Professional Documents
Culture Documents
Cardiology
Myocardial Infarction
A 52-year-old man comes to the ER with 1 hour of severe chest pain on exertion. He
is nauseated and diaphoretic with slight shortness of breath. The pain does not
change with respiration or bodily position. Exam shows normal vitals, clear lungs,
no murmurs, and no tenderness.
• Pneumonia
• Pneumothorax
• Pulmonary embolus
• Pleuritis
• Pericarditis
• Pericarditis only
• when lying back causes more pain
• Costochondritis only
EKG shows 2 mm of ST segment elevation in V2-V4
Cardiac Enzymes
Cardiac Enzymes
Begins to Lasts
Elevate
CPK-MB 4-6 hr 2 days
Troponin 4-6 hr 1-2 wk
Myoglobin 1-4 hr s
LDH 12-24 hr s
Best Answers:
• Myoglobin
CPK-MB is sensitive and specific, but not as sensitive as myoglobin or as specific as troponin.
Special Circumstances
• Angioplasty
o Patients with major bleeding or risk of bleeding
o Patients who can’t receive thrombolytics for any reason
o Patients failing thrombolytics and progressing to hemodynamic instability
o Equal in efficacy to thrombolytics
Special Circumstances
• ACE Inhibitor
o Patients with decreased left ventricle function or CHF
• Lidocaine
o Never as prophylaxis
o All patients who develop major vertricular arrhythmias (ventricular tachycardia
or fibrillation)
Pacemakers
A 67-year-old woman comes to the ER with 1-2 hours of severe shortness of breath.
She has a history of two MIs in the past. She comes with a pizza in one hand and a
bag of Doritos in the other, and she is chewing a sausage. Her respiration rate is 34;
BP, 130/82; and PUD, 18. Jugulovenous distention is present. Chest: rales to apices.
Heart:3/6 systolic murmur at Apex 1. S3 gallop. Abd: Enlarged liver.3+ Edema of
lower extremities to mid-thigh.
• Positive inotropes
• Dobutamine
• Amrinone
• Ace inhibitors - IV
• Nitroprusside
Congestive Heart Failure
• Ace inhibitors
• Diuretics
• Digoxin
• β − Blockers (carvedilol or metoprolol)
β − Blockers
• Reduce mortality
• Increase ejection fraction
• Improve symptoms
Introduction to Antibiotics
Introduction to Antibiotics
• Penicillins:
o Oxacillin
o Cloxacillin
o Dicloxacillin
o Nafcillin
• First-generation cephalosporins:
o Cefazolin
o Cephalexin
o Cephradine
o Cefadroxil
• Clindamycin
• Macrolides (erythromycin, clarithromycin, azithromycin): Used for minor, non-life-
threatening infections
• Vancomycin, Synercid, Linezolid: Used for gram-positive infections with life-
threatening allergy to penicillin and methicillin-resistant Staphylococcus
Gram-negative Bacilli
Gram-negative Bacilli
Anaerobes
• Clindamycin
• Penicillin (any penicillin EXCEPT the Ox/Clox/Diclox/Naf group)
• Metronidazole
• Imipenem
• Second-generation cephalosporins
• Beta-lactam/ Beta-lactamase inhibitor combinations
Antivirals
Antivirals
Influenza
• Oseltamivir, zanamivir
• Amantadine, rimantadine: Becoming archaeologic
Hepatitis B
• Lamivudine or interferon
Hepatitis C
Antifungals
• Amphotericin
Candida infections
• Azoles
• Fluconazole, ketoconazole, itraconazole
Onychomycosis
• Terbinafine, itraconazole
ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the
following clues:
Meningitis
• The patient also has photophobia and nuchal rigidity (stiff neck) on exam.
Encephalitis
ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the
following clues:
Abscess
Note: There is considerable overlap between these diseases. If the question state
that he has a stiff neck AND confusion/lethargy AND focal findings, then neither you
nor anyone else could determine the precise diagnosis.
Meningitis
Cultures
“What is the BEST - Most Accurate - Most Likely to lead to specific diagnosis” type
of question.
Meningitis
A 48-year-old man comes to the ER with 1 day of fever, headache, and nausea. He
has photophobia and a stiff neck. He has no focal neurological deficits or papilledema
and is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count
of 3,502, and a negative gram stain. Culture is sent.
Any type of meningitis can cause an elevated cell count; the differential on the cell count gives
more specific information.
Neutrophils – Bacterial:
• Rocky Mountain spotted fever: rash on wrists/ankles, moving centrally towards the
body
• Lyme: Facial palsy, target lesion rash (erythema migrans)
• Cryptococcus: HIV+ patients with <100 CD4 cells
• TB: Very high protein in CSF,and very low glucose, TB in lungs
• Viral: Everything negative; no particular association. Exclude the other causes
A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has
photophobia and a stiff neck. He has no focal neurological deficits or papilledema and
is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count of
3,502, and a negative gram stain. Culture is sent. The differential shows 92%
neutrophils.
A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has
photophobia and a stiff neck. He has no focal neurological deficits or papilledema and
is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count of
3,502, and a negative gram stain. Culture is sent. The differential shows 92%
neutrophils.
PPD Testing
PPD Testing
To screen the asymptomatic: do not use as primary method for diagnosing TB in acutely
symptomatic patients
• >10 mm induration, not erythema in most patients; >5 mm in HIV+ patients and close
contacts
• Always get CXR after a positive PPD
• Treatment for a positive PPD means INH alone
Treat all PPD+ patients if the risk of developing TB is greater than risk of hepatitis from the
isoniazid:
• A 32-year-old, HIV- physician from India who received BCG as a child and has never
been tested before. She has 12 mm of induration at health screening before starting
an internship in the US.
• A 47-year-old HIV+ man who had never been tested before and has 7 mm of
induration.
• A 95-year-old, HIV-, female nursing home resident who was PPD- last year and has
11 mm of induration this year.
• A 3,725-year-old Egyptian mummy who was PPD- last year and is PPD+ this year.
HIV
HIV
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
575, and his viral load is 1,000.
• Zidovudine (anemia)
• Didanosine (pancreas, neuropathy)
• Stavudine (pancreas, neuropathy)
• Zalcitabine (pancreas, neuropathy)
• Lamivudine
• Nelfinavir
• Ritonavir
• Indinavir
• Saquinavir
• Amprenavir
What to start?
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
275, and his viral load is 1,000.
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
575, and his viral load is 71,000.
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
175, and his viral load is 31,000
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is 45,
and his viral load is 31,000.
A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is 5,
and his viral load is 371,000
.
Any two nucleosides AND a protease inhibitor AND
trimethoprim/sulfamethoxazole AND azithromycin AND…
NOTHING!!
Microcytic Anemia
Microcytic Anemia
A 32-year- old woman presents with several weeks of fatigue. She complains of
nothing else. Initial CBC reveals an hematocrit of 28%.
Symptoms of anemia are largely based on severity not etiology. Iron deficiency
with hematocrit of 28% will give the same symptoms and the anemia of chronic
disease, folate deficiency, thalassemia, etc, with hematocrits of 28%.
After determining that the patient has anemia, the next most useful step is to
determine the cell size. This is the next easiest clue as to the etiology of the
anemia.
Low MCV
• Iron deficiency
• Anemia of chronic disease (can also be normocytic)
• Sideroblastic
• Thalassemia
High MCV
Normal MCV
• Hemolysis
What is the next best step in the management of this microcytic patient? (ie:
What is the best initial diagnostic test?)
Iron Studies
After the iron studies, how would you address other questions
about the specifics of the various low MCV anemias? (“What is
the most accurate diagnostic test?”)
Iron Deficiency
Sideroblastic anemia
What is the most specific test? Prussian blue stain for ringed sideroblasts
Thalassemia
What is the most specific test? Hemoglobin electrophoresis
Iron Deficiency
• Iron replacement
• Ferrous sulfate tablets
Chronic Disease
Sideroblastic anemia
• Pyridoxine
Thalassemia trait
• No therapy
Macrocytic Anemia
A 32-year-old woman presents with several weeks of fatigue. Initial CBC reveals an
hematocrit of 28%.
Symptoms of anemia are largely based on the severity not the etiology. Iron
deficiency with hematocrit of 28% will give the same symptoms and the anemia
of chronic disease, folate deficiency, thalassemia, etc, with an hematocrit of
28%.
A 32-year-old woman comes to the office with several weeks of fatigue. In addition,
she complains of a sensation of pins and needles in her hands and feet. She drinks
almost a quart of vodka per day. Initial CBC reveals an hematocrit of 28%. The MCV
is 120 (normal 80-100).
What is the next best step in the management of this macrocytic patient?
• Peripheral neuropathy
B12 Deficiency
Folate Deficiency
Hemolysis
Hemolysis
A 42-year-old man is admitted to the hospital because of weakness, fatigue, and dark
urine. On examination he appears jaundiced with scleral icterus. Initial CBC shows an
hematocrit of 28% with a normal MCV. His indirect bilirubin, LDH level and
reticulocyte count are all elevated.
All forms of hemolysis present with elevated LDH levels, reticulocyte count, and
indirect bilirubin. The dark urine can be either from hemoglobin filtered into the urine
in intravascular hemolysis or from the bilirubin alone. Sometimes the MCV can be
slightly elevated because reticulocytes are slightly larger.
Which clues in the history will tell you which type of hemolytic
anemia it is?
Which clues in the history will tell you which type of hemolytic
anemia it is?
An 87-year-old woman with a history of gout and osteoarthritis is found on the floor of
her apt. by her family. It is not clear how long she has been on the floor. She uses
NSAIDs for joint pain. In the ER she is found to be confused. Her temperature is 102
F, pulse is 117, and systolic BP blood is 92; rales are heard on lung examination. She
has a head CT with contrast to evaluate her confusion and receives penicillin and
gentamicin for her pneumonia. She has no urine output since admission. On hospital
day 2 her BUN and creatinine begin to rise.
The first step in evaluating a patient with acute renal failure is to determine whether
there is a problem inside the kidney (tubules, glomeruli, vascular) or with the
perfusion of the kidney (prerenal) or drainage out of the kidney (postrenal).
The fever, tachycardia, relatively low BP, and the fact that she was found on the
floor are all sufficient suggestions of pre-renal azotemia.
Do NOT assume that the decreased urine output described is from the renal failure. The renal
failure could simply be from decreased urine output and obstruction.
Damage to the kidney could affect tubules, glomeruli, or vasculature. It is NOT very
useful to think of the diseases as cortical or medullary. Glomerular diseases, eg,
lupus, Goodpasture, Alport syndrome, Berger disease, or even post-streptococcal
disease, are unlikely to occur this acutely and without other history of systemic
disease. The same is true of vascular diseases, eg, polyarteritis nodosa, Wegener
granulomatosis, TTP, HUS, or Henoch Schonlein purpura.
Intra-renal Damage (ATN)
Acute renal failure such as this is most often from tubular diseases, which are most
often from various toxins combined with possible ischemia from hypoperfusion.
An 87-year old woman with a history of gout and osteoarthritis is found on the floor
of her apartment by her family. It is not clear how long she has been on the floor. She
uses NSAIDs for joint pain. In the ER she is found to be confused. Her temperature is
102 F, pulse is 117, and systolic BP blood is 92; rales are seen on lung examination.
She has a heat CT with contrast to evaluate her confusion and receives penicillin
and gentamicin for her pheumonia. She has no urine output since admission. On
hospital day 2 her BUN and creatinine began to rise.
You could simply say that the tubular diseases are from toxins. However, since
the answers to questions concerning initial and best tests and treatments are
different, they must be subdivided so they can be addressed individually.
Direct Toxins
Gentamicin acts directly as a toxin to the kidney's tubule. Other drugs include
amphotericin, cisplatin, NSAIDs, and cyclosporine. Contrast agents also act in the
same way.
Best test: Exclude other causes of renal failure. There is no test to determine the
specific etiology of any toxin-mediated organ toxicity. Biopsy will NOT determine the
specific agent.
Direct Toxins:
Best therapy: Stop the offending agent. There is no specific therapy to reverse ANY
toxin-mediated organ damage beyond this. Dialysis does NOT reverse the damage; it
supports the patient while waiting for the kidneys to come back to life on their own.
Allergic Interstitial Nephritis:
Penicillin causes damage to the kidney, as it causes an allergic reaction against the
kidney tubule. Other drugs include sulfa drugs, allopurinol, phenytoin, rifampin and
NSAIDs.
Keys to recognizing this as the cause of the renal failure are fever and rash,
although these do not have to be present.
Best initial test: Measure blood and urinary eosinophils. IgE levels are not
sufficiently sensitive. Renal biopsy is the most accurate test but should seldom, if
ever, be used.
Best initial therapy: Stop the medications. Very severe cases can be treated with
steroids.
Crystals:
Uric acid crystals from the gout as well as from oxalate crystals from ethylene glycol
ingestion can also damage the tubules. Look for gout or ethylene glycol ingestion in
the history.
Therapy: Either allopurinol for gout or ethanol infusion for the ethylene glycol
ingestion.
Pigments:
Myoglobin from rhabdomyolysis and hemoglobin from hemolysis are directly toxic to
the tubule. The fact that this patient was found lying on the floor of her apartment is
suggestive of rhabdomyolysis. Clues to pigments as the cause of the renal failure are
hemolysis or muscle breakdown, as dark urine, on history.
Pigments:
Best initial tests: EKG to exclude signs of life-threatening hyperkalemia and
urinalysis to show dipstick positive for blood with no RBCs on the microscopic
examination.
Most accurate and specific tests: Myoglobin in urine and elevated CPK level in
blood for rhabdomyolysis.
Best initial therapy: Hydration and alkalinization of the urine with bicarbonate.
Hyponatremia
A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145)
Normal volume:
• Addison’s disease does not require free water to drive the sodium down.
• Psychogenic polydipsia
• Pseudohyponatremia
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Hypothyroidism
A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145). Physical examination reveals normal
skin turgor and no orthostasis, edema, or rales.
If a normal person’s sodium were suddenly driven below normal, the body’s response
would be to immediately shut off all ADH secretion, allowing the maximal amount of
free water to be released. The normal response would be to maximally dilute the
urine. The normal response to hyponatremia would be to have a urine osmolality at
the lowest possible amount. The range of urine osmolarity is 50-1200 mOsm/kg. The
normal response would be urine osmolarity around 50 mOsm/kg and urine osmolality
less than serum osmolarity. Urine sodium should also be low.
urine osmolality
A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145). Physical examination reveals normal skin
turgor and no orthostasis, edema, or rales. His serum osmolality is 250 mOsm/kg
(normal 280-300), urine osmolality is 425 mOsm/kg and urine sodium is 42
mEq/L.
• The urine osmolality in this patient is higher than the serum osmolality. Combined with
a high urine sodium level this is confirmatory of SIADH. We do not use ADH levels.
• Therapy for SIADH is divided as follows:
(>1-2 mEq/L/hr)
The patient described above has his sodium corrected by normal saline infusion and
a diuretic. His neurological symptoms resolve.
Demeclocycline to block the effect of the ADH at the level of the kidney tubule
on a chronic basis.
Hyperkalemia
A 27-year-old man presents to the ER at your hospital after having just taken the
physical exam to join the NY City Fire Department. As part of this exam he must do
50 push-ups followed by suddenly lifting a 175-lb bag of sand. He then has to run up
and down 3 flights of stairs and across a balance beam followed by 50 more push-
ups. He comes to see you because of severe muscle pain, muscle tenderness, and
dark urine developing over the next several hours.
The patient seems to have rhabdomyolysis on the basis of severe, sudden exertion.
Several tests are needed: CPK level, urinalysis looking for blood on dipstick, urine
microscopic exam, potassium level, and possibly urine myoglobin level. However, you
must choose the MOST URGENT test. No matter how high the CPK level is,
hyperkalemia is more immediately life-threatening. Even if the potassium level is
elevated, it is more important to know whether there are EKG abnormalities from the
hyperkalemia, which mean he will suddenly die of an arrhythmia.
The original potassium level (on entry, before therapy) comes back at 7.9 mEq/L. His
CPK level is markedly elevated at 48,000 and the urinalysis is dipstick positive for
blood, but no RBCs are seen on microscopic exam.
What is the NEXT best step in management?
Overdose
A 25-year-old medical student gets very depressed while preparing for USMLE Step
2. After finishing studying at midnight she takes a bottle of pills at 12:15 am in an
attempt to commit suicide. She removes the label from the bottle so no one can
determine what she took. After 12:15 she finds that her last practice test score was
87% and she will easily pass. She walks across the street to the ER at 12:30 am to
seek treatment.
Gastric emptying with ipecac has limited utility because it must be given within the
first hour of management. Do NOT give ipecac with ingestions of caustic substances
since they will burn the GI tract and mouth on their way out.
Do NOT answer “toxicology screen.” This takes too long to come back to be useful
and it will not change management. No matter what pills she took, the initial answer in
the first hour of management is to empty the stomach.
Why NOT the gastric lavage?
Gastric lavage with an oropharyngeal hose is not very useful, and most awake
patients do not need this and will not tolerate it. Use gastric lavage in patients with an
acute overdose who have an altered mental status in the first hour after a pill
ingestion. You cannot give ipecac to these patients because they will aspirate.
• Perform endotracheal intubation with gastric lavage to protect the airway when
the patient has altered mental status.
Activated charcoal
A 25-year-old medical student gets very depressed while preparing for USMLE Step
2. After finishing studying at midnight she takes a bottle of pills at 12:15 am in an
attempt to commit suicide. She removes the label from the bottle so no one can
determine what she took. At 12:30 am she finds that her last practice test score was
87% and she will easily pass. She walks across the street to the ER at 1:00 am to
seek treatment.
The patient is confused, disoriented, lethargic, sleepy, and
obtunded and is not thinking so well.
• Naloxone
• Thiamine
• Dextrose
Although you will want to intubate the patient to perform gastric lavage,
you must FIRST give the naloxone, thiamine, and dextrose. If the
patient took an opiate or is hypoglycemic she will awaken immediately.
You will NOT have to do lavage then because the problem will have
been solved.
She awakens after being given the naloxone, dextrose and thiamine.
What is the NEXT best step in management?
After this management, then toxicology and specific drug levels are used to determine
the specific etiology of the overdose.