mometasone Triamcinolone
Or Increase dose of ICS LABA Salmeterol Or Formoterol
MTBS2CK p.131132
Asthma/Treatment
Zafirlukast is hepatotoxic and has been associated with Churg-Strauss syndrome
Management of Acute Exacerbation
Step#1: determine severity of asthma exacerbation, quantified by Decreased peak expiratory flow (PEF) ABG with evidence of increased A-a Aa gradient or CO2 retention
MTBS2CK p.131
MTBS2CK p.133
Asthma/Treatment Management of Acute Exacerbation Oxygen Albuterol (often nebulized to ensure adequate delivery to lungs) +/- inhaled anticholinergic (e.g., ipratropium) Corticosteroids: need 4-6 4 6 hours to begin to work work, so give right away Epinephrine injections are no more effective than albuterol and have more adverse systemic effects
PEF is an approximation of FVC No precise normal value Based predominantly on height and age, not weight PEF is used in acute assessment by y seeing g how much difference theres from patients usual PEF when stable
MTBS2CK p.133
MTBS2CK p.133
Asthma/Treatment Anticholinergics Role of ipratropium and tiotropium in asthma management unclear In general, ipratropium should be used, but doesnt work as rapidly as albuterol Epinephrine Rarely used and only as a drug of last resort
Asthma/Treatment Magnesium Some modest effect in bronchodilation Not as effective as albuterol, ipratropium, or steroids, but it does help Magnesium g helps p bronchospasm. p Magnesium is used only in acute, severe asthma exacerbation not responsive to several rounds of albuterol while waiting for steroids to take effect.
MTBS2CK p.132133
MTBS2CK p.133
Asthma/Treatment Adverse Effects of Chronic Systemic Corticosteroids Should be a last resort because of very harsh adverse effects such as Osteoporosis Cataracts Adrenal suppression and fat redistribution Hyperlipidemia, hyperglycemia, acne, and hirsutism (particularly in women) Thinning of skin, striae, and easy bruising
Asthma/Treatment
High-dose inhaled steroids rarely lead to adverse effects associated with prednisone
MTBS2CK p.132
MTBS2CK p.132
Asthma/Treatment 47-year-old man with history of asthma comes to ED with several days of increasing SOB, cough, and sputum production. RR is 34. He has diffuse expiratory wheezing and prolonged expiratory phase. Which would you use as the best indication of the severity of his asthma? a. Respiratory rate b. Use of accessory muscles Subjective c. Pulse oximetry Hypoxia, until imminent respiratory failure d. Pulmonary function testing Short of breath e. Pulse rate Adds nothing
The following are not effective in acute exacerbations Theophylline Cromolyn and nedocromil (best with ith extrinsic t i i allergies ll i lik like h hay fever) Leukotriene modifiers Omalizumab Salmeterol
MTBS2CK p.133
MTBS2CK p.132.4
Asthma/Treatment
If no response to oxygen, albuterol, and steroids or develops respiratory acidosis (increased pCO2)
Consider endotracheal intubation and mechanical ventilation
ChronicObstructive PulmonaryDisease
MTBS2CK p.133
COPD/Definition
COPD/Definition
Characterized by airflow obstruction secondary to emphysema and/or chronic bronchitis Emphysema

Terminal airway destruction resulting in decreased elastic recoil of lungs
Normally, elastin fibers allow passive exhalation
MTBS2CK p.134
Chronic bronchitis
Productive cough for > 3 months/year for 2 consecutive years
Both
Part of COPD spectrum Results in decrease in FEV1 and FVC with increase in TLC
MTBS2CK p.134
COPD/Etiology
COPD/Presentation
Tobacco smoking Leads to almost all COPD Destroys elastin fibers Young and Y d a nonsmoker k , answer alpha-1 antitrypsin deficiency as most likely cause
SOB worsened by exertion Intermittent exacerbations with cough, sputum, and SOB often brought on by infection Barrel chest from air trapping Muscle wasting and cachexia
COPD now thought to have a component of systemic inflammation
MTBS2CK p.134
MTBS2CK p.134
COPD/DiagnosticTests
Best initial test: chest X-ray Increased anteriorposterior (AP) di diameter t Air trapping and flattened diaphragms
Most accurate diagnostic test: PFT Decreased FEV1, FVC, and FEV1/FVC ratio (< 70%) Increased TLC due to RV Decreased DLCO in emphysema p y (destruction of alveolar septae where capillaries are found) Incomplete improvement with albuterol Little or no worsening with methacholine
MTBS2CK p.134
MTBS2CK p.134
COPD/DiagnosticTests Reversibility with Inhaled Bronchodilators COPD generally associated with IRREVERSIBLE airway obstruction But COPD has a broad response to inhaled bronchodilators (e (e.g., g albuterol) Ranges from no reversibility to complete reversibility Reversibility in response to bronchodilators is: > 12% increase and 200 mL increase in FEV1
MTBS2CK p.134
Arterial blood gas (ABG) Acute exacerbations of COPD are associated with pCO2 and hypoxia
Respiratory acidosis may be present if theres there s insufficient metabolic compensation and bicarbonate level will be elevated to compensate In between exacerbations, not all those with COPD will retain CO2
MTBS2CK p.134
COPD/Treatment Improves Mortality and Delays Progression of Disease: only 2 interventions! Smoking cessation Oxygen therapy for hypoxia
PaO2 <55 or SaO2 <90% PaO2 <60 or SaO2 <90%
If patient also has pulmonary hypertension, cor pulmonale or polycythemia
EKG Right atrial hypertrophy and right ventricular hypertrophy A-fib or multifocal atrial tachycardia (MAT) Echocardiography Right atrial and right ventricular hypertrophy Pulmonary hypertension
Mortality benefit from oxygen is directly proportional to the number of hours that oxygen is used
MTBS2CK p.135
MTBS2CK p.135
COPD/Treatment Definitely Improves Symptoms (But Does Not Decrease Disease Progression) Short-acting beta agonists (e.g., albuterol) Anticholinergic agents: tiotropium, ipratropium Inhaled steroids Long-acting beta agonists (e.g., salmeterol) Pulmonary rehabilitation
COPD/Treatment Asthmatics not controlled with albuterol Inhaled steroid COPD not controlled with albuterol Anticholinergic (e.g., tiotropium) Inhaled steroid Inhaled anticholinergic agents are most effective in COPD
MTBS2CK p.135
MTBS2CK p.135
COPD/Treatment Possibly Improves Symptoms Theophylline Lung volume reduction surgery No Benefit Cromolyn C l Leukotriene modifiers (e.g., montelukast) When all medical therapy is insufficient, the answer is refer for transplantation
MTBS2CK p.135
COPDAcuteExacerbations/Treatment
Combination of bronchodilators and corticosteroid therapy
COPD exacerbation treatment is identical to asthma exacerbation treatment, but with less proven benefit
MTBS2CK p.136
COPDAcuteExacerbations/Treatment
Antibiotics For exacerbation of moderate to severe COPD

Defined as requiring hospitalization or having at least two of the three cardinal symptoms of a COPD flare Dyspnea Sputum production Sputum purulence
ChronicBronchitisAcuteExacerbations/ Treatment Antibiotics Although viruses cause 20-50% of episodes, coverage should be provided against Streptococcus pneumoniae, H. influenzae, and Moraxella catarrhalis
Macrolides: azithromycin, clarithromycin Cephalosporins: cefuroxime, cefixime Amoxicillin/clavulanic acid Quinolones: levofloxacin, moxifloxacin
Second-line Agents Doxycycline, TMP/SMX

MTBS2CK p.136
MTBS2CK p.136
COPDAcuteExacerbations/Treatment Criteria for Oxygen Use in COPD Although the hypoxic drive elimination concept is incorrect Avoid reflexively placing a patient with COPD on very high-flow 100% nonrebreather mask Use only as much oxygen necessary to raise pO2 above 90% saturation The idea of eliminating hypoxic drive is not accurate. Dyspneic, hypoxic patients with COPD must get oxygen
MTBS2CK p.136
Bronchiectasis & AssociatedConditions
Bronchiectasis/Definition Uncommon disease from chronic destruction, remodeling, and dilation of the large bronchi Permanent anatomic abnormality that cannot be reversed or cured
Bronchiectasis/Etiology
Single MCC Cystic fibrosis: 50% of cases Other causes are Infections
TB ( (and non-tuberculous mycobacterium) y ) Pneumonia (staph or repeated aspiration)
Panhypogammaglobulinemia and immune deficiency
MTBS2CK p.136
Source: Yale Rosen, commons.wikimedia.org
MTBS2CK p.137
Bronchiectasis/Etiology
Bronchiectasis/DiagnosticTests
Foreign body or tumors Allergic bronchopulmonary aspergillosis (ABPA) Collagen vascular such as RA Immotile cilia syndrome y ( (Kartagener g syndrome) These conditions result in repeated and persistent lung infections
MTBS2CK p.137
Best initial test Chest X-ray shows

Dilated, thickened bronchi, sometimes with tram-tracks, which is thickening of bronchi
Most accurate test High-resolution CT, general rule of thumb

Sizable airways are larger in diameter than corresponding adjacent bronchial arteries
MTBS2CK p.137
Impossible to diagnose bronchiectasis without imaging study such as CT
Sputum culture
Only way to determine specific bacterial etiology
MTBS2CK p.137
Source: Thomas P. Eberle
MTBS2CK p.137
Bronchiectasis/Treatment
1. Chest physiotherapy (cupping and clapping) and postural drainage

Essential for dislodging plugged-up bronchi
AllergicBronchopulmonaryAspergillosis (ABPA)
2. Treat each episode of infection as it arises

Same antibiotics as for COPD exacerbations Only difference is inhaled antibiotics seem to have some efficacy
Hypersensitivity to fungal antigens that colonize bronchial tree Almost exclusively with asthma and atopic disorders Look for
Asthmatic with recurrent episodes of brown-flecked sputum and transient infiltrates on X-ray
3. Surgical resection
Focal lesions
MTBS2CK p.138
Cough, wheezing, hemoptysis, bronchiectasis

MTBS2CK p.138
AllergicBronchopulmonaryAspergillosis (ABPA)/DiagnosticTests
AllergicBronchopulmonaryAspergillosis (ABPA)/Treatment
Peripheral eosinophilia Skin test reactivity to aspergillus antigens Precipitating p g antibodies to aspergillus p g on blood test Elevated serum IgE levels Pulmonary infiltrates on chest X-ray or CT
MTBS2CK p.138
1. Oral steroids (prednisone) for severe cases

Inhaled steroids arent effective for ABPA
2. Itraconazole or voriconazole orally for recurrent episodes i d Inhaler cant deliver high enough dose steroids to be effective in ABPA
MTBS2CK p.138
CysticFibrosis(CF)/Etiology Autosomal recessive from mutation that codes for chloride transport
Known as CF transmembrane conductance regulator (CFTR)
CysticFibrosis/Etiology Leads to abnormally thick mucus in

General Growth failure (malabsorption) Vitamin deficiency states Vitamins A,D,E,K Nose & Sinuses Nasal polyps Sinusitis Liver Hepatic steatosis Portal hypertension Gallbladder Biliary cirrhosis Neonatal obstructive jaundice Cholelithiasis Lungs Bronchiectasis Bronchitis Broncholitis Pneumonia Atelectasis Hemoptysis Pneumothorax Reactive airway disease Cor pulmonale Respiratory failure Mucoid impaction of the bronchi Allergic bronchopulmonary aspergillosis
Mutations in CFTR g gene damage g chloride and water transport across apical surface of epithelial cells in exocrine glands throughout the body
MTBS2CK p.138139
Source: Mucoviscidose.PNG: Mirmillon, commons.wikimedia.org
Heart Right ventricular hypertrophy Pulmonary artery dilation

Source: Maen K Abu Househ, commons .wikimedia.org
MTBS2CK p.139
10
CysticFibrosis/Etiology
Bone Hypertrophic osteoarthropathy Clubbing Arthritis Osteoporosis Spleen Hypersplenism Stomach GERD Pancreas Pancreatitis Insulin I li d deficiency fi i Symptomatic hyperglycemia Diabetes Reproductive Infertility Aspermia, absence of vas deferens Amenorrhea Delayed puberty
Source: Maen K Abu Househ, commons .wikimedia.org
CysticFibrosis/Etiology Damaged mucus clearance decreases ability to get rid of inhaled bacteria
Intestines Meconium ileus Meconium peritonitis Rectal prolapse Intussusception Volvulus Fibrosing colonopathy (strictures) Appendicitis Intestinal atresia Distal intestinal obstruction syndrome Inguinal hernia MTBS2CK p.139
Neutrophils in CF dump tons of DNA into airway secretions clogging them up
MTBS2CK p.139
CysticFibrosis/Etiology
CysticFibrosis/Presentation Over 1/3 CF patients are adults Look for

Young adult with chronic lung disease
Cough Sputum py Hemoptysis Bronchiectasis Wheezing Dyspnea
And Recurrent episodes of infection
Sinus pain and polyps are common

Source: nih.gov
MTBS2CK p.139
CysticFibrosis/Presentation
CysticFibrosis/Presentation Recurrent pancreatitis Distal intestinal obstruction Biliary y cirrhosis
GastrointestinalInvolvement
Meconium ileus: infants with abdominal distention Pancreatic insufficiency (in 90%) with steatorrhea and vitamin A, D, E, and K malabsorption
Genitourinary Involvement Men are often infertile

95% have azoospermia, vas deferens missing in 20%
Women are infertile because

Chronic lung disease alters menstrual cycle And Thick cervical mucus blocks sperm entry
MTBS2CK p.139
Islets spared, beta cell function is normal until much later in life
MTBS2CK p.139
11
CysticFibrosis/DiagnosticTests Most accurate test: increased sweat chloride test Pilocarpine increases acetylcholine levels increases sweat production
Chloride levels in sweat > 60 mEq/L in CF on repeated testing establishes diagnosis
CysticFibrosis/DiagnosticTests
Sputum Culture
Nontypable Haemophilus influenzae Pseudomonas aeruginosa Staphylococcus aureus Burkholderia cepacia
Genotyping, not as accurate as increased sweat chloride level

Because there are so many different types of mutations leading to CF
MTBS2CK p.139
MTBS2CK p.140
CysticFibrosis/Treatment
1. Antibiotics are routine
Eliminating colonization: difficult Sputum culture: essential to guide therapy Inhaled aminoglycosides: almost exclusively limited to CF
CysticFibrosis/Treatment Gross hemoptysis Rigid bronchoscopy

Unsuccessful
2. Inhaled recombinant human deoxyribonuclease ( hDN (rhDNase) )

Breaks down massive amounts of DNA in respiratory mucus that clogs up airways
Embolization Interventional radiology Place patient bad lung-side down

Helps prevent bleeding into healthier lung, which is providing most of oxygen exchange
3. Inhaled bronchodilators
Albuterol
4. Lung transplantation
MTBS2CK p.140
CommunityAcquiredPneumonia/Definition
Pneumonia Part1
Community-acquired pneumonia (CAP)

Pneumonia occurring before hospitalization Or Within 48 hours of hospital admission
MTBS2CK p.140
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CAP/Definition
CAP/Etiology
Common Pathogens in CAP & Their Associations
Haemophilus influenzae COPD Klebsiella pneumoniae Alcoholism Diabetes Legionella Contaminated water sources Air conditioning Ventilation systems Coxiella burnetii Animals at time of giving birth Veterinarians Farmers
Most common infectious cause of death in U.S. MCC: Streptococcus pneumoniae
Mycoplasma pneumoniae Young Healthy patients
Staphylococcus aureus Recent viral infection (influenza)
Anaerobes
Poor dentition Aspiration
Chlamydophila pneumoniae
Chlamydia psittaci Birds
Hoarseness MTBS2CK p.140 MTBS2CK p.141
CAP/Presentation All forms of pneumonia present with Fever and cough Severe infection Associated with dyspnea Distinguished by abnormalities of
Vital signs (tachycardia, hypotension, tachypnea) Or Mental status
CAP/Presentation Abdominal pain or diarrhea can occur with infection in lower lobes irritating intestines through diaphragm
Legionella is particularly known for causing diarrhea
Chills or rigors are sometimes a sign of bacteremia

S. pneumo would be most common
Dyspnea, high fever, and abnormal chest X-ray are main ways to distinguish pneumonia from bronchitis
MTBS2CK p.141
Chest pain (often pleuritic) occurs from inflammation of pleura Hypothermia is as bad as fever in terms of pathologic significance
MTBS2CK p.141
CAP/Presentation
CAP/Presentation Organism-specific Associations on Presentation
USMLE S2 may play abnormal breath sounds as part of multimedia and ask you to recognize them Dullness to percussion if theres effusion Bronchial breath sounds and egophony consolidation of air spaces
MTBS2CK p.141
Klebsiella pneumoniae Hemoptysis from necrotizing disease disease, currant jelly sputum
Mycoplasma pneumoniae Dry cough, rarely severe bullous severe, myringitis
Pneumocystis AIDS with <200 CD4 cells
Legionella Anaerobes Foul-smelling sputum, rotten eggs

MTBS2CK p.141
Gastrointestinal symptoms Abdominal pain, diarrhea, or CNS symptoms Headache & confusion
13
CAP/Presentation
CAP/Presentation
Dry or non-productive cough Mycoplasma Viruses Coxiella Pneumocystis Chlamydia
Preferentially involve interstitial space Air spaces of alveoli empty

Thats why theres less sputum production! Specific sputum colors are useless in determining etiology
MTBS2CK p.142
MTBS2CK p.142
CAP/DiagnosticTests
CAP/DiagnosticTests
Best initial test for all respiratory infections

Chest X-ray: but cant determine specific etiology
Atypical pneumonia Organism not visible on Gram stain and not culturable on standard blood agar
Mycoplasma Chlamydophila Legionella Coxiella And Viruses
MTBS2CK p.142
Sputum Gram stain and sputum culture

Best ways to first determine specific etiology Many organisms wont be detected
MTBS2CK p.142
30-50% of cases of CAP
CAP/DiagnosticTests
CAP/DiagnosticTests
Chest X-ray Bilateral interstitial Nonproductive infiltrates with cough Mycoplasma X-rays lag behind Viruses clinical findings
Coxiella Pneumocystis Chlamydia
Right middle lobe infiltrate characteristic of bacterial pneumonia. Source: Nirav Thakar, MD
1st chest X-ray can be falsely negative in 10-20%
MTBS2CK p.142
MTBS2CK p.143
14
CAP/DiagnosticTests
CAP/DiagnosticTests
Blood Cultures are positive 5-15% of CAP Particularly with S. pneumoniae! Sputum Gram stain is adequate if: > 25 WBCs and < 10 epithelial cells
MTBS2CK p.143
Interstitial infiltrates leave the air space empty. This chest x-ray can be consistent with PCP, Mycoplasma, viruses, and Chlamydia. Source: Craig Thurm, MD
MTBS2CK p.143
CAP/DiagnosticTests
CAP/DiagnosticTests Tests Done in Severe Disease with an Unclear Etiology, or Those Not Responding to Treatment Thoracentesis
Any new large effusion should be analyzed Empyema
Infected pleural effusion Acts like abscess Only improves if drained with chest tube
MTBS2CK p.143
Chest CT and MRI show Greater definition of abnormalities found on chest X-ray But Wont W t determine d t i specific ifi microbiologic i bi l i etiology In infectious diseases radiologic test is never the most accurate test
MTBS2CK p.143
Source: nih.gov
CAP/DiagnosticTests Etiology of pleural effusions Transudative
CAP/DiagnosticTests
Empyema
LDH > 60% of serum OR Protein > 50% of serum pH < 7.2, 7 2 +gram stain stain, +culture +culture, or frank pus
Exudative
Secondary to Increased PCWP Or Decreased intravascular oncotic pressure
Secondar to Secondary Increased vascular permeability
New, large effusions secondary to pneumonia should be tapped

MTBS2CK p.143
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CAP/DiagnosticTests
CAP/DiagnosticTests S. pneumo can be tested via urine antigen

Specific Diagnostic Tests by Organism Mycoplasma pneumoniae Pneumocystis jiroveci (PCP) Bronchoalveolar lavage (BAL) Legionella Rising serologic titers Urine antigen, Culture on charcoalyeast extract
Bronchoscopy
Only needed if sputum stain and culture and blood cultures dont yield an organism and patients condition is worsening despite empiric therapy Exception is pneumocystis pneumonia
PCR Cold agglutinins Serology Special culture media

MTBS2CK p.144
Chlamydophila pneumoniae, Chlamydia psittaci & Coxiella burnetii
MTBS2CK p.143144
CAP/Treatment
CAP/Treatment
Rare to have specific organism identified at time treatment is initiated If case describes organism on Gram stain treatment is directed towards that organism Most important step is determining severity of disease.
Determines location in which to place patient
MTBS2CK p.144
Severity of disease, not the etiology drives initial therapy
Mycoplasma & Chlamydophila, rarely confirmed because they are simply treated empirically
MTBS2CK p.144
CAP/Treatment
Outpatient Treatment Previously healthy or no antibiotics in past 3 months and mild symptoms Comorbidities or antibiotics in past 3 months
CAP/Treatment Inpatient Treatment Respiratory fluoroquinolone: levofloxacin or moxifloxacin Or Ceftriaxone and azithromycin
Macrolide - Azithromycin or clarithromycin Or Doxycycline

MTBS2CK p.144
Respiratory fluoroquinolone Levofloxacin Or Moxifloxacin
Almost all infectious diseases are initially treated empiricallythat is, without a specific etiology
MTBS2CK p.144
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CAP/Treatment Reasons to Hospitalize 80% safely treated outpatient with oral antibiotics Severe disease is defined as a combination of
Hypotension (systolic < 90 mmHg) Respiratory rate > 30/min pO2 < 60 mmHg, pH < 7.35 Elevated BUN > 30 mg/dL, Sodium <130 mmol/L
MTBS2CK p.145
CAP/Treatment
Glucose >250 mg/dL Pulse > 125/min Confusion Temperature > 104F 65 or comorbidities such as cancer, COPD, CHF, renal failure, or liver disease
Hypoxia and hypotension as single factors are a reason to hospitalize a patient
Chest X-ray does not guide admission cannot tell severity of hypoxia
MTBS2CK p.145
CAP
CURB 65 Confusion Uremia Respiratory Distress BP low
65-year-old woman is hospitalized with CAP. Sputum Gram stain: Gram-positive diplococci. Sputum culture doesnt grow a specific organism. Chest X-ray: lobar infiltrate and large effusion. Shes placed on ceftriaxone and azithromycin. Thoracentesis: marked elevated LDH and protein level with 17,000 WBC/L. Blood cultures grow Streptococcus pneumoniae with minimal inhibitory concentration (MIC) to penicillin i illi < 0 0.1 1 g/mL. / L Oxygen O saturation t ti 96% on room air. i BP 110/70, T 102F, Pulse 112. What is the next step in management? a. Repeated thoracentesis Will add nothing b. Placement of chest tube for suction c. Add ampicillin to treatment No benefit d. Place patient in ICU No need for chest tube e. Consult pulmonary Will add nothing
MTBS2CK p.145
CAP/Treatment
CAP/Treatment
MTBS2CK p.146
Pleural effusion with a large meniscus sign. Only a fluid sample from thoracentesis can determine the specific cause. Source: Craig Thurm, MD
MTBS2CK p.146
Effusion should be freely mobile and from a layer when the patient lies on her side. Source: Nishith Patel.
17
CAP/Treatment
CAP/Treatment Pneumococcal Vaccination Everyone > 65 should receive vaccination with 23 polyvalent vaccine Chronic heart Liver Vaccinated as soon as Kidney their underlying disease is apparent, regardless Or of age Lung disease
Including asthma
MTBS2CK p.146
Hydropneumothorax is both abnormal air and fluid (effusion) in the pleural space. Chest tube drainage is the most effective way to remove this condition. Source: Albert Takem, MD.
MTBS2CK p.146
CAP/Treatment
CAP/Treatment
Pneumococcal Vaccination Other reasons to vaccinate

Functional or anatomic asplenia (e.g., sickle cell disease) Hematologic malignancy (leukemia, lymphoma) Immunosuppression: diabetes mellitus, alcoholics, corticosteroid users, AIDS or HIV positive CSF leak and cochlear implantation recipients
Pneumococcal Vaccination Generally healthy: single dose at 65 If first vaccination was given before 65 or with other conditions previously described a second dose should also described, be given 5 years after first dose Healthcare workers do not need pneumococcal vaccine
MTBS2CK p.147
MTBS2CK p.146147
HealthcareAssociatedPneumoniaor HospitalAcquiredPneumonia(HAP)/Definition
Pneumonia Part2
Pneumonia developing > 48 hours after admission g incidence of Gram Much higher negative bacilli such as E. coli or Pseudomonas
MTBS2CK p.147
18
HAP/Treatment Main difference in management is

Macrolides (azithromycin or clarithromycin) are unacceptable as empiric therapy
HAP/Treatment
Centered around therapy for Gram-negative bacilli

Antipseudomonal cephalosporins: cefepime or ceftazidime Or Antipseudomonal penicillin: piperacillin/tazobactam Or Carbapenems: imipenem, meropenem, or doripenem
MTBS2CK p.147
Piperacillin and ticarcillin always used in combination with beta-lactamase inhibitor (e.g., ( g tazobactam or clavulanic acid)
MTBS2CK p.147
VentilatorAssociatedPneumonia/Definition
VAP/Diagnosis
Mechanical ventilation interferes with normal mucociliary clearance of respiratory tract (e.g., ability to cough) Positive pressure is tremendously damaging to normal ability to clear colonization Ventilator-associated pneumonia (VAP) has an incidence as high as 5% per day in first few days on ventilator
Because of multiple countercurrent illnesses (e.g., CHF) even a diagnosis of VAP can be hard to establish Look for
Fever and/or rising WBC count New infiltrate on chest X-ray Purulent secretions coming from endotracheal tube
MTBS2CK p.147
MTBS2CK p.147
VAP/DiagnosticTests
VAP/DiagnosticTests
Least accurate but easiest to do Tracheal aspirate Bronchoalveolar lavage (BAL) Most accurate but dangerous Protected brush specimen Tip of p bronchoscope covered when passed through nasopharynx, then uncovered only inside lungs Much more specific, decreased contamination
Sputum culture: nearly worthless

Due to colonization of endotracheal tube (ET)
Diagnosis of specific etiology is extremely difficult on ventilator
Suction catheter placed l d into i t ET and d aspirates contents below trachea when catheter is past end of tube
Bronchoscope placed deeper in lungs where there arent supposed to be organisms Can be contaminated when passed through the nasopharynx
MTBS2CK p.148
MTBS2CK p.148
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VAP/DiagnosticTests
VAP/Treatment
Combine 3 different drugs Cephalosporin (ceftazidime or cefepime) Or Penicillin (piperacillin/tazobactam) Or Carbapenem (imipenem, meropenem, or doripenem) d i ) Aminoglycoside (gentamicin or tobramycin or amikacin) Vancomycin Or Linezolid
1. Antipseudomonal beta-lactam PLUS 2. Second antipseudomonal agent PLUS
MTBS2CK p.148
Subcutaneous emphysema is air abnormally leaking into soft tissue of the chest wall. Chest tube placement may cause air to leak into soft tissues of the chest wall. Source: Birju Shah, MD.
3. Methicillin-resistant antistaphylococcal agent

MTBS2CK p.148149
VAP/Treatment
Patient hospitalized for head trauma and subdural hematoma is intubated for hyperventilation and subsequent craniotomy. Several days after admission hematemesis ensues and stomach stress ulcers are found. Lansoprazole is started. VAP develops, placed on imipenem, linezolid, and gentamicin. Phenytoin, started prophylactically. Three days later creatinine rises followed by seizures . Repeat head CT shows no changes. h What is the most appropriate next step in management? a. Switch phenytoin to carbamazepine Less likely to cause renal failure (RF) b. Stop lansoprazole Not likely to cause RF c. Stop imipenem d. Stop linezolid Not likely to cause RF e. Perform an electroencephalogram Will add nothing
Change initial therapy for VAP if specific etiology is identified
MTBS2CK p.149
MTBS2CK p.149
LungAbscess/Etiology
LungAbscess/Etiology
Rare because of prompt treatment of aspiration pneumonia Occurs only with

Large-volume Large ol me aspiration of oral/phar oral/pharyngeal ngeal contents, usually with poor dentition, who isnt adequately treated
Large-volume aspiration occurs from

Stroke with loss of gag reflex Seizures Intoxication Endotracheal intubation
Aspiration pneumonia happens in the right upper lobe when lying flat
MTBS2CK p.149
MTBS2CK p.149
20
LungAbscess/Presentation
LungAbscess/DiagnosticTests
Look for
Person with one of these risk factors presenting a chronic infection developing over several weeks with large-volume sputum that is foul smelling because of anaerobes
Best initial test: chest X-ray

Cavity, possibly with air-fluid level
Chest CT is more accurate Only lung biopsy can establish specific microbiologic etiology Sputum culture is the wrong answer for diagnosing a lung abscess. Everyones sputum has anaerobes from mouth flora.
MTBS2CK p.150
Weight loss is common
MTBS2CK p.150
LungAbscess/DiagnosticTests
LungAbscess/Treatment
Clindamycin is best to cover lung abscess
Cavity consistent with an abscess with a thick wall and an air-fluid level. Source: Alejandro de la Cruz, MD.
MTBS2CK p.150
MTBS2CK p.150
PneumocystisPneumonia(PCP)/Etiology
PCP/Presentation
Agent causing PCP has been renamed P. jiroveci instead of P. carinii Almost exclusively in patients with AIDS whose CD4 cell count is < 200/L and who arent aren t on prophylactic therapy
Also occurs in chronically immunosuppressed patients, especially those on long term high dose steroids
Look for
Patient with AIDS presenting with dyspnea on exertion, dry cough, and fever
Question will often suggest or directly state that CD4 count is low (< 200/L) and that patient isnt on prophylaxis
MTBS2CK p.150
MTBS2CK p.150
21
PCP/DiagnosticTests
PCP/DiagnosticTests
Best initial test

Chest X-ray showing bilateral interstitial infiltrates Or ABG looking for hypoxia or an increased A-a gradient
Sputum stain: quite specific if its positive

If positive, there is no need to do further testing If negative, bronchoscopy as the best diagnostic test
LDH levels are always elevated Most accurate test

Bronchoalveolar lavage
MTBS2CK p.150
Normal LDH means DONT answer PCP as the most likely diagnosis
MTBS2CK p.150151
PCP/DiagnosticTests
PCP/Treatment
Best initial therapy for both treatment and prophylaxis
Trimethoprim/sulfamethoxazole (TMP/SMX)
S2CK asks what is the most likely diagnosis, not what is the for sure diagnosis
Add steroids to decrease mortality if PCP is severe Severe PCP: pO2 < 70 or A-a gradient > 35 Atovoquone
Alternative to TMP/SMX if mild PCP, meaning g there is only mild hypoxia
Cannot distinguish PCP from Mycoplasma, Chlamydophila, or viruses by X-ray alone. However, in HIV, PCP is most likely with interstitial infiltrates
If toxicity from TMP/SMX switch to either

Clindamycin and primaquine Or Pentamidine
MTBS2CK p.151
MTBS2CK p.151
PCP/Treatment HIV-positive African American man is admitted with dyspnea, dry cough, high LDH, and pO2 of 63 mmHg. He is started on TMP/SMX and prednisone. On 3rd hospital day he develops severe neutropenia and rash. He has anemia and smear shows bite cells. What is the most appropriate next step in management?
a. Stop TMP/SMX Need to treat Will not help acute b. Begin antiretroviral medications opportunistic infection c. Switch TMP/SMX to intravenous pentamidine IV for active d. Switch TMP/SMX to aerosol pentamidine disease e. Switch TMP/SMX to clindamycin and primaquine
MTBS2CK p.151
Often students will see 2 correct treatments and think theres a mistake in the question. question If there are 2 correct treatments, look for a contraindication to one of them.
Contraindicated due to G6PD
MTBS2CK p.152
22
PCP/Prophylaxis AIDS with CD4 count < 200/L Rash Or Neutropenia
PCP/Treatment
1. TMP/SMX
2. Atovoquone or Dapsone
Always choose therapy based first on efficacy, not adverse effects
Aerosol pentamidine: not used as second-line therapy for prophylaxis

Due to less efficacy than either atovoquone or dapsone
Dapsone is contraindicated in those with G6PD deficiency
MTBS2CK p.152
MTBS2CK p.152
HIV-positive woman with 22 CD4 cells/L is admitted with PCP and is treated successfully with TMP/SMX. Prophylactic TMP/SMX and azithromycin are started. She is then started on antiretroviral medication and her CD4 rises to 420 cells for last 6 months. What is the most appropriate next step in management? p TMP/SMX And azithromycin a. Stop y because CD4 b. Stop both TMP/SMX and azithromycin Cannot stop antiretrovirals; c. Stop all medications and observe CD4 will d. Stop all medications if the PCR-RNA viral load is undetectable CD4 will ; antiretrovirals maintain CD4 e. Continue all the medications No prophylaxis needed f. Stop the azithromycin And TMP/SMX because CD4
MTBS2CK p.152
Tuberculosis
Tuberculosis(TB)/Etiology
Tuberculosis/Etiology Almost all patients with TB have 1+ established risk factors

Recent immigrants (in past 5 years) Prisoners HIV positive Healthcare workers Close contact of someone with TB Steroid use Hematologic malignancy Alcoholics Diabetes mellitus
Due to Mycobacterium tuberculosis Initial infection most commonly leads to latent TB Most symptomatic cases due to
Reactivation R ti ti of f latent l t t infection i f ti rather th than primary exposure
Pulmonary TB most common, but can affect any organ system

MTBS2CK p.152
MTBS2CK p.153
23
Tuberculosis/Presentation Look for

Previously listed risk factors presenting with fever, cough, sputum, weight loss, hemoptysis, and night sweats
Tuberculosis/DiagnosticTests Best initial test: chest X-ray as with all respiratory infections Sputum stain and culture specifically for acid-fast bacilli (mycobacteria) must be done 3 times to fully exclude TB g acid-fast stains, , but clinical suspicion p If 3 negative high
Bronchoscopy with BAL or pleural biopsy
Symptoms are almost always > 3 weeks in duration You cannot answer TB as diagnosis without a clear risk factor, a cavity on chest X-ray or a positive smear
PPD skin testing is never best test for TB in symptomatic patient

MTBS2CK p.153154
MTBS2CK p.153
Tuberculosis/DiagnosticTests Most common finding: cavitary upper lobe infiltrate
Tuberculosis/Treatment Smear positive: begin therapy with 4 drugs

Rifampin, isoniazid, pyrazinamide, and ethambutol (RIPE)
Ethambutol not needed if known from start of therapy that organism is sensitive to all TB medications
Ethambutol: given as part of 4-drug empiric therapy prior to knowing sensitivity of organism
After using RIPE for first 2 months

Stop ethambutol and pyrazinamide And Continue rifampin and isoniazid for next 4 months
MTBS2CK p.153
Chest x-ray with upper lobe disease consistent with TB. Source: Craig Thurm, MD.
MTBS2CK p.154
Tuberculosis/Treatment
Tuberculosis/Treatment
Standard of care: 6 months total of therapy Treatment is extended to 9 months for

Osteomyelitis Miliary tuberculosis Meningitis Pregnancy or any other time pyrazinamide isnt used
Toxicity of Therapy All TB medications cause hepatoxicity Dont stop them unless transaminases rise i 3 3-5 5 ti times upper limit li it of f normal l
MTBS2CK p.154
MTBS2CK p.154
24
AdverseEffectsofAntituberculosisTherapy Rifampin
Toxicity
Tuberculosis/Treatment Ethambutol Optic neuritis/ color vision i i Use of Steroids Glucocorticoids decrease risk of constrictive pericarditis in those with pericardial involvement Decrease neurologic complication in TB meningitis
Isoniazid
Pyrazinamide
Red color to body secretions

Treatment
Peripheral neuropathy
Hyperuricemia
Pregnant patients shouldnt receive pyrazinamide Use pyridoxine to prevent No treatment unless symptomatic Decrease dose in renal failure
MTBS2CK p.154
None, benign finding

MTBS2CK p.154
LatentTuberculosis/PPDTesting
LatentTuberculosis/PPDTesting What Is Considered a Positive Test? Only induration is counted towards a positive test Erythema is irrelevant Induration > 5 mm
HIV-positive patients Glucocorticoid users Close contact with active TB patients Abnormal calcifications on chest X-ray Organ transplant recipients
Indications for PPD Testing Not a general screening test for whole population Only those in risk groups previously described should be screened PPD testing isnt useful in those who are symptomatic or those with abnormal chest X-rays
MTBS2CK p.154
MTBS2CK p.155
LatentTuberculosis/PPDTesting Induration > 10 mm

Recent immigrants (past 5 years) Prisoners Healthcare workers Close contacts with TB patients Hematologic malignancy malignancy, alcoholics alcoholics, DM
LatentTuberculosis/PPDTesting Two-Stage Testing If patient never had a PPD skin test before, a second test is indicated within 1-2 weeks if first test is negative
1st test maybe falsely negative
Induration > 15 mm
Those with no risk factors
If 2nd test is negative: truly negative If 2nd test is positive: first test was false negative If the first test is positive, a second test isnt necessary
MTBS2CK p.155
Everyone with a reactive PPD test should have a chest X-ray to exclude active disease
MTBS2CK p.155
25
LatentTuberculosis/PPDTreatment
LatentTuberculosis/PPDTreatment
Treatment for a Positive PPD After active TB has been excluded with a chest X-ray, patients should receive 9 months of isoniazid Positive PPD confers a 10% lifetime risk of TB Isoniazid results in 90% reduction in risk; after isoniazid lifetime risk of TB goes from 10% to 1%
Those at high risk (e.g., healthcare workers), should have a PPD annually to screen for conversion Majority of risk for developing active TB lies within first 2 years after conversion Once PPD is positive, itll always be positive in future
MTBS2CK p.155
MTBS2CK p.155
LatentTuberculosis/PPDTreatment PPD testing is one of the hardest and most misunderstood tests on USMLE S2 CK. Reread preceding section and forget what youve learned in the past.
SolitaryPulmonaryNodule& InterstitialLungDisease
Previous BCG has no effect on these recommendations. If PPD is positive, the patient must take isoniazid for 9 months even if he or she had BCG.
MTBS2CK p.155
SolitaryPulmonaryNodule For Step 2, be sure to know when biopsy is appropriate!

QualitiesofBenignandMalignantPulmonaryNodules Benign <30yearsold Nochangeinsize Nonsmoker Smoothborder Small,<1cm Normallung Adenopathy() Dense,centralcalcification NormalPETscan
MTBS2CK p.156
SolitaryPulmonaryNodule Best initial step in all lung lesions is to compare size with old X-rays Biopsy all enlarging lung lesions, particularly p y if they y are rapidly p y enlarging g g However, doubling in size < 30 days more likely to be infectious than malignant (think about clinical scenario to decide)
Malignant >40yearsold Enlarging Smoker Spiculated(spikes) Large,>2cm Atelectasis Adenopathy(+) Sparse,eccentriccalcification AbnormalPETscan
MTBS2CK p.156
26
SolitaryPulmonaryNodule
HighProbabilityLesions/Management
When many features are described under malignant

Resect (remove) lesion Sputum cytology, needle biopsy, and PET scanning shouldnt be done because a negative ti t test ti is lik likely l false f l negative ti
If resection is one of the choices, then its the answer
Source: Lange123 at the German language Wikipedia, commons.wikimedia.org
MTBS2CK p.156
IntermediateProbabilityLesions/ Management
IntermediateProbabilityLesions/ Management Sputum cytology

If positive, this is highly specific, the most appropriate next step in management is resection of lesion If negative cytology doesnt exclude malignancy
There are some gray or inconclusive aspects of solitary pulmonary nodule such as
Age range gap (between 30 and 40) Or Size ( (between 1 cm and 2 cm) )
Definition of intermediate probability
Bronchoscopy or transthoracic needle biopsy

Each is the most appropriate next step in most patients with intermediate probability of malignancy Bronchoscopy for central lesions Transthoracic biopsy for peripheral lesions
MTBS2CK p.156
MTBS2CK p.156
Diagnostic test question in intermediate lesions; clear answer must be present. Choice of test may not be clear, but adverse effects are always clear. clear Most common adverse effect of a transthoracic biopsy is pneumothorax.
Positron emission tomography (PET scan) Tells whether content of lesion is malignant without biopsy Malignancy has increased uptake of tagged glucose Sensitivity of PET scan is 85 - 95% Negative scan points away from malignancy
MTBS2CK p.157
MTBS2CK p.157
27
SolitaryPulmonaryNodule
Video-assisted thoracic surgery (VATS) VATS is both more sensitive and more specific than all other forms of testing Frozen section in operating room allows for immediate conversion to an open thoracoscopy and lobectomy if malignancy is found
MTBS2CK p.157
Benign pulmonary nodules often represent scar from previous infection

Immigrant, think TB SW United States, think coccidioidomycosis y Ohio River Valley, think histoplasmosis
InterstitialLungDisease/Definition Diseases characterized by inflammation and/or fibrosis of interalveolar septum Fibrosis causes Impaired gas exchange Increased lung stiffness And Decreased lung compliance & expansion
MTBS2CK p.157
Source: Ed Uthman. commons.wikimedia.org
InterstitialLungDisease/Etiology Specific Causes of Interstitial Lung Disease Idiopathic pulmonary fibrosis (IPF) and other idiopathic interstitial pneumonias Collagen vascular disease Granulomatous disorders Hypersensitivity disorders Pneumoconiosis Radiation Drugs: bleomycin, busulfan, amiodarone, methylsergide, nitrofurantoin, cyclophosphamide
MTBS2CK p.157
InterstitialLungDisease/Etiology TypesofPneumoconioses Exposure Coal Sandblasting,rock mining,tunneling Shipyard py workers, ,p pipe p fitting,insulators Cotton Electronicmanufacture Moldysugarcane Disease Coalworkerspneumoconiosis Silicosis Asbestosis Byssinosis Berylliosis Bagassosis
InterstitialLungDisease/Presentation All forms of pulmonary fibrosis, regardless of etiology, present with

Dyspnea worsening on exertion Hypoxia worsening on exertion Fine rales or crackles on examination Loud P2 heart sound (if pulmonary HTN present) Clubbed fingers
Inflammatory infiltration with white cells is reversible (treatable), whereas fibrosis is irreversible
Biopsy shows granulomas in berylliosis

28
InterstitialLungDisease/DiagnosticTests
InterstitialLungDisease/Diagnostictests
Best initial test: always chest X-ray High resolution CT scan is more accurate than chest X-ray Most accurate test: lung biopsy Echocardiography E h di h will ill often ft show h pulmonary HTN and possibly right ventricular hypertrophy
MTBS2CK p.158
PCP. Source: commons.wikimedia.org
InterstitialLungDisease/Diagnostictests
InterstitialLungDisease/DiagnosticTests PFTs Restrictive lung disease with proportional decrease FEV1, FVC, TLC, and RV all , but since everything is decreased, the FEV1/FVC ratio will be normal DLCO Decreased in proportion to severity of alveolar septal thickening
MTBS2CK p.158
Severe, long-standing interstitial fibrosis produces thick walls between alveoli that give the appearance of honeycombing. Source: Craig Thurm, MD.
MTBS2CK p.158
InterstitialLungDisease/Treatment Most types of interstitial lung diseases are untreatable Biopsy shows
White cell or inflammatory infiltrate; prednisone should be used Mostly y fibrosis ( (e.g., g IPF), ) steroids typically yp y NOT effective
InterstitialLungDisease/ HypersensitivityPneumonitis
Specific type of interstitial lung disease caused by pulmonary hypersensitivity reaction to certain environmental antigens Inflammation from hypersensitivity reaction results in alveolar thickening and granuloma formation
MTBS2CK p.158
Of all causes of pneumoconioses, berylliosis is most likely to respond to steroids

Due to granulomas (sign of inflammation)
MTBS2CK p.158
29
InterstitialLungDisease/ HypersensitivityPneumonitis Most common antigens causing hypersensitivity pneumonitis include

Antigens from feathers (bird fanciers lung) MAI antigen (hot tub lung) Spores of actinomyces from moldy hay (farmers l lung) ) Spores of actinomyces from compost (mushroom workers lung) Spores of actinomyces from air conditioners (air conditioner lung)
Presentation Acutely
Fever, dyspnea, severe cough Within 4-6 hours of antigen exposure
Or Chronically
Progressive dyspnea on exertion, fine rales, pulmonary fibrosis
Treatment Corticosteroids help to reduce inflammation AVOID O ONGOING O GO G EXPOSURE OSU to inciting agent
Sarcoidosis& ThromboembolicDisease
Sarcoidosis/Definition/Etiology
Sarcoidosis/Presentation Look for

Young African American woman with SOB on exertion and occasional fine rales on lung exam, but without wheezing of asthma
More common in African American women Idiopathic inflammatory disorder predominantly of lungs, lungs but can affect most of the body Characterized by noncaseating granulomas
MTBS2CK p.159
Erythema y nodosum and lymphadenopathy y p p y on chest X-ray hands you diagnosis question
MTBS2CK p.159
30
Sarcoidosis/Presentation
Brain complications Eye problems (burning, itching, tearing or pain) Salivary glands Enlarged lymph nodes in neck & chest Heart complications Granulomas (inflamed lumps in lungs) Liver enlargement Spleen enlargement Enlarged lymph nodes in chest near windpipe and lungs Scarring and granulomas in lung Lupus pernio (painful skin sores on face) Skin lesions on back, arms, neck, face, and scalp
Also presents with

Constitutional symptoms: fever, malaise, weight loss Arthritis Parotid gland enlargement Facial pals palsy Heart block and restrictive cardiomyopathy CNS involvement Iritis and uveitis
Erythema nodosum (itchy and painful rashes) on the lower legs and ankles
MTBS2CK p.159
Source: National Heart, Lung, and Blood Institute, commons.wikimedia.org
Sarcoidosis/DiagnosticTests Chest X-ray: best initial test Hilar lymphadenopathy > 95% with sarcoidosis Parenchymal involvement can also be present in combination with lymphadenopathy
CXR can reveal bilateral hilar lymphadenopathy only Hilar lymphadenopathy with parenchymal disease Or Parenchymal disease alone (depending on stage of disease)
Answer sarcoidosis when chest X-ray or CT shows hilar adenopathy in generally healthy African American woman Although liver and kidney granulomas are very common on autopsy, they are rarely symptomatic
MTBS2CK p.159
MTBS2CK p.159
Sarcoidosis/DiagnosticTests
Sarcoidosis/DiagnosticTests
Lymph node biopsy: most accurate test

Granulomas are noncaseating
Elevated ACE level: 60% Hypercalciuria: 20% Hypercalcemia: yp 5%

Granulomas in sarcoidosis make vitamin D
PFTs: restrictive lung disease

Decreased FEV1, FVC, and TLC with a normal FEV1/FVC ratio
Source: Jmh649, commons.wikimedia.org
MTBS2CK p.159
31
Sarcoidosis/Treatment
ThromboembolicDisease/Definition
Prednisone: drug of choice

Few patients fail to respond
Pulmonary emboli (PE) and deep venous thrombosis (DVT) are treated as same disease PE From DVT vessels of legs in 70% of cases and pelvic veins in 30%, but since risks and treatment are the same they can be discussed simultaneously
Asymptomatic hilar adenopathy doesnt need to be treated
MTBS2CK p.159
MTBS2CK p.160
ThromboembolicDisease/Etiology Virchows triad outlines conditions that predispose to venous TE

Immobility CHF Recent surgery Trauma T Surgery Recent fracture
ThromboembolicDisease/Presentation Look for Sudden onset SOB with clear lungs on examination and normal chest X-ray Other findings in PE
Tachypnea, tachycardia, cough, and hemoptysis Leg pain from DVT Pleuritic chest pain from lung infarction Fever can arise from any cause of clot or hematoma Extremely severe emboli will produce hypotension
MTBS2CK p.160
Factor V Leiden mutation Any malignancy leads to DVT
MTBS2CK p.160
ThromboembolicDisease/DiagnosticTests
Most questions about PE concern diagnostic testing and treatment
ThromboembolicDisease/DiagnosticTests Chest X-ray Usually normal in PE Most common abnormality is atelectasis Wedge Wedge-shaped shaped infarction (Hampton hump), and oligemia of one lobe (Westermark sign) are much less common than simple atelectasis
MTBS2CK p.160161
There is no single, uncomplicated diagnostic test for PE y, EKG, , and ABG are best initial tests Chest X-ray, In PE, the main issue is to know Whats the most common finding? And Whats the most common abnormality when theres an abnormality?
MTBS2CK p.160
EKG Usually shows sinus tachycardia Most common abnormality is nonspecific p ST-T wave changes Only 5% will show right axis deviation, RV hypertrophy or RBBB
32
ThromboembolicDisease/DiagnosticTests ABG Hypoxia and respiratory alkalosis ( pH and p CO2) with normal chest X-ray is extremely suggestive of PE
65-year-old woman with recent hip replacement has acute onset of SOB and tachycardia. Chest X-ray normal. Hypoxia on ABG, increased A-a gradient, EKG with sinus tachycardia. What is the most appropriate next step in management? a. Intravenous unfractionated heparin b. Thrombolytics Hemodynamically unstable & acute RV failure Anticoagulants contraindicated, c. Inferior I f i vena cava filter filt recurrent emboli & RV dysfunction d. Embolectomy If heparin ineffective & persistent e. Spiral CT scan hypotension, hypoxia, tachycardia f. Ventilation/perfusion (V/Q) scan If initial labs suggestive, treat! g. Lower-extremity Doppler studies Dont wait to confirm PE h. D-dimer Poor specificity
MTBS2CK p.161
Frequent wrong answer is to choose S1, Q3, T3 as the most common abnormality on EKG
MTBS2CK p.161
Spiral CT scan Also called CT angiogram Standard of care in diagnostic testing to confirm presence of PE after X-ray, EKG and ABG EKG, Specificity is excellent (> 95%) However, sensitivity is 85%, it can miss 15% of clots
MTBS2CK p.161
Chest spiral CT scan with radiocontrast agent showing multiple filling defects both at the bifurcation and in the pulmonary arteries. Source: James Heilman, MD, commons.wikimedia.org
ThromboembolicDisease/DiagnosticTests Ventilation/Perfusion (V/Q) scan May reveal segmental areas of mismatch High probability scans have no clot (false positive) in 15% Low probability scans have a clot (false negative) in 15% Interpret results in combination with clinical suspicion Chest X-ray must be normal for V/Q scan to have any degree of accuracy. Do a spiral CT if chest X-ray is abnormal.
MTBS2CK p.161162
V/Q or ventilation perfusion scanning is still very useful in evaluating pulmonary emboli. A positive test is an area that is ventilated with decreased perfusion. Source: Nishith Patel.
MTBS2CK p.161
33
D-dimer Test is very sensitive (better than 97% negative predictive value) Specificity poor. Any clot or bleeding elevates D-dimer level Negative test excludes clot Positive test doesnt mean anything
D-dimer is answer when pretest probability of PE is low and you need a simple, noninvasive test to exclude thromboembolic disease
MTBS2CK p.162
MTBS2CK p.162
ThromboembolicDisease/DiagnosticTests Lower extremity (LE) Doppler study If LE Doppler positive, no further testing needed Only 70% of PEs originate in legs, so itll miss 30% of cases You dont need a spiral CT or V/Q scan to confirm a PE if theres there s a clot in legs because they wont won t change therapy Patient still needs heparin and 6 months of warfarin
Spiral CT negative V/Q or LE Doppler negative withhold therapy with heparin LE D Dopplers l are a good d test if V/Q and spiral CT do not give clear diagnosis
MTBS2CK p.162
MTBS2CK p.162
ThromboembolicDisease/DiagnosticTests Angiography Most accurate test Nearly 100% specificity and a false negative rate < 1% Unfortunately, theres 0.5% mortality, which is high if you consider the tens of thousands of tests a year that are needed to exclude PE in all cases
When testing for PE, angiography is rarely done

Thrombus (labeled A) causing a central obstruction in the left main pulmonary artery. ECG tracing shown at bottom. Source: Aung Myat and Arif Ahsan, commons.wikimedia.org
MTBS2CK p.162
34
ThromboembolicDisease/Treatment
Heparin Best initial therapy Warfarin should be started simultaneously with heparin to
Achieve Achie e therapeutic therape tic INR of 2 to 3 times normal as quickly as possible
When is an inferior vena cava (IVC) filter the right answer? Contraindication to the use of anticoagulants (e.g., melena, CNS bleeding) Recurrent emboli while on heparin or fully therapeutic warfarin (INR of 23) Right ventricular (RV) dysfunction with an enlarged RV on echo. In this case, the next embolus, even if seemingly small, could be potentially fatal
MTBS2CK p.162
MTBS2CK p.162
When are thrombolytics the right answer? Hemodynamically unstable patients (e.g., hypotension and tachycardia) Acute RV dysfunction Contraindicated in p patients with recent surgery or bleeding No specific time limit in which to use thrombolytics as there is in stroke or MI
MTBS2CK p.162
When are direct-acting thrombin inhibitors (argatroban, lepirudin) the answer? Heparin-induced thrombocytopenia When is aspirin the answer? Never
MTBS2CK p.162163
PulmonaryHypertension/Definition
PulmonaryHypertension, ObstructiveSleepApnea,& AcuteRespiratory DistressSyndrome
Lung or pulmonary circulation normally extremely low pressure

Systolic 25 mmHg Diastolic 8 mmHg Mean 15 mmHg
MTBS2CK p.163
35
PulmonaryHypertension/Definition
PulmonaryHypertension/Etiology
Classified as either Primary

Idiopathic dysfunction of pulmonary arteries
Secondary causes include

L sided-heart failure (MCC) ( ) Intracardiac L R shunting Hypoxic vasoconstriction from chronic lung disease (e.g., COPD) Thromboembolic disease
MTBS2CK p.163
Chronic hypoxemia leads to pulmonary HTN, which results in more hypoxemia
MTBS2CK p.163
PulmonaryHypertension/Presentation Dyspnea and fatigue Syncope (exertional!) Chest pain (exertional!) Wide splitting of S2 with loud P2 or tricuspid and pulmonary valve insufficiency Sign of right right-sided sided heart failure Its impossible to know that pulmonary HTN is causing dyspnea without tests
PulmonaryHypertension/DiagnosticTests
ChestXrayand CT
Best initial tests Showing dilation of proximal pulmonary arteries with narrowing or pruning of distal vessels
Source: tmcr.usuhs.mil
MTBS2CK p.163
MTBS2CK p.163
RightheartorSwanGanzcatheter Most accurate test And Most precise method to measure pressures
EKG Right axis deviation, right atrial and ventricular hypertrophy Echocardiography RA and RV hypertrophy; Doppler estimates pulmonary artery (PA) pressure
MTBS2CK p.163
V/Q scanning Identifies chronic PE as cause of pulmonary HTN CBC Shows polycythemia from chronic hypoxia
MTBS2CK p.163
36
PulmonaryHypertension/Treatment
PulmonaryHypertension/Treatment
1. Correct underlying cause when one is clear 2. Idiopathic disease is treated with
Inhaled or intravenous prostacyclin analogues (pulmonary arterial vasodilators): epoprostenol, treprostinil, iloprost, beraprost Endothelin antagonists: bosentan Phosphodiesterase inhibitors: sildenafil Calcium-channel blockers
Only if demonstrated to be responsive to them during right heart catheterization
Oxygen slows progression, particularly with COPD Only lung transplantation is curative for idiopathic pulmonary HTN
MTBS2CK p.164
MTBS2CK p.164
ObstructiveSleepApnea(OSA)/Definition
ObstructiveSleepApnea(OSA)/Presentation
Cessation of airflow due to upper airway obstruction during sleep Obesity Ob it i is most t commonly identified cause
Source: Habib M'henni, commons.wikimedia.org
Patients present with daytime somnolence and history of loud snoring Other symptoms include
Headache Impaired memory and judgment Depression HTN Erectile dysfunction
MTBS2CK p.164
MTBS2CK p.164
ObstructiveSleepApnea Risk factors include

Male gender Obesity Large uvula/tongue And Retrognathia (recession of mandible)
ObstructiveSleepApnea/Treatment
Arrhythmias and erythrocytosis are common Can lead to pulmonary HTN and RV failure Most accurate test is polysomnography (sleep study)
Shows multiple episodes of apnea
MTBS2CK p.164
1. Weight loss and avoidance of alcohol 2. Nasal continuous positive airway pressure (nasal CPAP) 3. Surgical widening of airway (uvuloplatopharyngoplasty) if this fails 4. Avoid use of sedatives
MTBS2CK p.164
37
AcuteRespiratoryDistressSyndrome(ARDS)/ Definition Acute respiratory failure from overwhelming lung injury or systemic disease Characterized by Severe hypoxia Poor lung compliance And Noncardiogenic pulmonary edema
ARDS is caused by endothelial injury at level of alveolus, making lung cells leaky so that alveoli fill up with fluid
MTBS2CK p.164165
ARDS/Etiology
ARDS is idiopathic Large number of illnesses and injuries are associated with alveolar epithelial cell and capillary endothelial cell damage Illnesses and injuries associated with developing ARDS include
Sepsis or aspiration Lung contusion/trauma Near-drowning Burns or pancreatitis
MTBS2CK p.165
ARDS/DiagnosticTests
Chest X-ray shows bilateral infiltrates quickly become confluent (white out) Air bronchograms are common
MTBS2CK p.165
Source: Samir , commons.wikimedia.org
Defined as having PaO2/FiO2 ratio < 200

The FIO2 is expressed as a decimal (e.g., room air with 21% oxygen = 0.21) If pO2 is 105 on room air (21% oxygen or 0.21), then the ratio of pO2/FIO2 is 500 (i.e., 105/.21) If pO2 (as measured on ABG) is 70 while breathing 50% oxygen, the ratio is 70/0.5 or 140
ARDS is associated with normal findings on right heart catheterization Wedge pressure is normal (< 18 mmHg)
Air bronchograms are a sign of dense consolidation of the lung air space. This is a case of pneumococcal pneumonia that left only the air space in the larger bronchi open or air bronchograms. Source: Omid Edrission, MD.
MTBS2CK p.165
MTBS2CK p.165
38
ARDS/Treatment
ARDS/Treatment Positive end-expiratory pressure (PEEP) is used when patient is undergoing mechanical ventilation to FIO2 Levels of FIO2 > 50% are toxic to lungs Maintain plateau pressure < 30 cm of water measured on ventilator No treatment is proven to reverse ARDS. Dont forget to treat the underlying cause.
Low tidal volume mechanical ventilation is the best support while waiting to see if lungs will recover
Use 6 mL/kg of tidal volume
Steroids aren arent t clearly beneficial in most cases

They may help in late-stage disease in which pulmonary fibrosis develops
MTBS2CK p.166
MTBS2CK p.166
39
CancerScreening PreventativeMedicine
BreastCancer CervicalCancer ColonCancer ProstateCancer LungCancer
BreastCancerScreening
Mammography screening tool of choice Start at 50 years old When reward is highest Starting at 40 is controversial MRI, MRI CT CT, and US are adjuvant screening
Self-examination not recommended. Never the correct answer on S2CK.
Which of the following is most likely to benefit an asymptomatic patient with multiple first-degree relatives with breast cancer? a. b. c c. d. e. f. Tamoxifen Most familial breast ca. NOT BRCA BRCA testing Aromatase inhibitors Unproven in prevention Effective but to lesser degree Dietary modification Performed in breast cancer patients HER-2/neu testing Estrogen/progesterone Performed in breast cancer patients receptor testing
MTBS2CK p.356
MTBS2CK p.356
TAMOXIFEN Greater risk: DVT/PE and endometrial cancer Less risk: Fractures Remember! Better to be ALIVE with a DVT than DEAD with normal legs
CanSTOPmammographyatage75
HER-2/neu positive patients treated with trastuzumab if you HAVE cancer! Not a prophylactic!
CervicalCancerScreening
ColonCancerScreening
Papanicolaou test = Pap Smear

Start at age 21 Done every 3 years, with cytology, until 30 years old After age 30, if HPV testing added, then every 5 years Stop at age 65 with adequate screening history and low risk
MTBS2CK p.357
Colonoscopy
The most accepted screening test Start at 50 years All other testing Repeat every 10 years modalities are inferior to Exceptions colonoscopy Family history 1st-degree relative 40 or ten years earlier Whichever is EARLIER! HNPCC: 3 relatives, 2 generations, 1 premature Start at 25 and do colonoscopy every 1-2 years
MTBS2CK p.357
Katsumi M. Miyai, M.D., Ph.D., Regents of the University of California. Used with permission.
ColonCancerScreening
ProstateCancerScreening
Familial Adenomatous Polyposis

Sigmoidoscopy at age 12, then every year
Personal History of Polyps

Repeat p every y 3-5 y years
Theres no test that reduces mortality Prostate Specific Antigen (PSA) Doesnt reduce mortality Useful in tracking current disease Digital Rectal Exam (DRE) Doesnt reduce mortality
PSAs require a conversation with the patient regarding pros and cons
MTBS2CK p.357358
LungCancerScreening
SummaryofPreventiveMedicineKeyPoints
Not recommended at this time Chest radiograph, CT scan, MRI, PET, etc. All have their purpose but NOT in screening
Any question asking who and when to screen for lung cancer is a trick
Mammography >50 to age 75 Tamoxifen for multiple 1st degree relatives BRCA is NOT clear! Pap smear interval to 5 years after age 30, if combined with HPV testing No lung or prostate screening clearly effective
MTBS2CK p.358
MTBS2CK p.358
LipidScreening Different by age and gender

Men start at 35 yo Women start at 45 yo Frequency depends on CVD status
NonCancerScreeningand Prevention
LipidScreening Hypertension:DiagnosisandControl DiabetesMellitus OtherScreenings
What is the test?

Cholesterol panel
Total CHL, HDL, LDL LDL guides therapy usually We do NOT know what to do with Triglycerides!
MTBS2CK p.358
LipidScreening Normal Values?

Determined by whats tolerable given risk
LipidScreening Goals of Therapy

HDL Cholesterol > 40
Interventions
Diet, Exercise, Pharmacology
0-1 Risk:
Diet at LDL >160 Drugs at LDL >190
Goals differ based on comorbidities

Diabetes HTN Coronary disease or equivalent
Coronary Artery Disease (CAD) equivalents: Carotid disease, peripheral arterial disease (PAD), diabetes mellitus, and aortic disease
MTBS2CK p.358
2 or more risks
Diet at LDL >130 Drugs at LDL >160
For CAD and Equivalents

LDL Cholesterol < 100 Both diet and drugs
Possibly < 70 for CAD combined with Diabetes!
MTBS2CK p.358
Hypertension All adults (>18) should be screened at every visit At least every two years HTN
Elevated BP at 2 separate occasions Not clear what to do about Pre-hypertension
DiabetesScreening Who is screened?

Those with CHD Hypertension is the clearest risk to screen for DM
Test
FastingBloodGlucose(FBG) OralGlucose ToleranceTest(OGTT) HemoglobinA1C
Diabetes 126mg/dL 200mg/dL 6.5%
MTBS2CK p.358
MTBS2CK p.359
Osteoporosis Bone density 2.5 SDs below average Recommendation

Every woman screened at 65 yo Dual-Energy X-ray Absorptiometry (DEXA) scan
OtherScreenings Abdominal Aortic Aneurysms

All men 65 -75 ANY smoking history Receive abdominal ultrasounds at least once
Osteoporosis Fractures Increased Mortality
Tobacco (traditional or smokeless)

Employ the Five-As Ask, Advise, Attempt, Assist, Arrange
Intimate Partner Violence

Not to be overlooked
MTBS2CK p.361
MTBS2CK p.361
AlcoholDependence Alcohol
Know difference between dependence and abuse CAGE Questions
Do they feel the need Cut down? Do they feel Annoyed with criticism of drinking? Have they ever felt Guilty by their drinking? Do they ever need an Eye-opener?
Vaccinations
InfluenzaandPneumococcal Varicella HepatitisA&B Tetanus Meningococcal
MTBS2CK p.361362
InfluenzaVaccination Influenza A and B

Strains circulating in previous year Inactivated (killed) injection
PneumococcalVaccine 23-valent Pneumococcal Polysaccharide Vaccine Protects against Streptococcal pneumoniae Who gets it?
Chronically ill
Respiratory, heart, kidney, and liver diseases
Who gets it?

Everybody Every year Healthcare workers, workers pregnant women women, elders
INFLUENZA VACCINE Every person Every year
Immunocompromised
Asplenia
Elderly: 65 yo
Revaccination after 5 years
MTBS2CK p.359
MTBS2CK p.359
Varicella&HerpesZosterVaccination Live attenuated vaccine against varicella virus Who gets Chicken Pox vaccination?
ALL adults seronegative for varicella infection
VaricellaVaccination
Who gets Herpes Zoster vaccination?

ALL adults 60 yo
Reduces incidence and severity
Herpes Zoster vaccine Chicken Pox vaccine

Different strengths and indications
Vaccines given to persons 60 to prevent zoster have 18 times viral antigens of pediatric vaccines
MTBS2CK p.360
HepatitisVaccination
HepatitisA Fecaloraltransmission Infectionrelatedtopoor hygieneandcrowding Nocarrierstate Low mortality/morbidity HepatitisAVaccine Chronicliverdisease MSMorIVdrugusers Infectedclosecontacts Travelers
MTBS2CK p.360
HepatitisVaccination
HepatitisB Percutaneous,perinatal, andsexualroutes (+)Carrierstate 10%developchronic disease HepatitisBVaccine ChronicLiverdisease MSMorIVdrugusers Infectedclosecontacts Healthcareworkers Dialysispatients
MTBS2CK p.360
HepatitisBVaccine DIABETESisanindication!
TetanusVaccine Tetanus Toxoid booster every 10 years One Tdap (Tetanus Acellular Pertussus) should be one of them Five years after a dirty wound
MeningococcalVaccination Quadrivalent conjugate polysaccharide vaccine

A,C,Y,W
Very efficacious Who gets it?

ALL children age 11 Adults:
Asplenia or equivalent immunodeficiency Epidemic settings (military, college dormitories)
MTBS2CK p.360
MTBS2CK p.360
ImportantDefinitions
Prevalence: Incidence: Sensitivity (SN): Total number of diseased patients in the population. Number of NEW cases during a specified period of time. Probability that person with disease has a positive test. Probability that person without disease has a negative test. Of those with a positive test, what proportion have disease?
Epidemiology
Sensitivity&Specificity PositiveandNegativePredictiveValues ChangingtheCutoff? ImportantFormulas
Specificity (SP): Positive Predictive Value (PPV):
Negative Predictive Of those with a negative test, what proportion do not have disease? Value (NPV):
The2x2Table
(+) D (+) Test a (-) D b
The2x2Table:SensitivityandSpecificity
(+) D (+) Test a (-) D b
(-) ( ) Test est
(-) ( ) Test est
Sensitivity (SN):
Probability that person with disease has a positive test. = a / (a+c)
The2x2Table:SensitivityandSpecificity
(+) D (+) Test a (-) D b
The2x2Table:PPVandNPV
(+) D (+) Test a (-) D b
(-) ( ) Test est
(-) ( ) Test est Positive Predictive Value (PPV):
Specificity (SP):
Probability that person without disease has a negative test. = d / (b+d)
Of those with a positive test, what proportion have disease? = a / (a+b)
The2x2Table:PPVandNPV
(+) D (+) Test a (-) D b
The2x2Table:SN,SP,PPV,NPV
(+) D (+) Test a (-) D b PPV a / (a+b) NPV d / (c+d)
(-) ( ) Test
(-) ( ) Test
Negative Predictive Of those with a negative test, what proportion do not have disease? Value (NPV): = d / (c+d)
SN a / (a+c)
SP d / (b+d)
FormulasList
Sensitivity (SN): Specificity (SP): Positive Predictive Value (PPV): a / (a + c) d / (b + d) a / (a + b) a b
EpidemiologyinPractice
Disease c d
No disease
Negative g Predictive d / (c + d) Value (NPV): False Negative Ratio: False Positive Ratio: c / (a + c) or (1 SN) b / (b + d) or (1 SP) Test Cutoff
Positive Test Disease No disease Disease
Negative Test No disease
Test Cutoff
Test Cutoff
MovingtheCutoff
Positive Test Disease
Negative Test No disease Disease No disease
Test Cutoff
Test Cutoff
MovingtheCutoff
MovingtheCutoff
Test Cutoff
Test Cutoff
Howdoesthisaffect:SP,SN,PPV,NPV?
Positive Test Negative Test
ImportantEpidemiologyConcepts
(+) D (-) D b a
(+)T
Disease No disease
Sensitivity and specificity are independent of disease prevalence

Characteristics of test
(-)T
Positive Test Negative Test
PPV and NPV are dependent on disease prevalence
SN:
Disease No disease
SP: PPV: NPV:
ImportantEpidemiologyConcepts When using a particular test:

Raising the Cutoff
Increases Sensitivity and NPV Decreases Specificity and PPV
FormulasList
Sensitivity (SN): Specificity (SP): Positive Predictive Value (PPV): Negative Predictive Value (NPV): False Negative Ratio: False Positive Ratio: Positive Likelihood Ratio: Negative Likelihood Ratio: a / (a + c) d / (b + d) a / (a + b) d / (c + d) c / (a + c) or (1 SN) b / (b + d) or (1 SP) (SN) / (1 SP) (1 SN) / SP
Lowering the Cutoff

Increases Specificity and PPV Decreases Sensitivity and NPV
Epidemiology
Sensitivity&Specificity PositiveandNegativePredictiveValues Changingthecutoff? ImportantFormulas
Xrays RADIOLOGY
MatthewKinney,MD
OrthopedicResident UniversityofCaliforniaSanDiego
ChestXrayIndications Subjective pulmonary complaints

Cough SOB/dyspnea Pleuritic chest pain Hemoptysis
ChestXrayIndications Objective pulmonary findings

Rales (Crackles) Rhonchi Wheezing Hyperresonance/ yp dullness to percussion Chest wall tenderness Tracheal deviation SVC syndrome
JVD Plethora
Source: James Heilman, MD
MTBS2CK p.491
MTBS2CK p.491
ChestXrayViews Posterior/anterior (PA) films

Standard CXR positioning Patient must be capable of standing
ChestXrayViews Anterior/posterior (AP) films

Necessary for immobile patients
ICU Paralysis
Source: Mikael Hggstrm
MTBS2CK p.491
MTBS2CK p.491
ChestXrayViews Lateral
Useful to localize lesion found on PA films Most sensitive test for pleural effusion
ChestXrayViews Lateral decubitus

Patient lies on side Useful to evaluate pleural effusions
Source: Nicholas Lange
MTBS2CK p.492
Source: Zachary M Alexander
MTBS2CK p.491
ChestXrayFindings Lobar pneumonia
ChestXrayFindings Solitary pulmonary nodule
Source: Nicholas Lange
Source: Zachary M Alexander
MTBS2CK p.491
MTBS2CK p.491
ChestXrayFindings Pleural effusion
ChestXrayFindings Pneumothorax
Source: Magnus Manske Source: John Yasmer
MTBS2CK p.491
MTBS2CK p.491
ChestXrayFindings Free air under diaphragm
AbdominalXrayIndications Small bowel obstruction

Mechanical obstruction Ileus
Source: Brian Johnston
MTBS2CK p.491
MTBS2CK p.492
AbdominalXrayViews Abdominal plain film

Erect view of abdomen
AbdominalXrayViews Kidneys, ureters, and bladder (KUB)

Supine view of abdomen
Source: Nevit Dilmen
Source: Nevit Dilmen
MTBS2CK p.492
MTBS2CK p.492
AbdominalXrayFindings Small Bowel Obstruction

Mechanical obstruction
BoneXrayIndications Fracture Bone tumor evaluation Osteomyelitis Skeletal Survey

Trauma Child abuse
Air fluid levels

Source: Stephanie A Bernard Source: James Heilman, MD
MTBS2CK p.492
MTBS2CK p.492
BoneXrayFindings Osteomyelitis
Periosteal elevation Osteolysis
Surrounded by ring of sclerosis
ComputedTomography(CT)
Note: XR findings are delayed (2 weeks)

MRI is positive earlier
MTBS2CK p.492
CTBasics
Definition Computed Tomography Large series of 2D X-rays around a single axis of rotation to create 3D image
Increased detail clarity Windowing capability
NoncontrastHeadCTIndications Severe head trauma

Loss of consciousness Altered mental status
Stroke
Hemorrhagic Ischemic
Drawbacks High doses of radiation Often requires IV contrast

Anaphylaxis risk Renal damage
Consider 1-2 liters of fluids, NaHCO3, and/or
Intracranial bleeding
Subdural hematoma Epidural hematoma
NAC if mild renal insufficiency
Medication contraindications (metformin)

MTBS2CK p.493
NoncontrastHeadCT Bone - bright white Blood - bright white CSF - dark black
NoncontrastHeadCTFindings Ischemic Stroke

Darkening of brain parenchyma Blurred Gray-White Junction Mass effect
Source: Andrew Ciscel
Source: Lucien Monfils
MTBS2CK p.493
MTBS2CK p.493
NoncontrastHeadCTFindings Hemorrhagic Stroke

Bright, localized area corresponding to bleed Mass effect Gray-white junction intact
NoncontrastHeadCTFindings Subdural Hematoma Crescent-shaped, bright white region

Not confined by skull sutures Adjacent j to skull
Mass effect
Source: commons.wikimedia.org Source: James M. Grimson
MTBS2CK p.493
MTBS2CK p.493
NoncontrastHeadCTFindings Epidural Hematoma Biconvex, bright white region

Adjacent to skull Confined by skull sutures
ContrastHeadCTIndications Infection
Meningitis Abscess
Tumor
Primary Cancer Brain Metastasis
Mass effect
Source:Hellerhoff,commons.wikimedia.org
MTBS2CK p.493
MTBS2CK p.493
ContrastHeadCTFindings Tumor
Primary tumor: Single lesion
Bright white Mass effect Identical to abscess
ContrastHeadCTFindings Tumor
Metastasis: Often multiple lesions
Bright white Found mostly at gray-white junction Mass effect
MTBS2CK p.493
MTBS2CK p.493
AbdominalCTIndications Retroperitoneal structure pathology

Pancreatitis Adrenal gland tumors
AbdominalCTViews
Appendicitis Diverticulitis Nephrolithiasis Abdominal viscera masses

Liver tumors
Splenic laceration NOTE: Use both oral and IV contrast

AbdominalCTFindings Pancreatitis
Irregular pancreatic outline Pancreatic enlargement Retroperitoneal fluid
AbdominalCTFindings Appendicitis
Appendix enlargement (> 6mm) Wall thickening Fat stranding
Appendix dilatedto15 mmthat doesntfillwith contrast.

Source: James M Grimsom
MTBS2CK p.493
MTBS2CK p.493
Source:AndrewSellers
AbdominalCTFindings Diverticulitis Localized bowel wall thickening Fat stranding Evidence of diverticulae Note: If advanced, abscess may be present
AbdominalCTFindings Nephrolithiasis Evidence of hydronephrosis Visible calcification in (if obstructing) urinary tract Note: No oral or IV contrast
Source: Phil Kang
MTBS2CK p.493
Source:Hellerhoff,commons.wikimedia.org
MTBS2CK p.493494
ChestCTIndications Mass lesions

Lung Mediastinum
NormalChestCT
Lung pathology
Interstitial lung disease Sarcoidosis Bronchiectasis Cavitary lesions
Pulmonary embolism
Source: Brendan T Doherty
MTBS2CK p.494
MTBS2CK p.494
MRIBasics Definition Magnetic Resonance Imaging

1) Magnetic field aligns H20 molecular dipoles 2) RF waves are applied, which alters proton spin 3) When waves are stopped, the protons relax to their natural spin -- producing a measurable signal Upshot: Allows visualization of tissue based on water content Best test for evaluating soft tissue
MagneticResonanceImaging, Ultrasonography,&Nuclear Medicine
Drawbacks
Long scans requiring complete immobility Certain metal implants are contraindicated Small bore tubes claustrophobia + body mass issues
MTBS2CK p.494
MRIIndications CNS pathology

Brain/spinal cord tumors MS Specific regions of the head Sinuses Orbits
MRIFindings Primary Brain Tumor Contrast enhancing Solitary lesion Mass effect
Musculoskeletal disease
Osteomyelitis Soft tissue injury Nerve compression Herniated disc disease Brachial plexus injury
Source: Steven J. Goldstein
MTBS2CK p.494
MTBS2CK p.494
MRIFindings Multiple Sclerosis Contrast-enhanced Demyelinated plaques appear white
MRIFindings Spinal Disc Herniation Disc extruding from IV space Compression of spinal cord
MTBS2CK p.494
Source: Jeffery Hirsch
MTBS2CK p.494
USBasics Definition Ultrasonography

Sound waves of a certain frequency emitted Echoes return based on specific tissue properties Dense objects (e.g., stones, tissue) reflect waves better than fluid/air Scanner measures echoes and creates image based on differences in object density
Ultrasonography
Drawbacks
Poor at visualizing structures beyond bone Poor at visualizing structures beyond air Body habitus affects image quality
MTBS2CK p.494495
USIndications Gallstone disease Renal disease

PCKD Hydronephrosis Note: CT preferred for kidney stones
USFindings Cholecystitis
Presence of gallstone Stone in lumen Silhouette Gall bladder wall thickening Pericholestatic fluid Sonographic Murphys sign
Source: Joseph Lagrew
Gynecologic evaluation
PCOS Uterine evaluation Pregnancy evaluation Ectopic pregnancy
Pancreatic disease (via endoscopic US)

NuclearScansBasics Definition
Radiolabeled molecules localize to specific organs Emission detected and allow for visualization of organ function PET scan = Glucose Cholescintigraphy = HIDA V/Q scan
Source: Jeffrey Hirsch
NuclearMedicine
MTBS2CK p.495
NuclearScanTypes HIDA (Hepatobiliary) scan
NuclearScanTypes Ventilation/perfusion (V/Q) scanning
V
Source: Jonathan Sexton
Source: Kieran Maher
MTBS2CK p.495
MTBS2CK p.495
NuclearScanTypes Bone scan

Uptake into osteoblasts Useful for detecting area of high bone turnover Occult cancer metastasis
Indium scan
Uptake into WBCs Useful in detecting fever of unknown origin (FUO)
Gallium scan
Uptake with iron metabolism Useful for detecting FUO and some cancers
Nuclear Ventriculography
Used to measure cardiac ejection fraction
MTBS2CK p.495
RHEUMATOLOGY
NiketSonpal,MD
Osteoarthritis,Gout,& Pseudogout
Osteoarthritis/Definition
Osteoarthritis/Etiology
Osteoarthritis or degenerative joint disease (DJD) Chronic, slowly progressive, erosive damage to joint surfaces Loss of articular cartilage
Incidence directly proportional to increasing age and trauma to joint

Contact sports with trauma
Obesity increases DJD

DJD is, by far, the MCC of joint disease.
MTBS2CK p.167
MTBS2CK p.167
Osteoarthritis/Presentation
Osteoarthritis/Presentation
Most commonly symptomatic in weightbearing joints Hand is affected, but isnt as great a cause of disability Distal interphalangeal (DIP) joints are > proximal interphalangeal joints (PIP) and metacarpophalangeal joints (MCP)
Crepitations of involved joints are common Effusion is rare Stiffness is of short duration (<15 min) DIP enlargement: l t Heberdens H b d nodes d PIP enlargement: Bouchards nodes
MTBS2CK p.167
MTBS2CK p.167
Osteoarthritis
Heberdens nodes (DIP joint)
Osteoarthritis/DiagnosticTests
Erythrocyte sedimentation rate
Bouchards nodes (PIP joint)
Complete blood count t
Normal Lab Tests
Antinuclear antibody tib d
Rheumatoid factor
Richard Usatine, M.D. Used with permission
MTBS2CK p.167
Dense subchondral bone
Osteoarthritis
Joint space narrowing
X-rays y Show:
Osteophytes
Bone cysts
MTBS2CK p.168
Source: Russell A. Patterson
Osteoarthritis/Treatment
Absence of inflammation, normal lab tests, and short duration of stiffness distinguishes DJD from RA
1. Weight loss and moderate exercise 2. Acetaminophen: best initial analgesic 3. NSAIDs: used if symptoms arent controlled with acetaminophen; toxicity - GI bleeding 4. Capsaicin p cream 5. Hyaluronic acid injections 6. Intra-articular steroids 7. Joint replacement Glucosamine and
chondroitin sulfate are no more effective than placebo.
MTBS2CK p.168
MTBS2CK p.168
Gout/Definition/Etiology
Gout/Etiology
Idiopathic
Overproduction
Defect in urate metabolism 90% of cases in men Can be from:

Overproduction or Underexcretion
Enzyme deficiency
Increased cell turnover
Renal Insufficiency
Underexcretion
Acidosis
Thiazides or ASA
Gout/Presentation
Gout
Man who develops sudden, excruciating pain, redness, and tenderness of big toe at night after binge drinking with beer Fever is common Hard to distinguish initial gouty attack from infection without arthrocentesis Metatarsal phalangeal (MTP) joint of great toe most frequently affected Also in ankles, feet, and knees
MTBS2CK p.168
Gout/Presentation Chronic Gout Tophi: tissue deposits of urate crystals with foreign body reaction Most often tophi occur in cartilage, subcutaneous tissues, bone, and kidney Often take years to develop Uric acid kidney stones occur in 5% to 10% of patients Long asymptomatic periods between attacks are common
Gout/DiagnosticTests Most accurate test:

Aspiration of joint
Needle-shaped crystals with negative birefringence on polarized light microscopy

Commons.Wikimedia.org. used with permission
Tophi can occur anywhere in the body.
MTBS2CK p.169
MTBS2CK p.169
Gout/DiagnosticTests
Gout/DiagnosticTests
WBC joint fluid elevated 2,000 to 50,000/L Predominantly neutrophils Infected joint has redness, warmth, and tenderness Its essential to tap joint to exclude infection Protein and glucose levels in synovial fluid dont help answer the most likely diagnosis question
Uric acid levels: elevated at some point in 95% of patients Single level during an acute attack normal in 25% Acute attacks = ESR and leukocytosis
MTBS2CK p.169
MTBS2CK p.169
Gout/DiagnosticTests X-rays:
Gout/Treatment Acute Attack NSAIDs superior to colchicine as best initial therapy Corticosteroids injection: single joint , oral: multiple joints Steroids (e (e.g., g triamcinolone) is answer when:
No response to NSAIDs Contraindication to NSAIDs such as renal insufficiency
Normal in early disease Erosions of cortical bone happen later
Contraindication questions are always clear

Source: Wikimedia.org
MTBS2CK p.169
MTBS2CK p.169
ChronicManagement
Management 1) Diet
Decrease consumption of alcohol, particularly beer; lose weight Decrease high-purine foods
Gout/Treatment
2) Stop thiazides, aspirin, and niacin 3) Colchicine is effective at preventing second attack of gout 4) Probenecid and sulfinpyrazone increase the excretion of uric acid in kidney (uricosuric) 5) Allopurinol decreases production of uric acid
MTBS2CK p.169170
Colchicine gives diarrhea and bone marrow suppression (neutropenia). Probenecid, NSAIDs, and sulfinpyrazone are contraindicated in renal insufficiency. Allopurinol is safe with renal injury.
MTBS2CK p.170
Gout/Treatment Adverse Effects of Chronic Treatment Hypersensitivity (rash, hemolysis, allergic interstitial nephritis) occurs with uricosuric agents and allopurinol Colchicine can suppress white cell production Toxic epidermal necrolysis or Stevens-Johnson Stevens Johnson syndrome may occur from allopurinol Dont start uricosuric agents or allopurinol during acute attacks of gout. If the patient is already on allopurinol you can safely continue it.
MTBS2CK p.170
CalciumPyrophosphateDepositionDisease (Pseudogout)/Definition/Etiology
Calcium-containing salts depositing in articular cartilage Most common risk

Hemochromatosis and hyperparathyroidism
CPDD can occur:

Diabetes Hypothyroidism Wilson disease
MTBS2CK p.170
CalciumPyrophosphateDepositionDisease (Pseudogout)/Presentation
CalciumPyrophosphateDepositionDisease (Pseudogout)/DiagnosticTests
CPDD differs from gout in that large joints such as the knee and wrist are affected, but not particularly the first MCP of the foot It differs from DJD in that DIP and PIP arent affected
Uric acid levels normal X-ray: calcification of cartilaginous structures Most accurate test is arthrocentesis, which reveals p positively y birefringent g rhomboidshaped crystals Synovial fluid: elevated level of WBCs 2,000 to 50,000/L - nonspecific
MTBS2CK p.170
MTBS2CK p.170
Pseudogout
Pseudogout
Source Wikimedia Source: Boma O. Afiesimama
CalciumPyrophosphateDepositionDisease (Pseudogout)/DiagnosticTests
Disease DJD
Characteristic History Older,slow, worsewithuse
Physical Findings
SynovialFluid Analysis
You cannot confirm a diagnosis of CPDD without aspiration of the joint.

Gout
DIP,PIP,hip, <200WBCs, andknees osteophytesand jointspace narrowing 1st bigtoe 2,00050,000 WBCs,negatively birefringent needles
Men,acute, bingedrinking
MTBS2CK p.170
MTBS2CK p.171
Disease CPDD
Characteristic History
Physical Findings
SynovialFluid Analysis 2,00050,000 WBCs,positively birefringent rhomboids
Disease Septic arthritis
Characteristic History Highfever, veryacute
Physical Findings Singlehot joint
SynovialFluid Analysis >50,000 neutrophils, cultureoffluid
Hemochromatosis, Wristsand hyperparathyroidism knees
Rheumatoid Young,female, arthritis morningstiffness betterwithuse
Multiplejoints Anticyclic ofhandsand citrulinated feet peptide(anti CCP)
MTBS2CK p.171
MTBS2CK p.171
CalciumPyrophosphateDepositionDisease (Pseudogout)/Treatment
Best initial therapy: NSAIDs Severe disease not responsive to NSAIDs give intra-articular steroids (e g triamcinolone) (e.g., Colchicine helps prevent subsequent attacks as prophylaxis between attacks
LowBackPain&Lumbar SpinalStenosis
MTBS2CK p.171
LowBackPain/Etiology
LowBackPain
Low back pain is No. 1 complaint in US DJD on X-ray or MRI of the spine is nearly universal in those > 50 years totally nonspecific
What Is the Most Likely Diagnosis? If all diseases described in the following are excluded, patient has simple low back pain from lumbosacral strain (idiopathic) No imaging studies and no treatment beyond NSAIDs
Most frequently tested issue is who shouldnt get an imaging study

CompressionoftheSpinalCord
Malignancy or infection compressing spinal cord is a neurological emergency that needs urgent identification and treatment Look for a history of cancer with sudden onset of focal neurological deficits (e.g., sensory level)
Compression at 10th thoracic vertebra leads to sensory loss below the umbilicus Point tenderness at spine with percussion of vertebra is highly suggestive of cord compression Hyperreflexia is found below level of compression
MTBS2CK p.171
MTBS2CK p.172
DiskHerniation(Sciatica)
Epidural abscess is most often from Staphylococcus aureus Epidural abscess presents in same way as cord compression from cancer, but theres there s high fever and markedly elevated ESR
Herniations at L4/5 and L5/S1 level account for 95% of all disk herniations The straight leg raise (SLR) test is pain going into the buttock and below the knee when the leg is raised > 60 degrees
Although only 50% of those with a positive SLR actually have a herniated disk; sensitivity is 90% A negative SLR excludes herniation with 95% sensitivity
MTBS2CK p.172
MTBS2CK p.172
NerveRootInnervation
Nerveroot Motordeficit Reflex affected(lost) Sensoryarea affected
LowBackPain/DiagnosticTests
L4
Dorsiflexion offoot Dorsiflexion oftoe Eversionof foot
Kneejerk
Innercalf
L5
None
Inner forefoot Outerfoot
S1
Anklejerk
Imaging required for cord compression, epidural abscess, ankylosing spondylitis, and cauda equina syndrome Best initial test for cancer with compression, infection, and fractures is plain X-ray Most accurate test is MRI CT scan is used as most accurate test if theres a contraindication to MRI (e.g., pacemaker) Intrathecal contrast must be given to increase accuracy (CT myelogram)
MTBS2CK p.172
MTBS2CK p.172
LowBackPain/DiagnosticTests Imaging in disk herniation is controversial We recommend you answer no MRI for just low back pain and a positive SLR alone Neurological deficits = MRI
ClassificationofBackPain
Diagnosis Cord Compression Historytoanswer MostLikelyDiagnosis Historyofcancer PhysicalFindings Vertebraltenderness, sensorylevel, hyperreflexia Sameascord compression Bilaterallegweakness, saddleareaanesthesia
Epiduralabscess
Fever highESR Fever,
Caudaequina
Bowelandbladder incontinence, erectiledysfunction
MTBS2CK p.172173
Source: Nirav Thakur, MD.
MTBS2CK p.173
ClassificationofBackPain
Diagnosis Ankylosing spondylitis Historytoanswer MostLikelyDiagnosis Underage40,pain worsenswithrest andimproveswith activity Pain/numbnessof medialcalforfoot PhysicalFindings Decreasedchest mobility
LowBackPain/Treatment
Chemotherapy for Lymphoma
Systemic Glucocorticoids Gl ti id Lossofkneeandankle reflexes,positive straightlegraise
Cord Compression p
Diskherniation
Radiation for Solid Tumors
MTBS2CK p.173
MTBS2CK p.174
MRSA
Acute Neurologic Deficits
Vancomycin Linezolid
Beta-lactam antibiotics when organism is sensitive Gentamicin = synergy with staph Surgical drainage for larger collections
Thi k of Think f epidural id l abscess b lik like endocarditis d diti Use vancomycin as initial empiric therapy Switch to oxacillin if its sensitive Drain it if the infection is large enough to produce neurological deficits or it doesnt respond to antibiotics alone
Epidural p Abscess
Systemic Glucocorticoids
MSSA
Oxacillin Nafcillin Cefazolin
MTBS2CK p.174
MTBS2CK p.174
Cauda equina syndrome: surgical decompression Disk herniation (sciatica): NSAIDs with continuation of ordinary activities Steroid injection into epidural space achieves rapid id and dd dramatic ti b benefit fit f for th those with ith sciatica Surgery rarely needed The most common wrong answer for sciatica is bed rest.
MTBS2CK p.174
Man with a history of prostate cancer comes to the emergency department with severe back pain and leg weakness. He has tenderness of the spine, hyperreflexia, and decreased sensation below his umbilicus. What is the most appropriate next step? a. Dexamethasone b. MRI Save neurons before seeing them c. X-ray Low specificity d. Radiation Not fast enough e. Flutamide Not fast enough to save neurons f. Ketoconazole Not fast enough to stop androgens g. Finasteride Not fast enough to stop androgens h. Leuprolide Dangerous with peripheral blockade i. Biopsy Only if cause unclear j. Orchiectomy Best long-term treatment
MTBS2CK p.174175
LumbarSpinalStenosis/Presentation
Most commonly tested point: no imaging studies in patients without focal neurological abnormalities or with simple lumbosacral strain
Look for a person > 60 with back pain while walking, radiating into buttocks and thighs bilaterally Pain described as worse when walking downhill, and better when sitting, but the pedal pulses and ankle/brachial index are normal
Spinal stenosis can simulate peripheral arterial disease, but vascular studies are normal.
MTBS2CK p.175
MTBS2CK p.175
LumbarSpinalStenosis/Presentation
LumbarSpinalStenosis/Treatment
Unsteady gait and leg weakness when walking also occur About have diminished lower extremity reflexes Pain is less with activities in which patient is leaning forward (e.g., cycling)
The only test is MRI Weight loss and steroid injections into the lumbar epidural space improve 25% to 50% of cases Surgical correction to dilate the spinal canal is needed in 75% of patients
MTBS2CK p.175
MTBS2CK p.175
Fibromyalgia
Fibromyalgia,CarpalTunnel Syndrome,&Dupuytren Contracture
What Is the Most Likely Diagnosis? Look for young woman with chronic musculoskeletal pain and tenderness with trigger points of focal tenderness at trapezius, medial fat pad of knee, and lateral epicondyle Cause is unknown Pain occurs at many sites (neck, shoulders, back, and hips) with:
Stiffness, numbness, and fatigue Headaches Sleep disorder
MTBS2CK p.176
Fibromyalgia/DiagnosticTests
Fibromyalgia/Treatment
No test to confirm fibromyalgia Based on complex of symptoms, trigger points at predictable points All lab tests are normal (e.g., ESR, Creactive protein protein, rheumatoid factor (RF), (RF) and CPK levels)
Best initial therapy is amitriptyline Other treatments are milnacipran and pregabalin Milnacipran is an inhibitor of serotonin and norepinephrine reuptake and is approved specifically for the management of fibromyalgia Trigger point injections with local anesthetic are also sometimes used Steroids are the wrong answer for fibromyalgia.
MTBS2CK p.176
MTBS2CK p.176
10
CarpalTunnelSyndrome/Definition
CarpalTunnelSyndrome/Etiology
Amyloidosis
Acromegaly Hypothyroidism
Peripheral neuropathy from compression of median nerve as it passes under the flexor retinaculum Pressure on nerve interferes with its sensory and motor function
Median Nerve Compression
Pregnancy
Rheumatoid Arthritis
Diabetes
MTBS2CK p.176
MTBS2CK p.176
CarpalTunnelSyndrome
CarpalTunnelSyndrome/DiagnosticTests
What Is the Most Likely Diagnosis? Look for pain in hand affecting the palm, thumb, index finger, and radial half of ring finger, muscle atrophy of thenar eminence Pain is worse at night and more frequent in those whose work involves prolonged use of the hands (e.g., typing)
Tinel sign: reproduction of pain and tingling with tapping or percussion of the median nerve
IMC 2010 DxR Development Group, Inc. All Rights Reserved.
MTBS2CK p.177
MTBS2CK p.177
Phalen sign: reproduction of symptoms with flexion of wrists to 90 degrees
Most accurate diagnostic tests are electromyography and nerve conduction testing
Sensory symptoms happen before motor symptoms.

IMC 2010 DxR Development Group, Inc. All Rights Reserved.
MTBS2CK p.177
MTBS2CK p.177
11
CarpalTunnelSyndrome/Treatment
Management Best Initial
Wrist Splints Immobilization to relieve pressure NSAIDS
DupuytrenContracture Hyperplasia of palmar fascia leading to nodule formation and contracture of fourth and fifth fingers Genetic predisposition and association with alcoholism and cirrhosis Patients lose ability to extend fingers, which is more often cosmetic embarrassment than functional impairment Triamcinolone injection Surgical release when function is impaired
Avoid Manual Activity Steroid St id Injection is used if splints and NSAIDs dont control Surgery Can be curative by mechanically decompressing the tunnel such as with cutting open the flexor retinaculum
MTBS2CK p.177
MTBS2CK p.177
DupuytrenContracture
SportsMedicine& Osteoporosis
RotatorCuffInjury
RotatorCuffInjury
Damage to rotator cuff of muscles, tendons, and bursae around shoulder leads to inability to flex or abduct the shoulder It presents with pain in shoulder thats that s worse at night when lying on affected shoulder There can be severe tenderness at the insertion of the supraspinatus
MTBS2CK p.177
MRI is the most accurate test Treat with NSAIDs, rest, and physical therapy Steroids Surgery
MTBS2CK p.177
12
PatellofemoralSyndrome
PatellofemoralSyndrome
Cause of anterior knee pain secondary to trauma, imbalance of quadriceps strength, or meniscal tear Pain in front of knee or underneath patella Particularly bad when walking up or down stairs Worse just after starting to walk after having been seated for a prolonged period It improves after walking
Crepitus, joint locking, and instability X-rays: normal Most cases respond to physical therapy and strength training with cycling Knee K b braces d dont t help h l Theres nothing to fix surgically
MTBS2CK p.178
MTBS2CK p.178
PlantarFasciitis
PlantarFasciitis
Very severe pain in bottom of foot near calcaneus where fascia inserts Pain worst in the morning and improves with walking a few steps Point tenderness @ the fascia inserts at the calcaneus
MTBS2CK p.178
PlantarFasciitis
Osteoporosis
Treatment consists of stretching exercises, arch supports, and NSAIDs Steroid injection is performed if these dont solve problem Surgical release of plantar fascia is rarely necessary X-ray of the foot is not useful in plantar fasciitis. There is no correlation with the presence of heel spurs.
MTBS2CK p.178
Look for an older person, more often a woman, with vertebral fractures leading to loss of height or wrist fracture Asymptomatic, fractures are found on routine screening with bone densitometry, which is recommended for all women > 65
Osteoporosis gives spontaneous fractures of weight-bearing bones.
MTBS2CK p.198
13
Osteoporosis/DiagnosticTests
Osteoporosis/Treatment
Most accurate test is bone densitometry (DEXA) scanning Osteopenia: bone density (T-score) is between 1 and 2.5 standard deviations below normal Osteoporosis: T-score > 2.5 standard deviations < normal
1. Vitamin D and calcium are the best initial therapy 2. Bisphosphonates (alendronate, risendronate, ibandronate) 3 Estrogen replacement 3. 4. Raloxifene
MTBS2CK p.198
MTBS2CK p.198
1. Teriparatide is an analogue of PTH that stimulates new bone matrix formation 2. Used as a nasal spray, calcitonin decreases vertebral fractures risk
Bisphosphonates are very rarely associated with osteonecrosis of the jaw. Bisphosphonates that have prolonged contact with the esophagus can cause esophagitis (pill esophagitis).
When multiple treatment options are presented, choose vitamin D, calcium, and bisphosphonates.
Teriparatide has caused osteosarcoma in rats. It has also caused hypercalcemia.
MTBS2CK p.198
MTBS2CK p.198
RheumatoidArthritis/Definition/Etiology
RheumatoidArthritis,Systemic LupusErythematosus,& p p p Syndrome y Antiphospholipid
RA is an autoimmune disorder predominantly of joints More common in women
MTBS2CK p.178
14
RheumatoidArthritis/Definition/Etiology
RheumatoidArthritis/Presentation
PIP Hands MCP Hands
Chronic synovitis leads to overgrowth, or pannus formation, which damages all the structures surrounding the joint (bone, ligaments, tendons, and g ) cartilage)
Morning stiffness of multiple small, inflamed joints is key to diagnosis.
MTBS2CK p.178
Morning Stiffness > 30 min
Bilateral Symmetrical
Rheumatoid Nodules
Rheumatoid Arthritis
Vasculitis
Episcleritis
Lung nodules and effusions
MTBS2CK p.178
RheumatoidArthritis/Presentation
RheumatoidArthritis/Presentation Boutonniere and swan neck are classic deformities of the hands
C1 and C2 laxity - subluxation Baker cyst Pericarditis and pleural disease Carpal tunnel syndrome
DIP is spared in RA. DIP involvement happens in DJD.
MTBS2CK p.179
MTBS2CK p.179
Source: Nirav Thakur, MD.
RheumatoidArthritis
RheumatoidArthritis/DiagnosticTests
Rheumatoid factor (RF) in 70% to 80% RF is rather nonspecific Anti-cyclic citrulinated peptide (antiCCP) is > 80% sensitive and > 95% specific
MTBS2CK p.179
15
Elevated ESR or C-reactive protein Anemia: normocytic Arthrocentesis on initial presentation excludes crystal disease or infection if diagnosis isnt clear Modest elevation in lymphocytes Sicca syndrome: dry eyes, mouth, and other mucous membranes
MTBS2CK p.179
Felty syndrome: RA Splenomegaly Neutropenia Caplan syndrome: RA Pneumoconiosis Lung nodules

MTBS2CK p.180
RheumatoidArthritis/Treatment
The most important issue in RA is stopping the progression of the disease. Any patient with erosive disease or X-ray abnormalities needs at least methotrexate to slow disease progression. The MCC of death in RA is coronary artery disease.
Disease-Modifying Antirheumatic Drugs (DMARD) Neither NSAIDs nor steroids stop RA from progressing Any patient with erosive RA needs DMARD as part of initial therapy
MTBS2CK p.180
MTBS2CK p.180
RheumatoidArthritis/Treatment Patient with long-standing RA is to have coronary bypass surgery. Which is most important prior to surgery?
a. Cervical spine X-ray Already diagnosed to have RA b Rheumatoid factor b. Doesnt change outcomes c. Extra dose of methotrexate Nonspecific test d. ESR e. Pneumococcal vaccination Has nothing to do with surgery
Erosive disease means: Joint space narrowing Physical deformity of joints X-ray y abnormalities
MTBS2CK p.180
MTBS2CK p.180
16
Methotrexate Best initial DMARD Adverse effects are:

Liver toxicity Bone marrow suppression Pulmonary toxicity
Tumor Necrosis Factor (TNF) Inhibitors (infliximab, adalimumab, etanercept) TNF inhibitors are first line as DMARDS Toxicity of anti anti-TNF TNF drugs:
Reactivation of TB Infection
MTBS2CK p.181
MTBS2CK p.181
Rituximab RA as a DMARD by removing CD20+ lymphocytes from circulation Excellent long-term +/- methotrexate
Hydroxychloroquine Rare as monotherapy as a DMARD More often used in combination with methotrexate as a DMARD Toxic to retina
Hydroxychloroquine leads to retinal toxicity. Do a dilated eye exam.

Symptomatic Control of RA NSAIDs are the best initial therapy for the pain of RA Steroids also work in a matter of hours to control the pain of RA secondary to inflammation Steroids for 2 purposes
NSAIDS arent working Bridge
MTBS2CK p.181
Use TNF inhibitors as a DMARD with methotrexate after methotrexate fails Adverse effects are mandatory for you to know Steroids dont prevent the progression of RA.
MTBS2CK p.181182
17
AdverseEffectsofRAMedications
Drug AntiTNF Hydroxychloroquine Sulfasalazine Rituximab Goldsalts Methotrexate
MTBS2CK p.182
Adverseeffect Reactivationoftuberculosis Ocular Rash,hemolysis y Infection Nephroticsyndrome Liver,lung,marrow
JuvenileRheumatoidArthritisor AdultStillDisease
Definition/Etiology Juvenile rheumatoid arthritis (JRA) is very difficult to define and theres no known etiology
MTBS2CK p.182
JuvenileRheumatoidArthritisor AdultStillDisease/Presentation
Presentation The most important feature of JRA is the presence of high, spiking fever (often > 104 104F) F) in a young person that has no clearly identified etiology, but is associated with a rash
Features of JRA rash: Often only with fever spikes Salmon colored On chest and abdomen Other features of JRA: Splenomegaly Pericardial effusion Mild joint symptoms
MTBS2CK p.182
MTBS2CK p.182
SystemicLupusErythematosus
Laboratory Abnormalities No clear diagnostic test; anemia and leukocytosis often present ANA is normal Ferritin level markedly elevated Treatment Half of cases improve with aspirin or NSAIDs If theres no response then use steroids
MTBS2CK p.183
Definition/Etiology Autoimmune disorder Inflammation diffusely through body
MTBS2CK p.183
18
Presentation Diagnosis of SLE is based on 4 of 11 known manifestations of disease Four skin-related manifestations:
1. Malar rash 2. Discoid rash 3. Photosensitivity 4. Oral ulcers
Alopecia is common in SLE, but isnt one of the official diagnostic criteria.
MTBS2CK p.183
Presentation Joint: arthritis is present in 90% X-ray is normal Serositis: inflammation of pleura and pericardium i di chest h t pain i
Presentation Renal: any degree of abnormality can occur from mild proteinuria to end-stage renal disease requiring dialysis
Most common g glomerulonephritis p is membranous Red cell casts and hematuria occur
Neurologic: symptoms include psychosis, seizures, or stroke from vasculitis

Pneumonia, alveolar hemorrhage, and restrictive lung disease happen in SLE, but arent criteria for diagnosis g of the disease.
Ocular findings arent part of formal diagnostic criteria: Photophobia Retinal lesions ( (cotton wool spots) Blindness
MTBS2CK p.183
MTBS2CK p.184
19
Presentation Hematologic: hemolytic anemia is part of diagnostic criteria, but anemia of chronic disease is more commonly found Lymphopenia, leukopenia, and thrombocytopenia are also seen
Presentation Immunologic (laboratory) abnormalities - criteria include positive ANA, or any one of the following:
Anti-double-stranded DNA Anti-Sm False positive test for syphilis Positive LE cell preparation
MTBS2CK p.184
MTBS2CK p.184
Additional findings: Mesenteric vasculitis Raynaud phenomenon Antiphospholipid syndromes
Diagnostic tests ANA: found in 95% to 99% of cases Anti-double-stranded DNA (60%) and anti-Sm (30%):
Found Fo nd onl only in SLE Extremely specific for SLE
MTBS2CK p.184
MTBS2CK p.184
Diagnostic tests Decreased complement levels:

Correlate with disease activity Drop further with acute disease exacerbations
Anti-SSA and anti-SSB: found in 10% to 20% of cases

Add little to diagnosis Tests most often found in Sjgren syndrome (65% of cases) Dont treat asymptomatic ANA
MTBS2CK p.184
34-year-old woman with history of SLE is admitted with pneumonia and confusion. As youre wrestling with the decision over a bolus of high-dose steroids in a person with an infection, you need to determine if this is a flare of lupus or simply an infection with sepsis causing confusion. Which of the following will help you the most?
a. Rise in anti-Sm Level doesnt change in acute disease b. Rise in ANA Level doesnt change in acute disease c. Decrease in complement and rise in anti-DS DNA d. MRI of the brain MRI doesnt diagnose regardless e. Response to steroids Not diagnostic
MTBS2CK p.184185
20
Treatment Acute lupus flare treated with high-dose boluses of steroids Hydroxychloroquine can control mildly chronic disease Lupus nephritis may need steroids either alone or in combination with cyclophosphamide or mycophenolate Only way to determine the severity of lupus nephritis is kidney biopsy Belimumab decreases symptoms
MTBS2CK p.185
Treatment Urinalysis is insufficient to determine severity of lupus nephritis Biopsy is the only way to diagnose simple glomerulosclerosis or scarring of the kidney, which will not respond to therapy
Young patients most commonly die of infection. In older patients, accelerated atherosclerosis makes MI the MCC of death.
MTBS2CK p.185
AntiphospholipidSyndrome/Definition
AntiphospholipidSyndrome
Idiopathic disorder with IgG or IgM antibodies made against negatively charged phospholipids The 2 main types are:
Lupus anticoagulant Anticardiolipin antibodies
Presentation/Diagnostic Tests Thromboses of both arteries and veins as well as recurrent spontaneous abortions Elevation of aPTT with a normal prothrombin time (PT) and normal INR APL = clotting + elevated aPTT and normal PT
MTBS2CK p.185
MTBS2CK p.185
Presentation/Diagnostic Tests False positive VDRL or RPR with a normal FTA Anticardiolipin antibodies - spontaneous abortion Lupus anticoagulant - elevated aPTT Best initial test is mixing study
Diagnostic Tests If the elevation in aPTT is from a clotting factor deficiency then aPTT will come down to normal If the APL syndrome antibody is present in plasma then aPTT remains elevated Most M t specific ifi test t t for f lupus l anticoagulant ti l ti is Russell viper venom test (RVVT) RVVT is prolonged with APL antibodies and doesnt correct on mixing with normal plasma
MTBS2CK p.185186
MTBS2CK p.186
21
AntiphospholipidSyndrome/Treatment
Thromboses (DVT or PE) treated with heparin and warfarin as you would any other form of thrombosis with an INR of 2 to 3 Lifelong vs. 6 months primary occurrence Recurrent thrombotic episodes are treated lifelong
USMLE S2 CK questions have to be unequivocally clear. If an area is controversial, USMLE will avoid it and ask only what is clear clear. The exam will not trick you.
MTBS2CK p.186
MTBS2CK p.186
Warfarin or steroids are wrong answers for preventing spontaneous abortion. Steroids arent effective.
Warfarin is contraindicated in pregnancy secondary to teratogenicity.
Scleroderma,Polymyositis,& Dermatomyositis
MTBS2CK p.186
Scleroderma(SystemicSclerosis)
Limited scleroderma is also known as CREST syndrome: Calcinosis Raynaud Esophageal h ld dysmotility tilit Sclerodactyly Telangiectasia
What is the most likely diagnosis? Look for a young (20s to 40s) woman (3 times more likely than men) with fibrosis of the skin and internal organs (e.g., lung kidney lung, kidney, and GI tract)
MTBS2CK p.186
MTBS2CK p.187
22
Scleroderma/Presentation
RaynaudSyndrome
Raynaud syndrome: increased vascular reactivity of fingers beginning with pain and pallor (white) or cyanosis (blue) followed by reactive hyperemia (red) Skin manifestations: fibrosis of hands, face, neck, k and d extremities; t iti t telangiectasia l i t i and d abnormalities of pigmentation occur
MTBS2CK p.187
Scleroderma
MTBS2CK p.187
Scleroderma/Presentation
Scleroderma/DiagnosticTests
GI: esophageal dysmotility with GERD, large-mouthed diverticuli of small and large bowel Renal: sudden hypertensive crisis Lung: fibrosis leading to restrictive lung disease and pulmonary hypertension Cardiac: myocardial fibrosis, pericarditis, and heart block; lung disease gives right ventricular hypertrophy
ANA: positive in 85% to 90%, but nonspecific ESR: usually normal SCL-70: most specific test (antitopoisomerase) Anticentromere: present in half of those with CREST syndrome Anticentromere antibodies are extremely specific for CREST syndrome.
MTBS2CK p.187
MTBS2CK p.187
23
Scleroderma/Treatment
PolymyositisandDermatomyositis
Penicillamine is ineffective Renal crisis: ACE inhibitors Esophageal dysmotility: PPIs for GERD Raynaud: calcium-channel blockers Pulmonary fibrosis: cyclophosphamide improves dyspnea and PFTs Pulmonary hypertension is treated like primary pulmonary hypertension with bosentan or ambrisentan (endothelin antagonist) or Sildenafil
MTBS2CK p.187
Presentation Proximal muscle weakness They dont affect facial or ocular muscles as occurs in myasthenia gravis Dysphagia
MTBS2CK p.188
Presentation Dermatomyositis presents with: Malar involvement Shawl sign: erythema of face, neck, shoulders, , upper pp chest, , and back Heliotrope rash: edema and purplish discoloration of eyelids Gottron papules: scaly patches over the back of hands, particularly PIP and MCP joints
MTBS2CK p.188
Commons.Wikimedia.org. used with permission Commons.Wikimedia.org. used with permission
24
PolymyositisandDermatomyositis/ Presentation
Dermatomyositis is associated with cancer in 25% of cases. Common sites are: Ovary y Lung GI Lymphoma
Diagnostic Tests Best initial test is CPK and aldolase Most accurate test is muscle biopsy ANA is frequently positive MRI Electromyography
MTBS2CK p.188
MTBS2CK p.188
Treatment Steroids are usually sufficient When patient is unresponsive or intolerant of steroids, use: Methotrexate Azathioprine IVIG Mycophenolate Hydroxychloroquine helps skin lesions
MTBS2CK p.188189
SjgrenSyndrome, Vasculitis,&Seronegative Spondyloarthropathies
SjgrenSyndrome/Definition/Etiology
SjgrenSyndrome/Presentation
Idiopathic autoimmune disorder secondary to antibodies predominantly against lacrimal and salivary glands 90% of those affected are women Sjgren syndrome is associated with:
RA SLE Primary biliary cirrhosis Polymyositis Hashimoto thyroiditis
MTBS2CK p.189
Sjgren presents with dryness of mouth and eyes Keratoconjunctivitis sicca Need to constantly drink water Dysphagia D h i Dental caries
MTBS2CK p.189
25
SjgrenSyndrome/Presentation
SjgrenSyndrome/DiagnosticTests
Less common manifestations are: Vasculitis Loss of vaginal secretions Lung disease leads to dyspareunia. Pancreatitis Renal tubular acidosis (20%)
Best initial test is called a Schirmer test Most accurate test is a lip or parotid gland biopsy Reveal lymphoid infiltration in salivary glands
Lymphoma is the most dangerous complication of Sjgren

SjgrenSyndrome/DiagnosticTests
SjgrenSyndrome/Treatment
Best initial test on blood: SS-A and SS-B These are also called Ro and La and each are present in about 65% of patients
SLE is associated with SS-A and SS-B in 10% to 20% of cases Other abnormalities that are present, but are nonspecific: ANA, RF, anemia, leukopenia, and eosinophilia
MTBS2CK p.190
Best initial therapy is to water the mouth Use frequent sips of water, sugar-free gum, and fluoride treatments Artificial tears to avoid corneal ulcers Pilocarpine and cevimeline increase acetylcholine t l h li , the th main i stimulant ti l t t to produce d saliva Cevimeline increases rate of saliva production No cure Evaluate for lymphoma
MTBS2CK p.190
Vasculitis
PolyarteritisNodosa/Definition
Etiology unknown Symptoms develop over weeks to months All vasculitides give:
Fever Fe er Malaise/fatigue Weight loss Arthralgia/myalgia
MTBS2CK p.190
Polyarteritis nodosa (PAN) is a disease of small- and medium-sized arteries leading to a diffuse vasculitis that inexplicably spares the lungs Chronic hepatitis B and C are associated with PAN
MTBS2CK p.190
26
PolyarteritisNodosa/Presentation
Common Features of PAN Renal: glomerulonephritis without a biopsy cant be diagnosed

UA isnt enough to confirm its PAN
Gastrointestinal: abdominal pain is worsened by eating from vasculitis of mesenteric vessels

Bleeding also occurs Nausea and vomiting are common
Neurological: any large peripheral nerve can be involved Peroneal neuropathy leading to foot drop Look for a stroke in a young person
MTBS2CK p.190191
Skin: lower extremity ulcers are most common; livedo reticularis, purpura, nodules, and rarely gangrene occur
Lung is spared in PAN
MTBS2CK p.191
PolyarteritisNodosa/DiagnosticTests
Mononeuritis Multiplex Mononeuritis multiplex is multiple peripheral neuropathies of nerves large enough to have a name
Most accurate test is a biopsy of a symptomatic site Angiography of renal, mesenteric, or hepatic artery shows abnormal dilation or beading. P-ANCA is present in < 20% Test all PAN patients for hepatitis B and C.
MTBS2CK p.191
MTBS2CK p.191
PolyarteritisNodosa/Treatment
PolymyalgiaRheumatica
Prednisone and cyclophosphamide Treat hepatitis when found
Polymyalgia rheumatica (PMR) occurs in those over age 50 with:

Pain and stiffness in shoulder and pelvic girdle muscles Difficulty combing hair and rising from chair Elevated ESR Normochromic, normocytic anemia
No Lab Findings CPK and aldolase are normal Steroids even at low doses great response
27
GiantCell(Temporal)Arteritis
GiantCell(Temporal)Arteritis
The difference is the presence of: Visual symptoms Jaw claudication (pain in jaw when chewing) Scalp tenderness Headache Symptoms in other arteries such as decreased arm pulses, bruits near the clavicles, or aortic regurgitation
MTBS2CK p.191192
ESR and C-reactive protein are elevated Most accurate test is a biopsy of affected artery (e.g., temporal artery) Treat with prednisone Starting high-dose prednisone quickly is more important than waiting for biopsy
Blindness is irreversible.
MTBS2CK p.192
WegenerGranulomatosis
WegenerGranulomatosis/Diagnostic Tests
Presents with:
Sinusitis Otitis media Mastoiditis Oral and gingival involvement
Best initial test is antineutrophil cytoplasmic antibody (ANCA) Most accurate test is a biopsy Cytoplasmic antibodies are also called CANCA.
C-ANCA = anti-proteinase-3 antibodies P-ANCA = anti-myeloperoxidase antibodies Wegener: C-ANCA Churg-Strauss and microscopic polyangiitis: P-ANCA
MTBS2CK p.192
Wegener is also associated with skin, joint, and eye lesions Look for combination of upper and lower respiratory tract findings in association with renal insufficiency
MTBS2CK p.192
WegenerGranulomatosis/Diagnostic Tests
WegenerGranulomatosis/Treatment
When asked about the best test for Wegener, lung biopsy is better than renal biopsy with sinus biopsy being the least accurate When all 3 are in the choices choose lung biopsy
Treat with prednisone and cyclophosphamide The clue to answering the most likely diagnosis question is unresolving diagnosis pneumonia not better with antibiotics. You will not first think of Wegener when presented with the case.
MTBS2CK p.192
MTBS2CK p.192
28
ChurgStraussSyndrome
HenochSchnleinPurpura
Pulmonary-renal syndrome, ChurgStrauss also has: Asthma Eosinophilia Biopsy Bi i is the th most t accurate t test t t Treat with prednisone and cyclophosphamide
Vasculitis more frequently seen in children, Henoch-Schnlein purpura (HSP) is characterized by involvement of:
GI tract: p pain, , bleeding g Skin: purpura Joint: arthralgia Renal: hematuria
MTBS2CK p.193
MTBS2CK p.193
HenochSchnleinPurpura
HenochSchnleinPurpura When the case describes leukocytoclastic vasculitis on biopsy, the answer is Henoch-Schnlein purpura. Leukoplastic reactions are painless, palpable purpura of buttocks and legs
MTBS2CK p.193
Source: Shreya Patel and Nishith Patel
HSP is most often a clinical diagnosis; however, biopsy is the most accurate test
Serum IgA levels are the wrong answer. They Th are unreliable when testing for Henoch-Schnlein purpura.
MTBS2CK p.193
HenochSchnleinPurpura/Treatment
Cryoglobulinemia
Most cases resolve spontaneously Steroids if there are severe extrarenal mainfestations associated with renal failure
Most commonly associated with chronic hepatitis C +/- endocarditis and/or Sjgren syndrome Dont confuse cryoglobulins with cold agglutinins
Both are IgM antibodies

Neither respond to steroids
MTBS2CK p.193
MTBS2CK p.194
29
DifferencesbetweenCryoglobulinsandColdAgglutinins Cryoglobulins Associatedwith HepatitisC Coldagglutinin EBV,Mycoplasma, Lymphoma Hemolysis
Cryoglobulinemia Lab tests show a positive rheumatoid factor and cold precipitable immune complexes Steroids NOT effective Treat the underlying cause, especially hepatitis C, with interferon and ribavirin Despite the rarity of the condition, the USMLE loves cryoglobulinemia questions.
Manifestations
Jointpain Glomerulonephritis Purpuricskinlesions Neuropathy Interferon, Ribavirin,and boceprevir (or telaprevir)
Treatment
MTBS2CK p.194
Staywarm Rituximab, cyclophosphamide, cyclosporine
SLE decreased C3 or 3 letters (SLE) = C3 Hep C decreased C4 or 4 letters (Hep C) = C4 .

MTBS2CK p.194
BehetSyndrome
BehetSyndrome
The most common Behet questions are:

What is the most likely diagnosis? What is pathergy? pathergy ?
Pathergy: sterile skin pustules from minor trauma (e.g., needle stick)
MTBS2CK p.194
Asian or Middle Eastern person with painful oral and genital ulcers +/erythema Also with:
Ocular lesions leading to uveitis and blindness Arthritis CNS lesions mimicking multiple sclerosis
MTBS2CK p.194
BehetSyndrome/Treatment
SeronegativeSpondyloarthropathies
Corticosteroids To wean patients off of steroids, use:

Azathioprine Cyclophosphamide Colchicine C l hi i Thalidomide
The 3 types of seronegative spondyloarthropathies are:
Ankylosing spondylitis Psoriatic arthritis Reactive arthritis (Reiter syndrome)
MTBS2CK p.195
MTBS2CK p.195
30
Men < 40 years: Involvement of spine and large joints Negative rheumatoid factor (hence the name seronegative) Enthesopathy (inflammation where tendons and ligaments attach to bones) Uveitis HLA-B27
Corticosteroids arent a good treatment for seronegative spondyloarthropathy
D Despite it th the association i ti with ith HLA HLA-B27, B27 this is never the best initial or most accurate test for seronegative spondyloarthropathies.
MTBS2CK p.195
MTBS2CK p.195
AnkylosingSpondylitis/Diagnosis
AnkylosingSpondylitis/Diagnosis
Young man with low backache and stiffness of his back has pain that radiates to buttocks with flattening of the normal lumbar curvature and decreased chest expansion Eventually E t ll th the spine i will ill not t expand di in any direction Enthesopathy occurs at the Achilles tendon Look for back pain worsened by rest and relieved by activity
MTBS2CK p.195
Other Findings of Ankylosing Spondylitis Transient peripheral arthritis of knees, hips, and shoulders (50%) Cardiac: atrioventricular block in 3% to 5%; aortic insufficiency Uveitis
Bamboo spine is a late finding with fusion of vertebral joints.
MTBS2CK p.195
AnkylosingSpondylitis/DiagnosticTests
Best initial test is an X-ray of sacroiliac (SI) joint Most accurate test is an MRI MRI detects abnormalities years before the X X-ray ray becomes abnormal ESR is elevated in 85%
MTBS2CK p.196
MTBS2CK p.196
31
AnkylosingSpondylitis
HLA B27 is not a confirmatory diagnostic test since 8% of general population is positive Treatment Exercise p program g and NSAIDs are best initial treatment If NSAIDs are insufficient, use anti-TNF drugs (e.g., etanercept, adalimumab, or infliximab)
MTBS2CK p.196
Source: Conrad Fischer, MD.
MTBS2CK p.196197
PsoriaticArthritis
PsoriaticArthritis
Psoriatic arthritis 80% will have preceding psoriasis Besides SI joint involvement, characteristic findings are: Sausage digits from enthesopathy Nail pitting
MTBS2CK p.197
MTBS2CK p.197
PsoriaticArthritis/DiagnosticTests
PsoriaticArthritis/Treatment
ESR is elevated nonspecific Best initial test is an X-ray of the joint showing a pencil in a cup deformity
NSAIDs are best initial therapy Methotrexate used when question describes severe disease or no response to NSAIDs Anti-TNF Anti TNF agents are the answer when methotrexate doesnt control disease Steroids are a wrong choice
MTBS2CK p.197
MTBS2CK p.197
32
ReactiveArthritis(ReiterSyndrome)
ReactiveArthritis/Diagnosis
Reactive arthritis occurs secondary to: Inflammatory bowel disease (equal sex incidence) Sexually transmitted infection (far greater in men) GI infection (Yersinia, Salmonella, Campylobacter)
Look for triad of: Joint pain Ocular findings (uveitis, conjunctivitis) Genital G it l abnormalities b liti ( (urethritis, th iti balanitis) Keratoderma
blennorhagicum is a skin lesion unique to reactive arthritis that looks like pustular psoriasis.
MTBS2CK p.197
MTBS2CK p.198
ReactiveArthritis/Diagnosis
ReactiveArthritis/DiagnosticTests/Treatment
No specific test for reactive arthritis Rule out septic joint Treat underlying cause/use NSAIDs Sulfasalazine > NSAIDS
Antibiotics dont reverse reactive arthritis once joint pain has started.
Source: commons.wikimedia.org. Used with permission
MTBS2CK p.198
SepticArthritis
SepticArthritis,Gonococcal Arthritis,&Osteomyelitis
Definition Septic arthritis is an infection of joint space Etiology Septic arthritis is relatively rare in an undamaged joint Risk of infection is directly proportional to degree of joint damage
MTBS2CK p.199
33
SepticArthritis
EtiologyofSepticArthritis Etiology Frequency
Etiology (contd) Osteoarthritis (DJD) provides slight risk RA has greater risk Greatest risk is with prosthetic joint Bacteremia can spread into joint space, space which is why endocarditis and injection drug use causes septic arthritis
Staphylococcus Streptococcus Gramnegative rods
40% 30% 20%
MTBS2CK p.199
MTBS2CK p.199
SepticArthritis/Presentation
SepticArthritis/DiagnosticTests
Joint is warm, red, and immobile often with palpable effusion Chills and fever happen because of bacteremia
Best initial and most accurate test is aspiration of the joint with a needle (arthrocentesis); X-ray, CT, and MRI arent useful and are the wrong answers Joint fluid shows:
Leukocytosis: more than 50,000 to 100,000 cells, predominantly neutrophils Gram stain: positive (50%) Gram-negative bacilli; (75%) with Staphylococcus Synovial fluid culture: 70% to 90% sensitive Blood cultures: 50% sensitive
MTBS2CK p.199
MTBS2CK p.199
SepticArthritis
OtherOptionsforTreatmentofSepticArthritis Gramnegative bacilli Grampositivecocci (sensitive) Grampositive cocci(resistant)
Treatment Ceftriaxone and vancomycin are best initial empiric therapy
Quinolones Aztreonam Cefotaxime Piperacillin Aminoglycosides
Oxacillin Cefazolin Piperacillinwith Tazobactam
Linezolid Daptomycin Ceftaraline Tigecycline
MTBS2CK p.199
MTBS2CK p.200
34
SepticArthritis/Treatment
SepticArthritis
Adjust antibiotics according to culture results.

If Staphylococcus p y is sensitive, , vancomycin is associated with a worse outcome than betalactam antibiotic (e.g., oxacillin or cefazolin). Switch drugs if organism is sensitive.
Prosthetic Joint Infection Infected prosthetic joint gives a warm, red, immobile, and tender joint Must do imaging
MTBS2CK p.200
MTBS2CK p.200
SepticArthritis
SepticArthritis
Prosthetic Joint Infection (contd) MRI difficult to perform with prosthetic joints because they are made of metal If there is lucency around implantation of the joint on radiologic imaging or if joint is physically loose, infection is likely present at implantation site
Treatment of Infected Prosthetic Joint Remove joint, treat with antibiotics for 6 to 8 weeks, and then replace joint The most common organism for recently placed artificial joints is Staphylococcus epidermidis.
MTBS2CK p.200
MTBS2CK p.200
GonococcalArthritis(Gonorrhea)
GonococcalArthritis/DiagnosticTests
The difference in presentation from septic arthritis is:

Polyarticular involvement Tenosynovitis (inflammation of tendon sheaths, making finger movement painful) Petechial rash
Detecting gonorrhea is much more difficult than detecting Staphylococcus, Streptococcus, and Gram-negative bacilli of septic arthritis
Gonococcal arthritis is more frequent during menses.

35
SynovialFluidAnalysisforInfectiousArthritis Testsensitivity Leukocytosis Gramstain C l Culture Bloodcultures Septicarthritis >50,000100,000cells/L 5070%sensitive 90%sensitive ii 50%sensitive Gonococcalarthritis 30,00050,000cells/L 25%sensitive <50%sensitive ii <10%sensitive
GonococcalArthritis/DiagnosticTests
In order to reach maximum sensitivity, multiple diffuse sites must be cultured for gonorrhea such as: Pharynx What tells you to Rectum Rectum culture everywhere? Urethra Rash Cervix Tenosynovitis
Polyarticular involvement
MTBS2CK p.201
MTBS2CK p.201
GonococcalArthritis/Treatment
Osteomyelitis/Definition/Etiology
Ceftriaxone, cefotaxime, or ceftizoxime is the best empiric therapy for disseminated gonorrhea Fluoroquinolones are not the best initial therapy If recurrent gonorrhea infection is described, test for terminal complement deficiencya favorite subject of USMLE Step 2 CK.
Osteomyelitis is an infection of bone Staphylococcus aureus is MCC Children get osteomyelitis through hematogenous spread, but adults get it from a contiguous (nearby) infection Salmonella is the most commonly identified organism in patients with sickle cell disease.
MTBS2CK p.201
MTBS2CK p.201
Osteomyelitis/DiagnosticTests
Best initial test is an X-ray Most accurate test is a biopsy If X-ray is normal, the most appropriate next step in management is MRI CT scan isnt very y useful
When is ESR the answer? To follow the response to therapy

MTBS2CK p.202
Source: Eva M. Smietana
36
Osteomyelitis/Treatment
When is culturing the drainage the answer? Never. You cannot reliably distinguish superficial colonization from whatever organism is inside the bone causing the bone infection. Bone scan is the answer only if you want to get an MRI and its contraindicated (pacemaker).
MTBS2CK p.202
Osteomyelitis takes weeks to progress Must biopsy MSSA Oxacillin, cefazolin, nafcillin, or ceftriaxone MRSA Vancomycin or linezolid
MTBS2CK p.202
Gram-negative bacilli such as E. coli are treated with fluoroquinolones (e.g., ciprofloxacin)
Its essential to confirm the sensitivity of the organism prior to treating with ciprofloxacin
Ciprofloxacin is the only oral therapy for osteomyelitis, but should be used only if the organism is confirmed as a sensitive Gram-negative bacillus.
MTBS2CK p.202
Toxicity of Quinolones Fluoroquinolones can cause Achilles tendon rupture

They are also contraindicated in pregnancy and children because they interfere with bone growth
MTBS2CK p.202
37
Surgery
MatthewKinney,MD OrthopedicResident UniversityofCaliforniaSanDiego
PreoperativeEvaluation, PostoperativeEvaluation,& VascularSurgery
PreoperativeEvaluation Objective: Identify factors that increase risk of complications in perioperative period Age Cardiac history
#1 predictor of perioperative complications
PreoperativeEvaluation
Cardiovascular Pulmonary y Renal
Diabetes status
Risk equivalent to Coronary disease
History of
Pulmonary disease Renal disease Stroke
MTBS2CK p.379
PreoperativeEvaluation/Cardiac Must obtain detailed cardiac history Look for indicators of previous MI or CHF Recent MI
Defer surgery for 6 months Follow-up stress test to ensure adequate perfusion
PreoperativeEvaluation/Cardiac Management If age < 35 and no history of cardiac disease

EKG
If history of cardiac disease (MI, CHF)

EKG Stress testing
Ensure appropriate cardiac perfusion
Evidence of CHF (JVD, edema)

Patients with EF < 35% at increased risk ACE-Is, B-blockers, spironolactone must be optimized Proven to decrease overall mortality!!!
Echocardiography
Monitor EF Evaluate structural damage
MTBS2CK p.379
MTBS2CK p.380
PreoperativeEvaluation/Pulmonary
71-year old man undergoing femoro-popliteal bypass for severe claudication of left leg which causes unbearable pain with exercise. Past medical/surgical history is significant for remote appendectomy and insulin-dependent type 2 DM. What preoperative testing is recommended? a.Basic Metabolic Panel (BMP) only High cardiac risk b.BMP + EKG c. BMP + EKG + PFTs Must get stress test/ECHO d.BMP + EKG + Exercise Stress Test Cannot exercise e.BMP + EKG + Thallium Stress Test
Must evaluate for history of lung disease (including smoking) PFTs required for all patients with known lung disease
Vital capacity - most important predictor of perioperative complications
MTBS2CK p.380
PreoperativeEvaluation/Pulmonary
PreoperativeEvaluation/Pulmonary Must evaluate for history of lung disease (including smoking) PFTs required for all patients with known lung disease
Vital capacity - most important predictor of perioperative complications
Smokers
PFTs Smoking cessation for 6-8 weeks preoperatively
Nicotine patch acceptable
MTBS2CK p.380
PreoperativeEvaluation/Renal Renal disease increases surgical risk

Intravascular fluid losses occur during surgery Results in hypoperfusion of kidneys Physiologic response to decreased intravascular volume is activation of Renin-Angiotensin system Constricts renal vasculature
PostoperativeEvaluation
FeverAssessment Complications
Renal hypoperfusion correlates with increased mortality Management

Aggressive IV hydration beginning 24 hours pre-op Dialysis patients must be dialyzed 24 hours pre-op
MTBS2CK p.380
PostOperativeFever
WIND WATER WALKING POD WOUND WEIRD
PostOpComplications/Confusion
Confused Patient Obtain ABG, CXR, CBC
Evidence of Hypoxemia Abnormal ABG Evidence of Infection Abnormal CBC
1-2
Atelectasis #1 Pneumonia CXR -Sputum Culture (if pneumonia suspected) -Incentive spirometry -Antibiotics Vanc. + Pip/Tazo
3-5
5-6
DVT Thrombophlebitis (IV site infection) Doppler US Anti-coagulation Heparin p Warfarin Replace IVs
8-15
Drug Reaction Deep Abscess D/C likely medication CT Scan Drainage of Abscess
Changes on CXR?
Yes No
UTI Urinalysis Nitrite + Leukocyte Esterase + Antibiotics MTBS2CK p.400
Incision-site Infection Cellulitis Physical Exam Erythema Pus Swelling Abscess Incision/Drainage Antibiotics
Culture Likely Sources Blood (Bacteremia) Urine (UTI)
Atelectasis vs. Pneumonia Incentive spirometry Antibiotics

MTBS2CK p.401
Consider PE Spiral CT
Treat with empiric Antibiotics
AdultRespiratoryDistressSyndrome Etiology Endothelial damage allows fluid to fill alveoli

Prevents O2/CO2 exchange, acts as shunt
AdultRespiratoryDistressSyndrome
Signs/Symptoms HR, RR
Labored breathing (accessory muscle use) Fever may be present
Diagnosis ABG: pO2, pCO2 CXR: Bilateral pulmonary infiltrates

MS-4 USU Teaching File, Uniformed Services University
MTBS2CK p.401
AdultRespiratoryDistressSyndrome
PulmonaryEmbolism
Treatment Mechanical ventilation

Maximize Positive End-Expiratory Pressure (PEEP)
Etiology
Passage of a venous blood clot to lungs
Origin: Deep leg vein > 90%
Clot lodges in lung vasculature

Prevents O2/CO2 exchange
Source: nlm.nih.gov
MTBS2CK p.401
PulmonaryEmbolism
Risk Factors Stasis: Immobility (post-surgical, travel, etc.), obesity Endothelial damage: Surgery, trauma Hypercoagulability yp g y: Oral contraceptive p pills (OCP), malignancy, genetic disorder Signs/Symptoms HR, RR, Temp Pleuritic chest pain
MTBS2CK p.401
62-year-old woman with no significant PMH undergoes right total hip replacement 3 days ago. Recovery is uncomplicated until 30 minutes ago, she reported moderate SOB and chest pain with deep inspiration. Whats the next step in evaluating this patient?
a. b. c. d. e.
EKG only Insensitive for pulmonary embolism EKG + V/Q Scan No reported contrast allergy EKG + Spiral CT scan EKG + D-Dimer Sensitive, but not specific EKG + Heparin Injection Must diagnose PE first
PulmonaryEmbolism Diagnosis ABG

pO2, pCO2
PulmonaryEmbolism
EKG
Nonspecific ST-segment and T wave changes
Most common
S1
S1-Q3-T3
Q3
T3
MTBS2CK p.401

pO2, pCO2
PulmonaryEmbolism
EKG
Most common
S1-Q3-T3
Infrequent during acute PE Can be found in massive acute PE and cor pulmonale
Spiral CT
MTBS2CK p.401

pO2, pCO2
PulmonaryEmbolism
EKG
Most common
Treatment Respiratory support Anticoagulation

Heparin acutely, bridge to warfarin longterm IVC filter (if anticoagulation contraindicated)
S1-Q3-T3
Infrequent during acute PE Can be found in massive acute PE and cor pulmonale
Spiral CT
Consider V/Q scan (if IV contrast allergy)
Vascular
AbdominalAorticAneurysm AorticDissection Claudication
69-year-old male with 50 pack-year smoking history is brought to the ER by his wife who reports he seems confused. He feels weak and has pain in middle of abdomen. He is a pale, elderly male in moderate distress. BP of 84/55, pulse 120. Palpable, pulsatile mass in patients abdomen. Whats the most likely diagnosis? a. b. c. d. Ruptured peptic ulcer Would expect peritoneal signs Hemorrhagic gastritis Would expect hematemesis Hemorrhagic pancreatitis Would expect flank bruising Ruptured abdominal aortic aneurysm
MTB S2CK - p. 399
AbdominalAorticAneurysm Etiology Weakening of aortic wall secondary to atherosclerosis

Aortic diameter expands > 1.5x normal Involves all layers of vessel wall (True Aneurysm) 90% arise from infrarenal aorta
AbdominalAorticAneurysm Risk Factors Male > Female Age Hypertension, Hyperlipidemia Smoking Si Signs/Symptoms /S t Frequently asymptomatic May report pulsatile abdominal mass
MTBS2CK p.399
Source: csm.ornl.gov
MTBS2CK p.399
AbdominalAorticAneurysm Diagnosis CT/MRI

Provides determination of level and surrounding structures
AorticDissection Treatment 3.0-4.0 cm

US every 2-3 years
4.0-5.4 cm
US or CT every 6-12 months
Etiology Tearing of aortic intima forms false lumen

Blood flows into false f lumen, extends tear
Sopurce: J. Heuser commons.wikimedia.org
Ultrasound for size measurements
5.5 cm, asymptomatic

Surgical repair
MTBS2CK p.399
AorticDissection/Etiology
AorticDissection
Can occur in ascending or descending aorta
Risk Factors Male > Female Age > 40 Hypertension (#1 risk factor) ) Marfans disease, Ehlers-Danlos syndrome
Signs/Symptoms Sudden onset, tearing chest pain

Radiates to the back
Elevated BP
May be asymmetric (R > L)
Sopurce: J. Heuser commons.wikimedia.org
AorticDissection/Diagnosis
AorticDissection
Demonstration of dissection on imaging CXR

Widening of mediastinum
Source: NNMC
AorticDissection/Diagnosis
AorticDissection
Demonstration of dissection on imaging CXR

Widening of mediastinum
Transesophageal ECHO (TEE)

Acute chest pain and/or clinically unstable
MRA
Chronic chest pain and hemodynamically stable
Treatment Ascending dissection = Emergent surgery Descending dissection = Medical therapy

Beta-Blockers (#1) Anti-hypertensive meds
CT angiogram
TEE and MRI contraindicated
Claudication Etiology Atherosclerotic plaques prevent sufficient perfusion to extremities (lower > upper)
Associated with smoking, DM, hyperlipidemia
Claudication/Management
Medical
Risk Modification Smoking cessation (#1) Graded exercise Pharmacologic therapy Cilostazol Cil t l Antiplatelet agents: Aspirin, Clopidogrel
Symptoms Calf/leg pain with exercise

Relieved by rest
Diagnosis Ankle-Brachial Index

< 0.9 = pathologic < 0.4 = symptomatic
Percutaneous
Stenting, angioplasty
Surgical
Trauma/ABCAssessment Initial assessment rely on ABC algorithm
Shock
TraumaAssessment(ABCs) yp ofShock Types Hypovolemic Cardiogenic Neurogenic Septic Anaphylactic
Airway Breathing Circulation Disability (CNS) Exposure ABCs are a roadmap, but you must know what to do at each step
MTBS2CK p.380381
Trauma/ABCAssessment A = Airway Must assess for airway compromise

If patient can talk airway is clear Look for traumatic obstruction, evidence of smoke inhalation
Trauma/ABCAssessment
Concern for airway compromise? AMS Facial trauma Apnea
Yes Intubate
No
Evaluate need for intubation

Indications
Facial Trauma Altered Mental Status Apnea
Assess Breathing/ Oxygenation
Yes
Facial Trauma?
No
Cricothyroidotomy
Yes
Cervical Spine Injury?

No
Careful Orotracheal Intubation Flexible bronchoscopy

MTBS2CK p.381
Orotracheal Intubation
MTBS2CK p.381
Trauma/ABCAssessment B = Breathing Assess breath sounds Monitor oxygenation status with pulse oximetry
Goal is O2 Saturation > 90% If O2 Sat < 90% consider
a. Supplemental O2 via nasal cannula b. O2 face mask c. Intubation
Trauma/ABCAssessment
C = Circulation Evaluate pulses (distal first, proximal if absent) Manage hemorrhage sites
Direct pressure slows blood loss
Monitor blood pressure

If the patient is hypotensive, place 2 largebore IVs and begin aggressive fluid resuscitation Start with normal saline (only use blood products as secondary measure)
MTBS2CK p.381
Source:UusiAjaja, commons.wikimedia.org
MTBS2CK p.381
Trauma/ABCAssessment D = Disability (Altered Mental Status) Assessed with Glasgow Coma Scale
Eye Response (1-4) Verbal Response (1-5) Motor Response (1-6)
Score < 8 requires intubation E = Exposure Remove all clothing on patient

Assess for hidden injuries
Thorough physical examination
52-year-old woman ejected from her car during a high-speed motor vehicle accident . Upon arrival to ED, she complains of severe, left-sided chest pain. Pale, cool patient in severe distress. Heart rate 130 bpm, BP 86/44 mmHg. JVD along angle of jaw. Chest X-ray shows anterior rib fractures on the left. Which is the most likely diagnosis? a. Hypovolemic shock Would not see JVD b. Neurogenic shock c. Anaphylactic shock d. Cardiogenic shock Warm, flush patients e. Septic shock
MTBS2CK p.381
Shock Definition Inadequate perfusion/oxygenation that impairs organ function Signs/Symptoms Vitals Signs
Decreased BP Increased HR
TypesofShock Hypovolemic Causes: Hemorrhage (#1), Dehydration, Burns
CNS: Confusion, altered mental status Kidney: Decreased urine output, increased BUN/Cr ratio Liver: Massively elevated AST/ALT (Shock Liver) Heart: Chest pain, shortness of breath
Source: U.S. Navy photo by Mass Communication Specialist 2nd Class Michael Russell, public.navy.mil
TypesofShock/Hypovolemic Signs/Symptoms
Pale, cold Trauma
TypesofShock
Cardiogenic
Causes: MI (#1), CHF, arrhythmia Signs/Symptoms
Pale, cold Symptoms associated with MI (Chest pain, SOB) JVD
Lab Findings
CO = SVR = CVP = PCWP =
Lab Findings
SVR = CVP = PCWP = CO =
Treatment
Treat cardiac problem Do NOT give fluid!!!
Treatment
Aggressive IV fluid replacement Pressors
MTBS2CK p.382
MTBS2CK p.382
TypesofShock
TypesofShock Lab Findings

SVR = CVP = PCWP = CO =
Neurogenic
Causes: CNS damage (cervical/thoracic spinal cord - #1) Signs/Symptoms:
Warm, , flush Evidence of CNS damage (trauma)
Septic Causes: Infection

E. coli and S. aureus (most common organisms)
Treatment
Aggressive IV fluid delivery Pressors
Signs/Symptoms
Warm, flush Possible nidus of infection (UTI, pneumonia, wound)
Source: cdc.gov
MTBS2CK p.382
MTBS2CK p.382
TypesofShock/Septic
TypesofShock
Lab Findings SVR = CVP = CO = PCWP =
Treatment Broad-spectrum antibiotics Fluid and pressors Dopamine Norepinephrine
Anaphylactic Causes: Allergy (insects, food, medication) Signs/Symptoms

Warm, flush Wheezing, hives, associated evidence of allergic reaction
MTBS2CK p.382
MTBS2CK p.382
TypesofShock/Anaphylactic
ShockAlgorithm
Pale/Cold
Lab Findings
CVP = SVR = PCWP = CO =
Elevated
Is patient pale/cold or warm/flush?

Decreased
Warm/Flush
PCWP change?
Decreased
CO change?
Elevated
Treatment
Epinephrine
Cardiogenic Treat cardiac problem
Hypovolemic Fluid and pressors
Neurogenic Fluid and pressors
PCWP change?
Decreased No Change
Anaphylactic Epinephrine
Septic Antibiotics Fluids and pressors
MTBS2CK p.382
AbdominalTrauma
Trauma
AbdominalTrauma ThoracicTrauma PelvicTrauma
Penetrating Gunshot wounds Must do exploratory laparotomy in ALL patients Stab wounds If hemodynamically stable, do a FAST ultrasound scan If hemodynamically unstable, perform an exploratory laparotomy
10
AbdominalTrauma
AbdominalTrauma
Diaphragmatic Rupture
Cause
Penetrating or blunt trauma
Left > Right
Symptoms
Respiratory distress Kehrs sign = Left shoulder pain
Loops of Bowel
Diagnosis
CXR: Bowel loops in thorax
Absent Hemi-Diaphragm
MTBS2CK p.383
Source: Hariharan D, Singhal R, Kinra S, Chilton A, commons.wikimedia.org
AbdominalTrauma/Blunt
Splenic/Liver injury Causes Most commonly injured in blunt abdominal trauma

Spleen #1 Liver #2
Pancreatic Injury Causes Blunt trauma to epigastrum

Bike handlebars Car dashboard
Associated with lower rib fractures Signs/Symptoms Hypotension (due to hemorrhage) Kehrs sign
MTBS2CK p.383
Signs/Symptoms Cullens sign = Bruising around umbilicus
MTBS2CK p.383
AbdominalTrauma/Blunt Diagnosis FAST scan (ultrasound)

To evaluate for intraabdominal bleeding
Fluid = Blood
CT scan If negative FAST FAST, but suspect splenic rupture To evaluate retroperitoneal bleed
Source: Herbert L. Fred, MD and Hendrik A. van Dijk, commons.wikimedia.org
MTBS2CK p.383
MTBS2CK p.383
11
Management If hemodynamically stable

Close monitoring Serial abdominal exams IV fluids
33-year-old female jogging at night was struck by a drunk driver. She complains of severe abdominal pain that radiates to the back. Vital signs are stable. After ER work-up, patient is admitted for evaluation. Three days later, the following picture is taken.
If hemodynamically unstable
Exploratory laparotomy
MTBS2CK p.383
33-year-old female jogging at night was struck by a drunk driver. She complains of severe abdominal pain that radiates to the back. Vital signs are stable. After ER work-up, patient is admitted for evaluation. Three days later, the following picture is taken. What is the most likely diagnosis?
Source: Herbert L. Fred, MD and Hendrik A. van Dijk, commons.wikimedia.org
a. b. c. d. e.
Pancreatic pseudocyst Delayed appearance Hemorrhagic pancreatitis Ruptured AAA No pulsatile mass Aortic dissection Stable BP, no chest pain Splenic rupture Wrong side, no L shoulder pain
ThoracicTrauma Pneumothorax Etiology Air in pleural space pulmonary collapse Signs/Symptoms Chest pain Decreased breath sounds Hyperresonance to percussion Tracheal deviation toward affected side
ThoracicTrauma/Pneumothorax
Diagnosis CXR
Collapsed Lung Border
Treatment Chest tube
Source: John Yasmer
MTBS2CK p.384
MTBS2CK p.384
12
ThoracicTrauma TensionPneumothorax AMEDICALEMERGENCY Etiology

Chest wall defect acts as one-way valve
Air can enter pleural space, but cannot exit Resulting increase in pressure can compress vital structures Trachea, vena cava
Source: army.mil
ThoracicTrauma/TensionPneumothorax
Resulting from laceration of cervical trachea and mediastinal pleura Resulting from sucking wound of valvular type
a. Laceration of cervical trachea b. Laceration of mediastinal pleura c. Tension pneumothorax d. Collapsed lung e. Shift of heart f. Subcutaneous emphysema g. Partial collapse of contralateral lung
a. Valvular sucking wound of chest wall b. Tension pneumothorax c. Collapsed lung d. Cardiac shift to intact side e. Partial collapse of contralateral lung
MTBS2CK p.384
ThoracicTrauma/TensionPneumothorax Signs/Symptoms
Chest pain Hyperresonance Decreased breath sounds Tracheal deviation (away from affected side)
ThoracicTrauma
Diagnosis
CXR
Source: James G. Smirniotopoulos, M.D.
Treatment
Immediate needle decompression Chest tube placement
MTBS2CK p.384
Hemothorax Etiology Blood in pleural space Signs/Symptoms g y p Chest pain Absent breath sounds Dullness to percussion
MTBS2CK p.384
Source: army.mil
ThoracicTrauma/Hemothorax
ThoracicTrauma/Hemothorax
White-Out
Diagnosis CXR
Blunted costophrenic angle
CT scan Treatment Chest tube drainage Thoracotomy

Posteroanterior CXR made shortly after wounding and showing hemothorax 10 days later, after 6 thoracenteses, three 150 cc of blood and other fluid was removed
Source: army.mil
MTBS2CK p.384
13
Hemo/PneumothoraxDiagnosis
Symptoms
Chest Pain Decreased/Absent Breath Sounds
ThoracicTrauma
Pericardial Tamponade
Etiology
Trauma to pericardium
Broken ribs Penetrating trauma
Response to Percussion?
Dullness Hyperresonance Tracheal Deviation? Toward lung Away from lung
Signs/Symptoms
JVD Hypotension Decreased heart sounds
Hemothorax
Chest tube drainage
Pneumothorax
Chest tube
Tension pneumothorax
Immediate needle thoracotomy Chest tube
MTBS2CK p.384
ThoracicTrauma/PericardialTamponade Diagnosis
EKG
Electrical Alternans
ThoracicTrauma/PericardialTamponade Diagnosis
EKG
Electrical Alternans
ECHO
Diagnostic test of choice
Treatment
Pericardiocentesis
Source: army.mil
MTBS2CK p.384
MTBS2CK p.384
26-year-old man suffers blow to chest with a baseball bat. He is brought to the ED with severe right-sided chest pain and difficulty breathing. He is tachypneic at 26 breaths/minute, with a heart rate of 130 beats/minute, diminished breath sounds on the right, and left tracheal deviation. What is the next step in management?
14-year-old boy hits a pothole while riding his bike and falls directly onto the central bar. He presents to the ED with severe groin pain and swelling. Physical examination reveals blood at the urethral meatus and a high-riding prostate. What is the next appropriate step in management?
a. b. c. d. e.
Pericardiocentesis Not pericardial tamponade Chest X-ray Too slow. This is an emergency Needle thoracotomy Chest tube placement EKG Not indicated in this patient
a. a b. c. d. e.
Place a Foley Can C f further th damage d urethra th Get a retrograde urethrogram Empiric antibiotics Must assess urethral patency CBC and electrolytes Discharge the patient with reassurance
MTBS2CK p.385
14
AbdominalPainDifferentialDiagnosis
RUQ LUQ
TheAbdomen Part1
AbdominalPain MesentericIschemia EsophagealPathology GastricPerforation
Cholecystitis Splenic Rupture - Radiates to R shoulder - Radiates to L shoulder Cholangitis Ischemic Bowel Disease Perforated Ulcer Mid-Epigastrum Pancreatitis Peptic Ulcer Disease Aortic Dissection - Radiates to back
RLQ
Appendicitis Ovarian Torsion () Ectopic Pregnancy () Diverticulitis (Cecal)
MTBS2CK p.387
LLQ
Diverticulitis (Sigmoid) Sigmoid Volvulus Ovarian Torsion () Ectopic Pregnancy ()
ChronicMesentericIschemia
66-year-old man in the ED with acute onset, severe abdominal pain. Abdominal exam benign, without guarding or rebound tenderness. White count 18,000/mm3 (4,500-11,000/mm3), lactic acid 4.2 mg/dL (4.5 to 19.8 mg/dL). Only medication is coumadin. Whats the most appropriate next step in management? a. MRI scan of f th the abdomen bd T k too Takes t long l b. Exploratory Laparotomy c. Colonoscopy Risk of bowel perforation d. Oral antibiotics Doesnt treat primary concern e. EKG Symptoms not consistent with cardiac etiology
Etiology Mesenteric artery atherosclerosis insufficient blood flow to bowel

Patients often have other atherosclerotic diseases
Angina Claudication
MTBS2CK p.385386
A lack of blood flow causes ischemia to the bowel wall and sloughing of the mucosa. Source: Niket Sonopal, MD.
ChronicMesentericIschemia
ChronicMesentericIschemia Diagnosis CT abdomen (initial test)

Fast, non-invasive
Signs/Symptoms Diffuse, postprandial abdominal pain

Severe, crampy, associated nausea Due to O2 requirement by gut after meals May lead to weight loss due to fear of eating
Bloody diarrhea Progressive disease begins with mild ischemia, progresses to full occlusion of blood flow
MTBS2CK p.386
CT angiography is most accurate Treatment Surgical revascularization via arterial bypass

NPO Hydration with IV fluids Bowel prep 24 hours preceding surgery
Nitrates may provide short-term symptom improvement

MTBS2CK p.386
15
AcuteMesentericIschemia
Etiology Acute occlusion of mesenteric arteries

Most commonly the superior mesenteric Causes:
Embolism secondary to A A-fib fib (#1)
MTBS2CK p.386
Source: Mikael Hggstrm from original image created and uploaded by Dr. I-Chen Tsai, commons.wikimedia.org
AcuteMesentericIschemia Signs/Symptoms Sudden onset, severe abdominal pain

Pain out of proportion to exam
Etiology Acute occlusion of mesenteric arteries

Most commonly the superior mesenteric Causes:
Embolism secondary to A A-fib fib (#1) Acute thrombus formation on atherosclerotic plaque
Diagnosis Labs: WBC, pH, Lactate Abdominal X-ray/CT

Air in bowel wall (Pneumatosis ( Intestinalis) Edema Ileus
Nausea, , vomiting g Bloody diarrhea
Results in bowel infarction

Splenic flexure (#1) and hepatic flexure (#2) are most common sites
MTBS2CK p.386
CT angiography (Most accurate)
Treatment
Emergent Laparotomy Resection of necrotic bowel
Mesenteric artery thromboembolism. Source: Joel McFarland, Medpix 28818
MTBS2CK p.386
16
AcuteMesentericIschemia 52-year-old woman, alcoholic, with severe chest pain after an episode of persistent vomiting. No blood in vomitus, only stomach contents. Exam reveals crepitus over upper anterior chest wall. What is the next step?
a. b. c. d. e. Ethanol level Not useful in this case Chest X-Ray Will not show esophageal rupture Upper Endoscopy Risk further perforation Barium Esophagogram Not water-soluble Gastrografin Esophagogram
Source: haitham alfalah, commons.wikimedia.org
MTBS2CK p.387
EsophagealInjuries
MucosalTear MalloryWeissSyndrome EsophagealPerforation BoerhaaveSyndrome
Cause
Vomiting/Retching Alcoholics Hematemesis Odynophagia
Symptoms
Location Diagnosis
Gastroesophageal junction
Gastrografin esophagogram Noleakage Treatment Supportive Cauterizationifnecessary Complications Rare

MTBS2CK p.387388
Iatrogenicis#1(Endoscopy) Vomiting/Retching Alcoholics Retrosternal chestpain Severe,acuteonset RadiatestoLshoulder SubcutaneousEmphysema Distalesophagus LeftPosterolateral Aspect Gastrografin esophagogram Leakage EmergentSurgery Highmortality(25%) Acutemediastinitis Veryhighmortality
57-year-old male with BMI of 37 (18.5-24.9 normal) presents to ED with weakness. Vomiting large amounts of blood twice in last hour and passing one bright red stool. He has persistent pain in his mid-abdomen. Takes omeprazole for heartburn. BP 100/60, HR 120. What is the diagnosis? a Gastric Perforation No a. N bl bleed. d P Peritoneal it l signs. i b. Hemorrhagic ulcer c. Boerhaaves syndrome No hematemesis d. Diverticulosis No hematemesis e. Acute mesenteric ischemia No hematochezia
GastricPerforation Etiology Secondary to peptic ulcer disease

Increased production of gastric acid, combined with compromise of stomach lining results in ulcer formation
GastricPerforation Risk Factors H. Pylori infection NSAIDs Burns Trauma Head trauma Cancer Ethanol Tobacco
Source: User:KGH, commons.wikimedia.org
MTBS2CK p.388
MTBS2CK p.388
17
GastricPerforation
GastricPerforation/SignsandSymptoms
Pathophysiology
Perforation
Ulcer completely erodes through visceral wall
Gastric contents are released into abdominal cavity Result is damage to peritoneal structures Peritonitis (anterior + posterior ulcers) Pancreatitis (posterior ulcers)
MTBS2CK p.388
Acute onset mid-epigastric abdominal pain

Hemorrhage
Ulcer erodes into gastroduodenal artery
More common than gastric perforation Seen with posterior ulcers Requires upper endoscopy to evaluate/treat bleed
May radiate to right shoulder (phrenic nerve involvement) Worsening over time
Peritoneal signs (if any delay in seeking t t treatment) t)

Rigidity Guarding Rebound tenderness
MTBS2CK p.389
GastricPerforation
GastricPerforation
Management 1) Make Patient NPO
Prevents further extrusion of gastric contents into peritoneal cavity
Diagnosis Upright chest X-ray

Free air under diaphragm
2) Place NG Tube
Suction gastric contents Mitigates risk from newly-formed newly formed acid
Abdominal CT
3) Medical Management
Broad-spectrum antibiotics to combat infection IV fluids in preparation for surgery
4) Emergent Surgery
Exploratory laparotomy - Repair perforation
MTBS2CK p.389
MTBS2CK p.389
TheAbdomen Part2
AbdominalAbscess InflammatoryGIConditions AbdominalObstruction
16-year-old boy comes with new onset RLQ pain. He reports vague, mid-abdominal pain for last day, but when he awoke this morning it was much sharper and had changed location. He displays guarding and rebound tenderness, and palpation of LLQ hurts on right side. WBC count of 16,000/mm3 (4,5003) 11 000/ 11,000/mm What is the next step in management?
a. b. c. d. Abdominal X-ray Non-specific findings Colonoscopy Risk of perforation RLQ Ultrasound Non-specific findings Laparoscopic Appendectomy
MTBS2CK p.389
18
RightLowerQuadrantPain
Age > 60 yo?
Yes No
AbdominalAbscess Cause Surgical complication (#1) Inflammatory disease Trauma Signs/Symptoms Abdominal pain/distension Non-specific symptoms
Fever/chills GI symptoms nausea/vomiting, diarrhea
Cecal Diverticulitis
Make NPO, Place NG Tube Broad-Spectrum Abx
Male
Male or Female?
Female
Order -HCG, Pelvic US Appendicitis

Emergent Laparoscopic Appendectomy
Normal Elevated or Abnormal
Ovarian Torsion
Doppler US to diagnosis Laparoscopic surgery
Ectopic Pregnancy
Emergent Surgery
Rectal fullness
MTBS2CK p.390
AbdominalAbscess Diagnosis Abdominal CT

Visual evidence of abscess Information about surrounding structures
AbdominalAbscess
Source: Joel McFarland, Medpix 28716
MTBS2CK p.390
AbdominalAbscess Diagnosis Abdominal CT

Visual evidence of abscess Information about surrounding structures 78-year-old woman with severe LLQ pain, fever, and anorexia of one day. Shes had dark, tarry stools in the past. The patients husband brings in a medication list, which includes a stool softener and iron supplements. She displays guarding and rigidity. What is the diagnosis? a Ectopic pregnancy Patient a. P ti t is i postmenopausal t l b. Acute appendicitis Rare in elderly, RLQ in location c. Cholecystitis RUQ pain d. Acute diverticulitis e. Acute pancreatitis Central abd pain, radiates to back
CBC
May show elevated WBC count
Treament Broad-Spectrum Antibiotics Incision + Drainage

Percutaneous (CT-guided) versus Open
MTBS2CK p.390
19
InflammatoryGIConditions
Appendicitis
Cause Fecolith obstructing appendiceal orifice Anorexia Fever Periumbilical Pain RLQ Phys.Exam CTScan
Pancreatitis
Alcohol Gallstone obstructing pancreaticduct N/V Fever AbdominalPain Radiatesto back Amylase/Lipase CTScan(#1)
Diverticulitis
Fecal obstructionof bowelwallout pouchings N/V Fever LLQ Pain
Cholecystitis
Gallstone obstructingcystic duct N/V Fever RUQ pain Worsewith inspiration Ultrasound Fluid,Stones, ThickWall HIDAscan(#1) Laparoscopic Removal Perforation
Symptoms
Diagnosis
CTScan
Treatment
Laparoscopic Removal
IVFluids NPO Pseudocyst
Complication Abscess
Antibiotics(x1) Resection(if recurrent) Abscess
55 year-old man presents to the ED with severe, intermittent abdominal pain and nausea/vomiting. He cannot recall when he last passed flatus, but is certain he didnt have a bowel movement this morning. He has type 1 diabetes and had an open appendectomy in his 30s. Temperature of 101.8. Loud, high-pitched bowel sounds noted on auscultation. An abdominal plain film shows a partial small bowel obstruction. What is the best next step in management? a. Prescribe a laxative Will not relieve obstruction (may worsen) b. Place an NG-tube c. Emergent exploratory laparotomy Medical management first d. Prescribe antibiotics No evidence of bowel perforation e. Perform a colonoscopy Will not relieve obstruction
MTBS2CK p.391
BowelObstruction
BowelObstruction
Pathophysiology
A mechanical or functional obstruction of intestines
Leads to fluid/gas accumulation proximal to site of f obstruction Resulting pressure increase leads to
1. Pain 2. Decreased perfusion (and risk of necrosis)
Causes/RiskFactors
Obstruction can be partial or complete
Partial = GI contents are able to pass obstruction site Complete = No avenue for passage
Represents a much more severe condition
Adhesions from previous abdominal surgery

#1 in developed countries
Neoplasms Intussusception = Telescoping bowel

Most frequently seen in pediatric population
Hernia
#1 in undeveloped countries
Volvulus = Twisting of bowel on its mesentery Crohns disease

MTBS2CK Only p.393
Foreign bodies Intestinal atresia = Blind Pouch

Only seen in neonates
MTBS2CK p.392
BowelObstruction
BowelObstruction
Signs/Symptoms Severe, crampy abdominal pain

Colicky in nature
Diagnosis Labs
WBC, Lactate, pH
Nausea/vomiting Fever High-pitched, Tinkling bowel sounds

MTBS2CK p.392393
Abdominal X-ray
Air-fluid levels, dilated loops of bowel
20
BowelObstruction Signs/Symptoms Severe, crampy abdominal pain

Colicky in nature
BowelObstruction Diagnosis Labs

WBC, Lactate, pH
Management 1) Make Patient NPO
Prevents further increase in bowel pressure
Abdominal X-ray
Air-fluid levels, dilated loops of bowel
Nausea/vomiting Fever High-pitched, Tinkling bowel sounds
2) Place an NG Tube (w/suction)

Lowers bowel pressure proximal to obstruction
Abdominal CT w/ oral contrast (#1)

Clear transition zone correlates with obstruction
3) Medical Management
IV Fluids Volume is lost due to third-spacing
4) Surgical Decompression (if indicated)

Complete obstruction (Emergent) Lack of improvement with medical management
MTBS2CK p.393
MTBS2CK p.392393
FracturesAlgorithm
Pain Swelling Bony deformity
Orthopedics
FractureTypes Upper pp Extremity yInjuries j BackPain FatEmbolism CompartmentSyndrome KneeInjuries
X-rays
Closed (skin intact)
Management
Open (skin puncture)
MTBS2CK p.393394
FractureTypes Stress Fractures Cause

Overuse injury secondary to repetitive insult to bone
FracturesTypes
Presentation Clue
High-performance athlete Common sites
1. Metatarsals 2. Tibia
Diagnosis
CT/MRI
Treatment
Rest and rehabilitation
MTBS2CK p.394
Compression Fractures Cause Vertebral fracture associated with poor bone quality Osteoporosis p ( (classical example) p ) Presentation Clue Elderly patient with back pain 33% thoracic spine, 33% thoracolumbar, 33% lumbar
MTBS2CK p.394
Diagnosis
Presentation
Symptoms:
Timing:
Acute onset with trauma
Neurovascular exam Closed reduction Surgery (ORIF) Emergency surgery (I&D)
21
FracturesTypes/CompressionFractures
FracturesTypes
Diagnosis X-ray CT, if inconclusive Treatment Controversial

MTBS2CK p.394
PathologicFractures
Cause
Fracture in bone weakened by disease
Metastatic cancer Multiple myeloma Pagets disease
Diagnosis
X-ray
Treatment
Treat fracture ID & treat primary disease
Presentation Clue
Patient with fracture after minimal trauma
MTBS2CK p.394
UpperExtremityInjuries
UpperExtremityInjuries/ClavicleFracture Workup
X-ray Careful distal neurovascular exam
Must rule out subclavian artery/brachial plexus injury
Clavicle Fracture Cause History of fall Blunt shoulder trauma Presentation Clue Pain over anterior shoulder Clavicle step-off
Treatment
Arm sling
Source: Mark D. Travis
MTBS2CK p.395
MTBS2CK p.395
Anterior Shoulder Dislocation Cause Fall on outstretched hand Sports, blunt trauma Signs/Symptoms Severe shoulder pain, swelling Arm is held in external rotation
UpperExtremityInjuries/ AnteriorShoulderDislocation Diagnosis X-ray, MRI (if necessary) Careful distal neurovascular exam Must rule out axillary artery or nerve injury Treatment Reduction w/sling immobilization
MTBS2CK p.395
Source: Daniel Patrick Moloney
MTBS2CK p.395
22
Posterior Shoulder Dislocation Cause

History of seizure or electric shock
UpperExtremityInjuries/ PosteriorShoulderDislocation
Diagnosis
XR, MRI (if necessary)
Signs/Symptoms g y p
Severe shoulder pain, swelling Arm is held in internal rotation
Treatment
Reduction w/sling immobilization
MTBS2CK p.395
MTBS2CK p.395
Source: Medpix 20030
19-year old with persistent wrist pain of 3 days duration. Pain began when he braced himself from a fall. Right wrist is notable for point tenderness and mild swelling at base of dorsal aspect of thumb, but no deformity. An X-ray is shown on the next slide.
Source: Medpix 6094
UpperExtremityInjuries 19-year old with persistent wrist pain of 3 days duration. Pain began when he braced himself from a fall. Right wrist is notable for point tenderness and mild swelling at base of dorsal aspect of thumb, but no deformity. An X-ray is shown below. What is the best next step in management? Trigger finger Cause
Inflammation of finger flexor pulley system
Leads to catching/locking of flexor tendon
Signs/Symptoms
Lone digit caught in flexion
Popping sensation if digit is manually extended
Scaphoid may be fractured a. Reassurance b. MRI Scan Unnecessary, worse than CT c. Thumb Spica Cast d. Amputation No indication e. Open Reduction + Internal Fixation No fracture (yet)
Moderatesevere pain
Diagnosis
Clinical Exam
Treatment
Corticosteroid injection
MTBS2CK p.395
23
DupuytrensContracture Cause
Thickening of palmar fascia, leading to flexion contracture
Digits cannot fully extend
UpperExtremityInjuries/ DupuytrensContracture
Risk Factors
Male > Female Age > 40 Northern European descent
Diagnosis Di i
Clinical Exam
Treatment
Surgery
MTBS2CK p.395
MTBS2CK p.395
BackPain A 66-year-old man comes to his PCP with bilateral leg pain of several months duration. The pain seems to be worst when he has to walk several blocks, and improves when he sits down. Leaning forward (on a bench, shopping cart, etc.) alleviates the pain. He is a non-smoker. What is the most appropriate next diagnostic step?
a. b. c. d. e. Lower Extremity XR Useful for bony trauma Doppler US of the calf Useful for DVT evaluation Ankle-Brachial Indices Diagnoses claudication Spine MRI Leg MRI Useful for soft-tissue injury/stress fractures
Spinal Stenosis Cause Arthritic changes result in narrowing of spinal canal Lumbar #1, Cervical #2 Symptoms Neck/Back Pain Bilateral leg/buttock pain + numbness Pseudo-claudication Worse with walking, improves with spine flexion
BackPain/SpinalStenosis
BackPain
Diagnosis MRI Treatment NSAIDs vs. surgery g y
Herniated Disk Disease Cause Intervertebral disk herniates, compressing spinal nerve root
Often associated with lifting injury Most frequently seen in elderly Symptoms
Electric Pain following a dermatome distribution
Source: nih.gov, commons.wikimedia.org
24
BackPain/HerniatedDiskDisease
BackPain/HerniatedDiskDisease Diagnosis Clinical Exam (Straight Leg Raise)

Consider MRI if red flags present
Treatment NSAIDS, Activity Modification

Source: user:debivort, commons.wikimedia.org
Source:Mjorter, commons.wikimedia.org
BackPain
BackPain
RedFlags ConcernforMetastasisorAbscess
Pain not relieved by rest

Not worse with activity
Fever Neurological deficits

Bowel/Bladder incontinence Abnormal reflexes
Management MRI to evaluate for mass lesion Emergent glucocorticoids if neurological findings
Night pain Constant, dull pain > 6 weeks
History of Cancer
FatEmbolism AMedicalEMERGENCY
22-year-old woman was struck by a car 3 days ago while walking her dog. The impact broke her femur, which required immediate surgical repair. This morning the patient is confused and has difficulty catching her breath. ABG shows PaO2 55 mmHg, and exam reveals a petechial rash. What is the most likely diagnosis? a. Myocardial infarction No rash b. Pancreatitis Expect abdominal pain c. Rhabdomyolysis No hypoxemia d. Fat embolism
Etiology Traumatic long bone fracture (#1 = Femur) Releases marrow fat into circulation Fat vesicles are too large to pass through capillaries Result is vascular occlusion
H&E stain, lungs blood vessel with fibrinoid material and an optical empty space indicative of the presence of lipid. Source: Boris L Kanen, Ruud JLF Loffeld, commons.wikimedia.org
MTBS2CK p.396
MTBS2CK p.396
25
FatEmbolism
FatEmbolism Diagnosis ABG: PO2 < 60 mmHg CBC: Decreased platelet count Chest X-ray: Infiltrates Urinalysis: Fat droplets in urine T t Treatment t Respiratory Support
Goal O2 Sat > 90% Consider intubation/mechanical ventilation if severely hypoxic
Signs/Symptoms Onset 0-5 days after fracture Respiratory Distress (V/Q mismatch) SOB Tachypnea yp Confusion (Involves brain vasculature) Petechial Rash (Involves skin capillaries) Chest wall, upper extremities
MTBS2CK p.396
MTBS2CK p.396
CompartmentSyndrome
CompartmentSyndrome/Signs&Symptoms
Early Findings Pain Severe, worse with muscle stretch Pallor Pale skin from blood flow
MTBS2CK p.396397
Pathophysiology
Injury occurs, resulting in Pressure builds, swelling leading to severe tissue compression Fracture #1 (tibial,
forearm) Nerves Burns Muscle Crush injuries Vessels (Reperfusion syndrome) Resulting damage can
The 6 Ps
Late Findings Pulselessness Absent distal pulses (ominous finding)
Parathesias Pins and needles nerve involvement
Poikilothermia Cold, due to decreased blood flow
In closed compartment (fascial sheath, cast), theres no escape for increasing pressure
MTBS2CK p.396
lead to Volkmanns ischemic contracture, limb loss, or death
Paralysis Inability to move distal musculature
CompartmentSyndrome
KneeInjuries Basic Principles

Ligamentous/meniscal knee injuries have similar symptoms
Knee Pain Swelling Instability The key factor is time course in which symptoms present
Treatment AMedicalEMERGENCY
Surgical fasciotomy Releases compartment p pressure
Pay attention to mechanism of injury! Physical exam provides clues to etiology

Special tests for each type of knee injury
Diagnostic test of choice is always MRI

MTBS2CK p.397
Source: Sarte, commons.wikimedia.org
26
KneeInjuries
Mechanismof Injury Symptom Onset Exam Maneuver Management
MCL/LCL Traumato Immediate Injury contralateral aspectofknee ACLTear Twistingor directimpact
Medial/Lateral Conservative Instability
Immediateand AnteriorDrawer Arthroscopic Repair Severe sign LachmanTest Repairvs. Conservative management
Immediatebut Posterior PCLTear Forced Hyperextension Mild Drawersign
22-year-old hockey star is checked by an opposing player, and his leg gets tangled as he falls. He experiences a popping sensation in his left knee, which immediately swells. The team physician performs a physical exam and notes a positive anterior drawer sign as well as medial knee instability. He recommends an MRI to evaluate the likely ACL and MCL tears. What other structure will likely be injured on MRI?
Meniscal TwistingInjury Delayed(1224 Jointline Conservative hours) tenderness Tear McMurrays Clicking/Locking
MTBS2CK p.398
a. b. c. d.
Lateral Collateral Ligament Different injury mechanism Lateral Meniscus Medial Meniscus Posterior Cruciate Ligament
MTBS2CK p.398
27

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Allergy&Immunology Allergy&Immunology

Anaphylaxis Angioedema Urticaria AllergicRhinitis PrimaryImmunodeficiency Disorders

Anaphylaxis Anaphylactoid Reactions

Causes of anaphylaxis = causes of any allergic event

Characterized by Hypotension Tachycardia Respiratory: stridor Rash

The best initial treatment is A Airway Protection

Source: Fashad Bagheri. MD

Angioedema Angioedema is sudden swelling of

Hereditary angioedema is a genetic disorder Glucocorticoids dont work

Angioedema/Tests The best initial test...

Angioedema/Treatment Airway Acute Tx Long Term Tx

3 types of hereditary angioedema

Ensure airway protection first

Fresh frozen plasma Ecallantide E ll tid

Androgens Danazole And Stanazole

2 L 2. Leukotriene k ti receptor t antagonists

B cells are present but decreased Igs Decrease in all Ig subtypes

LOW B cells output, normal T cells

CommonVariableImmunodeficiency(CVID) Recurrent sinopulmonary infections Frequent episodes of

Other manifestations are

Antigen Stimulation Decreased response

Normal T cells normal B cells decline with age

Aphthous ulcers And Inflammation of nares is common

Abnormal nitroblue tetrazolium testing

LOW B & T cells Analogous to HIV

CoronaryArtery Disease Part1

Can be used interchangeably with:

early in morning, ST segment elevation

Risk factors are most important with equivocal or uncertain histories

Women > men eventually die of heart disease

immeasurable, no evidence of proven benefit

with high LDL, DM, and HTN

What Is the Most Likely Diagnosis? Ischemic pain

Diabetes mellitus Tobacco smoking Hypertension Hyperlipidemia Weight loss

Fixing all of them is good. But Not as fast as smoking cessation!

Characteristics of Ischemic Pain

Ifthecase describes. Chestwalltenderness Radiationtoback, unequalblood pressurebetween arms

Answerasmost likelydiagnosis Costochondritis Aorticdissection

Duration Stable angina: > 2 - < 10 min ACS: > 10 - 30 min

Provoking factors Physical activity, activity cold cold, emotional stress

Alleviating factors Rest

NOT tender NOT positional NOT pleuritic

Associated symptoms SOB, nausea, diaphoresis, dizziness, lightheadedness, fatigue

Radiation Neck, lower jaw and teeth, arms, shoulders

Painworsewithlying flat,betterwhen sittingup

,cough, g , Badtaste, hoarseness

Response p toPPIs; ;or liquidantacids

CoronaryArtery Disease Part2

to the emergency department

uncertain & EKG not diagnostic

Persantine (dipyridamole) or adenosine with nuclear isotopes (e.g., thallium or sestamibi) Or

Dipyridamole may provoke bronchospasm. Avoid in asthmatics.

Chest pain (likelihood of CHD is high)

Nuclear and Echo:

Exercise stress test

Stress echocardiogram or nuclear stress test

3 vessel disease, left main or 2 vessel disease in diabetics CABG

CAD/Treatment USMLE Step 2 CK is most concerned that you know:

CoronaryArtery Disease Part3

Medications that lower mortality

Step 2 will not test dosing Route of administration is tested

Statins (HMG-CoA reductase inhibitors)

CAD with LDL > 100 mg/dL