Causes of Clubbing Causes of Hepatomegaly o Hepatoma

Respiratory Infection
Cancer Viral Causes of Splenomegaly
- Bronchogenic Ca -Hepatitis - Infection
-Lung Mets - EBV Bacterial Subacute
-Pleural Mesothelioma Bacterial bacterial endocarditis
- Oseophageal cancer -Weils disease (leptospiro.) Viral - CMV, EBV
COPD - Syphilis Parasite - Malaria
Tuberculosis Parasitic Haematological
Suppurative Lung Disease -Hydatid cyst Lymphoproliferative
- Lung Abscess -Schistosomiasis, - Lymphoma
- Empyema -Amoebic abscess, - Chronic LL
- Bronchiectasis - Malaria Myeloproliferative disease
- Leishmaniasis
Cystic Fibrosis
Malignancy - Myelofibrosis
Interstitial Lung disease
Hepatocellular carcinoma -Chronic ML
- Sarcoidosis
- Fibrosing alveolitis Metastases GI, Lung, breast -Polycythemia vera
- Asbestosis etc. and melanomas -Essential thrombo.
Pulmonary AV fistuala Hematologic Thalassemia
Myeloproliferative Sickle cell
Cardiovascular -Myelofibrosis Vascular congestion
Congenital Cyanotic Heart -CML Cirrhosis
disease Lymphoma Hepatic vein
- Tetralogy of Fallot (ToF) -Hodgkins obstruction
- Coarctation of aorta - Non-Hodgkins Connective Tissue
- Pulmonary stenosis (critical) Leukaemia RA, SLE
-ALL Storage disorders
Subacute Bacterial endocarditis
-AML Gauchers disease
Eisenmengers syndrome
Sickle cell Niemann-Pick disease
Left Atrial myxoma
-Hepatic sequestration Infiltrative
Isolated Toe clubbing -Extramedullary
- PDA with Shunt reversal Amyloidosis
haematopoiesis
- Called Eisenmenger PDA Sarcoidosis
Hepatic congestion
Abdomen Cardiac failure
Causes of Massive Splenomegaly
Liver Cirrhosis Hepatic vein thrombosis
(>8cm)
Neoplasm Storage disorders
Infection
- Colorectal Ca Wilsons
Visceral Leishmaniasis
- Gastric Ca Haemochromatosis
(Kala-azar)
- GI lymphoma Gauchers
Infiltrative Malaria
- Hepatoma Schistosomiasis
Inflammatory BD Sarcoidosis
Amyloidosis Haematologic
- Crohns Disease Myeloproliferative
- Ulcerative colitis Biliary obstruction; e.g. Pancreatic
Ca - CML, Myelofibrosis
Malabsorption Sickle cell
- Celiac disease Fatty Liver (NASH)
Early cirrhosis -Splenic Sequestration in
- Whipples disease the young, HbSC disease
- Cystic Fibrosis Whipples disease
- Intestinal Polyposis
Causes of Pulsatile liver Storage Disorder
Other
Tricuspid regurgitation o Gauchers
Hyperthyroidism
Idiopathic Tropical (Africa
- Particularly Graves
& South-East Asia)
Idiopathic
Causes of Tender Hepatomegaly Causes of Moderate Splenomegaly
Thymoma
Hepatitis (4 -8 cm)
Thalassemia Lymphoproliferative disorders
Rapid liver enlargement
o Rt heart failure Hodgkins disease
o Budd-Chiari Chronic lymphoytic
leukemia,
Syndrome
Cirrhosis with portal hypertension
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 Other Hormonal
Causes of Hepatsplenomealy - Sarcoidosis hypothyroidism
List is essentially the same as exogenous steroids
splenomegaly alone. Common Localized Lynphadenopahy pregnancy
causes include estrogen
- Chronic leukemias Causes of Ascites
- Lymphoproliferative disorders Portal (SAAG > 1.1g/dL)
- Cirrhosis with portal HTN Exudative (Protein > Causes of Jaundice
- Myelofibrosis 2.5g/L) Unconjugated
o Budd-Chiari Prehepatic
Causes of Palpable Kidneys o CCF Hemolytic anemia
Thin individual Transudative (Protein < - Sickle Cell Anemia -
AD Polycystic kidney disease - Hereditary Spherocytosis
2.5g/dL)
Maligancy o Cirrhosis - Hereditary Elliptocytosis
- Renal Cell Cancer Gilberts syndome
o Hepatic failure
- Wilms Tumour Hematoma resorption
Non-Portal (SAAG < 1.1g/dL)
(Nephroblastoma)
Exudative (Protein >
Hydronephrosis (Can be Conjugated
2.5g/dL)
bilateral rarely) Hepatic
o Intra-abdominal
Renal Cyst / Abscess Viral Hepatits A B, C
Amyloidosis (Can be bilateral malignancy Leptospirosis
o Intra-abdominal
rarely) Hepatic Abscess
Hypertrophy of a single infection e.g. Tb Post Hepatic
o Pancreatitis Choledocholithiasis
functioning kidney
Transudative (Protein < Ascending Cholangitis
Nephropathy
o HIV 2.5g/dL) Sclerosing cholangitis
o Sickle cell o Nephrotic Pancreatits
o Diabetes Syndrome Cancer at head of Pancreas or
o Protein-losing Ampule
Iliac Fossa enteropathy Methastatic cancer
Renal Transplant (May have o Severe Foreign body in CBD eg. worm
cushinoid features 2nd to steroids malnutrition with
anasarca Causes of Tachpnea/SOB
Generalized Lymphadenopathy Cardiovascular
Infection Causes of Local Edema acute MI
Viral inflammation /infection CHF/LV failure
-HIV, Ebstein Barr virus, venous or lymphatic obstruction aortic stenosis
CMV, Measles, Mumps, thrombophlebitis mitral stenosis
Rubella, Viral Hepatitis, chronic lymphangitis elevated pulmonary venous
Bacterial pressure
resection of regional lymph
- IE, Tb, Syphilis
nodes
Fungal Respiratory
filariasis
- Histoplasmosis Airway disease
Protozoal asthma
Some Causes of Generalized Edema
-Toxoplasmosis, COPD exacerbation
Increased hydrostatic pressure
- Filariasis upper airway obstruction
Increased fluid retention
- Leishmaniasis (foreign body, mucus
Malignancy Cardiac causes e.g. CHF
Hepatic causes e.g. plugging, anaphylaxis)
o Leukaemia Parenchymal lung disease
cirrhosis
-ALL, CLL ARDS
o Lymphoma Renal causes e.g. acute
and pneumonia
-Hodgkins, Non-Hodgkins interstitial lung disease
Metastatic Solid Tumour chronic renal failure
Vasodilators (especially CCBs) Pulmonary vascular dis.
Connective Tissue Disease
Refeeding edema PE
RA, SLE
pulmonary HTN
Drugs
Decreased oncotic pressure pulmonary vasculitis
- Phenytoin, hydrallazine,
Hypoalbuminemia Pleural disease
- allopurinol
2
 pneumothorax Miscellaneous facial/upper extremity edema
pleural effusion Impaired coagulation (SVC compression)
Pulmonary endometriosis paraneoplastic syndromes (e.g.
Neuromuscular and chest wall disorders myasthenia gravis (thymomas))
C-spine injury Mediastinal Mass
polymyositis, myasthenia gravis,
Guillain-Barri syndrome Investigations
kyphoscoliosis Etiology and Pathophysiology
CXR (compare to previous)
Anxiety/psychosomatic diagnosis is made by location CT with contrast (provides
Severe anemia and patients age information regarding anatomic
anterior compartment location, density, relation to
Causes of Cough (sternum to anterior border of mediastinal vascular structures)
Airway Irritants pericardium) - more likely to be MRI specifically indicated
Inhaled smoke, dusts, fumes malignant in the evaluation of neurogenic
Aspiration astric contents o 5 Ts Thymoma tumours
(GERD) Thyroid enlargement ultrasound (best for assessment
Oral secretion (goiter) of structures in close proximity
Foreign body Teratoma to the heart and pericardium)
Postnasal drip Thoracic aortic radionuclide scanning 131I
Airway Disease aneurysm (for thyroid), Gallium (for
URTI including postnasal drip Tumours (lymphoma, lymphoma)
and sinusitis parathyroid, biochemical studies thyroid
Acute or chronic bronchitis esophageal, function, serum calcium,
Bronchiectasis angiomatous) phosphate, parathyroid
Neoplasm o lymphoma, lipoma, hormones, AFP, beta-hCG
External compression by node pericardial cyst biopsy (mediastinoscopy,
or mass lesion middle compartment (anterior percutaneous needle aspiration)
Asthma to posterior pericardium)
COPD o pericardial cyst, Management
Parenchymal Disease bronchogenic
Pneumonia cyst/tumour,
depends on the diagnosis
Lung abscess lymphoma, lymph
decide if the lesion should be
node enlargement,
Interstitial lung disease excised (most isolated benign
aortic aneurysm
CHF masses should be removed)
posterior compartment
Drug-induced (e.g. ACE inhibitor) needle aspiration of suspected
(posterior pericardium to
benign cystic lesion
vertebral column)
Differentials of Hemoptysis resection via minimally
o neurogenic tumours,
Airway Disease invasive video assisted
meningocele, enteric
Acute or chronic bronchitis procedures (bronchogenic
cysts, lymphomas,
Bronchiectasis cysts, localized neurogenic
diaphragmatic hernias,
Bronchogenic CA tumours)
esophageal tumour,
Bronchial carcinoid tumour exploration via sternotomy or
aortic aneurysm
Parenchymal Disease thoracotomy
Pneumonia diagnostic biopsy rather than
TB major operation if mass is
Lung abscess likely to be a lymphoma, germ
Miscellaneous: Signs and Symptoms cell tumour, or unresectable
Goodpastures syndrome invasive malignancy
Idiopathic pulmonary 50% asymptomatic (most of post-op
hemosiderosis these are benign); when radiotherapy/chemotherapy if
Vascular Disease symptomatic, 50% are malignant
PE malignant
Elevated pulmonary venous chest pain, cough, dyspnea, Bronchogenic Cancer
pressure: recurrent respiratory infections
LVF hoarseness, dysphagia, Pathological Classification
Mitral stenosis Horners syndrome,
Vascular malformation

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 bronchogenic cancer (90% of lung, hilum, mediastinum, o biopsy: bronchoscopy,
primary lung cancers) (for pleura: pleural effusion, percutaneous,
characteristics, see Table 24 atelectasis, wheezing mediastinoscopy
below) pericardium: pericarditis, staging work-up
o classified into small pericardial tamponade o blood work: LFTs,
cell lung cancer esophageal compression: calcium, ALP
(SCLC) and non- dysphagia o imaging: CXR, CT
SCLC (NSCLC i.e. phrenic nerve: paralyzed thorax and abdomen,
adenocarcinoma, diaphragm bone scan,
squamous cell, large recurrent laryngeal nerve: neuroimaging
cell), hoarseness o invasive:
bronchioalvelolar superior vena cava syndrome: bronchoscopy,
cancer (BAC) obstruction of SVC causing mediastinoscopy,
o incidence of neck and facial swelling, as mediastinotomy,
adenocarcinoma is well as dyspnea and cough thoracotomy
increasing o other symptoms
lymphoma associated with SVC Therapy for Bronchogenic
secondary metastases: breast, compression: Cancer
colon, prostate, kidney, thyroid, hoarseness, tongue
stomach, cervix, rectum, testes, swelling, epistaxis, chemotherapy (no role for
bone, melanoma and hemoptysis chemo alone, only in
o physical findings combination with other
Risk Factors include dilated neck treatments)
veins, increased o cisplatin and etoposide
cigarette smoking: 85% of lung number of collateral o paclitaxel, vinorelbine,
cancer related to smoking veins covering the
and gemcitabine are
asbestos 5x increased risk, anterior chest wall,
new NSCLC therapies
asbestos + smoker 80-90x cyanosis, edema of the
o new biologics, e.g.
increased risk face, arms, and chest,
epidermal growth
radiation: radon, uranium Pembertons sign
factor inhibitor
(especially if smoker) o milder symptoms if
(Gefitinib)
arsenic, chromium, nickel obstruction is above
o complications:
the azygos vein
genetic damage acute: tumour
lung apex (Pancoast tumour):
parenchymal scarring: lysis
Horners syndrome, brachial
granulomatous disease, fibrosis, syndrome,
plexus palsy, most commonly
scleroderma infection,
C8 and T1 nerve roots
passive exposure to cigarette bleeding,
rib and vertebrae: erosion myelosuppres
smoke
distant metastasis to brain, sion,
air pollution: exact role is
bone, liver, adrenals hemorrhagic
uncertain
paraneoplastic syndromes cystitis
HIV
o a group of disorders (cyclophosph
associated with amide),
Signs and Symptoms malignant disease, not cardiotoxicity
related to the physical (doxorubicin)
cough (75%); beware of effects of the tumour , renal
chronic cough that changes in itself toxicity
character o most often associated (cisplatin),
dyspnea (60%) with SCLC peripheral
chest pain (45%) neuropathy
hemoptysis (35%) Investigations (vincristine)
other pain (25%) chronic:
clubbing (21%) initial diagnosis neurologic
constitutional signs: anorexia, o imaging: CXR, CT damage,
weight loss, fever, anemia chest + upper leukemia,
abdomen, PET scan, second
Presentation by Location of bone scan primary
Tumour Extension o cytology: sputum neoplasms

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 radiotherapy cirrhosis o chylothorax: occurs
surgery nephrotic syndrome when the thoracic duct
o only chance for cure is pulmonary embolism (may is disrupted and chyle
resection when tumour cause transudative or exudative accumulates in the
is still localized effusion) pleural space, due to
o contraindications if peritoneal dialysis, trauma, tumour
any evidence of local hypothyroidism, CF, o hemothorax: due to
extension or urinothorax rupture of a blood
metastases vessel, commonly by
patients with Exudative Pleural Effusions trauma or tumours
surgically other
resectable o pneumothorax
Pathophysiology: increased
disease must permeability of pleural capillaries or (spontaneous,
undergo medi lymphatic dysfunction traumatic, tension)
astinal node o pleural thickening
sampling (chronic infection,
since CT etiology
neoplasm,
thorax is not inflammatory)
accurate infectious
in 20-40% of o parapneumonic Appearance of Fluid
cases effusion (associated
poor with bacterial
Bloody - trauma, malignancy
pulmonary pneumonia, lung
White - chylothorax, empyema
status (i.e. abscess
Black - aspergillosis, amoebic liver
unable to o empyema (bacterial,
abscess
tolerate fungal, TB), TB
Yellow-green - rheumatoid pleurisy
resection of pleuritis, viral
Viscous - malignant mesothelioma
lung) infection
Ammonia odour - urinothorax
palliative care for end-stage
Food particles - esophageal rupture
disease malignancy
Analysis of Pleural Effusion
o lung carcinoma (35%) Protein, LDH - transudate vs.
o lymphoma (10%) exudate
Pleural Effusion o metastases: breast Gram stain, Ziehl-Nielsen stain
Light's criteria - a pleural effusion is
(25%), ovary, kidney (TB), culture - looking for
likely exudative if at least one of the
mesothelioma specific organisms
following exists:
vascular/cardiac Cell count differential -
1. The ratio of pleural fluid
o collagen vascular neutrophils vs. lymphocytes
protein to serum protein is
greater than 0.5 diseases: RA, SLE (lymphocytic TB, lymphoma)
2. The ratio of pleural fluid LDH o pulmonary embolism, Cytology - malignancy,
and serum LDH is greater than after coronary artery infection
0.6 bypass surgery Glucose (low) RA, TB,
3. Pleural fluid LDH is greater intra-abdominal empyema, malignancy,
than 2/3 times the normal upper o subphrenic abscess esophageal rupture
limit for serum o esophageal perforation Rheumatoid factor, ANA,
(elevated pleural fluid complement - collagen
Transudative Pleural Effusions amylase) vascular disease
Pathophysiology: alteration of o pancreatic disease Amylase - pancreatitis,
systemic factors that affect the (elevated pleural fluid esophageal perforation,
formation and absorption of pleural amylase) malignancy
fluid (i.e. increased capillary o Meigs syndrome pH - empyema <7.2, TB and
hydrostatic pressure, decreased (ascites and mesothelioma <7.3
plasma oncotic pressure) hydrothorax Blood - mostly traumatic,
associated with an malignancy, PE with infusion,
ovarian fibroma or TB
etiology
other pelvic tumour Triglycerides - chylothorax
trauma from thoracic duct leakage,
congestive heart failure

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 mostly due to trauma, lung CA,
or lymphoma
Signs and Symptoms
dyspnea: varies with size of
effusion and underlying lung
function
pleuritic chest pain
often asymptomatic
inspection: trachea deviates
away from effusion, ipsilateral
decreased expansion
percussion: decreased tactile
fremitus, dullness
auscultation: decreased breath
sounds, bronchial breathing and
egophony at upper level,
pleural friction rub
Investigations
CXR
o must have >250 ml of
pleural fluid for
visualization
o lateral: small effusion
leads to blunting of
posterior costophrenic
angle
o PA: blunting of lateral
costophrenic angle
o dense opacification of
lung fields with
concave meniscus
o decubitus: fluid will
shift unless it is
loculated
o supine: fluid will
appear as general
haziness
thoracentesis: indicated if
pleural effusion is a new
finding
o risk of re-expansion
pulmonary edema if 2
L of fluid is removed
o inspect for colour,
character, and odour of
fluid
o analyze fluid
pleural biopsy: indicated if
suspect TB, mesothelioma, or
other malignancy (and if
cytology negative)
U/S: detects small effusions
and can guide thoracentesis
treatment depends on cause,
drainage if symptomatic
CT can be helpful in
differentiating parenchymal
from pleural abnormalities
Treatment
thoracentesis
treat underlying cause
Obstructive Lung Disease
Characterized by obstructed
airflow, decreased (decreased
FEV1 ) flow rates (most marked
during expiration), air trapping
(increased RV/TLC), and
hyperinflation (increased FRC,
TLC)
Differential diagnosis includes
asthma, chronic obstructive
pulmonary disease (COPD),
cystic fibrosis (CF), and
bronchiectasis
Flow rate
FEV1 - decreased
FVC - decreased
FEV1/FVC - decreased
FEF25-75 - decreased
Lung Volumes
TLC - decreased
FRC - decreased
VC - decreased
RV - decreased
RV/TLC - N
Restrictive Lung Disease
Characterized by decreased
lung compliance and lung
volumes
Differential diagnosis includes
interstitial lung disease,
neuromuscular disease, chest
wall disease, pleural disease,
and parenchymal disease
(pulmonary fibrosis)
Flow rate
FEV1 - decreased or N
FVC - decreased
FEV1/FVC - increased or N
FEF25-75 - increased or N
Lung Volumes
6
TLC - decreased
FRC - decreased
VC - decreased
RV - decreased
RV/TLC - N
Asthma Controlled?
daytime symptoms <4 days/wk
no asthma-related absence from
work/school
night-time symptoms, <1
night/wk
beta-2 agonist use <4 times/wk
normal physical activity
FEV1 or PEF >90% of personal
best
mild, infrequent exacerbations
PEF diurnal variation <10-15%
Risk Factors for Poor Asthma
Control
Previous Non-Fatal Episodes
night time symptoms >1
night/week
frequent ER visits
ICU admission
prior intubation
Omnious Features
use of beta2 agonists >3
times/day
loss of consciousness
during asthma attack
silent chest
FEV1 or PEF (peak
expiratory flow) <60%
limited activities of daily
living
Asthma Signs and Symptoms
tachypnea,
wheezing,
chest tightness,
cough (especially nocturnal),
sputum production
Red Flags in Asthma
fatigue
silent chest
diminished expiratory effort
Decreased LOC
silent chest
Respiratory Distress in Asthma
inability to speak
nasal flaring,
 tracheal tug
cyanosis
accessory muscle use,
intercostal indrawing
pulsus paradoxus
Ventolin (Salbutomo) in Asthma
Adult
2.5-5 mg via hand-held nebulizer or
metered-dose inhaler (MDI) with
spacer (holding chamber) q20min
for 3 doses, then 2.5-10 mg q1-4h
prn; dilute 2.5 mg in 3-4 mL of
saline or use premixed nebules
Pediatric
0.15 mg/kg (minimum dose 2.5
mg) via hand-held nebulizer or
using a metered-dose inhaler (MDI)
with spacer (holding chamber)
q20min for 3 doses, then 0.15-0.3
mg/kg up to 10 mg q1-4h prn
Atrovent (Ipratropium) in Asthma
Adult
Nebulizer: 0.5 mg q20min for 3
doses then prn
MDI: 8 puffs q20min prn up to 3 h
Pediatric
Nebulizer: 0.25-5 mg q20min for 3
doses, then prn
MDI: 4-8 puffs q20min up to 3 h
Emphysema (Pink Puffer)
Symptoms
dyspnea ( exertion)
minimal cough
tachypnea
decreased exercise tolerance
Signs
pink skin
pursed-lip breathing
accessory muscle use
cachectic appearance due to
anorexia + increased work of
breathing
hyperinflation/barrel chest,
hyperresonant percusion
decreased breath sounds
decreased diaphragmatic
excursion
Investigations
PFT:
decreased FEV1, decreased
FEV1/FVC
increased lung volume
decreased DCO
CXR:
increased AP diameter
flat hemidiaphragm (on
lateral CXR)
decreased heart shadow
increased retrosternal space
bullae
decreased peripheral
vascular markings
Bronchitis (Blue Bloater)
Symptoms
chronic productive cough
purulent sputum
hemoptysis
Signs
mild dyspnea initially
cyanotic (2o to hypoxemia and
hypercapnia)
peripheral edema from RVF (cor
pulmonale)
crackles, wheezes
prolonged expiration if
obstructive
frequently obese
Investigations
PFT: decreased FEV1, decreased
FEV1/FVC, N TLC,
increased or N DCO
CXR: AP diameter normal
increased bronchovascular
markings enlarged heart
with cor pulmonale
Treatment of Stable COPD
Prolong survival
Smoking cessation: nicotine
replacement
vaccination: influenza
prophylaxis, pneumovax
home oxygen: to prevent cor
pulmonale and decrease
mortality if used >15 hrs/day -->
indications: PaO2 <55 mmHg;
O2 saturation <89% consistently
Symptomatic relief
Bronchodilators: mainstay of
current drug therapy, used in
combination
Anticholinergics (e.g.
ipratropium bromide,
tiotropium bromide)
Short acting beta2-agonists
(e.g. salbutamol, terbutaline)
7
Long acting beta2-agonists
(e.g. salmeterol, formoterol)
may delay hospitalization
Theophylline increases
collateral ventilation,
mucociliary clearance, and may
reduce airway inflammation;
used as 4th line
Side effects include:
nervous tremor, nausea
/vomiting/diarrhea,
tachycardia, arrhythmias,
sleep changes, headache,
gastric acid, toxicity
Corticosteroids
chronic treatment of COPD
with systemic glucocorticoids
should be avoided
COPD airways are usually
inflamed, but not generally
responsive to steroids
inhaled steroids used in
spirometric responsive
symptomatic patients. Trial of 6
wks to 3 months. If FEV1
improves 20%, inhaled steroids
can be used in the long term.
However, long term benefits
have yet to be determined.
Consider use in patients with
FEV1 <35% (GOLD
guidelines)
surgical treatment
lung reduction surgery:
bullectomy of emphysematous
parts of lung to improve
ventilatory function, associated
with higher mortality in certain
risk groups (FEV1 <20%)
o lung transplant
Others
patient education, eliminate
respiratory irritants/allergens
(occupational/environmental),
exercise rehabilitation to
improve physical endurance
Causes of interstitial Lung
Disease
Upper Lung Disease
Farmer's lung
Ankylosing spondylitis
Sarcoidosis
 Silicosis
Neurofibromatosis
TB (miliary)
Eosinophilic granuloma
(histiocytosis)
Lower Lung Disease
Bronchiolitis obliterans with
organizing pneumonia (BOOP)
Asbestosis
Drugs (nitrofurantoin,
hydralazine, INH, amiodarone,
many chemo drugs)
Aspiration
Scleroderma
Hamman Rich (interstitial
pulmonary fibrosis)
Rheumatologic disease
Signs and Symptoms
SOB, especially on exertion
dry crackles
dry cough
cyanosis
clubbing (only in IPF and
asbestosis)
features of cor pulmonale
note that signs and symptoms
vary with underlying disease
process
Investigations
CXR/high resolution CT
o decreased lung
volumes, reticular,
nodular, or
reticulonodular pattern
(nodular <3 mm),
Kerley B lines,
hilar/mediastinal
adenopathy
o diffuse ground-glass
appearance early in
disease progresses to
honey-combing late in
disease
o DDx: pulmonary
fibrosis, interstitial
pulmonary edema
(CHF), PCP, TB
(miliary), sarcoidosis,
pneumoconiosis,
lymphangitic
carcinomatosis
o DDx of cystic lesions:
end-stage emphysema,
PCP, histiocytosis X, Respiratory centre stimulation
lymphangiomyomatosi CNS disorders
s hepatic failure
PFTs Gram-negative sepsis
o restrictive pattern: drugs (ASA, progesterone,
decreased lung theophylline, catecholamines,
volumes (VC and psychotropics)
TLC) and compliance pregnancy
o normal or increased anxiety
FEV1/FVC (>70- pain
80%), i.e. flow rates mechanical hyperventilation
are actually normal or (excessive mechanical
supernormal when ventilation)
corrected for absolute
lung volume DIFFERENTIAL DIAGNOSIS OF
o DCO decreased due to RESPIRATORY ACIDOSIS
less surface area for Characterized by increased PaCO2
gas exchange secondary to hypoventilation
pulmonary vascular
disease respiratory centre depression
ABGs (decreased RR)
o initially may be drugs (anesthesia, sedatives,
normal narcotics)
o with progression of trauma
disease, hypoxemia increased ICP
and decreased PaCO2 encephalitis
may be present stroke
Other central apnea
o bronchoscopy, supplemental O2 in chronic
bronchoalveolar CO2 retainers (i.e. COPD)
lavage, lung biopsy Neuromuscular disorders (decreased
o c-ANCA (Wegners), TV)
anti-GBM myasthenia gravis
(Goodpastures), ESR, Guillain-Barr syndrome
ANA (lupus), RF poliomyelitis
(RA), serum- muscular dystrophies
precipitating
ALS
antibodies to inhaled
myopathies
organic antigens
(hypersensitivity chest wall disease (obesity,
kyphoscoliosis)
pneumonitis)
Airway obstruction (asthma, foreign
body) (decreased FEV)
Parenchymal disease
COPD
pulmonary edema
pneumothorax
pneumonia
DIFFERENTIAL DIAGNOSIS OF pneumoconiosis
RESPIRATORY ALKALOSIS acute respiratory distress
Characterized by decreased PaCO2 syndrome (ARDS)
secondary to hyperventilation Mechanical hypoventilation
(inadequate mechanical ventilation)
Hypoxemia
pulmonary disease (pneumonia, Anion Gap Metabolic Acidosis
edema, PE, interstitial fibrosis) MUDPILES
severe anemia Methanol
heart failure Uremia
high altitude Diabetic ketoacidosis
8
Paraldehyde
Isopropyl alcohol / Iron / INH
Lactic acidosis
Ethylene glycol
Salicylates
Causes of Non-Anion Gap
Metabolic Acidosis: HARDUP
Hyperalimentation
Acetazolamide
RTA
Diarrhea
Ureteroenteric fistula
Pancreaticoduodenal fistula
Metabolic Alkalosis
Requires initiating event and
maintenance factors
Initiating event
GI (vomiting, NG) or renal loss
of H
exogenous alkali (oral or
parenteral administration), milk
alkali syndrome
diuretics (contraction
alkalosis): decreased excretion
of HCO3, decreased ECF
volume, therefore increased
[ HCO3]
posthypercapnia: renal
compensation for respiratory
acidosis is HCO3 retention,
rapid correction of respiratory
disorder results in transient
excess of HCO3
Maintenance factors
volume depletion: increased
proximal reabsorption of
NaHCO3 and increased
aldosterone
hyperaldosteronism (1o or 2o):
distal Na reabsorption in
exchange for K and H excretion
leads to HCO3 generation,
aldosterone also promotes
hypokalemia
hypokalemia: transcellular K/H
exchange, stimulus for
ammoniagenesis and HCO3
generation
Approach to Acid-Base Status
1. What is the pH acidemic (pH Cardiac
<7.35), alkalemic (pH >7.45), or arrhythmias (PAB, PVB, SVT,
normal (pH 7.35-7.45) VT)
mitral valve prolapse
2. What is the primary disturbance? valvular heart disease
hypertrophic cardiomyopathy
Endocrine
metabolic: change in HCO3 and
pH in same direction thyrotoxicosis
pheochromocytoma
respiratory: change in HCO3
and pH in opposite direction hypoglycemia
Systemic
fever
3. Has there been appropriate
compensation? (Table 7 below) anemia
Drugs
tobacco,
metabolic compensation occurs
caffeine,
over 2-3 days reflecting altered
alcohol,
renal HCO3
epinephrine,
production/excretion
ephedrine,
respiratory compensation
through ventilation control of aminophylline, atropine
PaCO2 occurs immediately Psychiatric
panic attack
inadequate compensation may
indicate a second acid-base
Causes of Bradycardia
disorder
Physiologic
4. If there is metabolic acidosis, Athlete
what is the anion gap and osmolar Elderly
gap? Pathologic
Heart block
Hypothermia
anion gap = [Na] - [Cl] -
[ HCO3]; normal = 10-15 Hypothyroidism
mmol/L Sick sinus syndrome
osmolar gap = measured Raised intracranial
osmolarity calculated pressure
osmolarity = measured Drugs
(2[Na] + glucose + urea); -blockers
normal = 10 Ca2+-channel blockers
(Verapamil, Diltiazem)
5. If anion gap is increased, is the Digoxin toxicity
change in bicarbonate the same as
the change in anion gap?
Differentials of Chest Pain
*can be fatal acutely
if not, consider a mixed picture Pulmonary
pneumonia
Ventilatory Failure pulmonary embolism (PE)*
Wont Breathe pneumothorax/hemothorax*
respiratory centre depression empyema
hypothyroid pulmonary neoplasm
sleep apnea bronchiectasis
Cant Breathe TB
neuromuscular disorders Cardiac
airway obstruction
MI/angina*
parenchymal disease
myocarditis
pericarditis/Dresslers
syndrome*
Causes of Tachcardia/Palpitations cardiac tamponade*
9
Gastrointestinal
esophageal: spasm, GERD,
esophagitis, ulceration,
achalasia, neoplasm
PUD
gastritis
pancreatitis
biliary colic
Mediastinal
lymphoma
thymoma
Vascular
dissecting aortic aneurysm
Surface structures
costochondritis
rib fracture
skin (bruising, shingles)
breast
Risk Factors for Atherosclerosis
Major
smoking
family history (FHx) of MI
(first degree male relative <55
or first degree female relative
<60)
diabetes mellitus (DM)
hypertension (HTN
Minor
hyperlipidemia
obesity
male,
postmenopausal female
sedentary lifestyle
hyperhomocysteinemia
Sym. & Signs of Left Heart Failure
dyspnea, orthopnea, PND peripheral
fatigue , syncope, systemic
hypotension, cool extremities
slow capillary refill, peripheral
cyanosis, pulsus alternans
mitral regurgitation, S3
edema, cough and crackles
Sym. & Signs of Left Heart Failure
Right heart failure can mimic most
of the symptoms of forward left
heart failure if decreased RV output
leads to LV underfilling).
Elevated JVP with Abdinal JR and
Kussmauls sign, hepatomegaly
tricuspid regurgitation, S3 (right-
sided),pulsatile liver
Complicatons of MI
ACT RAPID Apex beat (location & character)
Arrhythmias (SVT, VT, VF) Tapping Palpable S1 (Think MS)
Congestive cardiac failure Thrusting LV Hypertrophy
Thromboembolic disorders eg. Displaced Dilatation from volume
stroke, (DVT, PE later on) overload eg. AR, MR R to L shunt
Rupture (ventricle - Tampanade, or Cardiomyopathy
septum - VSD, papillary muscle - Impalpable Obesity, effusion and
Regurgitation) Hyperinflation
Aneurysm (ventricle)
Pericarditis Palpable P2
Infaction (a second one) Pulmonary hypertension
Death/ Dressler's syndrome
Shock Features of First heart sound
Loud: mitral stenosis,
Precipitants of Heart Failure Soft: mitral incompetence
HTN (common)
Endocarditis/environment (e.g. heat Features of Second heart sound
wave)
Anemia Soft: Aortic or pulmonary stenosis
Rheumatic heart disease and other Loud: Systemic (A2) or P. HTN
valvular disease (P2)
Thyrotoxicosis Wide Fixed split: ASD
Failure to take meds (very common) Paradoxical Fixed Split: Delayed
Arrhythmia (common)
LV or early RV emptying
Infection/ischemia/infarction (common)
Lung problems (PE, pneumonia,
COPD)
Endocrine (pheochromocytoma,
Causes of Mitral regurgitation
hyperaldosteronism)
Dietary indiscretions (common) Ring
Dilated cardiomyopathy
Hypertensive heart disease
Cause Irregularly irregular pulse
Ischemic cardiomyopathy
Atrial Fibrillation Leaflet
Rheumatic mitral disease Mitral valve prolapse
(esp Mitral Stenosis) RHD
Aortic Stenosis IE
HTN Chordae
Thyrotoxicosis rupture
Ischemic heart disease Papillary muscle
Drugs Ischemia / rupture
o Alcohol Connective tissue disease
CCF, Cardiomyopathy Marfans syndome
Atrial Flutter
Mitral Regurge
Causes of Collapsing Pulse
Fever
Anemia
Thyrotoxicosis
Aortic regurgitation
Pregnancy Etiology
Exercise Annulus LV dilatation/
aneurysm (CHF, DCM,
Left Parasternal Heave
L Atrial enlargement (2nd to severe myocarditis), IE abscess, MV
annulus calcification
MR)
RV Enlargement w/ Pulmon. HTN Leaflets - Congenital cleft
Severe LV Enlargement leaflets, myxomatous
degeneration (MVP, Marfans
syndrome), RHD, collagen VD
10
 Chordae: acute MI,
myxomatous degeneration,
Trauma/tear, IE
Papillary muscle/LV Wall:
infarction/ischemia/rupture,
aneurysm, HOCM
Pathophysiology
Reduced CO => increased LV &
LA pressure => LV & LA
dilatation => CHF & pulmonary
HTN
Symptoms
Dyspnea, PND, orthopnea,
palpitations, peripheral edema
Physical Exam
Displaced, hyperdynamic apex
(LV dilataton), +/- left
parasternal lift (LAE with MR),
apical thrill
Auscultation: holosystolic
murmur at apex, radiating to
axilla (also sometimes to base
or back if jet is directed
posteriorly) +/- mid-diastolic
rumble (often no MS), S1
normal or soft, loud S2 (if
pulmonary HTN), S3 usually
present.
Severity gauged by LVD, S3,
diastolic flow rumble.
Investigations
ECG: LAE, left atrial delay
(bifid P waves), +/- LVH
CXR: LVH, LAE, pulmonary
venous HTN
Echo: severity of MR, (LV
function - EF, LA/LV),
(leaflets flail, vegetations
etc.)
Card. Cath: Assess coronaries,
assess flow and contours in
LA, Prominent LA V
wave on Swan-Ganz
Treatment
Asymptomatic: serial Echos, IE
prophylaxis.
Symptomatic: decrease preload
(diuretics)and decrease afterload
(ACEIs) for severe MR & poor
surgical candidate; stabilize
acute MR with vasodilators b/f
surgery
Surgery if: acute MR with CHF,
papillary muscle rupture, NYHA
class III-IV CHF, AFib, LVEF
<60%, increasing LV size,
earlier surgery if valve
repairable
Surgical Options
Valve repair: >75% of pts with
MR & myxomatous MV disease
(MVP). Annuloplasty rings,
leaflet repair, chordae
transfers/shorten/replacement
Valve replacement: failure of
repair, heavily calcified annulus
Advantage of Repair: low rate of
endocarditis, no anticoagulation,
less chance of re-operation
Causes of Aortic Incompetence
Ring
Left ventricular dilatation
HTN
Valve
RHD
IE
Bicuspid aortic valve
Root
Marfans
Syphilitic Aortitis
Aortic dissection
Takayasus aortitis
Ankylosing spondylitis,
seronegative arthritides
RA, SLE
Trauma
Aortic Incompetence
Etiology
Supravalvular:
Aortic root disease (Marfans,
atherosclerosis & dissecting
aneurysm, connective tissue
disease)
Valvular:
Congenital (bicuspid AV, large
VSD), IE
11
Acute Onset: IE, aortic dissection,
trauma, failed prosthetic valve
Pathophysiology
Volume overload => LV
dilatation => increased SV, high
sBP & low dBP => increased
wall tension => pressure
overload => LVH (low dBP =>
decreased coronary perfusion)
Symptoms
(Usually only becomes
symptomatic late in disease
when LV failure develops)
Dyspnea, orthopnea, PND,
syncope, angina.
Physical Exam
Waterhammer pulse, bisferiens
pulse, Difference in femoral-
brachial systolic BP > 20 (Hills
test wide pulse pressure)
hyperdynamic apex, displaced
PMI, heaving apex
Auscultation: early
decrescendo diastolic murmur
at LLSB (cusp See this more
due to RHD) or RLSB (aortic
root), best heard sitting,
leaning forward, on full
expiration. Soft S1, absent S2,
S3 (late)
Investigations
ECG: LVH, LAE
CXR: LVH, LAE, aortic root
dilatation
Echo/TTE: Gold standard.
Quantify AR, leaflet or aortic
root anomalies. Visualize
regurge into LV.
Radionuclide scan: Sensitive to
decreased LV function (EF
doesnt increase w/ exercise
Cath: if >40 yrs and surgical
candidate - to assess for
ischemic heart disease
Exercise testing: hypotension
with exercise
Treatment
Asymptomatic: serial Echos,
afterload reduction (ACEIs if
normal LV function)
Symptomatic: avoid exertion,
treat CHF
Surgery if: NYHA class III-IV
 CHF, LVEF < 50% with/without
symptoms, increasing LV size
Surgical Options
Valve replacement:Most Cases.
Valve types include mechanical,
bioprosthetic, homograph and
sometimes pulmonary autograph
Valve repair: limited role. repair
of valves to improve coaptation
Aortic root replace (Bentall
proced.):when ascending aortic
aneurysm present, valved
conduit used
Other Signs in Aortic Regurge
Large-volume, 'collapsing' pulse
also known as:
Watson's water hammer pulse
Corrigan's pulse (rapid upstroke
and collapse of the carotid artery
pulse) low diastolic and
increased pulse pressure
de Musset's sign (head nodding in
time with the heart beat)
Quincke's sign (pulsation of the
capillary bed in the nail)
Traube's sign (systolic and diastolic
murmurs described as 'pistol shots'
heard over the femoral artery when
it is gradually compressed)
Duroziez's sign (a double sound
heard over the femoral artery when
it is compressed distally)
Mller's sign (pulsations of uvula)
Austin Flint murmur, a soft mid-
diastolic rumble heard at the apical
area. It appears when regurgitant jet
from the severe aortic insufficiency
renders partial closure of the
anterior mitral leaflet.
Mitral Stenosis
Etiology
Rheumatic disease most
common cause; Lung carcinoid,
Mitral annular calcification,
Lupus. Congenital rarely
Pathophysiology
MS => fixed CO & Left atiral
enlargement => increased LA
pressure => pulmonary vascular
resistance & CHF; worse with
Afib (no atrial kick), tachycardia
(decreased atrial emptying time)
& pregnancy (increased
preload)
Symptoms
SOBOE, orthopnea, fatigue,
palpitations, peripheral edema,
malar flush (Pulm. Htn), pinched
and blue facies (severe MS).
Hemoptysis (late). If TR or RVF
then hepatic enlargement/pulsatility,
ascites, peripheral edema.
Physical Exam
Irregular pulse if AFib ( no A
wave on JVP), left parasternal
lift, palpable diastolic thrill at
apex (tapping apex not
displaced)
Auscultation: mid-diastolic
rumble at apex, best with bell
in LLD position following
exertion, No radiation. Loud S1
(valves not pliable), OS
following loud P2 (heard best
during expiration). Crackles. If
pulm. Htn present look for
loud /palpable P2, Pulmonary
Regurge (Graham Steell
murmur). It may also be
associated with MR and TR.
Long murmur & short A2-
Opening snap interval correlate
with worse MS
Investigations
ECG: Normal S rhythm/AFib,
LAE (P mitrale), RVH,
RAD
CXR: L atrial enlargement (LA
appendage, double
contour, carina splaying)
Pulmonary Congestion
(Kerley B lines), MV
calcification, Flattened
left heart border.
Echo/TTE: Thickened calcified
valve, fused leaflets, LAE,
12
PAP, TR
Cath: concurrent CAD if >40
yrs (male) or >50 yrs (female)
Treatment
Avoid exertion, fever (increased
LA pressure), treat AFib (rate
control, cardioversion) and CHF,
increase diastolic filling time
(beta-blockers, digitalis). IE
prophylaxis? Anticoagulation
previous embolus.
Surgery if: NYHA class III-IV
CHF, failure of medical therapy
(usually MVA <1.2 cm2),
Worstening P Htn, systemic
embolization, IE, severe life
style limitations
Surgical Options
Percutaneous balloon
valvuloplasty: young rheumatic
pts & good leaflet morphology,
asymptom pts with mod-sev
MS, new-onset AFib, pulmon
HTN
Contraindication: Left atrial
thrombus, mod-sev MR
Open Mitral Commissurotomy:
If mild calcif +leaflet/chordal
thickening. Best if valve
repairable
Open Mitral Commissurotomy:
Rarely done in North A.
Above steps have Restenosis in
50% pts in 8yrs
Valve replacement: immobile
leaflets/mod-sev calcification &
severe scarred leaflets, MR
Aortic stenosis
Causes:
Congenital (bicuspid >
unicuspid valve), calcification
(wear and tear), rheumatic
disease
Pathophysiology
Outflow obstruction =>
increased EDP => concentric
LVH => LV failure =>
 concentric CHF, subendocardial
ischemia
Symptoms
Triad of Exertional angina,
syncope (fixed CO or
arrythmias) and dyspnea. PND,
orthopnea, peripheral edema
Physical Exam
Narrow pulse pressure, brachial-
radial delay, pulsus parvus et
tardus, sustained PMI
Auscultation: crescendo-
decrescendo Systolic ejection
murmur radiating to R
clavicle & carotid (may have
thrill at neck), musical quality at
apex (Gallavardin phenomenon),
thrill in 2nd RICS, S4 (early in
disease), soft S2 w/paradoxical
splitting, S3 (late)
Complications:
Recurrent PE, pulmonary
infections pneumonia and
bronchitis, LA thrombus
(Systemic embolic to kidney,
brain, spleen, arm)
Investigations
ECG: LVH & strain, LBBB,
LAE, AFib
CXR: post-stenotic aortic root
dilatation, calcified valve,
LVH, LAE, CHF (later)
ECHO:
Test of choice. Reduced
valve area (RVA) pressure
gradient (PG), LVH,
reduced LV function
Card Cath:
Rule out CAD before
surgery esp. with cases of
angina. Also in inconclusive
ECHO - PG, RVA
Treatment
Asymptomatic:
Serial Echos, avoid exertion
?IE prophylaxis
Symptomatic: avoid
nitrates/arterial dilators &
ACEIs in severe AS
Surgery if: symptomatic, LV
dysfunction or in moderate AS
when other cardiac surgery is
done
Surgical Options
Valve replacement : Procedure of
choice. aortic rheumatic valve
disease & trileaflet valve
Open/Balloon valvuloplasty:
Repair may be possible in children.
Rarely done in adults Temporizing
in Pregnancy, patient stabilization
or as palliative if people with
comordities.
Tricuspid Regurg
RHD
I.E. (esp in IV drug abuse)
Pulm HTN
Carcinoid syndrome
Rt ventricular failure
Tricuspid Regurge
Etiology
RV dilatation, IE (IV drug use),
rheumatic disease,
congenital (Ebstein anomaly),
carcinoid
Pathophysiology
RV dilatation => TR => further
RV dilatation => right heart
failure
Symptoms
Peripheral edema, fatigue,
palpitations
Physical Exam
Large V waves in JVP (CV,
+ve abdomino jugular reflux,
Kussmauls sign (JVP with
inspiration), holosystolic
murmur at LLSB accentuated by
inspiration, left parasternal lift,
hepatomegaly +/- systolic
pulsations, edema, ascites
Investigations
ECG: RAE, RVH, AFib
CXR: RAE, RV enlargement
Echo: diagnostic
Treatment
13
Preload reduction (diuretics)
Surgery if: usually only if other
surgery needed (e.g. MVR)
Surgical Options
Annuloplasty, i.e. repair (rarely
replacement)
Tricuspid Stenosis
Etiology
Rheumatic disease, congenital,
carcinoid, fibroelastosis; usually
accompanied by MS
Pathophysiology
Increased RA pressure => right
heart failure => decreased CO
and fixed on exertion
Symptoms
Peripheral edema, fatigue,
palpitations
Physical Exam
Prominent A waves in JVP, +ve
abdominojugular reflex,
Kussmauls sign, diastolic
rumble 4th left intercostals
space
Investigations
ECG: RAE
CXR: dilatation of RA without
pulmonary artery enlargement
Echo: diagnostic
Treatment
Preload reduction (diuretics)
Surgery if: usually only if other
surgery needed (e.g. MVR)
Surgical Options:
Commissurotomy
Valve Replace: if severely
diseased valve. Bioprosthesis
preferred
Pulmonary Stenosis

Symptoms
Chest pain, syncope, fatigue,
peripheral edema
Physical Exam
Early diastolic murmur at LLSB,
Etiology Graham Steell (diastolic)
Usually congenital, rheumatic murmur 2nd and 3rd LICS
disease (rare), carcinoid increasing with inspiration
Pathophysiology Investigations
Increased RV pressure => RV ECG: RVH
hypertrophy => right heart CXR: prominent pulmonary
failure arteries if pulmonary HTN;
enlarged RV
Symptoms echo: diagnostic
Chest pain, syncope, fatigue,
peripheral edema Treatment
Rarely requires treatment; valve
Physical Exam replacement if severe
Systolic murmur at 2nd LICS
accentuated by inspiration, Surgical Options
Pulmonary valve replacement
pulmonary ejection click, right-
sided S4
Mitral Valve Prolapse
Investigations Etiology
ECG: RVH Myxomatous degeneration of
CXR: prominent pulmonary chordae; thick, bulky leaflets
arteries enlarged RV that crowd orifice; Marfans
echo: diagnostic syndrome; pectus excavatum,
straight back syndrome, other
Treatment MSK abnormalities; <3% of
Balloon valvuloplasty if severe population, F=M
symptoms
Pathophysiology
Surgical Options MV displaced into LA during
Percutaneous or open balloon systole; no causal mechanisms
valvuloplasty found for symptoms
Pulmonary Regurge Symptoms
Prolonged, stabbing chest pain,
dyspnea, anxiety/panic,
palpitations, fatigue, presyncope
Physical Exam
Ausculation: mid-systolic click
(billowing of mitral leaflet into
LA; tensing of redundant valve
Etiology tissue); mid to late systolic
Pulmonary HTN, IE, rheumatic murmur at apex, accentuated by
disease, tetrology of Fallot, post- Valsalva or squat-to-stand
repair maneuvers
Pathophysiology Investigations
Increased RV volume => ECG: non-specific ST-T wave
increased wall tension => RV changes, PSVT, ventricular
hypertrophy => right heart ectopy
failure
14
Echo: systolic displacement of
thickened MV leaflets into LA
Treatment
Asymptomatic: no treatment;
reassurance
Symptomatic: beta-blockers and
avoidance of stimulants
(caffeine) for significant
palpitations, anticoagulation if
systemic emboli
Surgical Options
None unless symptomatic and
significant MR
Tetralogy of Fallot
10% of all CHD, most common
cyanotic heart defect diagnosed
beyond infancy
Embryologically, a single defect
with hypoplasia of the conus
causing:
VSD, right ventricle (RV) outflow
tract obstruction (RVOTO),
overriding aorta and RVH
degree of RVOTO directly
determines the direction and
degree of shunt and therefore
the extent of clinical cyanosis
and degree of RVH
infants may initially have a
L>R shunt and therefore are not
cyanotic but the RVOTO is
progressive, resulting in
increasing R>L shunting with
hypoxemia and cyanosis
history: hypoxic spells
primary pathophysiology is
hypoxia, leading to increased
pulmonary vascular resistance
(PVR) and decreased systemic
resistance, occurring in
exertional states (e.g. crying,
exercise)
paroxysm of rapid and deep
breathing, irritability and crying
hyperpnea, increasing cyanosis
often leading to deep sleep and
decreased intensity of murmur
(decreased flow across
RVOTO)
peak incidence at 2-4 months of
age
 o if severe may lead to
seizures, loss of
consciousness, death
(rare)
o management: O2,
knee-chest position,
fluid bolus, morphine
sulfate, propanolol
physical exam:
single loud S2 due to severe
pulmonary stenosis (i.e RVOTO)
investigations:
ECG: RAD, RVH
CXR: boot shaped heart (small
PA, RVH), decreased
pulmonary vasculature, right
aortic arch (in 20%)
treatment: surgical repair within
first two years of life, or earlier if
marked cyanosis, spells, or severe
RV outflow tract obstruction
Ventricular Septal Defect (VSD)
most common congenital heart
defect (30-50% of CHD)
Small VSD (majority)
history: asymptomatic, normal
growth and development
physical exam: early systolic to
holosystolic murmur, best
heard at left lower sternal
border (LLSB)
investigations: ECG and CXR
are normal
treatment: most close
spontaneously, do not need
surgical closure even if remains
patent
Moderate-to-large VSD
natural history: secondary
pulmonary hypertension, CHF
by 2 months of age
history: delayed growth and
development, decreased
exercise tolerance, recurrent
URTIs or asthma
episodes, CHF
physical exam: holosystolic
murmur at LLSB with thrill,
mid-diastolic rumble at apex,
size of VSD is inversely related
to intensity of murmur
investigations:
o ECG: left ventricular
hypertrophy (LVH),
left atrial hypertrophy
(LAH), RVH
o CXR: increased
pulmonary
vasculature,
cardiomegaly, CHF
treatment: treatment of CHF
and surgical closure by 1 year
of age
Patent Ductus Arteriosus (PDA)
patent vessel between
descending aorta and left
pulmonary artery
epidemiology
o functional closure
within first 15 hours of
life, anatomical
closure within first
days of life
o 5-10% of all
congenital heart
defects
o common in premature
infants (1/3 of infants
<1750 grams)
o natural history:
spontaneous closure
common in premature
infants, less common
in term infants
history: may be asymptomatic
or have apneic or bradycardic
spells, poor feeding, accessory
muscle use
physical exam: tachycardia,
bounding pulses, hyperactive
precordium, wide pulse
pressure, continuous
machinery murmur, best heard
at left infraclavicular area
investigations:
o ECG: may show LAH,
LVH, BVH
o CXR: normal to
mildly enlarged heart,
increased pulmonary
vasculature, prominent
pulmonary artery
15
o diagnosis by
echocardiography
(Echo)
treatment:
o indomethacin
(Indocid) PGE1
antagonist (PGE1
maintains
ductus arteriosus
patency) in premature
infants if necessary
o catheter or surgical
closure if PDA is
contributing to
respiratory
compromise or
persists beyond 3rd
month of life
Coarctation of the Aorta (Chilren)
narrowing of aorta almost
always at the level of the ductus
arteriosus
commonly associated with
bicuspid aortic valve (50%);
Turner syndrome (35%)
few have high BP in infancy
(160-200 mmHg systolic) but
this decreases as collaterals
develop
if severe, presents with shock in
the neonatal period when the
ductus closes
history: often asymptomatic
physical exam: upper extremity
systolic pressures of 140-145
mmHg, decreased blood pressure
and weak/absent pulses in lower
extremities, radial-femoral delay,
absent or systolic murmur with late
peak at apex, left axilla, and left
back
investigations:
ECG-RVH early in infancy, LVH
later in childhood
prognosis and treatment
o if associated with
other lesions (e.g.
PDA, VSD) can cause
CHF
 o complications: o CXR: dilated post- Lower Motor Exam Check
hypertension stenotic pulmonary List
o management: balloon artery Look at attitude of limb,
arterioplasty or treatment: surgical repair if Neurocutaneous lesion,
surgical correction in critically ill or severe PS, or if Spontaneous or induced
symptomatic neonate, presence of symptoms in older fasciculations.
give prostaglandins to infants/children Do clonus at knees as well
open up PDA for systemic venous return re-
stabilization enters systemic circulation
Causes of Proximal Myopathy
directly
Congenital
Aortic Stenosis (children) most prominent feature is
Muscle dystrophy
cyanosis (O2 sat <75%)
Inflammatory
valvular (75%), subvalvular differentiate between cardiac
Polymyositis
(20%), supravalvular and and other causes of cyanosis
with hyperoxic test Dermatomyositis
idiopathic hypertrophic Polymyalgia rheumatica
subaortic stenosis (IHSS) (5%) o obtain preductal, right
Endocrine
history: often asymptomatic but radial ABG in room
air, repeat ABG after Cushings Syndrome
may be associated with CHF, (including iatrogenic)
exertional chest pain, syncope the child inspires
100% oxygen Diabetes Mellitus
or sudden death
o if PaO2 improves to Hypothyroidism /
physical exam: SEM at upper Hyperthyroidism
right sternal border (URSB) greater than 150
mmHg, cyanosis less Acromegaly
with aortic ejection click at the
likely cardiac in origin Addisons disease
apex
survival depends on mixing via Conns syndrome
treatment
o surgical repair if infant shunts (e.g. ASD, VSD, PDA) Hyperparathyroidism /
hypoparathyroidism
with critical aortic
JVP Metabolic
stenosis or older child
Osteomalacia
with symptoms or A Rt atrial contraction
peak gradient >50 Hypokalemia
C bulging of tricuspid Hypercalcemia
mmHg
valve into Rt atrium on Toxic
o exercise restriction
ventricular contraction Alcohol
required
x descent lowering Rt Vitamin E
atrial pressure as tricuspid Organophosphate
Pulmonary Stenosis (Children) ring moves down Drugs
V atrial filling Corticosteroids
valvular (90%), subvalvular, or y descent opening of Amiodarone
supravalvular tricuspid valve Vincristine
usually part of other congenital ventricular filling Paraneoplastic
heart lesions (e.g. Tetralogy of
Carcinomatous
Fallot) or in association with Raised JVP with normal neuromyopathy
other syndromes (e.g. waveform Rt heart Dermatomyositis
congenital rubella, Noonan failure; fluid overload
syndrome) Raised JVP with absent
critical pulmonic stenosis: pulsation SVC Causes of Spastic Paraparesis
inadequate pulmonary blood obstruction
flow, dependent on ductus for HAM/TSP
Absent a wave A. Fib
oxygenation, progressive Spinal cord compression
Large a wave pulm HTN
hypoxia and cyanosis Multiple Sclerosis
pulm stenosis, tricuspid
history: spectrum from Subacute Combined
stenosis
asymptomatic to CHF Degeneration of the cord
Cannon a wave complete
physical exam: wide split S2 on (Vit B12 def)
heart block
expiration, SEM at ULSB, Transverse Myelitis
CV wave tricuspid
pulmonary ejection click Parasagittal Meningioma
regurgitation
investigations: HIV-associated
o ECG: RVH myelopathy
Tabes dorsalis

16
 SLE Compression (e.g. post
Nutritional communication artery
Causes of Spastic Hemiplegia
Vit B1 Deficiency aneurysm)
CVA Vit B6 Deficiency Abducens Nerve
Tumour Vit B12 deficiency
Brown-Sequard Vit E Deficiency DM
Endocrine HTN
Causes of Flaccid paraparesis
Diabetes Mellitus Vasculitis
Poliomyelitis Acromegaly Causes of Facial Weakness
Guillain-Barre Heavy metal upper motor neuron
Motor Neuron Disease Lead TIA/stroke
Spina bifida Mercury post-ictal hemiparesis
Botulism Drugs tumour
Cauda equina syndrome Isoniazid
infection: otitis media,
Phenytoin mastoiditis, Epstein-Barr
Metronidazole virus (EBV), herpes zoster
Flaccid Hemiplegia Methotrexate virus (HZV), Lyme
Acute CVA disease, HIV
Plexopathy Peripheral Neuropathy (DANG
THE RAPIST) lower motor neuron

Sensory Exam Check List DM, Uremia

Amyloidosis infection: otitis media,
Look for Ulcers, U. Cath or Diaper
Nutritional (Vit B1, 6, 12 def) mastoiditis, Epstein-Barr
Do light touch, sharp touch, Guillain-Barre virus (EBV), herpes zoster
Proprioception (toe and ankle) Toxins & drugs (lead, mercury, virus (HZV), Lyme
organophosphate, metronidazole, disease, HIV
Causes of Sensory Disturbance isoniazid, ethambutol, vincristine, idiopathic (Bells
amiodarone) palsy)
stroke
Hereditary (Friedrichs ataxia, sarcoid
tumour
porphyria, Charcot-marie-tooth) neuropathy (DM)
multiple sclerosis
Endocrine (acromegaly) parotid gland
peripheral neuropathies
Rheumatoid & vasculitides (SLE,
B12 deficiency
RA, Polyarteritis nodosa, Sjogrens, Facial Nerve
Churg-Strauss)
Causes of a Sensory Level Bells palsy
Alcohol
(Sensation is lost below a Ipsilateral LMN facial
Paraproteinemia (Multiple
particular level) Bells phenomenon
myeloma) / Paraneoplastic (non-
Transverse myelitis metastatic manifestation) Hyperacusis
Spinal cord compression Infectious (HIV, Leprosy, Lyme o If nerve to
Spinal cord tumour disease, diphtheria, tetanus, stapedius is
botulism) involved
Cervical spondylosis Sarcoidosis Salivation
Traumatic injury to spinal cord Thyroid (hypothyroidism) Lacrimation
Causes of Ptosis
Causes of Peripheral Neuropathy Oculomotor Nerve
cranial nerve III palsy
Renal failure CN 3 motor nucleus at level of myasthenia gravis
Infection superior colliculus + Edinger- (uni/bilateral)
Westphal (parasympathetic Horners syndrome
HIV
peripheral fibres) passes b/w congenital/idiopathic
Leprosy
posterior cerebral & superior myotonic dystrophy
Lyme disease cerebellar arteries superior
Infiltrative (bilateral)
orbital fissure
Sarcoidosis Ischemia (e.g. Diabetic
Amyloidosis Causes of Facial Pain
mononeuropathy) sinusitis
Inflammatory o Pupillary sparing
Guillain-Barre dental disease
RA

17
 tic douloureux (Trigeminal
Neuralgia)
trigeminal neuropathic pain
(secondary to trigeminal
nerve injury or disease)
glossopharyngeal neuralgia
postherpetic neuralgia
atypical facial pain
multiple sclerosis
Causes of Vertigo
brainstem lesions (stroke,
MS)
cerebellar lesions
vertebrobasilar
insufficiency
drugs/alcohol
peripheral causes
Loss of Vision
Painful
Angle Closure Glaucoma
Trauma
Temporal Arteritis
Optic Neuritis
Minimal Pain
Retinal detachment
Central Retinal Artery
Occlusion
TIA/Stroke
Pseudotumour cerebri
Causes of Diplopia
Neuromuscular:
cranial nerve III/IV/VI
palsies (DM, tumour,
trauma, aneurysm)
brainstem pathology
(stroke, tumour, MS)
myasthenia gravis
Wernicke's encephalopathy
leptomeningeal disease
(e.g. meningitis)
Guillain-Barr
syndrome (e.g. Miller-
Fisher Variant)
Mechanical
thyroid ophthalmopathy
cavernous sinus pathology
trauma (e.g. orbital
fracture)
General Approach to Neuro Exam
State of Consciousness/Arousal
Glasgow Coma Scale
(EVM = 456)
reflexes: responses to pain
may include decerebrate
and decorticate posturing
Mental Status Exam
appearance, behaviour,
mood, affect, speech,
thought process, thought
content, perceptions,
insight, judgement
assess as is appropriate
throughout the interview
Cognition
Mini-Mental Status Exam
(MMSE), clock drawing,
Baycrest Neurocognitive
Assessment, MOCA
frontal lobe testing for
perseveration
Cranial Nerve Examination
Cranial Nerve Interpretation
CN1:
Unilateral loss of smell suggests
interior frontal lobe lesion
(avoid irritative stimuli which
stimulate CN5)
CN2:
Look at optic discs for edema
and optic atrophy
CN3/4/6:
Look for pupillary
abnormalities, ptosis, abnormal
eye movements
Drug reactions:
Bilaterally dilated fixed pupils
with anticholinergics (e.g. atropine,
mushrooms), but also seen in
herniation.
Bilaterally small fixed pupils with
morphine and related drugs, but also
seen in pontine lesion
Horners syndrome = ptosis,
miosis (anisocoria), anhydrosis (due
to interrupted sympathetic nerve
supply)
18
CN3 palsy = Ptosis,
Eye is down and out, +/-
impaired pupillary response
(suggests structural/compressive
cause)
CN4 Palsy:
Cant intort eye (also depresses
and adducts eye. Diplopia esp.
on downward and inward gaze.
Issues reading, going down
stairs
CN 6 Palsy:
Cant abduct eye
CN5
Absent corneal reflex may be
CN5 (ophth. N - sensory deficit)
or CN7 (motor deficit)
CN7:
Forehead sparing = upper motor
neuron lesion
CN9/10:
Dysarthria
Motor examination
Inspection:
Bulk, accessory movements,
tremor, fasciculations, etc.
Tone:
Assess for rigidity, spasticity,
Clonus
Power:
(0-5, 0: no contraction, 1:
flicker, 2: active movement
with gravity eliminated, 3:
active movement against
gravity, 4-,4, 4+: active
movement against gravity and
resistance, 5: full power)
Reflexes:
0 to 4+, 0: absent with
reenforcement, 1+: reduced, 2+:
normal, 3+: increased, 4+:
clonus present)
Motor System Interpretation
Ataxia may be due to cerebellar
disease, proprioceptive abnormality
Ataxia with eyes closed only is a
positive Rombergs sign suggesting
a loss of joint position
sense/peripheral neuropathy.
Ataxia with eyes open or closed
suggests cerebellar disease
Pronator drift - Suggests Sensory Exam Interpretation
hemiparesis or loss of position sense Hemisensory loss - with sensory
level or dissociation loss suggests
Spasticity - Indicates upper motor spinal cord lesion
neuron disease
Symmetrical distal sensory loss
Atrophy and fasciculations suggests polyneuropathy
-Indicates lower motor neuron
disease Loss of vibration sense suggests
peripheral neuropathy or posterior
Cogwheel rigidity - is seen in column lesion
extrapyramidal processes (e.g.
Parkinsons Disease) Impaired graphesthesia and
stereognosis with intact primary
Symmetrical weakness of proximal sensation indicates parietal lesion
muscles suggests myopathy; of
distal muscles suggests Other Stuff
polyneuropathy Dolls movement, if absent,
suggests pons or midbrain lesion or
Reflexes Interpretation very deep coma
Increased in upper motor neuron
disease Loss of vestibulo-ocular reflex
with caloric stimulation suggests
Decreased/absent in lower motor brain stem lesion or drug toxicity
neuron disease, myopathies or
neuromuscular junction disorders Absence seizures can be
precipitated by hyperventilation
Slow relaxation of knee or ankle
reflex is seen in hypothyroidism Characteristic skin lesions are
seen in neurocutaneaous syndromes
Babinski sign suggests an upper (e.g. neurofibromatosis, tuberous
motor neuron lesion but may be sclerosis complex, Sturge-Weber
seen following a seizure syndrome)
Sensory Examination Where is the Lesion ?
posterior columns Cortex and internal Capsule
Contralateral sensory & motor
vibration,
deficits
proprioception,
light touch)
Cortical lesions:
Spinothalamic Associated with aphasia,
pain neglect, extinction,
temperature graphaesthesia, visual loss
Cortical sensation (higher level dysfunctions) and
graphesthesia, astereognosia
stereognosis, Internal capsule lesions:
extinction, Associated with pure motor,
2-point discrimination pure sensory losses,
incoordination, absence of
Co-ordination cortical features
finger to nose, Common causes:
heel to shin, Seizure disorder (cortex only)
rapid alternating Coma
movements Stroke
Stance & Gait Cerebellum and Basal Ganglia
Romberg, Coordination Problems
tandem gait Cerebellar Lesions:
Abnormal intentional
19
Movements. Clumsiness,
unsteadiness, vertigo.
Tandem gait impairment,
nysatagmus, abnormal heel
to shin, dysdiadockinesis,
abnormal finger to nose and
rapid alternating movements
Basal Ganglia:
Tremor, bradykinesia,
cogwheel rigidity,
involuntary movements
Common Causes:
Cerebellar degeneration
Parkinsons disease
Stroke
Brainstem (unilateral)
Midbrain CN 3-4
Pons CN 6-7
Medulla CN 8-10
Bilateral motor abnormalities
(UMN pattern). Crossed
sensory signs (ipsilateral
face and contralateral body)
MIDBRAIN:
Diplopia, ptosis, pupillary
changes (large or midposition
and unreactive)
PONS:
LMN facial weakness,
quadriparesis in bilateral pontine
lesions, pinpoint pupils (why?)
MEDULLA:
lateral or medial medullary
syndromes
Common Causes
Cranial nerve palsies
Stroke
Unilteral Spinal Cord
Upper Motor neuron signs
Ipsilateral paralysis and
proprioceptive loss
Sensory level, bowel/bladder
dysfunction paraparesis
Contralateral pain-temperature
loss below the level of the
lesion in Brown-Sequard
syndrome
Common Causes :
Spinal Cord Syndromes
 sublcilincal seizure/ post- Toxins
Nerve Root ictal state Heavy metals
Radicular pain (sharp, electric, hypertensive Dementia
radiating) + sensory loss in encephalopathy Other psychiatric
dermatome/weakness in Metabolic (e.g. depression)
myotome or absent reflex diabetic ketoacidosis
hypoglycemia Mental Status Exam: ASEPTIC
Common Causes: electrolyte disturbance
Nerve root compression Appearance and behaviour
acid-base disturbance Speech
Disk herniation thiamine deficiency Emotion (mood and affect)
Systemic Perception
Peripheral Nerve
liver failure Thought content and process
Ipsilateral motor and sensory
renal failures Insight and judgment
deficits along a nerve
sepsis Cognition
distribution.
Focal CNS
LMN signs power, wasting,
abscess
reflexes, normal or tone)
In Polyneuropathy (distal
epidural/ subdural Rheumatology
hematoma Demographics: name, age,
weakness, glove and stocking
distribution of sensory loss) hemorrhage/ aneurysm occupation
hydrocephalus History
Common Causes: stroke SLE
Neuropathy tumour Joint pain (duration &
venous occlusion severity), swelling, redness,
Neuromuscluar Junction warmth
Proximal & symmetrical Glascow Coma Scale Chest pain
muscle weakness Eyes Open Photosensitivity
No sensory loss 4 = Spontaneously Seizure
Fatiguability (?Repeated 3 = To voice Change in personality
strength testing) 2 = To pain Recurrent early pregnancy
Diplopia, ptosis, bulbar 1 = No response losses
weakness Systemic Sclerosis
Best Verbal Response Cold numbness & pain
Common Causes: 5 = Answers questions appropriately in fingers; fingertips pale,
Myasthenia gravis 4 = Confused, disoriented then blue
Lambert-Eaton syndrome 3 = Inappropriate words Difficulty swallowing
Botulism 2 = Incomprehensible sounds RA
1 = No verbal response Difficulty dressing, undoing
Muscle buttons, washing, opening
Best Motor Response bottle, opening door
Proximal & symmetrical
6 = Obeys commands Morning stiffness
muscle weakness
5 = Localizes to pain Joint pain (duration &
No sensory loss
4 = Withdraws from pain severity), swelling, redness,
LMN signs wasting, normal 3 = Decorticate (flexion)
or reflexes, normal or tone stiffness, warmth
2 = Decerebrate (extension) Sjgrens
1 = No response
Common Causes: Dry eyes
Muscular dystrophies Dry mouth
Myopathies including Acute Confusional states Difficulty swallowing
polymyositis (delirium) Joint pain
Dermatomyositis I WATCH DEATH" Cold numbness & pain
Infectious in fingers; fingertips pale,
Altered Mental Status Withdrawal from drugs then blue
Coma Acute metabolic disorder Behets
Diffuse CNS Trauma Recurrent painful oral &
head trauma CNS pathology genital ulcers
infection Hypoxia Blurry vision, periorbital
inflammation/ vasculitis Deficiencies in vitamins pain
global cerebral ischemia Endocrinopathies
Acute vascular insults Examination
20
SLE b. Ask if they understand Renal impairment
Malar rash 4. Do you have any questions? Menorrhagia/amenorrhea
Oral ulcers 5. [Summarise] So, do you Constipation
Arthritis remember what we spoke about Anemia
Discoid rash today? ... Paresthesiaia
alopecia 6. This is a continuous education
Systemic Sclerosis process, unfortunately we cant Hypercalcemia
Taut skin; loss of wrinkling do everything in this session. 1. Calcium = Ca++ uptake
Further counselling will be (milk alkali syndrome)
telangiectasia
necessary & I would 2. Hyperparathyroidism (1
Sausage-shaped fingers
recommend that for your next hyperparathyroidism is
Wasting of thenar &
visit, you have a family associated with Ca++)
hypothenar eminences
member or loved one 3. Iatrogenic (drug induced as
Loss of pulp of digits accompany you. occurs with thiazides, or
Beaked nose lithium)
Radial furrowing Features of Hyperthyroidism 4. Metastasis (bone and
Oral cavity unable to admit General prostate metastasis can
3 of patients own fingers fatigue, heat intolerance, lead to Ca++)
RA irritability, fine tremor 5. Pagets disease of bone
Arthritis Cardiovascular 6. Addisons disease
Swan neck & Boutonnire tachycardia, atrial fibrillation, 7. Neoplasm as in metastasis
deformities; Z thumb palpitations elderly patients 8. ZE syndrome (MEN I - 1
Ulnar deviation may have only cardiovascular HPT)
Wasting of small muscles symptoms, commonly new onset 9. Excessive vitamin D intake
of hands atrial fibrillation 10. Excessive vitamin A intake
Rheumatoid nodules GI 11. Sarcoidosis
(palpate extensor surface weight loss with increased
of forearm) appetite, thirst, increased Psychiatry
Sjgrens frequency of bowel movements Multiaxial Assessment
Dry mucous membranes (hyperdefecation)
Axis I
Dental caries Neurology
o differential diagnosis
Arthritis proximal muscle weakness,
of DSM-IV clinical
Parotid gland enlargement hypokalemic periodic paralysis
disorders
Behets (common in Orientals)
GU Axis II
Oral & genital ulcers o personality disorders,
scant menses, decreased fertility
Sclera injection & mental retardation
excessive lacrimation Axis III
Dermatology
(uveitis) o general medical
fine hair, skin moist and warm,
vitiligo, soft nails with conditions that are
onycholysis (Plummers nails), potentially relevant to
DDx the understanding or
clubbing (acropachy), palmar
Osteoarthritis management of the
erythema, pretibial mxyedema
o DIP Heberdens mental disorder
MSK
nodes decreased bone mass, proximal Axis IV
o PIP - Bouchards muscle weakness o psychosocial and
nodes Hematology environmental issues
Gout leukopenia, lymphocytosis, Axis V
o Gouty tophi 1st splenomegaly, lymphadenopathy o global assessment of
metatarsophalang (occasionally in Gravesdisease functioning (GAF, 0 to
eal joint Signs and Symptoms of 100) incorporating
o Hypothyroidism effects of axes I to IV
HISFIRMCAP
Counselling Station Hypoventilation
1. Introduction Axis V: Global Assessment of
Intolerance to cold Functioning
2. So, what do you know about Slow HR
your condition? Fatigue 91- Superior functioning in a wide
3. [Educate & counsel based on Impotence 100 range of activities
info received prior] 81- Absent or minimal symptoms
a. Build rapport
21
90
If symptoms are present, they
71- are transient and expected
80 reactions to psychosocial
stressors
Some mild symptoms or some
61-
difficulty but generally
70
functioning well
51- Moderate symptoms or
60 difficulty
41-
Serious symptoms or difficulty
50
Some impairment in reality
31-
testing/communication,
40
impairment in several areas
Behaviour is influenced by
21- delusions/hallucinations or
30 serious impairment in
communication/judgment
Some danger of hurting self or
others or occasionally fails to
11-
maintain minimal hygiene or
20
gross impairment in
communication
Persistent danger of severely
hurting self or others or
1-
persistent inability to maintain
10
minimal personal hygiene or
serious suicidal act
0 Inadequate information
Mental Status Exam
General Appearance and
Behaviour
dress, grooming, posture, gait,
physical characteristics, body
habitus, apparent vs.
chronological age, facial
expression (e.g. sad,
suspicious)
psychomotor activity (agitation,
retardation), abnormal
movements or lack thereof
(tremors, akathisia, tardive
dyskinesia, paralysis), attention
level and eye contact, attitude
toward examiner (ability to
interact, level of co-operation)
Speech
rate (e.g. pressured, slowed),
rhythm/fluency, volume, tone,
articulation, quantity,
spontaneity
Mood and Affect
mood - subjective emotional
state; in patients own words
affect - objective emotional
state; described in terms of
quality (euthymic, depressed,
elevated, anxious), range (full,
restricted, flat, blunted),
stability (fixed, labile), mood
congruence, appropriateness,
intensity
Thought Process
coherence - coherent,
incoherent
logic - logical, illogical
stream
o goal-directed
o circumstantiality -
speech that is indirect
and delayed in
reaching its goal;
eventually comes back
to the point
o tangentiality - speech
is oblique or
irrelevant; does not
come back to the
original point
o loosening of
associations - illogical
shifting between
topics
o flight of ideas -
quickly skipping from
one idea to another
where the ideas are
marginally connected,
associated with mania
o word salad - jumble of
words lacking
meaning or logical
coherence
perseveration - repetition of
the same verbal or motor
response to stimuli
echolalia - repetition of
phrases or words spoken by
someone else
thought blocking - sudden
cessation of flow of thought
and speech
clang associations - speech
based on sound such as
rhyming or punning
22
neologism - use of novel words
or of existing words in a novel
fashion
Thought Content
suicidal ideation/homicidal
ideation
o low - fleeting
thoughts, no
formulated plan, no
intent
o intermediate - more
frequent ideation, well
formulated plan, no
active intent
o high - persistent
ideation and profound
hopelessness/anger,
well formulated plan
and active intent,
believes
suicide/homicide is the
only helpful option
available
obsession - recurrent and
persistent thought, impulse or
image which is intrusive or
inappropriate
o cannot be stopped by
logic or reason
o causes marked anxiety
and distress
o common themes:
contamination,
orderliness, sexual,
pathological
doubt/worry/guilt
pre-occupations, ruminations
(reflections/thoughts at length)
overvalued ideas- unusual/odd
beliefs that are not of
delusional proportions
magical thinking- belief that
thinking something will make it
happen; normal in kids
ideas of reference- similar to
delusion of reference but the
reality of the belief is
questioned
delusion - a fixed false belief
that is out of keeping with a
persons cultural or religious
background and is firmly held
despite incontrovertible proof
to the contrary
thought
insertion/withdrawal/broadcasti
 ng; delusions of control
belief that ones
thoughts/actions are controlled
by some external source
Perception
hallucination - sensory
perception in the absence of
external stimuli that is similar
in quality to a true perception;
auditory (most common),
visual, gustatory, olfactory,
tactile
illusion - misperception of a
real external stimulus
depersonalization - change in
self-awareness such that the
person feels unreal, detached
from his or her body, and/or
unable to feel emotion
derealization - feeling that the
world/outer environment is
unreal
Cognition
level of consciousness
orientation: time, place, person
memory: immediate, recent,
remote
global evaluation of intellect
(below average, average, above
average)
intellectual functions: attention,
concentration, calculation,
abstraction (proverb
interpretation, similarities test),
language, communication
Insight
patients ability to realize that
he or she has a physical or
mental illness and to
understand its implications
Judgment
ability to understand
relationships between facts
and draw conclusions that
determine ones action
Attitude to examiner
Types of Delusions
Persecutory - belief that others are
trying to cause harm
Delusions of reference -
interpreting publicly known
events/celebrities as having direct
reference to the patient
Erotomania - belief that another is
in love with you
Grandiose - belief of an inflated
sense of self-worth or power
Religious - belief of receiving
instructions/powers from a higher
being; of being a higher being
Somatic - belief that one has a
physical disorder/defect
Nihilistic - belief that things do not
exist;a sense that everything is
unreal
Psychosis
characterized by a significant
impairment in reality testing
delusions or hallucinations
(with/without insight into their
pathological nature)
behaviour so disorganized that
it is reasonable to infer that
reality testing is disturbed
Differentials of Psychosis
primary psychotic disorders:
schizophrenia,
schizophreniform, brief
psychotic, schizoaffective,
delusional disorder
mood disorders: depression
with psychotic features, bipolar
disorder (manic episode with
psychotic features)
personality disorders:
schizotypal, schizoid,
borderline, paranoid, obsessive-
compulsive
general medical conditions:
tumour, head trauma, dementia,
delirium, metabolic
substance-induced psychosis:
intoxication or withdrawal
DSM-IV-TR Diagnostic Criteria
for Schizophrenia
A. characteristic symptoms (active
phase): >2 of the following, each
present for a significant portion of
time during a 1-month period (or
less if successfully treated):
delusions **
23
hallucinations **
disorganized speech (e.g.
frequent derailment or
incoherence)
grossly disorganized or
catatonic behaviour
negative symptoms, e.g.
affective flattening, alogia
(inability to speak), or avolition
(inability to initiate and persist
in goal-directed activities)
**Note: only 1 symptom is required
if delusions are bizarre or
hallucinations consist of a voice
keeping a running commentary on
the person's behaviour or thoughts,
or 2 or more voices conversing with
each other
B. social/occupational dysfunction:
>1 major areas of functioning
(work, interpersonal relations, self-
care) markedly below the level
achieved prior to the onset of
symptoms
C. continuous signs of disturbance
for >6 months, including >1 month
of active phase symptoms; may
include prodromal or residual
phases
D. schizoaffective and mood
disorders excluded
E. the disturbance is not due to the
direct physiological effects of a
substance or a general medical
condition (GMC)
F. if history of pervasive
developmental disorder, additional
diagnosis of schizophrenia is made
only if prominent delusions or
hallucinations are also present for at
least 1 month
Subtypes
paranoid
o preoccupation with
one or more delusions
(typically persecutory
or grandiose) or
frequent auditory
hallucinations
 o relative preservation symptoms in criteria A pharmacological
of cognitive present in attenuated o acute treatment and
functioning and affect; form maintenance with
onset tends to be later antipsychotics
in life; believed to Good Prognositic Factors anticonvulsants
have the best Acute onset anxiolytics
prognosis Precipitating factors o management of side
catatonic Good cognitive functioning effects
o at least two of: motor Good premorbid functioning psychosocial
immobility (catalepsy No family history o psychotherapy
or stupor); excessive Presence of affective symptoms (individual, family,
motor activity Absence of structural brain group): supportive,
(purposeless, not abnormalities cognitive behavioural
influenced by external Good response to drugs therapy (CBT)
stimuli); extreme Good support system o assertive community
negativism (resistance treatment (ACT)
to Etiology - multifactorial: o social skills training,
instructions/attempts disorder is a result of interaction employment
to be moved) or between both biological and programs, disability
mutism; peculiar environmental factors benefits
voluntary movement genetic 50% concordance in o housing (group home,
(posturing, stereotyped monozygotic (MZ) twins; 40% boarding home,
movements, prominent if both parents have transitional home)
mannerisms); schizophrenia; 10% of
echolalia (repeating dizygotic (DZ) twins, siblings,
words/phrases of children affected Schizophreniform Disorder
anothers speech) neurochemistry - dopamine
or echopraxia hypothesis theory: excess diagnosis: criteria A, D & E of
(imitative repetition of activity in the mesolimbic schizophrenia are met; an
anothers dopamine pathway may episode of the disorder lasts at
movements, gestures mediate the positive symptoms least 1 month but less than 6
or posture) of psychosis (i.e. delusions, months
disorganized hallucinations, disorganized treatment: similar to acute
o disorganized speech speech and behaviour, and schizophrenia
and behaviour; flat or agitation) prognosis: better than
inappropriate affect neuroanatomy - decreased schizophrenia; begins and ends
o poor premorbid frontal lobe function, more abruptly; good pre- and
personality, early and asymmetric temporal/limbic post-morbid function
insidious onset, and function, decreased basal
continuous course ganglia function; subtle Brief Psychotic Episode
without significant changes in thalamus, cortex, diagnosis: acute psychosis
remissions corpus callosum, and (presence of 1 or more positive
undifferentiated ventricles; cytoarchitectural symptoms in criteria A1-4 of
o symptoms of criteria A abnormalities schizophrenia) lasting from 1
met, but does not fall neuroendocrinology day to 1 month, with eventual
into the 3 previous abnormal growth hormone, full return to premorbid level of
subtypes prolactin, cortisol, and functioning
residual adrenocorticotropic hormone can occur after a stressful event
o absence of prominent neuropsychology global or postpartum (see Postpartum
delusions, defects seen in attention, Mood Disorders)
hallucinations, language, and memory suggest treatment: secure
disorganized speech, lack of connectivity of neural environment, antipsychotics,
grossly disorganized networks anxiolytics
or catatonic behaviour indirect evidence of prognosis: good, self-limiting,
o continuing evidence of geographical variance, winter should return to pre-morbid
disturbance indicated season of birth, and prenatal function in about 1 month
by the presence of viral exposure
negative symptoms or
two or more Management of Schizophrenia
24
DSM-IV-TR Diagnostic Criteria
for Schizoaffective Disorder
A. uninterrupted period of illness
during which there is either a major
depressive episode (MDE), manic
episode, or a mixed episode
concurrent with symptoms meeting
criteria A for schizophrenia
B. in the same period, delusions or
hallucinations for at least 2 weeks
in the absence of prominent mood
symptoms
C. symptoms that meet criteria for a
mood episode are present for a
substantial portion of total duration
of active and residual periods of the
illness
D. the disturbance is not due to the
direct physiological effects of a
substance or GMC
treatment: antipsychotics,
mood stabilizers,
antidepressants
prognosis: between that of
schizophrenia and that of mood
disorder
DSM-IV-TR Diagnostic Criteria
for Delusional Disorder
A. non-bizarre delusions for at least
1 month
B. criterion A for schizophrenia
has never been met (though patient
may have tactile or olfactory
hallucinations if they are related to
the delusional theme)
C. functioning not markedly
impaired; behaviour not obviously
odd or bizarre
D. if mood episodes occur
concurrently with delusions, total
duration has been brief relative to
duration of the delusional periods
E. the disturbance is not due to the
direct physiological effects of a
substance or GMC
subtypes: erotomanic,
grandiose, jealous, persecutory,
somatic, mixed, unspecified
treatment: psychotherapy,
antipsychotics, antidepressants
prognosis: chronic, unremitting
course but high level of
functioning
Folstein Mini Mental State Exam
(MMSE) to assess Dementia:
Orientation (time and place) 5
points
Memory (immediate and delayed
recall) 5 points
Attention and Concentration
Language (comprehension, reading,
writing, repetition, naming)
Spacial ability (intersecting
pentagons)
Gross screen for cognitive
dysfunction: Total score is out of
30; <24 abnormal 20-24 mild, 10-19
moderate, <10 severe
See attached Form
DSM-IV-TR Diagnostic Criteria
for Dementia (Alzheimers Type)
A. the development of multiple
cognitive deficits manifested by
both
1. memory impairment
(impaired ability to learn new
information or to recall
previously learned information)
2. >1 of the following
cognitive disturbances:
o aphasia (language
disturbance)
o apraxia (impaired
ability to carry out
motor activities
despite intact motor
function)
o agnosia (failure to
recognize or identify
objects despite intact
sensory function)
o disturbance in
executive functioning
(i.e. planning,
organizing,
25
sequencing,
abstracting)
B. the cognitive deficits in Criteria
A1 and A2 each cause significant
impairment in social or
occupational functioning and
represent a significant decline from
a previous level of functioning
C. the course is characterized by
gradual onset and continuing
cognitive decline
D. the cognitive deficits in Criteria
A1 and A2 are not due to any of the
following:
1. other central nervous system
conditions that cause
progressive deficits in memory
and cognition
2. systemic conditions that are
known to cause dementia
3. substance-induced conditions
E. the deficits do not occur
exclusively during the course of a
delirium
F. the disturbance is not better
accounted for by another Axis I
disorder
Investigations (rule out reversible
causes)
standard: as in Delirium
as indicated: VDRL, HIV,
SPECT, CT head in dementia
indications for CT head, as in
Delirium section plus: age <60,
rapid onset (unexplained
decline in cognition or function
over 1-2 months), dementia of
relatively short duration (<2
years), recent significant head
trauma, unexplained
neurological symptoms (new
onset of severe
headache/seizures)
Management
 treat medical problems and
prevent others
provide orientation cues (e.g.
clock, calendar)
provide education and support
for patient and family (day
programs, respite care, support
groups, home care)
consider long-term care plan
(nursing home) and power of
attorney/living will
inform Ministry of
Transportation about
patients inability to drive
safely
consider pharmacological
therapy
o cholinesterase
inhibitors (e.g.
donepezil (Aricept))
for mild to severe
disease
o glutamatergic NMDA
receptor antagonist
(e.g memantine) for
moderate to severe
disease
o low-dose neuroleptics
(haloperidol,
risperidone) and
antidepressants if
behavioural or
emotional symptoms
prominent - start low
and go slow
o reassess
pharmacological
therapy every 3
months
Substance Abuse History
Validatedscreeningquestionnaire
(Alcohol):
CeverfelttheneedtoCut drinking
downondrinking?
A ever felt Annoyed at
criticism of your drinking?
G ever feel Guilty about your
drinking?
E ever need a drink first thing
in morning (Eye opener)?
formen,ascoreof>2isa GI: gastritis, dyspepsia, pancreatitis,
positivescreenandforwomen, liver disease, bleeds, diarrhea,
ascoreof>1isapositive
screen
ifpositiveCAGE,thenassess
furthertodistinguishbetween
problemdrinkingandalcohol
dependence
General Assessment
Whenwasthelastdrink?
Doyouhavetodrinkmoreto
getthesameeffect?
Doyougetshakyornauseous
whenyoustopdrinking?
Haveyouhadawithdrawal
seizure?
Howmuchtimeandeffortdo
youputintoobtainingalcohol?
Hasyourdrinkingaffectedyour
abilitytowork,gotoschool,or
haverelationships?
Haveyousufferedanylegal
consequences?
Hasyourdrinkingcausedany
medicalproblems?
Moderate Drinking
Men: 2 or less/day
Women: 1 or less/day
Elderly: 1 or less/day
Drinking Problem
Drinking above the recommended
guidelines, associated with:
Drinking to or reduce
depression or anxiety
Loss of interest in food
Lying/hiding drinking habits
Drinking alone
Injuring self or others while
intoxicated
Were drunk more than three or
four times last year
Increasing tolerance
Withdrawal symptoms: feeling
irritable, resentful,
unreasonable when not
Experiencing medical, social,
or financial problems caused by
drinking
Adverse Medical Conditions -
alcohol
26
oral/esophageal cancer
Cardiac: hypertension, alcoholic
cardiomyopathy
Neurologic: Wernicke-Korsakoff
syndrome, peripheral neuropathy
Hematologic: anemia,
coagulopathies
Other: trauma, insomnia, family
violence, anxiety/depression,
social/family dysfunction, sexual
dysfunction, fetal damage
Investigations
GGT and MCV for baseline
and follow-up monitoring
AST, ALT (usually, AST:ALT
approaches 2:1 in an alcoholic)
CBC (anemia,
thrombocytopenia), PT
(decreased clotting factors
production by liver)
Management
intervention should be
consistent with patients
motivation for change
(motivational interviewing)
regular follow-up is crucial
10% of patients in alcohol
withdrawal will have seizures
or delirium tremens
Alcoholics Anonymous/12-step
program
outpatient/day programs
for those with chronic,
resistant problems
family treatment (Al-Anon,
Alateen, screen for
spouse/child abuse)
in-patient program if:
dangerous or highly
unstable home
environment
severe medical/psychiatric
problem
addiction to drug that may
require in-patient
detoxification
refractory to other
treatment programs
Non Pharmacological
behaviourmodification:
hypnosis,relaxation
training,aversiontherapy,
 assertivenesstraining,
operantconditioning
supportiveservices:half
wayhouses,detoxification
centres,Alcoholics
Anonymous
psychotherapy,
motivationalinterviewing
medicationsimportantas
adjunctivetreatment:
SSRIs,ondansetron,
topiramate
pharmacologic
diazepam for withdrawal
disulfiram (Antabuse)
o blocks conversion
of acetaldehyde to
acetic acid (which
leads to flushing,
headache,
nausea/vomiting,
hypotension if
alcohol is
ingested)
naltrexone
o competitive
opioid antagonist
that reduces
cravings and
pleasurable
effects of drinking
o note: prescription
opioids become
ineffective; may
trigger withdrawal
in opioid-
dependent
patients
Signs of Alcohol withdrawl
(Delerium Tremens)
Autonomic hyperactivitiy
(diaphoresis, tachycardia, increased
respiration)
Hand tremor
Insomnia
Psychomotor agitation
Anxiety
Nausea or vomiting
Grand mal seizures
Visual/tactile/auditory
hallucinations
Persecutory delusions
Management of Alcohol Withdrawal
Monitor using the Clinical Institute
Withdrawal Assessment for Alcohol
(CIWA-A) scoring system. Areas of
assessment include
nausea and vomiting
paroxysmal sweats
tactile disturbances
visual disturbances
tremor
anxiety
auditory disturbances
headache, fullness in head
agitation
o orientation and
clouding of sensorium
all categories are scored from
0-7 (except:
orientation/sensorium 0-4),
maximum score of 67
mild <10
moderate 10-
20
severe >20
basic treatment protocol using
CIWA-A scale
o diazepam 20 mg PO
q1-2h prn until CIWA-
A <10 points; tapering
dose not required
o observe 1-2 h after last
dose and re-assess on
CIWA-A scale
o thiamine 100 mg IM
then 100 mg PO OD
for 3 days
o supportive care
(hydration and
nutrition)
if history of withdrawal
seizures
o diazepam 20 mg q1h
for minimum of three
doses regardless of
subsequent CIWA
scores
if history of seizure disorder or
multiple withdrawal seizures
despite diazepam, use anti-
seizure medication (e.g.
Dilantin)
if oral diazepam not tolerated
o diazepam 2-5 mg
IV/min maximum
10-20 mg q1h; or
lorazepam SL
if >65 yr or severe liver
disease, severe asthma, or
respiratory failure are present,
use short acting benzodiazepine
27
o lorazepam PO/SL/IM
1-4 mg q1-2h
if hallucinosis present
o haloperidol 2-5 mg
IM/PO q1-4h max
5 doses/day or atypical
antipsychotics
(olanzapine,
risperidone)
o diazepam 20 mg x 3
doses as seizure
prophylaxis
(haloperidol lowers
seizure threshold)
admit to hospital if:
o still in withdrawal
after >80 mg of
diazepam
o delirium tremens,
recurrent arrhythmias,
or multiple seizures
o medically ill or unsafe
to discharge home
Wernicke-Korsakoff Syndrome
alcohol-induced amnestic
disorders due to thiamine
deficiency
necrotic lesions
mammillary bodies,
thalamus, brain stem
Wernickes
encephalopathy (acute and
reversible): triad of
nystagmus (CN VI palsy),
ataxia and confusion
Korsakoffs syndrome
(chronic and only 20%
reversible with treatment):
anterograde amnesia and
confabulations; cannot
occur during an acute
delirium or dementia and
must persist beyond usual
duration of
intoxication/withdrawal
management
o Wernickes:
thiamine 100 mg
PO OD x 1-2
weeks
o Korsakoffs:
thiamine 100 mg
PO bid/tid x 3-12
mon
Prognosis
 relapse is common and should
not be viewed as failure
monitor regularly for signs of
relapse
25-30% of abusers exhibit
spontaneous improvement over
1 year
60-70% of individuals with
jobs and families have an
improved quality of life 1 year
post-treatment
Cocaine
Intoxication
elation, euphoria, pressured
speech, restlessness,
sympathetic stimulation (i.e.
tachycardia, mydriasis,
sweating)
prolonged use may result in
paranoia and psychosis
Overdose
medical emergency:
hypertension, tachycardia,
tonic-clonic seizures, dyspnea,
and ventricular arrhythmias
treatment with IV diazepam to
control seizures and propanolol
or labetalol to manage
hypertension and arrhythmias
Withdrawal
initial crash (1-48 hrs):
increased sleep, increased
appetite
withdrawal (1-10 wks):
dysphoric mood plus fatigue,
irritability, vivid, unpleasant
dreams, insomnia or
hypersomnia, psychomotor
agitation or retardation
complications: relapse, suicide
(significant increase in suicide
during withdrawal period)
management: supportive
management
Treatment of Chronic Abuse
optimal treatment not
established
psychotherapy, group therapy,
and behaviour modification
useful in maintaining
abstinence
studies of dopamine agonists to
block cravings show
inconsistent results
Complications
cardiovascular: arrhythmias,
MI, CVA, ruptured AA
neurologic: seizures
psychiatric: psychosis,
paranoia, delirium, suicidal
ideation
Ganja
marijuanaisthemostoftenused
illicitdrug
psychoactivesubstancedelta9
tetrahydrocannabinol(9THC)
smokingisthemostcommon
modeofselfadministration
intoxicationcharacterizedby
tachycardia,conjunctivalvascular
engorgement,drymouth,increased
appetite,increasedsenseofwell
being,euphoria/laughter,muscle
relaxation,impairedperformanceon
psychomotortasksincluding
driving
highdosescancause
depersonalization,paranoia,and
anxiety
maytriggerpsychosisand
schizophreniainpredisposed
individuals
chronicuseassociatedwith
toleranceandanapathetic,
amotivationalstate
cessationdoesnotproduce
significantwithdrawalphenomenon
treatmentofdependence
includesbehaviouraland
psychologicalinterventionsto
maintainanabstinentstate
Medical Uses of Ganja
Anorexia-cachexia (AIDS, cancer)
Spasticity, muscle spasms (multiple
sclerosis, spinal cord injury)
Levodopa-induced
dyskinesia (Parkinson's Disease)
Controlling tics and obsessive-
compulsive behaviour (Tourette's
28
syndrome)
Reducing intra-ocular pressure
(glaucoma)
Mood Disorders
Mood disorders are defined by the
presence of mood episodes
mood episodes represent a
combination of symptoms
comprising a predominant
mood state that is abnormal in
quality or duration; examples
include: major depressive,
manic, mixed, hypomanic
types of mood disorders
include:
o depressive (major
depressive disorder,
dysthymia)
o bipolar (bipolar I/II
disorder, cyclothymia)
o secondary to GMC,
substances,
medications
Secondary Causes of Mood
Disorders
infectious:
encephalitis/meningitis,
hepatitis, pneumonia, TB,
syphilis
endocrine: hypothyroidism,
hyperthyroidism,
hypopituitarism, SIADH
metabolic: porphyria,
Wilsons disease, diabetes
vitamin disorders:
Wernickes, beriberi,
pellagra, pernicious anemia
collagen vascular diseases:
SLE, polyarteritis nodosa
neoplastic: pancreatic cancer,
carcinoid, pheochromocytoma
cardiovascular:
cardiomyopathy, CHF, MI,
CVA
neurologic: Huntingtons
disease, multiple sclerosis,
tuberous sclerosis, degenerative
(vascular, Alzheimers)
drugs: antihypertensives,
antiparkinsonian, hormones,
steroids, antituberculous,
interferon, antineoplastic
medications
Medical Workup of Mood
Disorder
routine screening:
o physical examination
o complete blood count
o thyroid function test
o electrolytes
o urinalysis, urine drug
screen
addtional screening:
o neurological
consultation
o chest x-ray
o electrocardiogram
o CT scan
Risk Factors for Depression
sex:female>male
age:onsetin2550yearage
group
familyhistory:depression,
alcoholabuse,sociopathy
childhoodexperiences:lossof
parentbeforeage11,negative
homeenvironment(abuse,
neglect)
personality:insecure,
dependent,obsessional
recentstressors(illness,
financial,legal)
postpartum<6months
lackofintimate,confiding
relationshipsorsocialisolation
DSM-IV-TR Criteria for Major
Depressive Episode
A. >5 of the following
symptoms have been present
during the same 2-week period
and represent a change from
previous functioning; at least
one of the symptoms is either
1) depressed mood, or 2) loss
of interest or pleasure
(anhedonia) Note: Do not
include symptoms that are
clearly due to a general
medical condition, or mood-
incongruent delusions or
hallucinations
depressed mood most of the
day, nearly every day, as
indicated by either subjective
report or observation made by
others
markedly diminished interest or
pleasure in all, or almost all,
activities most of the day,
nearly every day
significant weight loss when
not dieting or weight gain, or
decrease or increase in
appetite nearly every day
insomnia or hypersomnia
nearly every day
psychomotor agitation or
retardation nearly every day
fatigue or loss of energy nearly
every day
feelings of worthlessness or
excessive or inappropriate guilt
(which may be delusional)
nearly every day (not merely
self-reproach or guilt about
being sick) more Major Depressive Episodes; to
diminished ability to think or
concentrate, or indecisiveness,
nearly every day
recurrent thoughts of death
(not just fear of dying),
recurrent suicidal ideation
without a specific plan, or a
suicide attempt or a specific
plan for committing suicide
B. the symptoms do not meet
criteria for a Mixed Episode
C. the symptoms cause
clinically significant distress or
impairment in social,
occupational, or other
important areas of functioning
D. the symptoms are not due to
the direct physiological effects
of a substance or a GMC
E. the symptoms are not better
accounted for by bereavement,
i.e. after the loss of a loved one,
the symptoms persist for longer
than 2 months or are
characterized by marked
functional impairment, morbid
preoccupation with
worthlessness, suicidal
ideation, psychotic symptoms,
or psychomotor retardation
Criteria for Depression (>5):
MSIGECAPS
29
M - Depressed Mood
S - Increased/decreased Sleep
I - Decreased Interest
G - Guilt
E - Decreased Energy
C - Decreased Concentration
A - Increased/decreased Appetite
P - Psychomotor
agitation/retardation
S - Suicidal ideation
MAJOR DEPRESSIVE
DISORDER
DSM-IV-TR Diagnostic Criteria
for Major Depressive Disorder
(MMD), Single Episode (vs.
Recurrent)
A. presence of a single Major
Depressive Episode (vs. Recurrent,
which requires presence of two or
be considered separate episodes,
there must be an interval of at least
2 consecutive months in which
criteria are not met for a MDE)
B. the Major Depressive Episode is
not better accounted for by
Schizoaffective Disorder and is not
superimposed on Schizophrenia,
Schizophreniform Disorder,
Delusional Disorder, or Psychotic
Disorder not otherwise specified
C. there has never been a Manic
Episode, a Mixed Episode, or a
Hypomanic Episode. Note: This
exclusion does not apply if all of the
manic-like, mixed-like, or
hypomanic-like episodes are
substance- or treatment-induced or
are due to the direct physiological
effects of a general medical
condition
Features/Specifiers
psychotic with hallucinations
or delusions
chronic - lasting 2 years or
more
catatonic - at least two of:
motor immobility; excessive
motor activity; extreme
negativism or mutism;
peculiarities of voluntary
 movement; echolalia or
echopraxia
melancholic - quality of mood
is distinctly depressed, mood is
worse in the morning, early
morning awakening, marked
weight loss, excessive guilt,
psychomotor retardation
atypical - increased sleep,
weight gain, leaden paralysis,
rejection hypersensitivity
postpartum
seasonal - pattern of onset at
the same time each year (most
often in the fall or winter)
Etiology
biological
genetic: 65-75% MZ twins; 14-
19% DZ twins
neurotransmitter dysfunction at
level of synapse (decreased
activity of serotonin,
norepinephrine, dopamine)
secondary to general medical
condition
psychosocial
psychodynamic (e.g. low self-
esteem)
cognitive (e.g. negative
thinking)
environmental factors (e.g. job
loss, diet (omega 3 fatty acids),
bereavement, history of abuse)
co-morbid psychiatric
diagnoses (e.g. anxiety,
substance abuse, mental
retardation, dementia, eating
disorder)
Treatment
biological: antidepressants,
lithium, antipsychotics,
anxiolytics, electroconvulsive
therapy (ECT), light therapy
psychological
o individual therapy:
psychodynamic,
interpersonal,
cognitive behavioural
therapy
o family therapy
o group therapy
social: vocational
rehabilitation, social skills
training
experimental: deep brain
stimulation, transcranial
magnetic stimulation, vagal
nerve stimulation
DSM-IV-TR Criteria for Manic
Episode
A. a distinct period of
abnormally and persistently
elevated, expansive, or irritable
mood, lasting >1 week (or any
duration if hospitalization is
necessary)
B. during the period of mood
disturbance, >3 of the
following symptoms have
persisted (4 if the mood is only
irritable) and have been present
to a significant degree:
o inflated self-esteem or
grandiosity
o decreased need for
sleep (e.g. feels rested
after only 3 hours of
sleep)
o more talkative than
usual or pressure to
keep talking
o flight of ideas or
subjective experience
that thoughts are
racing
o distractibility (i.e.
attention too easily
drawn to unimportant
or irrelevant external
stimuli)
o increase in goal-
directed activity
(either socially, at
work or school, or
sexually) or
psychomotor agitation
o excessive involvement
in pleasurable
activities that have a
high potential for
painful consequences
(e.g. engaging in
unrestrained buying
sprees, sexual
indiscretions, or
30
foolish business
investments)
C. the symptoms do not meet
criteria for a Mixed Episode
(see below)
D. the mood disturbance is
sufficiently severe to cause
marked impairment in
occupational functioning or in
usual social activities or
relationships with others, or to
necessitate hospitalization to
prevent harm to self or others,
or there are psychotic features
E. the symptoms are not due to
the direct physiological effects
of a substance (e.g. drug of
abuse, medication, or other
treatment) or a general medical
condition (e.g.
hyperthyroidism). Note:
Manic-like episodes that are
clearly caused by somatic
antidepressant treatment (e.g.
medication, electroconvulsive
therapy, light therapy) should
not count toward a diagnosis of
Bipolar I Disorder
Criteria for Mania (>3): GST PAID
Grandiosity
Sleep (decreased need)
Talkative
Pleasurable activities, Painful
consequences
Activity
Ideas (flight of)
Distractable
Mixed Episode
criterion met for both manic
episode and major depressive
episode (MDE) nearly every
day for 1 week
criteria D and E of manic
episodes are met
Hypomanic Episode
criterion A of a manic episode
is met, but duration is >4 days
criterion B and E of manic
episodes are met
episode associated with an
uncharacteristic decline in
functioning that is observable
by others
change in function is not
severe enough to cause marked
 impairment in social or
occupational functioning or to
necessitate hospitalization
absence of psychotic features
BIPOLAR I / BIPOLAR II
DISORDER
Bipolar I Disorder
o disorder in which at
least one manic or
mixed episode has
occurred
o commonly
accompanied by at
least 1 MDE but not
required for diagnosis
Bipolar II Disorder
o disorder in which
there is at least 1 MDE
and at least 1
hypomanic episode
o no past manic or
mixed episode
Risk Factors
slight increase in upper
socioeconomic groups
60-65% of bipolar patients have
family history of major mood
disorders
Treatment
biological: mood stabilizers,
anticonvulsants, antipsychotics,
antidepressants, ECT (Note:
Treatment of bipolar depression
must be done extremely
cautiously, as a switch from
depression to mania can result.
Monotherapy with
antidepressants should be
avoided)
psychological: supportive and
psychodynamic psychotherapy,
cognitive or behavioural
therapy
social: vocational
rehabilitation, leave of absence
from school/work, drug and
EtOH cessation, substitute
decision maker for finances,
sleep hygiene, social skills
training, education for family
members
Anxiety Disorders
Anxiety is a universal human
characteristic involving tension,
apprehension, or even terror, which
serves as an adaptive mechanism to
warn about an external threat by
activating the sympathetic nervous
system (fight or flight)
manifestations of anxiety can
be described along a continuum
of physiology, psychology, and
behaviour
physiology - main brain
structure involved is the
amygdala; neurotransmitters
involved include serotonin,
cholecystokinin, epinephrine,
norepinephrine, dopamine
psychology ones perception of
a given situation is distorted
which causes one to believe it
is threatening in some way
behaviour - once feeling
threatened, one responds by
escaping or facing the situation,
thereby causing a disruption in
daily functioning
anxiety becomes pathological
when
fear is greatly out of proportion
to risk/severity of threat
response continues beyond
existence of threat or becomes
generalized to other
similar/dissimilar situations
social or occupational
functioning is impaired
Differential Diagnosis
endocrine: hyperthyroidism,
pheochromocytoma,
hypoglycemia,
hyperadrenalism,
hyperparathyroidism
CVS: congestive heart failure,
pulmonary embolus,
arrhythmia, mitral valve
prolapse
respiratory: asthma,
pneumonia, hyperventilation
metabolic: vitamin B12
deficiency, porphyria
31
neurologic: neoplasm,
vestibular dysfunction,
encephalitis
substance-induced: intoxication
(caffeine, amphetamines,
cocaine), withdrawal
(benzodiazepines, alcohol)
Medical Workup of Anxiety
Disorder
routine screening: physical
examination, CBC, thyroid
function test, electrolytes,
urinalysis, urine drug screening
additional screening:
neurological consultation, chest
x-ray, electrocardiogram
(ECG), CT scan
DSM-IV-TR Diagnostic
Criteria for Generalized
Anxiety Disorder
A. excessive anxiety and worry
(apprehensive expectation),
occurring more days than not for at
least 6 months, about a number of
events or activities (such as work or
school performance)
B. the person finds it difficult to
control the worry
C. the anxiety and worry are
associated with >3 of the
following 6 symptoms (with at
least some symptoms present
for more days than not for the
past 6 months). Note: Only one
item is required in children
(1) restlessness or feeling
keyed up or on edge
(2) being easily fatigued
(3) difficulty concentrating
or mind going blank
(4) irritability
(5) muscle tension
(6) sleep disturbance
(difficulty falling or
staying asleep, or restless
unsatisfying sleep)
D. the focus of the anxiety and
worry is not confined to
 features of an Axis I disorder,
such as panic disorder, social
phobia, etc.
E. the anxiety, worry, or
physical symptoms cause
clinically significant distress or
impairment in social,
occupational, or other
important areas of functioning
F. the disturbance is not due to
the direct physiological effects
of a substance or a GMC and
does not occur exclusively
during a Mood Disorder, a
Psychotic Disorder, or a
Pervasive Developmental
Disorder
Treatment
psychotherapy, relaxation,
mindfulness, and CBT
caffeine and EtOH
avoidance, sleep hygiene
pharmacotherapy:
o benzodiazepines
(short term, low
dose, regular
schedule, long
half-life, no prn)
o buspirone (tid
dosing)
o others:
SSRIs/SNRI,
TCAs, beta-
blockers
combinations of above
DSM-IV-TR Diagnostic Criteria
for Post-Traumatic Stress
Disorder
A. the person has been exposed to a
traumatic event in which both of
the following were present:
(1) the person experienced,
witnessed, or was confronted
with an event or events that
involved actual or threatened
death or serious injury, or a
threat to the physical integrity
of self or others
(2) the person's response
involved intense fear,
helplessness, or horror. Note: In
children, this may be expressed
instead by disorganized or
agitated behaviour
B. the traumatic event is
persistently re-experienced in one
(or more) of the following ways:
(1) recurrent and intrusive
distressing recollections of the
event, including images,
thoughts, or perceptions. Note:
In young children, repetitive
play may occur in which
themes or aspects of the trauma
are expressed
(2) recurrent distressing dreams
of the event. Note: In children,
there may be frightening
dreams without recognizable
content
(3) acting or feeling as if the
traumatic event were recurring
(includes a sense of reliving the
experience, illusions,
hallucinations, and dissociative
flashback episodes, including
those that occur on awakening
or when intoxicated) Note: In
young children, trauma-specific
reenactment may occur
(4) intense psychological
distress at exposure to internal
or external cues that symbolize
or resemble an aspect of the
traumatic event
(5) physiological reactivity on
exposure to internal or external
cues that symbolize or resemble
an aspect of the traumatic event
C. persistent avoidance of stimuli
associated with the trauma and
numbing of general responsiveness
(not present before the trauma), as
indicated by three (or more) of the
following:
(1) efforts to avoid thoughts,
feelings, or conversations
associated with the trauma
(2) efforts to avoid activities,
places, or people that arouse
recollections of the trauma
32
(3) inability to recall an
important aspect of the trauma
(4) markedly diminished
interest or participation in
significant activities
(5) feeling of detachment or
estrangement from others
(6) restricted range of affect
(e.g. unable to have loving
feelings)
(7) sense of a foreshortened
future (e.g. does not expect to
have a career, marriage,
children, or a normal life span)
D. persistent symptoms of
increased arousal (not present
before the trauma), as indicated by
>2 of the following:
(1) difficulty falling or staying
asleep
(2) irritability or outbursts of
anger
(3) difficulty concentrating
(4) hypervigilance
(5) exaggerated startle response
E. duration of the disturbance
(symptoms in Criteria B, C, and D)
is >1 month
F. the disturbance causes clinically
significant distress or impairment in
social, occupational, or other
important areas of functioning
Treatment
CBT - systematic
desensitization, relaxation
techniques, thought stopping
pharmacotherapy
o SSRIs
o benzodiazepines (for
acute anxiety)
o first-line adjunct
atypical antipsychotics
(quetiapine,
olanzapine,
risperidone)
EMDR (eye movement
desensitization and
reprocessing): an experimental
method of reprocessing
memories of distressing events
by recounting them while using
 a form of dual attention
stimulation such as eye
movements, bilateral sound, or
bilateral tactile stimulation
DSM-IV-TR Diagnostic Criteria
for Panic Disorder without
Agoraphobia
A - Both 1 and 2
(1) recurrent unexpected panic
attacks: a discrete period of intense
fear or discomfort, in which >4 of
the following symptoms develop
abruptly and reach a peak within
10 minutes
palpitations, pounding heart, or
accelerated heart rate
sweating
trembling or shaking
sensations of shortness of
breath or smothering
feeling of choking
chest pain or discomfort
nausea or abdominal distress
feeling dizzy, unsteady,
lightheaded, or faint
derealization (feelings of
unreality) or depersonalization
(being detached from oneself)
fear of losing control or going
crazy
fear of dying
paresthesias (numbness or
tingling sensations), chills or
hot flushes
(2) at least one of the attacks has
been followed by 1 month (or
more) of >1 of the following:
persistent concern about having
additional attacks
worry about the implications of
the attack or its consequences
(e.g. losing control, having a
heart attack, "going crazy")
a significant change in behavior
related to the attacks
B. absence of agoraphobia
C. the panic attacks are not due to
the direct physiological effects of a
substance or GMC
D. the panic attacks are not better
accounted for by another mental
disorder, such as Social Phobia,
Specific Phobia, Obsessive-
Compulsive Disorder, Post-
Traumatic Stress Disorder,
Separation Anxiety Disorder
Treatment
supportive psychotherapy,
relaxation techniques
(visualization, box-breathing),
cognitive behavioural therapy
(correct distorted thinking,
desensitization/exposure
therapy)
pharmacotherapy
o benzodiazepines (short
term, low dose,
regular schedule, long
half-life, no prn)
o SSRIs/SNRI (start
low, go slow, aim high
since anxiety patients
are very sensitive)
o other antidepressants
(Trazodone,
Remeron, MAOIs;
avoid Wellbutrina)
Panic Disorder with Agoraphobia
Agoraphobia - anxiety about being
in places or situations from which
escape might be difficult (or
embarrassing) or where help may
not be available in the event of
having an unexpected panic attack
fears commonly involve
situations: being out alone,
being in a crowd, standing in a
line, or travelling on a bus
situations are avoided, endured
with anxiety or panic, or
require companion
treatment: as per panic disorder
Criteria for Panic Disorder (>4):
"STUDENTS FEAR the 3 Cs"
Sweating
Trembling
Unsteadiness, dizziness
Depersonalization, Derealization
Excessive heart rate, palpitations
33
Nausea
Tingling
Shortness of breath
Fear of dying, losing control, going
crazy
3 C's: Chest pain, Chills, Choking
Suicide
Risk Factors
Epidemiologic factors
age: increases after age 14;
second most common cause of
death for ages 15-24; highest
rates in persons >65 years
sex: male
race/ethnic background: white
or native Canadians on reserves
marital status:
widowed/divorced
living situation: alone; no
children <18 years old in the
household
other: stressful life events;
access to firearms
psychiatric disorders
mood disorders (15% lifetime
risk in depression; higher in
bipolar)
anxiety disorders (especially
panic disorder)
schizophrenia (10-15% risk)
substance abuse (especially
EtOH 15% lifetime risk)
eating disorders (5% lifetime
risk)
adjustment disorder
conduct disorder
personality disorders
(borderline, antisocial)
past history
prior suicide attempt
family history of suicide
attempt/completion
Symptoms associated with suicide
hopelessness
anhedonia
 insomnia
severe anxiety
impaired concentration
psychomotor agitation
panic attacks
Approach
Ideation Do you have thoughts
about ending your life,
committing suicide?
Passive would rather not be
alive but doesnt admit to idea
that involves act of initiation
o Id rather not wake up
o I wouldnt mind if a
car hit me
Active
o I think about killing
myself
Plan - Do you have a plan as to
how you would end your life?
Intent -You talk about wanting
to die, but are you planning to
do this? What has stopped you
from ending your life?
Past attempts - Highest risk if
previous attempt in past year,
ask about lethality, outcome,
medical intervention
Assessment of Suicidal
Ideation
Onsetandfrequencyof
thoughtsWhendidthisstart?
Howoftendoyouhavethese
thoughts?
Controloversuicidalideation
Canyoustopthethoughtsor
callsomeoneforhelp?
LethalityDoyouwanttoend
yourlife?Orgetareleasefrom
youremotionalpain
AccesstomeansHowwill
yougetagun?Whichbridgedo
youthinkyouwouldgoto?
TimeandplaceHaveyou
pickedadateandplace?Isitin
anisolatedlocation?
ProvocativefactorsWhat
makesyoufeelworse(e.g.
beingalone)?
ProtectivefactorsWhatkeeps
youalive(e.g.friends,family,
pets,faith,therapist)?
Final Arrangements - Have you
written a suicide note? Made a
will? Given away your
belongings?
Practised suicide or aborted
attempts - Have you put the gun
to your head? Held the
medications in your hand?
Stood at the bridge?
Ambivalence - There must be a
part of you that wants to live -
you came here for help
Assessment of Suicide Attempt
Setting isolated vs. others
present, chance of discovery
Planned vs. impulsive attempt,
triggers/stressors
Intoxication
Medical attention brought in
by another person vs. brought
in by self to ER
Time lag from suicide attempt
to ER arrival
Expectation of lethality, dying
Reaction to survival:
guilt/remorse vs.
disappointment/self-blame
Management
depends on the level of risk
identified
higher risk:
o patients with a plan,
access to lethal means,
recent social stressors,
and symptoms
suggestive of a
psychiatric disorder
should be hospitalized
immediately
o do not leave patient
alone; remove
potentially dangerous
objects from room
o if patient refuses to be
hospitalized, complete
form for involuntary
admission
lower risk: New stuff
o patients who are not
actively suicidal, with
no plan or access to
lethal means
34
o discuss protective
factors and supports in
their life, remind them
of what they live for
(as identified above),
promote survival skills
that helped them
through previous
suicide attempts
o make a safety plan -
an agreement that they
will not harm
themselves, that they
will try to avoid
alcohol, drugs, and
situations that may
trigger suicidal
thoughts, that they will
follow up with you at
a designated time, and
that they will contact a
health care worker,
call a crisis line or go
to an emergency
department if they feel
unsafe or if their
suicidal feelings return
or intensify
depression: hospitalize if severe
or if psychotic features are
present; otherwise outpatient
treatment with good supports
and SSRIs/SNRIs
alcohol-related: usually
resolves with abstinence for a
few days; if not, suspect
depression
personality disorders: crisis
intervention/confrontation, may
or may not hospitalize
schizophrenia/psychosis:
hospitalization
parasuicide/self-mutilation:
long-term psychotherapy with
brief crisis intervention when
necessary
proper documentation of the
clinical encounter and rationale
for management is essential

Atopic Dermatitis
subacute and chronic
eczematous reaction associated
with Type I (IgE-mediated)
hypersensitivity reaction
(release of histamine) and Th2
cellular response producing
prolonged severe pruritus
Etiology
associated with personal or
family history of atopy
(asthma, hay fever,
anaphylaxis, eosinophilia)
polygenic inheritance: one
parent >60% chance for child;
two parents >80% chance for
child
frequently affects infants,
children, and young adults
females only slightly more at
risk than males (1.3:1 over the
age of 2 years)
almost 15% of children in
developed countries under the
age of 5 are affected; half of
these cases are diagnosed by 1
year of age
half of all patients with AD are
over 18 years of age
the earlier the onset, the more
severe and persistent the
disease
long-term condition with 1/3 of
patients continuing to show
signs of AD into adulthood
childhood onset and hereditary
forms are associated with a
defect in the protein filaggrin
Signs and Symptoms
inflammation, lichenification,
excoriations are secondary to
relentless scratching
atopic palms: prominent palmar
creases
associated with
o keratosis pilaris
(hyperkeratosis of hair
follicles, chicken
skin)
o xerosis
o occupational hand
dryness
patients usually suffer from
three flares per year
Distribution
infant (onset at 2-6 months
old): face, scalp, extensor
surfaces
childhood (>18 months):
flexural surfaces
adult: hands, feet, flexures,
neck, eyelids, forehead, face,
wrists
Investigations
no prerequisite investigations to
diagnose atopic dermatitis
may consider: skin biopsy,
immunoglobulin serum levels
(often elevated serum IgE
level), patch testing, and skin
prick tests to look for contact or
environmental allergies
Treatment
majority of cases are mild and
easily managed
goal: reduce signs and
symptoms, prevent or reduce
recurrences, and provide long-
term management to prevent
progression from early disease
to full AD flare
treatment maximized (i.e. less
flare-ups, modified course of
disease) if diagnosis made early
and treatment plan
individualized
o individualized based
on age, severity, sites
and extent of
involvement, presence
of infection, previous
responses to therapy
reassure patients that although
there is no absolute cure, the
disease can be controlled
35
avoid triggers of AD: irritants
(detergents and solvents,
certain clothing, water
hardness), inappropriate
bathing habits (long hot
showers), microbes (S. aureus),
stress, sweating, contact
allergens, and environmental
aeroallergens (dust mites)
enhance barrier function of the
skin
o simplest and most
important aspect of
controlling AD
o involves regular
application of
moisturizers +/-
diluted corticosteroid
wet-wrap dressings
emollients
hydrate the
skin and
reduce
pruritus
o twice daily application
is recommended even
in absence of
symptoms, especially
after bathing or
swimming
bathing
promotes
hydration
when
followed by
the
application of
moisturizers
to the skin
consider psychological support
for some patients
Anti-inflammatory therapies
a) topical corticosteroids:
o effective, rapid
symptomatic relief for
acute flares
o different formulations
and potencies suitable
for nearly any area of
skin
o best applied
immediately after
bathing
o control inflammation
with a potent topical
steroid; prescribe a
milder one following
 resolution of acute associated infants - one cause of cradle
flare with their use cap
o systemic children may be generalized
immunosuppression Prognosis with flexural and scalp
may be needed in 50% clear by age 13, few involvement
severe cases persist >30 years of age adults - diffuse in areas of scalp
o flares may respond to margin with yellow to white
systemic anti- flakes, pruritus, and underlying
staphylococcal therapy erythema
side effects: sites: scalp, eyebrows,
skin atrophy, eyelashes, beard, face, trunk,
purpura, body folds, genitalia
striae, steroid Complications face: eyebrows, sides of nose,
acne, perioral posterior ears, glabella
dermatitis, infections are common: chest: over sternum
and glaucoma diagnose early and treat
when used appropriately (i.e. Treatment
around the antibiotic, antifungal,
eyes antiviral therapy);
b) topical immunomodulators infections must be resolved face: Nizoral cream OD + mild
o long-term before applying anti- steroid cream OD or bid
management inflammatory treatments scalp: salicylic acid in olive oil
o calcineurin inhibitors o topical mupirocin or Derma-Smoothe FS lotion
or fusidic acid is (peanut oil, mineral oil,
such as pimecrolimus
often sufficient fluocinolone acetonide 0.01%)
(Elidel) and
o oral antibiotics to remove dense scales, 2%
tacrolimus
(i.e. cloxacillin, ketoconazole shampoo
(Protopic)
cephalexin) for (Nizorale), ciclopirox (Stieprox
block
widespread S. ) shampoo, selenium sulfide
calcineurin
aureus infections (e.g. Selsun) or zinc pyrithione
and inhibit
(e.g. Head and Shoulders)
inflammatory
shampoo, steroid lotion (e.g.
cytokine Seborrheic Dermatitis betamethasone valerate 0.1%
transcription
lotion bid)
in activated
T-cells and
Greasy, erythematous, yellow,
other non-pruritic scaling papules HTLV Associated Dermatitis
inflammatory and plaques; occurs in areas
cells rich in sebaceous glands The average age of onset is
o significant adverse 2 years.
events may include Etiology The skin manifestations
skin burning and become less severe with
transient irritation age.
possible etiologic association Severe exudative dermatitis
o advantages of long-
with Pityrosporum ovale of the scalp, external ear,
term management of
(yeast) retroauricular areas, eyelid
AD over long-term
corticosteroid use: margins, paranasal skin,
rapid, Epidemiology neck, axillae and groins
sustained Generalized fine papular
effect in common in infants and at rash
controlling puberty Chronic watery nasal
pruritus increased incidence in discharge sometimes with
produce no immunocompromised patients crusting
skin atrophy e.g. HIV HTLV-1 seropositivity
safe for the in adults, can cause dandruff Staphylococcus aureus
face and neck (pityriasis sicca) and/or B-haemolytic
no significant streptococci commonly
systemic cultured from anterior nares
Signs and Symptoms
toxicities and skin

36
 Responds to antibiotics but
relapses if antibiotics
withdrawn
Lichen Planus
acute or chronic inflammation
of mucous membranes or skin
characterized by violaceous
papules, especially on flexural
surfaces
Epidemiology
association with hepatitis C
may be triggered by severe
emotional stress
Signs and Symptoms
small, polygonal, flat-topped,
shiny, violet papules; resolves
with hyperpigmented macules
Wickhams striae: greyish lines
over surface; pathognomonic
sites: wrists, ankles, mucous
membranes in 60% (mouth,
vulva, glans), nails, scalp
mucous membrane lesions:
lacy, whitish reticular network,
milky-white plaques/papules;
increased risk of SCC in
erosions and ulcers
nails: longitudinal ridging;
dystrophic
scalp: scarring alopecia
spontaneously resolves in
weeks or lasts for years (mouth
and shin lesions)
Koebner phenomenon:
develops in areas of trauma
Treatment
topical corticosteroids with
occlusion or intradermal steroid
injections
short courses of oral prednisone
(rarely)
photochemotherapy for
generalized or resistant cases
oral retinoids for erosive lichen
planus in mouth
Mnemonic
The 6 Ps of Lichen Planus
Purple, Pruritic, Polygonal,
Peripheral, Papules, Penis (i.e.
mucosa)
Pityriasis Rosea
Definition and Clinical Features
acute, self-limiting,
erythematous eruption
characterized by red, oval
plaques/patches with
central scales that do not
extend to edge of lesion
sites: trunk, proximal
aspects of arms and legs
long axis of lesions follows
parallel to ribs producing
Christmas tree
pattern on back
varied degree of pruritus
most start with a
herald patch which
precedes other lesions by
1-2 weeks
Etiology
suspected human herpes virus 7
Treatment
no treatment needed; clears
spontaneously in 6-12 weeks,
reassurance
topical corticosteroids when
post-inflammatory
pigmentation is a concern
Clinical Pearl
Secondary syphilis can present with
a non-pruritic papulosquamous
eruption but usually ALSO has
palmar lesions.
Psoriasis
Mnemonic
PSORIASIS: Pathophysiology
Pink papules/Plaques/Pinpoint
bleeding (Auspitz sign)/Physical
injury (Koebner phenomenon)
Silver scale/Sharp margins
37
Onycholysis/Oil spots
Rete Ridges with Regular elongation
Itching
Arthritis/Abscess
(Monro)/Autoimmune
Stratum corneum with nuclei
Immunologic
Stratum granulosum absent
Classification
plaque psoriasis
guttate psoriasis
erythrodermic psoriasis
pustular psoriasis
psoriatic arthritis
Differential Diagnosis
atopic dermatitis, mycosis
fungoides (cutaneous T-cell
lymphoma), seborrheic
dermatitis, tinea
PLAQUE PSORIASIS
a common chronic and recurrent
disease characterized by well-
circumscribed erythematous
papules/plaques with silvery-white
scales, mostly at sites of repeated
trauma
Pathophysiology
decreased epidermal transit
time from basal to horny layers
shortened cell cycle of psoriatic
and normal skin --> excess
keratinization with scales
Epidemiology
multifactorial inheritance
Clinical Pearl
Woronoffs Ring
Woronoffs ring: blanched halo that
surrounds psoriatic lesions after
topical or phototherapy treatments
Signs and Symptoms
 worse in winter (lack of sun
and humidity)
Koebner phenomenon
(isomorphic response):
induction of new lesion by
injury
Auspitz sign: bleeds from
minute points when scale is
removed
sites: scalp, extensor surfaces
of elbows and knees, trunk,
nails, pressure areas
usually non-pruritic
exacerbating factors: drugs
(lithium, ethanol, chloroquine,
beta-blockers), sunlight, stress,
obesity
Treatment
preventative measures: avoid
sunburns, avoid drugs that
exacerbate the condition (beta-
blockers, lithium, corticosteroid
rebound phenomenon,
interferon, etc.)
first-line treatment mainly
involves topical treatments,
usually prescribed if less than
5-10% of the body surfaces are
involved. If the affected area is
>10%, use topical medications
as adjuncts to phototherapy or
systemic drugs
systemic treatments should be
considered if:
o psoriatic lesions cover
>10% of the body
surface area
o unsuccessful topical
therapies
o disease is causing
psychological distress
GUTTATE PSORIASIS ("DROP-
LIKE")
Definition and Clinical Features
discrete, scattered salmon-pink
scaling papules
sites: generalized, sparing
palms and soles
often antecedent streptococcal
pharyngitis
Treatment
UVB phototherapy, sunlight,
lubricants
penicillin V or erythromycin if
Group A beta-hemolytic
Streptococcus on throat culture
ERYTHRODERMIC
PSORIASIS
Definition and Clinical Features
generalized erythema with fine
desquamative scale on surface
associated symptoms:
arthralgia, severe pruritus
may present in patient with
previous mild plaque psoriasis
aggravating factors: lithium,
beta-blockers, NSAIDs,
antimalarials, phototoxic
reaction, infection
Treatment
hospitalization, bedrest, IV
fluids, sun avoidance, monitor
fluid and electrolytes
treat underlying aggravating
condition
methotrexate, UV, oral
retinoids, biologicals
PUSTULAR PSORIASIS
Definition and Clinical Features
sudden onset of erythematous
macules and papules which
evolve rapidly into pustules,
very painful
can be generalized or localized
to palms/soles
patient usually has history of
psoriasis; may occur with
sudden withdrawal from steroid
therapy
Treatment
methotrexate, oral retinoids,
biologicals
PSORIATIC ARTHRITIS
38
5 categories
asymmetric oligoarthropathy
distal interphalangeal (DIP)
joint involvement
(predominant)
rheumatoid pattern
symmetric polyarthropathy
psoriatic arthritis mutilans
(most severe form)
predominant spondylitis or
sacroiliitis
Rheumathoid Arthritis
chronic, symmetric, erosive
synovitis of peripheral joints
(i.e. wrists, MCP joints, and
MTP joints)
characterized by a number of
extra-articular features
Clinical Pearl
Common Presentation
Morning stiffness >30 min, improves
with use
Symmetric joint involvement
Initially involves small joints of
hands and feet
Constitutional symptoms
Clinical Pearl
Criteria are 91-94% sensitive and
89% specific for RA.
Table 7. Diagnostic Criteria: RA
diagnosed if 4 or more of the
following 7 criteria present
(American Rheumatism
Association, 1987)
Criteria Definition
1. Morning Joint stiffness >1
stiffness hour for >6 weeks
At least 3 active
joints for >6 weeks;
2. Arthritis of
commonly involved
three or more
joints are PIP, MCP,
joint areas
wrist, elbow, knee,
ankle, MTP
At least one active
3. Arthritis of
joint in wrist, MCP
hand joints
or PIP for >6 weeks
4. Symmetric Bilateral
 involvement of PIP,
arthritis MCP, or MTP for >6
weeks
Subcutaneous
nodules over bony
5. Rheumatoid prominences,
nodules extensor surfaces or
in juxta-articular
regions
Found in 60-80% of
6. Serum RF
RA patients
Erosions or
periarticular
7. osteopenia, likely to
Radiographic see earliest changes
changes at ulnar styloid, 2nd
and 3rd MCP and
PIP joints
Signs and Symptoms
Etiology and Pathophysiology
autoimmune disorder, unknown
etiology
hallmark of RA is hypertrophy
of the synovial membrane
o outgrowth of activated
rheumatoid synovium
(pannus) into and over
the articular surface
results in destruction
of articular cartilage
and subchondral bone
two theories attempt to explain
chronic remissions and
exacerbations seen in RA
o sequestered Ag
o molecular
Common sites of joint
involvement in mimicry RA
variable course of
exacerbations and
remissions
morning stiffness >1 hr,
improves with use,
aggravated by rest
symmetric joint
involvement
signs of disease activity:
synovitis (assessed by
tender and swollen joint
count), elevated serum
markers of inflammation
such as ESR or CRP,
decreased grip strength,
increased pain
signs of mechanical joint
damage: loss of motion,
instability, deformity,
crepitus
constitutional symptoms:
profound fatigue; rarely
myalgia or weight loss
extra-articular features (see
Figure 7 below) and
radiographic damage
limitation of function and
decrease in global
functional status
39
Investigations
RF positive in 80% of patients
o non-specific, also seen
in other rheumatic
diseases (e.g. SLE,
Sjogrens), chronic
inflammation (e.g.
SBE, hepatitis, TB)
and 5% of healthy
population
anti-CCP (cyclic citrullinated
peptide): sensitivity (~80%)
increased disease activity is
associated with decrease Hb
(anemia of chronic disease),
increased platelets, elevated
ESR, CRP, and RF
Classification of Global
Functional Status in RA
(American College of
Rheumatology, 1991)
Class I: able to perform usual
ADLs (self-care, vocational,
avocational)
Class II: able to perform self-
care and vocational activities,
restriction of avocational
activities
Class III: able to perform self-
care, restriction of vocational
and avocational activities
Class IV: limited in ability to
perform self-care, vocational,
avocational activities
Complications of Chronic
Synovitis
joint deformities (see Figure 8
below)
o swan neck deformity,
boutonnire deformity
 o ulnar deviation of
MCP; radial deviation
of wrist joint
o hammer toe, mallet
toe, claw toe
o flexion contractures
atlanto-axial and subaxial
subluxation
o C-spine instability
o neurological
impingement (long
tract signs)
o difficult intubation
limited shoulder mobility,
spontaneous tears of the rotator
cuff leading to chronic spasm
tenosynovitis => may cause
rupture of tendons
Carpal Tunnel Syndrome
ruptured Bakers cyst
(outpouching of synovium
behind the knee); presentation
similar to acute DVT
decreased functional capacity
and early mortality
aquatic/aerobic/strengthening
exercise between flares),
assistive devices and patient
education
patients may need job
modification, time off work or
change in occupation
B) Medical
Treatment NSAIDs, DMARDs, and
corticosteroids are the mainstay
goals of therapy of pharmacological therapy
o control disease activity 1. Reduction of Inflammation and
o relieve pain and Pain
stiffness
o maintain function and NSAIDS individualize according to
lifestyle efficacy and tolerability
o prevent or control
joint damage
contraindicated or
o key is early diagnosis cautioned in some patients
and early intervention
with disease
analgesics
modifying anti-
rheumatic drugs
(DMARDs) add acetaminophen
opioid prn for synergistic
pain control
corticosteroids
Clinical Pearl
Poor prognostic features of RA local
include young age of onset, high RF o intra-articular
titer, elevated ESR, activity of >20 injections to
joints, and presence of EAF. control symptoms
in a specific joint
o eye drops for eye
Clinical Pearl involvement
Common Syndromes in RA
1. Sjogrens syndrome (sicca systemic (prednisone)
complex, dry eyes and mouth)
2. Caplans syndrome o low dose (5-10
(multiple pulmonary nodules and mg/day) useful
pneumoconiosis) for (a) short term
3. Feltys syndrome (arthritis, to improve
splenomegaly, neutropenia) symptoms if
NSAIDs
ineffective, (b) to
A) Education, occupational bridge gap until
therapy, physiotherapy, DMARD takes
vocational counselling effect or (c) for
refractory disease
o moderate to high
therapeutic exercise program
dose (20-60+
(isometrics and active ROM
mg/day) for
exercise during flares,
40
 cardiopulmonary
disease
o high dose (1
mg/kg/day) for
vasculitis
o do baseline
DEXA bone
density scan and
start
bisphosphonate,
calcium, and
vitamin D therapy
if using
corticosteroids >3
months at >7.5
mg/day
side effects: osteoporosis,
avascular necrosis (AVN),
hypertension, cataracts,
glaucoma, peptic ulcer
disease (PUD),
susceptibility to
infection, hypokalemia,
hyperglycemia,
hyperlipidemia, weight
gain, acne
cautions/contraindications:
active infection,
osteoporosis, hypertension,
gastric ulcer, diabetes, TB
2. Disease Modifying
Antirheumatic Drugs (DMARDs)
combination DMARDs are the
standard of care
start DMARDs within 3 months
of diagnosis to decrease disease
progression, symptoms and
signs
DMARDs reduce or prevent
joint damage, and are
associated with better long-
term disability index
delayed onset of action (may
take 8-12 weeks)
many DMARDs have potential
toxicities that require periodic
monitoring
if repetitive flares, progressive
joint damage, or ongoing
disease activity after 3 months
of maximal therapy > change or
add other DMARDs
mild and early stages:
o hydroxychloroquine or Signs and Symptoms
sulfasalazine
monotherapy preferred characterized by periods of
moderate to severe disease exacerbation and remission
(especially if unfavourable systemic
prognostic factors): o fever, malaise, fatigue,
o methotrexate is the lymphadenopathy,
gold standard weight loss
o single regimen with vascular
methotrexate or o Raynauds
leflunomide phenomenon,
o combination therapy: thrombosis, vasculitis,
methotrexate + livedo reticularis
sulfasalazine + (mottled
hydroxychloroquine; discolouration of skin
methotrexate + due to narrowing of
cyclosporine; blood
methotrexate + vessels, characteristic
leflunomide lacy or net-like
biologics: indicated if persistent appearance)
disease activity dermatologic
o commonly used after o maculopapular rash,
failure of other photosensitivity,
DMARDs; however, panniculitis
evidence suggests (inflammation of
benefit from use in subcutaneous fat and
early RA as well muscle tissue),
alopecia (hair loss),
Clinical Pearl urticaria, purpura,
Only DMARDs (not analgesics or oral, nasal, genital
NSAIDs) alter the course of RA! ulcers
ophthalmic
o conjunctivitis,
C) Surgical Therapy episcleritis,
keratoconjunctivitis,
synovectomy: debridement cytoid bodies (cotton
and/or removal of inflamed wool
synovium from individual exudates on
joints (surgical or fundoscopy =
radioactive) infarction of nerve cell
joint replacement (hip, layer of retina)
shoulder, knee) gastrointestinal
joint fusion (wrist, thumb, o pancreatitis, lupus
ankle, C-spine) enteropathy, hepatitis,
reconstruction (tendon hepatomegaly
repair) pulmonary
surgery indicated for o interstitial lung
structural joint damage disease, pulmonary
hypertension, PE,
SLE alveolar hemorrhage,
Diagnostic Criteria of SLE: MD pleuritis
SOAP BRAIN musculoskeletal
Malar rash Blood o arthralgias, arthritis,
Discoid rash Renal avascular necrosis,
Serositis Arthritis myositis
Oral ulcers Immune neurologic
ANA Neurologic o depression, personality
Photosensitivity disorder, cerebritis,
41
 transverse myelitis, o bisphosphonates, Cushingoid Faces and buffalo
seizures, headache, calcium, vitamin D to hump
peripheral neuropathy combat osteoporosis Adrenal suppression and
o antimalarials atrophy
Investigations (hydroxychloroquine Weight gain, Na and water
if no serious internal retention, K depletion
organ involvement => Infections, especially viral, TB
serologic hallmark is high titer
improves long term and fungal
ANA detected by
control and prevents Osteoporosis, aseptic bone
immunofluorescence
flares) necrosis, ruptured Achilles
ANA has high sensitivity (98%)
o NSAIDs Gastrointestinal
and therefore is a useful
gastroprotective agent Despespsia, Peptic ulcer
screening test, but poor
for arthritis (also and perforation
specificity
beneficial for pleuritis Pancreatitis
anti-dsDNA Ab (detected by
and pericarditis CNS
Crithidia test, Farr
radioimmunoassay) and anti- organ threatening disease euphoria
Sm Ab are specific for SLE o systemic steroids to Psychosis, increased
(95-99%) minimize end organ intracranial pressure,
a drop in anti-dsDNA titer and damage secondary to increased tendency to
normalization of serum inflammation high- epilepsy
complement (C3, C4) are dose oral Cataracts, increased intra ocular
useful to monitor response to prednisone/IV pressure
treatment in patients who are methylprednisolone in Amenorrhea, premature
clinically and serologically severe disease menopause
concordant o steroid sparing agents: Teratongenity (fetal cleft
azathioprine, palate)
lupus anticoagulant may cause
methotrexate, Rebound disease on reducing
increased risk of arterial and
mycophenolate dosage
venous clotting and increased
o IV cyclophosphamide Myopathy or muscle atrophy
PTT
for serious organ
involvement (e.g. Cataracts
Treatment any opacity of the lens
cerebritis or SLE
nephritis) most common cause of
principles of therapy: reversible blindness worldwide
o treat early and avoid types: nuclear sclerosis,
Side Effects of Steroids
long term steriod use cortical, posterior subcapsular
if possible (see Figure 16 below)
o if high doses of Local:
steroids necessary for Atrophy
Perioral dermatitis Etiology
long-term control add
steroid sparing agents Steroid acne
Rosacea acquired
and taper when
Contact dermatitis o age-related (over 90%
possible
o treatment is tailored to Tachyphylaxis (tolerance) of all cataracts)
o cataract associated
organ system involved
and severity of disease Systemic: with systemic disease
o all medications used to Dermatological (may have juvenile
Thin, fragile skin onset)
treat SLE require
Mild hirsutism diabetes
periodic monitoring
Bruising mellitus
for potential toxicites
metabolic
dermatologic Facial erythema
disorders
o preventative: use Increased sweating
(e.g.
sunscreen, avoid UV Impaired wound healing, Wilsons
light and estrogens Striae disease,
o topical steroids for Acne galactosemia,
rash, antimalarials Growth suppression in children homocystinur
musculoskeletal Hypertension ia)
Hyperlipidemia hypocalcemia
Hyperglycemia
42
 o traumatic (may be
rosette shaped)
o intraocular
Classification
inflammation (e.g.
uveitis)
o toxic (steroids,
phenothiazines)
o radiation
congenital
o present with altered
red reflex or
leukocoria
o treat promptly to
prevent amblyopia
Diabetic Retinopathy
most common cause of
blindness in young people in
North America
blurring of distance vision with
rise of blood sugar
consider DM if unexplained
retinopathy, cataract, EOM
palsy, optic neuropathy, sudden
change in refractive error
loss of vision due to
o progressive
microangiopathy,
leading to macular
edema
o progressive diabetic
retinopathy -->
neovascularization -->
traction --> retinal
detachment and
vitreous hemorrhage
o rubeosis iridis
(neovascularization of
the iris) leading to
neovascular glaucoma
(poor prognosis)
o macular ischemia
Clinical Pearl
Macular edema is the most common
cause of visual loss in patients with
background DR.
Background:
Clinical Pearl
altered vascular permeability
(loss of pericytes, breakdown
Presence of DR in:
of blood-retinal barrier,
Type 1 DM
thickening of basement
25% after 5 years
membrane)
60% after 10 years
retinal vessel closure >80% after 15 years
Type 2 DM
20% at time of diagnosis
60% after 20 years
non-proliferative: increased
vascular permeability and
retinal ischemia Screening Guidelines for Diabetic
o dot and blot Retinopathy
hemorrhages
o microaneurysms Type 1 DM
o hard exudates (lipid o screen for retinopathy
deposits) beginning annually 5
o macular edema years after disease
advanced non-proliferative onset
(or pre-proliferative): o screening not
o non-proliferative indicated before the
findings plus onset of puberty
o venous beading (in 2 Type 2 DM
of 4 retinal quadrants) o initial examination
o intraretinal shortly after diagnosis,
microvascular then repeat annually
anomalies (IRMA) in pregnancy
1 of 4 retinal o ocular exam in 1st
quadrants trimester, close
IRMA: follow-up throughout
dilated, leaky as pregnancy can
vessels within exacerbate DR
the retina o gestational diabetics
o cotton wool spots not at risk for
(nerve fibre layer retinopathy
infarcts)
proliferative Treatment
o 5% of patients with
diabetes will reach this Diabetic Control and
stage Complications Trial (DCCT)
o neovascularization: o tight control of blood
iris, disc, retina to sugar decreases
vitreous frequency and severity
o neovascularization of of microvascular
iris (rubeosis iridis) complications
can lead to blood pressure control
neovascular glaucoma focal laser for clinically
o vitreous hemorrhage significant macular edema
from bleeding fragile panretinal laser
new vessels, fibrous photocoagulation, for
tissue can contract proliferative diabetic
causing tractional retinopathy, reduces
retinal detachment neovascularization, hence
o increased risk of reducing the angiogenic
severe visual loss stimulus from ischemic retina
by decreasing retinal metabolic
demand --> reduces risk of
blindness
vitrectomy for vitreous
hemorrhage and retinal
detachment in proliferative
diabetic retinopathy which is
complicated by non-clearing
43
 vitreous hemorrhage or retinal
detachment
the diabetic retinopathy
vitrectomy study indicated that
vitrectomy before vitreous
hemorrhage does not improve
the visual prognosis
Lens Changes
earlier onset of senile nuclear
sclerosis and cortical cataract
may get hyperglycemic
cataract, due to sorbitol
accumulation (rare)
sudden changes in refraction of
lens: changes in blood glucose
levels (poor control) may cause
refractive changes by 3-4
diopters
Hypertensive Retinopathy
retinopathy is the most
common ocular manifestation
of hypertension
key features of chronic HTN
retinopathy: AV nicking, blot
retinal hemorrhages,
microaneurysms, cotton wool
spots
key features of acute HTN
retinopathy: retinal arteriolar
spasm, superficial retinal
hemorrhage, cotton-wool spots,
optic disc edema
Table 6. Keith-Wagener-Barker
Classification
Group Mild to moderate narrowing
1 or sclerosis of the arterioles
Group Moderate to marked
2 narrowing of the arterioles
Local and/or generalized
narrowing of arterioles
Exaggeration of the light
reflex
Arteriovenous crossing
changes
Group Retinal arteriolar narrowing
3 and focal constriction
Retinal edema
Cotton-wool patches
Hemorrhage
Group Same as group 3, plus
4 papilledema
Glaucoma
aqueous is produced by the
ciliary body and flows from the
posterior chamber to the
anterior chamber through the
pupil, and drains into the
episcleral veins via the
trabecular meshwork and the
canal of Schlemm
an isolated increase in IOP is
termed ocular hypertension (or
glaucoma suspect) and these
patients should be followed for
increased risk of developing
glaucoma (~10% if IOP = 20-
30 mmHg; 40% if IOP = 30-40
mmHg; and most if IOP >40
mm Hg)
average IOP is 15 3 mm
Hg (diurnal variation, higher in Features of Papilledema
a.m.) Engorged retinal veins
pressures >21 mmHg more Loss of cupping
likely to be associated with Pink disk with blurred margins
glaucoma; however, up to 50%
Cribosa not visible
of patients with glaucoma do
Flamed shaped hemorrhages
not have IOP >21mmHg
normal C:D (cup:disc) ratio
Causes of Papilledema
<0.4
central retinal vein occlusion
be suspicious of glaucoma if
systemic illness
C:D ratio >0.6, C:D ratio
difference between eyes >0.2 or HTN, vasculitis, hypercapnia
toxic/metabolic/nutritional
cup approaches disc margin
loss of peripheral vision most deficiency
commonly precedes central loss infiltration
sequence of events: gradual o neoplastic: leukemia,
pressure rise, followed by lymphoma, glioma
o non-neoplastic:
increased C:D ratio, followed
by visual field loss sarcoidosis
screening tests should include: pseudotumour cerebri
o medical and family o idiopathic signs and
history symptoms of increased
o visual acuity testing ICP, with a normal CT
o slit lamp exam to o usually in obese young
assess anterior women
chamber depth compressive
o ophthalmoscopy to o meningioma,
assess the disc features hemangioma, thyroid
o tonometry by ophthalmopathy
applanation or
indentation to measure Optic Atrophy
the IOP
o visual field testing Damage to the optic nerve from
many different kinds of pathologies.
Not a disease, but rather a sign of an
underlying condition
44
Causes:

glaucoma,
anterior ischemic optic
neuropathy,
retinal lesions eg.
chorioretinitis, intraocular
bleed
tumour, aneurism or pagets
disease pressing on the optic
nerve,
optic neuritis (retrobulbar
neuritis)
Lebers hereditary optic
neuropathy,
Congenital
Division of optic nerve
surgeryor trauma

Signs and symptoms:

low visual acuity,
peripheral vision impairment,
difficulty with colour vision,
pallor of the optic disc on
fundoscopy

Management:
optic nerve atrophy is an
irreversible condition, management
of the underlying condition is
crucial to prevent exacerbation

45