Causes of Clubbing

Respiratory
Cancer
- Bronchogenic Ca
-Lung Mets
-Pleural Mesothelioma
- Oseophageal cancer
COPD
Tuberculosis

Suppurative Lung Disease

- Lung Abscess
- Empyema
- Bronchiectasis
Cystic Fibrosis
Interstitial Lung disease
- Sarcoidosis
- Fibrosing alveolitis
- Asbestosis etc.
Pulmonary AV fistula

Cardiovascular
Congenital Cyanotic Heart
disease
- Tetralogy of Fallot (ToF)
- Coarctation of aorta
- Pulmonary stenosis (critical)
Subacute Bacterial endocarditis
Eisenmengers syndrome
Left Atrial myxoma
Isolated Toe clubbing
- PDA with Shunt reversal
- Called Eisenmenger PDA
Abdomen
Liver Cirrhosis
Neoplasm
- Colorectal Ca
- Gastric Ca
- GI lymphoma
- Hepatoma
Inflammatory BD
- Crohns Disease
- Ulcerative colitis
Malabsorption
- Celiac disease
- Whipples disease
- Cystic Fibrosis
- Intestinal Polyposis
Other
Hyperthyroidism
- Particularly Graves
Idiopathic
Thymoma
Thalassemia

Causes of Hepatomegaly
Infection
Viral
-Hepatitis - EBV
Bacterial
-Weils disease (leptospiro.)
- Syphilis
Parasitic
-Hydatid cyst
-Schistosomiasis,
-Amoebic abscess,
- Malaria
- Leishmaniasis
Malignancy
Hepatocellular carcinoma
Metastases GI, Lung, breast
and melanomas
Hematologic
Myeloproliferative
-Myelofibrosis
-CML
Lymphoma
-Hodgkins
- Non-Hodgkins
Leukaemia
-ALL
-AML
Sickle cell
-Hepatic sequestration
-Extramedullary
haematopoiesis
Hepatic congestion
Cardiac failure
Hepatic vein thrombosis
Storage disorders
Wilsons
Haemochromatosis
Gauchers
Infiltrative
Sarcoidosis
Amyloidosis
Biliary obstruction; e.g. Pancreatic
Ca
Fatty Liver (NASH)
Early cirrhosis
Whipples disease
Causes of Pulsatile liver
Tricuspid regurgitation
Causes of Tender Hepatomegaly
Hepatitis
Rapid liver enlargement

o
o
o

Rt heart failure
Budd-Chiari
Syndrome
Hepatoma

Causes of Splenomegaly
Infection
Bacterial Subacute
bacterial endocarditis
Viral - CMV, EBV
Parasite - Malaria
Haematological
Lymphoproliferative
- Lymphoma
- Chronic LL
Myeloproliferative disease
- Myelofibrosis
-Chronic ML
-Polycythemia vera
-Essential thrombo.
Thalassemia
Sickle cell
Vascular congestion
Cirrhosis
Hepatic vein
obstruction
Connective Tissue
RA, SLE
Storage disorders
Gauchers disease
Niemann-Pick disease
Infiltrative
Amyloidosis
Sarcoidosis
Causes of Massive Splenomegaly
(>8cm)
Infection
Visceral Leishmaniasis
(Kala-azar)
Malaria
Schistosomiasis
Haematologic
Myeloproliferative
- CML, Myelofibrosis
Sickle cell
-Splenic Sequestration in
the young, HbSC disease

Storage Disorder
o Gauchers
Idiopathic Tropical (Africa
& South-East Asia)
Causes of Moderate Splenomegaly
(4 -8 cm)

Lymphoproliferative disorders
Hodgkins disease

Chronic lymphoytic
leukemia,
Cirrhosis with portal hypertension
Causes of Hepatsplenomealy
List is essentially the same as
splenomegaly alone. Common
causes include
- Chronic leukemias
- Lymphoproliferative disorders
- Cirrhosis with portal HTN
- Myelofibrosis
Causes of Palpable Kidneys
Thin individual
AD Polycystic kidney disease
Maligancy
- Renal Cell Cancer
- Wilms Tumour
(Nephroblastoma)
Hydronephrosis (Can be
bilateral rarely)
Renal Cyst / Abscess
Amyloidosis (Can be bilateral
rarely)
Hypertrophy of a single
functioning kidney
Nephropathy
o HIV
o Sickle cell
o Diabetes
Iliac Fossa
Renal Transplant (May have
cushinoid features 2nd to steroids
Generalized Lymphadenopathy
Infection
Viral
-HIV, Ebstein Barr virus,
CMV, Measles, Mumps,
Rubella, Viral Hepatitis,
Bacterial
- IE, Tb, Syphilis
Fungal
- Histoplasmosis
Protozoal
-Toxoplasmosis,
- Filariasis
- Leishmaniasis
Malignancy
o Leukaemia
-ALL, CLL
o Lymphoma
-Hodgkins, Non-Hodgkins

Metastatic Solid Tumour

Connective Tissue Disease
RA, SLE
Drugs
- Phenytoin, hydrallazine,
- allopurinol
Other
- Sarcoidosis
Localized Lynphadenopahy
Causes of Ascites
Portal (SAAG > 1.1g/dL)
Exudative (Protein >
2.5g/L)
o Budd-Chiari
o CCF
Transudative (Protein <
2.5g/dL)
o Cirrhosis
o Hepatic failure
Non-Portal (SAAG < 1.1g/dL)
Exudative (Protein >
2.5g/dL)
o Intra-abdominal
malignancy
o Intra-abdominal
infection e.g. Tb
o Pancreatitis
Transudative (Protein <
2.5g/dL)
o Nephrotic
Syndrome
o Protein-losing
enteropathy
o Severe
malnutrition with
anasarca

Renal causes e.g. acute

and
chronic renal failure
Vasodilators (especially CCBs)
Refeeding edema
Decreased oncotic pressure
Hypoalbuminemia
Hormonal
hypothyroidism
exogenous steroids
pregnancy
estrogen
Causes of Jaundice
Unconjugated
Prehepatic
Hemolytic anemia
- Sickle Cell Anemia - Hereditary Spherocytosis
- Hereditary Elliptocytosis
Gilberts syndome
Hematoma resorption
Conjugated
Hepatic
Viral Hepatits A B, C
Leptospirosis
Hepatic Abscess
Post Hepatic
Choledocholithiasis
Ascending Cholangitis
Sclerosing cholangitis
Pancreatits
Cancer at head of Pancreas or
Ampule
Methastatic cancer
Foreign body in CBD eg. worm

Causes of Local Edema

inflammation /infection
venous or lymphatic obstruction
thrombophlebitis
chronic lymphangitis
resection of regional lymph
nodes
filariasis

Causes of Tachpnea/SOB
Cardiovascular
acute MI
CHF/LV failure
aortic stenosis
mitral stenosis
elevated pulmonary venous
pressure

Some Causes of Generalized Edema

Increased hydrostatic pressure
Increased fluid retention
Cardiac causes e.g. CHF
Hepatic causes e.g.
cirrhosis

Respiratory
Airway disease
asthma
COPD exacerbation

upper airway obstruction

(foreign body, mucus
plugging, anaphylaxis)

Parenchymal lung disease

ARDS
pneumonia
interstitial lung disease
Pulmonary vascular dis.
PE
pulmonary HTN
pulmonary vasculitis
Pleural disease
pneumothorax

pleural effusion

Neuromuscular and chest wall disorders

C-spine injury

polymyositis, myasthenia gravis,

Guillain-Barri syndrome
kyphoscoliosis

Anxiety/psychosomatic
Severe anemia
Causes of Cough
Airway Irritants
Inhaled smoke, dusts, fumes

Lung abscess
Miscellaneous:
Goodpastures syndrome
Idiopathic pulmonary
hemosiderosis
Vascular Disease
PE

Elevated pulmonary venous

pressure:
LVF
Mitral stenosis
Vascular malformation
Miscellaneous
Impaired coagulation
Pulmonary endometriosis
Mediastinal Mass
Etiology and Pathophysiology

Aspiration astric contents

(GERD)
Oral secretion
Foreign body
Postnasal drip
Airway Disease
URTI including postnasal drip
and sinusitis
Acute or chronic bronchitis
Bronchiectasis
Neoplasm

External compression by node

or mass lesion
Asthma
COPD
Parenchymal Disease
Pneumonia
Lung abscess
Interstitial lung disease
CHF
Drug-induced (e.g. ACE inhibitor)
Differentials of Hemoptysis
Airway Disease
Acute or chronic bronchitis
Bronchiectasis
Bronchogenic CA
Bronchial carcinoid tumour
Parenchymal Disease
Pneumonia
TB

diagnosis is made by location

and patients age
anterior compartment
(sternum to anterior border of
pericardium) - more likely to be
malignant
o 5 Ts Thymoma
Thyroid enlargement
(goiter)
Teratoma
Thoracic aortic
aneurysm
Tumours (lymphoma,
parathyroid,
esophageal,
angiomatous)
o lymphoma, lipoma,
pericardial cyst
middle compartment (anterior
to posterior pericardium)
o pericardial cyst,
bronchogenic
cyst/tumour,
lymphoma, lymph
node enlargement,
aortic aneurysm
posterior compartment
(posterior pericardium to
vertebral column)
o neurogenic tumours,
meningocele, enteric
cysts, lymphomas,
diaphragmatic hernias,
esophageal tumour,
aortic aneurysm

Signs and Symptoms

50% asymptomatic (most of

these are benign); when
symptomatic, 50% are
malignant
chest pain, cough, dyspnea,
recurrent respiratory infections
hoarseness, dysphagia,
Horners syndrome,
facial/upper extremity edema
(SVC compression)
paraneoplastic syndromes (e.g.
myasthenia gravis (thymomas))

Investigations

CXR (compare to previous)

CT with contrast (provides
information regarding anatomic
location, density, relation to
mediastinal vascular structures)
MRI specifically indicated
in the evaluation of neurogenic
tumours
ultrasound (best for assessment
of structures in close proximity
to the heart and pericardium)
radionuclide scanning 131I
(for thyroid), Gallium (for
lymphoma)
biochemical studies thyroid
function, serum calcium,
phosphate, parathyroid
hormones, AFP, beta-hCG
biopsy (mediastinoscopy,
percutaneous needle aspiration)

Management

depends on the diagnosis

decide if the lesion should be
excised (most isolated benign
masses should be removed)
needle aspiration of suspected
benign cystic lesion
resection via minimally
invasive video assisted
procedures (bronchogenic
cysts, localized neurogenic
tumours)
exploration via sternotomy or
thoracotomy

diagnostic biopsy rather than

major operation if mass is
likely to be a lymphoma, germ
cell tumour, or unresectable
invasive malignancy
post-op
radiotherapy/chemotherapy if
malignant

Bronchogenic Cancer
Pathological Classification

bronchogenic cancer (90% of

primary lung cancers) (for
characteristics, see Table 24
below)
o classified into small
cell lung cancer
(SCLC) and nonSCLC (NSCLC i.e.
adenocarcinoma,
squamous cell, large
cell),
bronchioalvelolar
cancer (BAC)
o incidence of
adenocarcinoma is
increasing
lymphoma
secondary metastases: breast,
colon, prostate, kidney, thyroid,
stomach, cervix, rectum, testes,
bone, melanoma

Presentation by Location of
Tumour Extension

Risk Factors

cigarette smoking: 85% of lung

cancer related to smoking
asbestos 5x increased risk,
asbestos + smoker 80-90x
increased risk
radiation: radon, uranium
(especially if smoker)
arsenic, chromium, nickel
genetic damage
parenchymal scarring:
granulomatous disease, fibrosis,
scleroderma
passive exposure to cigarette
smoke
air pollution: exact role is
uncertain
HIV

cough (75%); beware of

chronic cough that changes in
character
dyspnea (60%)
chest pain (45%)
hemoptysis (35%)
other pain (25%)
clubbing (21%)
constitutional signs: anorexia,
weight loss, fever, anemia

lung, hilum, mediastinum,

pleura: pleural effusion,
atelectasis, wheezing
pericardium: pericarditis,
pericardial tamponade
esophageal compression:
dysphagia
phrenic nerve: paralyzed
diaphragm
recurrent laryngeal nerve:
hoarseness
superior vena cava syndrome:
obstruction of SVC causing
neck and facial swelling, as
well as dyspnea and cough
o other symptoms
associated with SVC
compression:
hoarseness, tongue
swelling, epistaxis,
and hemoptysis
o physical findings
include dilated neck
veins, increased
number of collateral
veins covering the
anterior chest wall,
cyanosis, edema of the
face, arms, and chest,
Pembertons sign
o milder symptoms if
obstruction is above
the azygos vein
lung apex (Pancoast tumour):
Horners syndrome, brachial
plexus palsy, most commonly
C8 and T1 nerve roots
rib and vertebrae: erosion
distant metastasis to brain,
bone, liver, adrenals
paraneoplastic syndromes

Signs and Symptoms

a group of disorders
associated with
malignant disease, not
related to the physical
effects of the tumour
itself
most often associated
with SCLC

Investigations

initial diagnosis
o imaging: CXR, CT
chest + upper
abdomen, PET scan,
bone scan
o cytology: sputum
o biopsy: bronchoscopy,
percutaneous,
mediastinoscopy
staging work-up
o blood work: LFTs,
calcium, ALP
o imaging: CXR, CT
thorax and abdomen,
bone scan,
neuroimaging
o invasive:
bronchoscopy,
mediastinoscopy,
mediastinotomy,
thoracotomy

Therapy for Bronchogenic

Cancer

chemotherapy (no role for

chemo alone, only in
combination with other
treatments)
o cisplatin and etoposide
o paclitaxel, vinorelbine,
and gemcitabine are
new NSCLC therapies
o new biologics, e.g.
epidermal growth
factor inhibitor
(Gefitinib)
o complications:
acute: tumour
lysis
syndrome,
infection,
bleeding,
myelosuppres
sion,
hemorrhagic

cystitis
(cyclophosph
amide),
cardiotoxicity
(doxorubicin)
, renal
toxicity
(cisplatin),
peripheral
neuropathy
(vincristine)
chronic:
neurologic
damage,
leukemia,
second
primary
neoplasms

radiotherapy
surgery
o only chance for cure is
resection when tumour
is still localized
o contraindications if
any evidence of local
extension or
metastases
patients with
surgically
resectable
disease must
undergo medi
astinal node
sampling
since CT
thorax is not
accurate
in 20-40% of
cases
poor
pulmonary
status (i.e.
unable to
tolerate
resection of
lung)
palliative care for end-stage
disease

2.

3.

etiology

congestive heart failure

cirrhosis
nephrotic syndrome
pulmonary embolism (may
cause transudative or exudative
effusion)
peritoneal dialysis,
hypothyroidism, CF,
urinothorax

Exudative Pleural Effusions

Pathophysiology: increased
permeability of pleural capillaries or
lymphatic dysfunction
etiology

infectious
o parapneumonic
effusion (associated
with bacterial
pneumonia, lung
abscess
o empyema (bacterial,
fungal, TB), TB
pleuritis, viral
infection
malignancy
lung carcinoma (35%)
lymphoma (10%)
metastases: breast
(25%), ovary, kidney
mesothelioma
vascular/cardiac
o collagen vascular
diseases: RA, SLE
o
o
o

pulmonary embolism,
after coronary artery
bypass surgery
intra-abdominal
o subphrenic abscess
o esophageal perforation
(elevated pleural fluid
amylase)
o pancreatic disease
(elevated pleural fluid
amylase)
o Meigs syndrome
(ascites and
hydrothorax
associated with an
ovarian fibroma or
other pelvic tumour
trauma
o chylothorax: occurs
when the thoracic duct
is disrupted and chyle
accumulates in the
pleural space, due to
trauma, tumour
o hemothorax: due to
rupture of a blood
vessel, commonly by
trauma or tumours
other
o pneumothorax
(spontaneous,
traumatic, tension)
o pleural thickening
(chronic infection,
neoplasm,
inflammatory)
o

Transudative Pleural Effusions

Pathophysiology: alteration of
systemic factors that affect the
formation and absorption of pleural
fluid (i.e. increased capillary
hydrostatic pressure, decreased
plasma oncotic pressure)

Pleural Effusion
Light's criteria - a pleural effusion is
likely exudative if at least one of the
following exists:
1. The ratio of pleural fluid
protein to serum protein is
greater than 0.5

The ratio of pleural fluid LDH

and serum LDH is greater than
0.6
Pleural fluid LDH is greater
than 2/3 times the normal upper
limit for serum

Appearance of Fluid
Bloody - trauma, malignancy
White - chylothorax, empyema
Black - aspergillosis, amoebic liver
abscess
Yellow-green - rheumatoid pleurisy
Viscous - malignant mesothelioma
Ammonia odour - urinothorax
Food particles - esophageal rupture
Analysis of Pleural Effusion
Protein, LDH - transudate vs.
exudate
Gram stain, Ziehl-Nielsen stain
(TB), culture - looking for
specific organisms
Cell count differential neutrophils vs. lymphocytes
(lymphocytic TB, lymphoma)

Cytology - malignancy,
infection
Glucose (low) RA, TB,
empyema, malignancy,
esophageal rupture
Rheumatoid factor, ANA,
complement - collagen
vascular disease
Amylase - pancreatitis,
esophageal perforation,
malignancy
pH - empyema <7.2, TB and
mesothelioma <7.3
Blood - mostly traumatic,
malignancy, PE with infusion,
TB
Triglycerides - chylothorax
from thoracic duct leakage,
mostly due to trauma, lung CA,
or lymphoma

Signs and Symptoms

Investigations

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

CXR
o
o

o
o

must have >250 ml of

pleural fluid for
visualization
lateral: small effusion
leads to blunting of
posterior costophrenic
angle
PA: blunting of lateral
costophrenic angle
dense opacification of
lung fields with
concave meniscus

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
o

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
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

with cor pulmonale

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

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)
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

Investigations

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

o
o

Others

note that signs and symptoms

vary with underlying disease
process

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,
lymphangiomyomatosi
s
PFTs
o restrictive pattern:
decreased lung
volumes (VC and
TLC) and compliance
o normal or increased
FEV1/FVC (>7080%), i.e. flow rates
are actually normal or
supernormal when
corrected for absolute
lung volume
o DCO decreased due to
less surface area for
gas exchange
pulmonary vascular
disease
ABGs
o initially may be
normal
o with progression of
disease, hypoxemia
and decreased PaCO2
may be present
Other

bronchoscopy,
bronchoalveolar
lavage, lung biopsy
c-ANCA (Wegners),
anti-GBM
(Goodpastures), ESR,
ANA (lupus), RF
(RA), serumprecipitating
antibodies to inhaled
organic antigens
(hypersensitivity
pneumonitis)

DIFFERENTIAL DIAGNOSIS OF
RESPIRATORY ALKALOSIS
Characterized by decreased PaCO2
secondary to hyperventilation
Hypoxemia
pulmonary disease (pneumonia,
edema, PE, interstitial fibrosis)
severe anemia
heart failure
high altitude
Respiratory centre stimulation
CNS disorders
hepatic failure
Gram-negative sepsis
drugs (ASA, progesterone,
theophylline, catecholamines,
psychotropics)
pregnancy
anxiety
pain
mechanical hyperventilation
(excessive mechanical
ventilation)
DIFFERENTIAL DIAGNOSIS OF
RESPIRATORY ACIDOSIS
Characterized by increased PaCO2
secondary to hypoventilation
respiratory centre depression
(decreased RR)
drugs (anesthesia, sedatives,
narcotics)
trauma
increased ICP
encephalitis

stroke
central apnea
supplemental O2 in chronic
CO2 retainers (i.e. COPD)
Neuromuscular disorders (decreased
TV)
myasthenia gravis

Guillain-Barr syndrome
poliomyelitis
muscular dystrophies
ALS
myopathies
chest wall disease (obesity,
kyphoscoliosis)
Airway obstruction (asthma, foreign
body) (decreased FEV)
Parenchymal disease
COPD
pulmonary edema
pneumothorax
pneumonia
pneumoconiosis
acute respiratory distress
syndrome (ARDS)
Mechanical hypoventilation
(inadequate mechanical ventilation)
Anion Gap Metabolic Acidosis
MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isopropyl alcohol / Iron / INH
Lactic acidosis
Ethylene glycol
Salicylates

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

<7.35), alkalemic (pH >7.45), or
normal (pH 7.35-7.45)
2. What is the primary disturbance?

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

metabolic: change in HCO3 and

pH in same direction
respiratory: change in HCO3
and pH in opposite direction

3. Has there been appropriate

compensation? (Table 7 below)

metabolic compensation occurs

over 2-3 days reflecting altered
renal HCO3
production/excretion
respiratory compensation
through ventilation control of
PaCO2 occurs immediately
inadequate compensation may
indicate a second acid-base
disorder

4. If there is metabolic acidosis,

what is the anion gap and osmolar
gap?

anion gap = [Na] - [Cl] [ HCO3]; normal = 10-15

mmol/L
osmolar gap = measured
osmolarity calculated
osmolarity = measured
(2[Na] + glucose + urea);
normal = 10

5. If anion gap is increased, is the

change in bicarbonate the same as
the change in anion gap?

if not, consider a mixed picture

Ventilatory Failure
Wont Breathe
respiratory centre depression
hypothyroid
sleep apnea
Cant Breathe
neuromuscular disorders
airway obstruction
parenchymal disease

Causes of Tachcardia/Palpitations
Cardiac
arrhythmias (PAB, PVB, SVT,
VT)
mitral valve prolapse
valvular heart disease
hypertrophic cardiomyopathy
Endocrine
thyrotoxicosis
pheochromocytoma
hypoglycemia
Systemic
fever
anemia
Drugs
tobacco,
caffeine,
alcohol,
epinephrine,
ephedrine,
aminophylline, atropine
Psychiatric
panic attack
Causes of Bradycardia

Physiologic
Athlete
Elderly
Pathologic
Heart block
Hypothermia
Hypothyroidism
Sick sinus syndrome
Raised intracranial
pressure
Drugs
-blockers
Ca2+-channel blockers
(Verapamil, Diltiazem)
Digoxin toxicity
Differentials of Chest Pain
*can be fatal acutely
Pulmonary
pneumonia
pulmonary embolism (PE)*
pneumothorax/hemothorax*
empyema
pulmonary neoplasm
bronchiectasis
TB
Cardiac
MI/angina*
myocarditis

pericarditis/Dresslers
syndrome*
cardiac tamponade*
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 (rightsided),pulsatile liver
Complicatons of MI
ACT RAPID
Arrhythmias (SVT, VT, VF)
Congestive cardiac failure
Thromboembolic disorders eg.
stroke, (DVT, PE later on)
Rupture (ventricle - Tampanade,
septum - VSD, papillary muscle Regurgitation)
Aneurysm (ventricle)
Pericarditis
Infaction (a second one)
Death/ Dressler's syndrome
Shock
Precipitants of Heart Failure
HTN (common)
Endocarditis/environment (e.g. heat
wave)
Anemia
Rheumatic heart disease and other
valvular disease
Thyrotoxicosis
Failure to take meds (very common)

10

Arrhythmia (common)
Infection/ischemia/infarction (common)
Lung problems (PE, pneumonia,
COPD)
Endocrine (pheochromocytoma,
hyperaldosteronism)
Dietary indiscretions (common)

Cause Irregularly irregular pulse

Atrial Fibrillation
Rheumatic mitral disease
(esp Mitral Stenosis)
Aortic Stenosis
HTN
Thyrotoxicosis
Ischemic heart disease
Drugs
o Alcohol
CCF, Cardiomyopathy
Atrial Flutter
Causes of Collapsing Pulse

Fever
Anemia
Thyrotoxicosis
Aortic regurgitation
Pregnancy
Exercise

Left Parasternal Heave

L Atrial enlargement (2nd to severe
MR)
RV Enlargement w/ Pulmon. HTN
Severe LV Enlargement
Apex beat (location & character)
Tapping Palpable S1 (Think MS)
Thrusting LV Hypertrophy
Displaced Dilatation from volume
overload eg. AR, MR R to L shunt
or Cardiomyopathy
Impalpable Obesity, effusion and
Hyperinflation
Palpable P2
Pulmonary hypertension
Features of First heart sound
Loud: mitral stenosis,
Soft: mitral incompetence
Features of Second heart sound
Soft: Aortic or pulmonary stenosis
Loud: Systemic(A2) or P. HTN (P2)
Wide Fixed split: ASD

Paradoxical Fixed Split: Delayed

LV or early RV emptying

Causes of Mitral regurgitation

Ring
Dilated cardiomyopathy
Hypertensive heart disease
Ischemic cardiomyopathy
Leaflet
Mitral valve prolapse
RHD
IE
Chordae
rupture
Papillary muscle
Ischemia / rupture
Connective tissue disease
Marfans syndome
Mitral Regurge

Etiology
Annlus LV dilatation/
aneurysm (CHF, DCM,
myocarditis), IE abscess, MV
annulus calcification
Leaflets - Congenital cleft
leaflets, myxomatous
degeneration (MVP, Marfans
syndrome), RHD, collagen VD
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

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

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

Etiology
Supravalvular:
Aortic root disease (Marfans,
atherosclerosis & dissecting
aneurysm, connective tissue
disease)
Valvular:
Congenital (bicuspid AV, large
VSD), IE

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

Acute Onset: IE, aortic dissection,

trauma, failed prosthetic valve

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

11

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 femoralbrachial 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 middiastolic 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.

12

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 A2Opening 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,
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, brachialradial delay, pulsus parvus et
tardus, sustained PMI
Auscultation: crescendodecrescendo 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

13

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
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

pulmonary ejection click, rightsided S4

Investigations
ECG: RVH
CXR: prominent pulmonary
arteries enlarged RV
echo: diagnostic
Treatment
Balloon valvuloplasty if severe
symptoms
Surgical Options
Percutaneous or open balloon
valvuloplasty
Pulmonary Regurge

Etiology
Pulmonary HTN, IE, rheumatic
disease, tetrology of Fallot, postrepair
Pathophysiology
Increased RV volume =>
increased wall tension => RV
hypertrophy => right heart
failure
Symptoms
Chest pain, syncope, fatigue,
peripheral edema

Etiology
Usually congenital, rheumatic
disease (rare), carcinoid
Pathophysiology
Increased RV pressure => RV
hypertrophy => right heart
failure
Symptoms
Chest pain, syncope, fatigue,
peripheral edema
Physical Exam
Systolic murmur at 2nd LICS
accentuated by inspiration,

Physical Exam
Early diastolic murmur at LLSB,
Graham Steell (diastolic)
murmur 2nd and 3rd LICS
increasing with inspiration
Investigations
ECG: RVH
CXR: prominent pulmonary
arteries if pulmonary HTN;
enlarged RV
echo: diagnostic
Treatment
Rarely requires treatment; valve
replacement if severe
Surgical Options

14

Pulmonary valve replacement

Mitral Valve Prolapse
Etiology
Myxomatous degeneration of
chordae; thick, bulky leaflets
that crowd orifice; Marfans
syndrome; pectus excavatum,
straight back syndrome, other
MSK abnormalities; <3% of
population, F=M
Pathophysiology
MV displaced into LA during
systole; no causal mechanisms
found for symptoms
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
tissue); mid to late systolic
murmur at apex, accentuated by
Valsalva or squat-to-stand
maneuvers
Investigations
ECG: non-specific ST-T wave
changes, PSVT, ventricular
ectopy
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

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

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%)

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)

15

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
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

prognosis and treatment

o if associated with
other lesions (e.g.
PDA, VSD) can cause
CHF
o complications:
hypertension
o management: balloon
arterioplasty or
surgical correction in
symptomatic neonate,
give prostaglandins to
open up PDA for
stabilization

Aortic Stenosis (children)

valvular (75%), subvalvular

(20%), supravalvular and
idiopathic hypertrophic
subaortic stenosis (IHSS) (5%)
history: often asymptomatic but
may be associated with CHF,

the child inspires

100% oxygen
o if PaO2 improves to
greater than 150
mmHg, cyanosis less
likely cardiac in origin
survival depends on mixing via
shunts (e.g. ASD, VSD, PDA)

JVP

Pulmonary Stenosis (Children)

investigations:
ECG-RVH early in infancy, LVH
later in childhood

exertional chest pain, syncope

or sudden death
physical exam: SEM at upper
right sternal border (URSB)
with aortic ejection click at the
apex
treatment
o surgical repair if infant
with critical aortic
stenosis or older child
with symptoms or
peak gradient >50
mmHg
o exercise restriction
required

valvular (90%), subvalvular, or

supravalvular
usually part of other congenital
heart lesions (e.g. Tetralogy of
Fallot) or in association with
other syndromes (e.g.
congenital rubella, Noonan
syndrome)
critical pulmonic stenosis:
inadequate pulmonary blood
flow, dependent on ductus for
oxygenation, progressive
hypoxia and cyanosis
history: spectrum from
asymptomatic to CHF
physical exam: wide split S2 on
expiration, SEM at ULSB,
pulmonary ejection click
investigations:
o ECG: RVH
o CXR: dilated poststenotic pulmonary
artery
treatment: surgical repair if
critically ill or severe PS, or if
presence of symptoms in older
infants/children
systemic venous return reenters systemic circulation
directly
most prominent feature is
cyanosis (O2 sat <75%)
differentiate between cardiac
and other causes of cyanosis
with hyperoxic test
o obtain preductal, right
radial ABG in room
air, repeat ABG after

16

A Rt atrial contraction
C bulging of tricuspid
valve into Rt atrium on
ventricular contraction
x descent lowering Rt
atrial pressure as tricuspid
ring moves down
V atrial filling
y descent opening of
tricuspid valve
ventricular filling
Raised JVP with normal
waveform Rt heart
failure; fluid overload
Raised JVP with absent
pulsation SVC
obstruction
Absent a wave A. Fib
Large a wave pulm HTN
pulm stenosis, tricuspid
stenosis
Cannon a wave complete
heart block
CV wave tricuspid
regurgitation

Lower Motor Exam Check

List
Look at attitude of limb,
Neurocutaneous lesion,
Spontaneous or induced
fasciculations.
Do clonus at knees as well
Causes of Proximal Myopathy
Congenital
Muscle dystrophy
Inflammatory
Polymyositis
Dermatomyositis
Polymyalgia rheumatica
Endocrine

Cushings Syndrome
(including iatrogenic)
Diabetes Mellitus
Hypothyroidism /
Hyperthyroidism
Acromegaly
Addisons disease
Conns syndrome
Hyperparathyroidism /
hypoparathyroidism
Metabolic
Osteomalacia
Hypokalemia
Hypercalcemia
Toxic
Alcohol
Vitamin E
Organophosphate
Drugs
Corticosteroids
Amiodarone
Vincristine
Paraneoplastic
Carcinomatous
neuromyopathy
Dermatomyositis
Causes of Spastic Paraparesis

HAM/TSP
Spinal cord compression
Multiple Sclerosis
Subacute Combined
Degeneration of the cord
(Vit B12 def)
Transverse Myelitis
Parasagittal Meningioma
HIV-associated
myelopathy
Tabes dorsalis

Causes of Spastic Hemiplegia

CVA
Tumour
Brown-Sequard

Causes of Flaccid paraparesis

Poliomyelitis
Guillain-Barre
Motor Neuron Disease
Spina bifida
Botulism
Cauda equina syndrome

Flaccid Hemiplegia

Acute CVA
Plexopathy

Sensory Exam Check List

Look for Ulcers, U. Cath or Diaper
Do light touch, sharp touch,
Proprioception (toe and ankle)
Causes of Sensory Disturbance

stroke
tumour
multiple sclerosis
peripheral neuropathies
B12 deficiency

Causes of a Sensory Level

(Sensation is lost below a
particular level)
Transverse myelitis
Spinal cord compression
Spinal cord tumour

Cervical spondylosis
Traumatic injury to spinal cord
Causes of Peripheral Neuropathy
Renal failure
Infection
HIV
Leprosy
Lyme disease
Infiltrative
Sarcoidosis
Amyloidosis
Inflammatory
Guillain-Barre
RA
SLE
Nutritional
Vit B1 Deficiency
Vit B6 Deficiency
Vit B12 deficiency
Vit E Deficiency
Endocrine
Diabetes Mellitus
Acromegaly
Heavy metal
Lead
Mercury
Drugs

17

Isoniazid
Phenytoin
Metronidazole
Methotrexate

Peripheral Neuropathy (DANG

THE RAPIST)
DM, Uremia
Amyloidosis
Nutritional (Vit B1, 6, 12 def)
Guillain-Barre
Toxins & drugs (lead, mercury,
organophosphate, metronidazole,
isoniazid, ethambutol, vincristine,
amiodarone)
Hereditary (Friedrichs ataxia,
porphyria, Charcot-marie-tooth)
Endocrine (acromegaly)
Rheumatoid & vasculitides (SLE,
RA, Polyarteritis nodosa, Sjogrens,
Churg-Strauss)
Alcohol
Paraproteinemia (Multiple
myeloma) / Paraneoplastic (nonmetastatic manifestation)
Infectious (HIV, Leprosy, Lyme
disease, diphtheria, tetanus,
botulism)
Sarcoidosis
Thyroid (hypothyroidism)
Oculomotor Nerve
CN 3 motor nucleus at level of
superior colliculus + EdingerWestphal (parasympathetic
peripheral fibres) passes b/w
posterior cerebral & superior
cerebellar arteries superior
orbital fissure
Ischemia (e.g. Diabetic
mononeuropathy)
o Pupillary sparing
Compression (e.g. post
communication artery
aneurysm)
Abducens Nerve

DM
HTN
Vasculitis

Causes of Facial Weakness

upper motor neuron
TIA/stroke
post-ictal hemiparesis
tumour

infection: otitis media,

mastoiditis, Epstein-Barr
virus (EBV), herpes zoster
virus (HZV), Lyme
disease, HIV

lower motor neuron

infection: otitis media,

mastoiditis, Epstein-Barr
virus (EBV), herpes zoster
virus (HZV), Lyme
disease, HIV
idiopathic (Bells
palsy)
sarcoid
neuropathy (DM)
parotid gland

Facial Nerve
Bells palsy
Ipsilateral LMN facial
Bells phenomenon
Hyperacusis
o If nerve to
stapedius is
involved
Salivation
Lacrimation
Causes of Ptosis
cranial nerve III palsy

myasthenia gravis
(uni/bilateral)
Horners syndrome
congenital/idiopathic
myotonic dystrophy
(bilateral)

Causes of Facial Pain

sinusitis
dental disease
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. MillerFisher 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

18

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)
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
hemiparesis or loss of position sense
Spasticity - Indicates upper motor
neuron disease
Atrophy and fasciculations
-Indicates lower motor neuron
disease

Cogwheel rigidity - is seen in

extrapyramidal processes (e.g.
Parkinsons Disease)

Loss of vibration sense suggests

peripheral neuropathy or posterior
column lesion

Symmetrical weakness of proximal

muscles suggests myopathy; of
distal muscles suggests
polyneuropathy

Impaired graphesthesia and

stereognosis with intact primary
sensation indicates parietal lesion

Reflexes Interpretation
Increased in upper motor neuron
disease

Other Stuff
Dolls movement, if absent,
suggests pons or midbrain lesion or
very deep coma

Decreased/absent in lower motor

neuron disease, myopathies or
neuromuscular junction disorders

Loss of vestibulo-ocular reflex

with caloric stimulation suggests
brain stem lesion or drug toxicity

Slow relaxation of knee or ankle

reflex is seen in hypothyroidism

Absence seizures can be

precipitated by hyperventilation

Babinski sign suggests an upper

motor neuron lesion but may be
seen following a seizure

Characteristic skin lesions are

seen in neurocutaneaous syndromes
(e.g. neurofibromatosis, tuberous
sclerosis complex, Sturge-Weber
syndrome)

Sensory Examination
posterior columns
vibration,
proprioception,
light touch)
Spinothalamic
pain
temperature
Cortical sensation
graphesthesia,
stereognosis,
extinction,
2-point discrimination
Co-ordination
finger to nose,
heel to shin,
rapid alternating
movements
Stance & Gait
Romberg,
tandem gait
Sensory Exam Interpretation
Hemisensory loss - with sensory
level or dissociation loss suggests
spinal cord lesion
Symmetrical distal sensory loss
suggests polyneuropathy

19

Where is the Lesion ?

Cortex and internal Capsule
Contralateral sensory & motor
deficits
Cortical lesions:
Associated with aphasia,
neglect, extinction,
graphaesthesia, visual loss
(higher level dysfunctions) and
astereognosia
Internal capsule lesions:
Associated with pure motor,
pure sensory losses,
incoordination, absence of
cortical features
Common causes:
Seizure disorder (cortex only)
Coma
Stroke
Cerebellum and Basal Ganglia
Coordination Problems
Cerebellar Lesions:
Abnormal intentional
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
Nerve Root
Radicular pain (sharp, electric,
radiating) + sensory loss in
dermatome/weakness in
myotome or absent reflex

Common Causes:
Nerve root compression
Disk herniation
Peripheral Nerve
Ipsilateral motor and sensory
deficits along a nerve
distribution.
LMN signs power, wasting,
reflexes, normal or tone)
In Polyneuropathy (distal
weakness, glove and stocking
distribution of sensory loss)
Common Causes:
Neuropathy
Neuromuscluar Junction
Proximal & symmetrical
muscle weakness
No sensory loss

Fatiguability (?Repeated
strength testing)
Diplopia, ptosis, bulbar
weakness

Common Causes:
Myasthenia gravis
Lambert-Eaton syndrome
Botulism
Muscle
Proximal & symmetrical
muscle weakness
No sensory loss

LMN signs wasting, normal

or reflexes, normal or tone

Common Causes:
Muscular dystrophies
Myopathies including
polymyositis
Dermatomyositis
Altered Mental Status
Coma
Diffuse CNS
head trauma
infection
inflammation/ vasculitis
global cerebral ischemia

sublcilincal seizure/ postictal state

hypertensive
encephalopathy

20

Metabolic
diabetic ketoacidosis
hypoglycemia
electrolyte disturbance
acid-base disturbance
thiamine deficiency
Systemic
liver failure
renal failures
sepsis
Focal CNS
abscess
epidural/ subdural
hematoma
hemorrhage/ aneurysm
hydrocephalus
stroke
tumour
venous occlusion
Glascow Coma Scale
Eyes Open
4 = Spontaneously
3 = To voice
2 = To pain
1 = No response
Best Verbal Response
5 = Answers questions
appropriately
4 = Confused, disoriented
3 = Inappropriate words
2 = Incomprehensible sounds
1 = No verbal response
Best Motor Response
6 = Obeys commands
5 = Localizes to pain
4 = Withdraws from pain
3 = Decorticate (flexion)
2 = Decerebrate (extension)
1 = No response

Acute Confusional states

(delirium)
I WATCH DEATH"
Infectious

Withdrawal from drugs

Acute metabolic disorder
Trauma
CNS pathology
Hypoxia
Deficiencies in vitamins
Endocrinopathies
Acute vascular insults

Toxins
Heavy metals

Dementia
Other psychiatric
(e.g. depression)
Mental Status Exam: ASEPTIC
Appearance and behaviour
Speech
Emotion (mood and affect)
Perception
Thought content and process
Insight and judgment
Cognition

Rheumatology
Demographics: name, age,
occupation
History
SLE
Joint pain (duration &
severity), swelling, redness,
warmth
Chest pain
Photosensitivity
Seizure
Change in personality
Recurrent early pregnancy
losses
Systemic Sclerosis
Cold numbness & pain
in fingers; fingertips pale,
then blue
Difficulty swallowing
RA
Difficulty dressing, undoing
buttons, washing, opening
bottle, opening door
Morning stiffness
Joint pain (duration &
severity), swelling, redness,
stiffness, warmth
Sjgrens
Dry eyes
Dry mouth
Difficulty swallowing
Joint pain
Cold numbness & pain
in fingers; fingertips pale,
then blue
Behets
Recurrent painful oral &
genital ulcers
Blurry vision, periorbital
pain

Examination
SLE
Malar rash
Oral ulcers
Arthritis
Discoid rash
alopecia
Systemic Sclerosis
Taut skin; loss of
wrinkling
telangiectasia
Sausage-shaped fingers
Wasting of thenar &
hypothenar eminences
Loss of pulp of digits
Beaked nose
Radial furrowing
Oral cavity unable to admit
3 of patients own fingers
RA
Arthritis
Swan neck & Boutonnire
deformities; Z thumb
Ulnar deviation
Wasting of small muscles
of hands
Rheumatoid nodules
(palpate extensor surface
of forearm)
Sjgrens
Dry mucous membranes
Dental caries
Arthritis
Parotid gland enlargement
Behets
Oral & genital ulcers
Sclera injection &
excessive lacrimation
(uveitis)
DDx

Osteoarthritis
o DIP Heberdens
nodes
o PIP - Bouchards
nodes
Gout
o Gouty tophi 1st
metatarsophalang
eal joint
o

Counselling Station
1.

Introduction

21

2.

So, what do you know about

your condition?
3. [Educate & counsel based on
info received prior]
a. Build rapport
b. Ask if they understand
4. Do you have any questions?
5. [Summarise] So, do you
remember what we spoke about
today? ...
6. This is a continuous education
process, unfortunately we cant
do everything in this session.
Further counselling will be
necessary & I would
recommend that for your next
visit, you have a family
member or loved one
accompany you.
Features of Hyperthyroidism
General
fatigue, heat intolerance,
irritability, fine tremor
Cardiovascular
tachycardia, atrial fibrillation,
palpitations elderly patients
may have only cardiovascular
symptoms, commonly new onset
atrial fibrillation
GI
weight loss with increased
appetite, thirst, increased
frequency of bowel movements
(hyperdefecation)
Neurology
proximal muscle weakness,
hypokalemic periodic paralysis
(common in Orientals)
GU
scant menses, decreased fertility
Dermatology
fine hair, skin moist and warm,
vitiligo, soft nails with
onycholysis (Plummers nails),
clubbing (acropachy), palmar
erythema, pretibial mxyedema
MSK
decreased bone mass, proximal
muscle weakness
Hematology
leukopenia, lymphocytosis,
splenomegaly,
lymphadenopathy (occasionally
in Gravesdisease
Signs and Symptoms of
Hypothyroidism
HISFIRMCAP

Hypoventilation
Intolerance to cold
Slow HR
Fatigue
Impotence
Renal impairment
Menorrhagia/amenorrhea
Constipation
Anemia
Paresthesiaia
Hypercalcemia
1. Calcium = Ca++ uptake
(milk alkali syndrome)
2. Hyperparathyroidism (1
hyperparathyroidism is
associated with Ca++)
3. Iatrogenic (drug induced as
occurs with thiazides, or
lithium)
4. Metastasis (bone and
prostate metastasis can
lead to Ca++)
5. Pagets disease of bone
6. Addisons disease
7. Neoplasm as in metastasis
8. ZE syndrome (MEN I - 1
HPT)
9. Excessive vitamin D intake
10. Excessive vitamin A intake
11. Sarcoidosis

Psychiatry
Multiaxial Assessment
Axis I
o differential diagnosis
of DSM-IV clinical
disorders
Axis II
o personality disorders,
mental retardation
Axis III
o general medical
conditions that are
potentially relevant to
the understanding or
management of the
mental disorder
Axis IV
o psychosocial and
environmental issues
Axis V
o global assessment of
functioning (GAF, 0 to
100) incorporating
effects of axes I to IV

Axis V: Global Assessment of

Functioning
91- Superior functioning in a wide
100 range of activities
81Absent or minimal symptoms
90
If symptoms are present, they
71- are transient and expected
80 reactions to psychosocial
stressors
Some mild symptoms or some
61difficulty but generally
70
functioning well
51- Moderate symptoms or
60 difficulty
41Serious symptoms or difficulty
50
Some impairment in reality
31testing/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
11maintain minimal hygiene or
20
gross impairment in
communication
Persistent danger of severely
hurting self or others or
1persistent 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

22

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
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

23

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, obsessivecompulsive
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 **
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)

Subtypes

**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, selfcare) 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

paranoid
o preoccupation with
one or more delusions
(typically persecutory
or grandiose) or
frequent auditory
hallucinations
o relative preservation
of cognitive
functioning and affect;
onset tends to be later
in life; believed to
have the best
prognosis
catatonic
o at least two of: motor
immobility (catalepsy
or stupor); excessive
motor activity
(purposeless, not
influenced by external
stimuli); extreme
negativism (resistance
to
instructions/attempts
to be moved) or
mutism; peculiar
voluntary movement
(posturing, stereotyped
movements, prominent
mannerisms);
echolalia (repeating
words/phrases of
anothers speech)
or echopraxia
(imitative repetition of
anothers
movements, gestures
or posture)
disorganized
o disorganized speech
and behaviour; flat or
inappropriate affect
o poor premorbid
personality, early and
insidious onset, and
continuous course
without significant
remissions
undifferentiated
o symptoms of criteria
A met, but does not
fall into the 3 previous
subtypes
residual

24

absence of prominent
delusions,
hallucinations,
disorganized speech,
grossly disorganized
or catatonic behaviour
continuing evidence of
disturbance indicated
by the presence of
negative symptoms or
two or more
symptoms in criteria A
present in attenuated
form

Good Prognositic Factors

Acute onset
Precipitating factors
Good cognitive functioning
Good premorbid functioning
No family history
Presence of affective symptoms
Absence of structural brain
abnormalities
Good response to drugs
Good support system
Etiology - multifactorial:
disorder is a result of interaction
between both biological and
environmental factors
genetic 50% concordance in
monozygotic (MZ) twins; 40%
if both parents have
schizophrenia; 10% of
dizygotic (DZ) twins, siblings,
children affected
neurochemistry - dopamine
hypothesis theory: excess
activity in the mesolimbic
dopamine pathway may
mediate the positive symptoms
of psychosis (i.e. delusions,
hallucinations, disorganized
speech and behaviour, and
agitation)
neuroanatomy - decreased
frontal lobe function,
asymmetric temporal/limbic
function, decreased basal
ganglia function; subtle
changes in thalamus, cortex,
corpus callosum, and
ventricles; cytoarchitectural
abnormalities
neuroendocrinology
abnormal growth hormone,

prolactin, cortisol, and

adrenocorticotropic hormone
neuropsychology global
defects seen in attention,
language, and memory suggest
lack of connectivity of neural
networks
indirect evidence of
geographical variance, winter
season of birth, and prenatal
viral exposure

day to 1 month, with eventual

full return to premorbid level of
functioning
can occur after a stressful event
or postpartum (see Postpartum
Mood Disorders)
treatment: secure
environment, antipsychotics,
anxiolytics
prognosis: good, self-limiting,
should return to pre-morbid
function in about 1 month

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

Management of Schizophrenia

pharmacological
o acute treatment and
maintenance with
antipsychotics
anticonvulsants
anxiolytics
o management of side
effects
psychosocial
o psychotherapy
(individual, family,
group): supportive,
cognitive behavioural
therapy (CBT)
o assertive community
treatment (ACT)
o social skills training,
employment
programs, disability
benefits
o housing (group home,
boarding home,
transitional home)

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

Schizophreniform Disorder

diagnosis: criteria A, D & E of

schizophrenia are met; an
episode of the disorder lasts at
least 1 month but less than 6
months
treatment: similar to acute
schizophrenia
prognosis: better than
schizophrenia; begins and ends
more abruptly; good pre- and
post-morbid function

Brief Psychotic Episode

diagnosis: acute psychosis
(presence of 1 or more positive
symptoms in criteria A1-4 of
schizophrenia) lasting from 1

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)

25

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)

apraxia (impaired
ability to carry out
motor activities
despite intact motor
function)
agnosia (failure to
recognize or identify
objects despite intact
sensory function)
disturbance in
executive functioning
(i.e. planning,
organizing,
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

Validated screening questionnaire

(Alcohol):

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

26

C ever felt the need to Cut

down on drinking?
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)?
for men, a score of >2 is a
positive screen and for women,
a score of >1 is a positive
screen
if positive CAGE, then assess
further to distinguish between
problem drinking and alcohol
dependence

General Assessment
When was the last drink?
Do you have to drink more to
get the same effect?
Do you get shaky or nauseous
when you stop drinking?
Have you had a withdrawal
seizure?
How much time and effort do
you put into obtaining alcohol?
Has your drinking affected your
ability to work, go to school, or
have relationships?
Have you suffered any legal
consequences?
Has your drinking caused any
medical problems?
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
drinking
Experiencing medical, social,
or financial problems caused by
drinking

Adverse Medical Conditions alcohol

GI: gastritis, dyspepsia, pancreatitis,

liver disease, bleeds, diarrhea,
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
behaviour modification:
hypnosis, relaxation
training, aversion therapy,
assertiveness training,
operant conditioning
supportive services: halfway houses, detoxification
centres, Alcoholics
Anonymous
psychotherapy,
motivational interviewing
medications important as
adjunctive treatment:
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 opioiddependent
patients

Signs of Alcohol withdrawl

(Delerium Tremens)
Autonomic hyperactivitiy
(diaphoresis, tachycardia, increased

27

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 1020
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

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 antiseizure 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
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

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

28

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

Prognosis

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
marijuana is the most often used
illicit drug
psychoactive substance delta-9tetrahydrocannabinol (9-THC)
smoking is the most common
mode of self-administration
intoxication characterized by
tachycardia, conjunctival vascular
engorgement, dry mouth, increased
appetite, increased sense of wellbeing, euphoria/laughter, muscle
relaxation, impaired performance on
psychomotor tasks including
driving
high doses can cause
depersonalization, paranoia, and
anxiety

 may trigger psychosis and

schizophrenia in predisposed
individuals
chronic use associated with
tolerance and an apathetic,
amotivational state
cessation does not produce
significant withdrawal phenomenon

treatment of dependence
includes behavioural and
psychological interventions to
maintain an abstinent state

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 obsessivecompulsive behaviour (Tourette's
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

DSM-IV-TR Criteria for Major

Depressive Episode

Medical Workup of Mood

Disorder

routine screening:
o physical examination
o complete blood count
thyroid function test
electrolytes
urinalysis, urine drug
screen
addtional screening:
o neurological
consultation
o chest x-ray
o electrocardiogram
o CT scan
o
o
o

Risk Factors for Depression

sex: female > male
age: onset in 25-50 year age
group
family history: depression,
alcohol abuse, sociopathy
childhood experiences: loss of
parent before age 11, negative
home environment (abuse,
neglect)
personality: insecure,
dependent, obsessional
recent stressors (illness,
financial, legal)
postpartum <6 months

29

lack of intimate, confiding

relationships or social isolation

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 moodincongruent 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)
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

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

Treatment

Criteria for Depression (>5):

MSIGECAPS
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
more Major Depressive Episodes; to
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

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; 1419% DZ twins

neurotransmitter dysfunction at
level of synapse (decreased
activity of serotonin,
norepinephrine, dopamine)
secondary to general medical
condition

psychosocial

psychodynamic (e.g. low selfesteem)

30

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)

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

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 goaldirected 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
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
o

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

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)

slight increase in upper

socioeconomic groups

31

60-65% of bipolar patients have

family history of major mood
disorders

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

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

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
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)

(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

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:

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)

32

(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:

Treatment

buspirone (tid
dosing)
o others:
SSRIs/SNRI,
TCAs, betablockers
combinations of above
o

(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
(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

33

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, ObsessiveCompulsive Disorder, PostTraumatic 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)
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
Nausea
Tingling
Shortness of breath
Fear of dying, losing control, going
crazy
3 C's: Chest pain, Chills, Choking

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

Suicide

Approach

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

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

34

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
Onset and frequency of
thoughts - When did this start?
How often do you have these
thoughts?
Control over suicidal ideation Can you stop the thoughts or
call someone for help?
Lethality - Do you want to end
your life? Or get a release from
your emotional pain
Access to means - How will
you get a gun? Which bridge do
you think you would go to?
Time and place - Have you
picked a date and place? Is it in
an isolated location?
Provocative factors - What
makes you feel worse (e.g.
being alone)?
Protective factors - What keeps
you alive (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:
o patients who are not
actively suicidal, with
no plan or access to
lethal means
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

(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

New stuff

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

Distribution

associated with personal or

family history of atopy

35

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

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

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
flare
o systemic
immunosuppression
may be needed in
severe cases
o flares may respond to
systemic antistaphylococcal therapy
side effects:
skin atrophy,
purpura,
striae, steroid
acne, perioral
dermatitis,
and glaucoma
when used
around the
eyes
b) topical immunomodulators
o long-term
management

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 longterm 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
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

36

calcineurin inhibitors
such as pimecrolimus
(Elidel) and
tacrolimus
(Protopic)
block
calcineurin
and inhibit
inflammatory
cytokine
transcription
in activated
T-cells and
other
inflammatory
cells
significant adverse
events may include
skin burning and
transient irritation
advantages of longterm management of
AD over long-term
corticosteroid use:
rapid,
sustained
effect in
controlling
pruritus
produce no
skin atrophy
safe for the
face and neck
no significant
systemic
toxicities
associated
with their use

Prognosis
50% clear by age 13, few
persist >30 years of age

Complications

infections are common:

diagnose early and treat
appropriately (i.e.
antibiotic, antifungal,
antiviral therapy);
infections must be resolved
before applying antiinflammatory treatments

o
o

topical mupirocin
or fusidic acid is
often sufficient
oral antibiotics
(i.e. cloxacillin,
cephalexin) for
widespread S.
aureus infections

Seborrheic Dermatitis

Greasy, erythematous, yellow,

non-pruritic scaling papules
and plaques; occurs in areas
rich in sebaceous glands

scalp: salicylic acid in olive oil

or Derma-Smoothe FS lotion
(peanut oil, mineral oil,
fluocinolone acetonide 0.01%)
to remove dense scales, 2%
ketoconazole shampoo
(Nizorale), ciclopirox (Stieprox
) shampoo, selenium sulfide
(e.g. Selsun) or zinc pyrithione
(e.g. Head and Shoulders)
shampoo, steroid lotion (e.g.
betamethasone valerate 0.1%
lotion bid)

HTLV Associated Dermatitis

Etiology

possible etiologic association

with Pityrosporum ovale
(yeast)

Epidemiology

common in infants and at

puberty
increased incidence in
immunocompromised patients
e.g. HIV
in adults, can cause dandruff
(pityriasis sicca)

Signs and Symptoms

infants - one cause of cradle

cap
children may be generalized
with flexural and scalp
involvement
adults - diffuse in areas of scalp
margin with yellow to white
flakes, pruritus, and underlying
erythema
sites: scalp, eyebrows,
eyelashes, beard, face, trunk,
body folds, genitalia
face: eyebrows, sides of nose,
posterior ears, glabella
chest: over sternum

Treatment

face: Nizoral cream OD + mild

steroid cream OD or bid

The average age of onset is

2 years.
The skin manifestations
become less severe with
age.
Severe exudative dermatitis
of the scalp, external ear,
retroauricular areas, eyelid
margins, paranasal skin,
neck, axillae and groins
Generalized fine papular
rash
Chronic watery nasal
discharge sometimes with
crusting
HTLV-1 seropositivity
Staphylococcus aureus
and/or B-haemolytic
streptococci commonly
cultured from anterior nares
and skin
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

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

Epidemiology

association with hepatitis C

may be triggered by severe
emotional stress

Signs and Symptoms

37

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

suspected human herpes virus 7

Treatment

atopic dermatitis, mycosis

fungoides (cutaneous T-cell
lymphoma), seborrheic
dermatitis, tinea

no treatment needed; clears

spontaneously in 6-12 weeks,
reassurance
topical corticosteroids when
post-inflammatory
pigmentation is a concern

a common chronic and recurrent

disease characterized by wellcircumscribed erythematous
papules/plaques with silvery-white
scales, mostly at sites of repeated
trauma

Secondary syphilis can present with

a non-pruritic papulosquamous
eruption but usually ALSO has
palmar lesions.
Psoriasis

decreased epidermal transit

time from basal to horny layers
shortened cell cycle of psoriatic
and normal skin --> excess
keratinization with scales

GUTTATE PSORIASIS
("DROP-LIKE")

Definition and Clinical Features

multifactorial inheritance

Clinical Pearl
Woronoffs Ring

PSORIASIS: Pathophysiology

Woronoffs ring: blanched halo that

surrounds psoriatic lesions after
topical or phototherapy treatments

Classification
plaque psoriasis
guttate psoriasis
erythrodermic psoriasis
pustular psoriasis
psoriatic arthritis

preventative measures: avoid

sunburns, avoid drugs that
exacerbate the condition (betablockers, 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

Epidemiology

Mnemonic

Pink papules/Plaques/Pinpoint
bleeding (Auspitz sign)/Physical
injury (Koebner phenomenon)
Silver scale/Sharp margins
Onycholysis/Oil spots
Rete Ridges with Regular elongation
Itching
Arthritis/Abscess
(Monro)/Autoimmune
Stratum corneum with nuclei
Immunologic
Stratum granulosum absent

Pathophysiology

Clinical Pearl

PLAQUE PSORIASIS

Etiology

Differential Diagnosis

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

38

UVB phototherapy, sunlight,

lubricants
penicillin V or erythromycin if
Group A beta-hemolytic
Streptococcus on throat culture

ERYTHRODERMIC
PSORIASIS

Definition and Clinical Features

Treatment

discrete, scattered salmon-pink

scaling papules
sites: generalized, sparing
palms and soles
often antecedent streptococcal
pharyngitis

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
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

see earliest changes

at ulnar styloid, 2nd
and 3rd MCP and
PIP joints

Etiology and Pathophysiology

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
stiffness

Joint stiffness >1

hour for >6 weeks

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

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
Bilateral
4. Symmetric 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

Signs and Symptoms

6. Serum RF

Found in 60-80% of
RA patients

7.
Radiographic
changes

Erosions or
periarticular
osteopenia, likely to

39

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

Complications of Chronic
Synovitis

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

Class I: able to perform usual

ADLs (self-care, vocational,
avocational)
Class II: able to perform selfcare and vocational activities,
restriction of avocational
activities
Class III: able to perform selfcare, restriction of vocational
and avocational activities
Class IV: limited in ability to
perform self-care, vocational,
avocational activities

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

Treatment
goals of therapy
o
o
o
o
o

Classification of Global
Functional Status in RA
(American College of
Rheumatology, 1991)

40

control disease activity

relieve pain and
stiffness
maintain function and
lifestyle
prevent or control
joint damage
key is early diagnosis
and early intervention
with disease
modifying antirheumatic drugs
(DMARDs)

corticosteroids
Clinical Pearl

Poor prognostic features of RA

include young age of onset, high RF
titer, elevated ESR, activity of >20
joints, and presence of EAF.

local
o

osteoporosis, hypertension,
gastric ulcer, diabetes, TB
intra-articular
injections to
control symptoms
in a specific joint
eye drops for eye
involvement

2. Disease Modifying
Antirheumatic Drugs (DMARDs)

Clinical Pearl
Common Syndromes in RA

1. Sjogrens syndrome (sicca

complex, dry eyes and mouth)
2. Caplans syndrome
(multiple pulmonary nodules and
pneumoconiosis)
3. Feltys syndrome (arthritis,
splenomegaly, neutropenia)

A) Education, occupational
therapy, physiotherapy,
vocational counselling

therapeutic exercise program

(isometrics and active ROM
exercise during flares,
aquatic/aerobic/strengthening
exercise between flares),
assistive devices and patient
education
patients may need job
modification, time off work or
change in occupation

o
o

B) Medical

NSAIDs, DMARDs, and

corticosteroids are the mainstay
of pharmacological therapy

1. Reduction of Inflammation and

Pain

NSAIDS individualize according to

efficacy and tolerability

contraindicated or
cautioned in some patients

analgesics

add acetaminophen
opioid prn for synergistic
pain control

systemic (prednisone)

low dose (5-10

mg/day) useful
for (a) short term
to improve
symptoms if
NSAIDs
ineffective, (b) to
bridge gap until
DMARD takes
effect or (c) for
refractory disease
moderate to high
dose (20-60+
mg/day) for
cardiopulmonary
disease
high dose (1
mg/kg/day) for
vasculitis
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,

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 longterm 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
sulfasalazine
monotherapy preferred
moderate to severe disease
(especially if unfavourable
prognostic factors):
o methotrexate is the
gold standard
o single regimen with
methotrexate or
leflunomide
o combination therapy:
methotrexate +
sulfasalazine +
hydroxychloroquine;
methotrexate +
cyclosporine;
methotrexate +
leflunomide
biologics: indicated if persistent
disease activity
o commonly used after
failure of other
DMARDs; however,
evidence suggests
benefit from use in
early RA as well

Clinical Pearl
Only DMARDs (not analgesics or

41

NSAIDs) alter the course of RA!

C) Surgical Therapy

synovectomy: debridement
and/or removal of inflamed
synovium from individual
joints (surgical or
radioactive)
joint replacement (hip,
shoulder, knee)
joint fusion (wrist, thumb,
ankle, C-spine)
reconstruction (tendon
repair)
surgery indicated for
structural joint damage

SLE
Diagnostic Criteria of SLE: MD
SOAP BRAIN
Malar rash
Blood
Discoid rash
Renal
Serositis
Arthritis
Oral ulcers
Immune
ANA
Neurologic
Photosensitivity

Signs and Symptoms

characterized by periods of
exacerbation and remission
systemic
o fever, malaise, fatigue,
lymphadenopathy,
weight loss
vascular
o Raynauds
phenomenon,
thrombosis, vasculitis,
livedo reticularis
(mottled
discolouration of skin
due to narrowing of
blood
vessels, characteristic
lacy or net-like
appearance)
dermatologic
o maculopapular rash,
photosensitivity,
panniculitis
(inflammation of
subcutaneous fat and
muscle tissue),
alopecia (hair loss),

urticaria, purpura,
oral, nasal, genital
ulcers
ophthalmic
o conjunctivitis,
episcleritis,
keratoconjunctivitis,
cytoid bodies (cotton
wool
exudates on
fundoscopy =
infarction of nerve cell
layer of retina)
gastrointestinal
o pancreatitis, lupus
enteropathy, hepatitis,
hepatomegaly
pulmonary
o interstitial lung
disease, pulmonary
hypertension, PE,
alveolar hemorrhage,
pleuritis
musculoskeletal
o arthralgias, arthritis,
avascular necrosis,
myositis
neurologic
o depression, personality
disorder, cerebritis,
transverse myelitis,
seizures, headache,
peripheral neuropathy

venous clotting and increased

PTT
Treatment

Investigations

serologic hallmark is high titer

ANA detected by
immunofluorescence
ANA has high sensitivity
(98%) and therefore is a useful
screening test, but poor
specificity
anti-dsDNA Ab (detected by
Crithidia test, Farr
radioimmunoassay) and antiSm Ab are specific for SLE
(95-99%)
a drop in anti-dsDNA titer and
normalization of serum
complement (C3, C4) are
useful to monitor response to
treatment in patients who are
clinically and serologically
concordant
lupus anticoagulant may cause
increased risk of arterial and

42

principles of therapy:
o treat early and avoid
long term steriod use
if possible
o if high doses of
steroids necessary for
long-term control add
steroid sparing agents
and taper when
possible
o treatment is tailored to
organ system involved
and severity of disease
o all medications used to
treat SLE require
periodic monitoring
for potential toxicites
dermatologic
o preventative: use
sunscreen, avoid UV
light and estrogens
o topical steroids for
rash, antimalarials
musculoskeletal
o bisphosphonates,
calcium, vitamin D to
combat osteoporosis
o antimalarials
(hydroxychloroquine
if no serious internal
organ involvement =>
improves long term
control and prevents
flares)
o NSAIDs
gastroprotective agent
for arthritis (also
beneficial for pleuritis
and pericarditis
organ threatening disease
o systemic steroids to
minimize end organ
damage secondary to
inflammation highdose oral
prednisone/IV
methylprednisolone in
severe disease
o steroid sparing agents:
azathioprine,
methotrexate,
mycophenolate

IV cyclophosphamide
for serious organ
involvement (e.g.
cerebritis or SLE
nephritis)

Side Effects of Steroids

Local:
Atrophy
Perioral dermatitis
Steroid acne
Rosacea
Contact dermatitis
Tachyphylaxis (tolerance)
Systemic:
Dermatological
Thin, fragile skin
Mild hirsutism
Bruising
Facial erythema
Increased sweating
Impaired wound healing,
Striae
Acne
Growth suppression in children
Hypertension
Hyperlipidemia
Hyperglycemia
Cushingoid Faces and buffalo
hump
Adrenal suppression and
atrophy
Weight gain, Na and water
retention, K depletion
Infections, especially viral, TB
and fungal
Osteoporosis, aseptic bone
necrosis, ruptured Achilles
Gastrointestinal
Despespsia, Peptic ulcer
and perforation
Pancreatitis
CNS
euphoria
Psychosis, increased
intracranial pressure,
increased tendency to
epilepsy
Cataracts, increased intra ocular
pressure
Amenorrhea, premature
menopause
Teratongenity (fetal cleft
palate)
Rebound disease on reducing

dosage
Myopathy or muscle atrophy

Cataracts
any opacity of the lens
most common cause of
reversible blindness worldwide
types: nuclear sclerosis,
cortical, posterior subcapsular
(see Figure 16 below)

Etiology

acquired
o age-related (over 90%
of all cataracts)
o cataract associated
with systemic disease
(may have juvenile
onset)
diabetes
mellitus
metabolic
disorders
(e.g.
Wilsons
disease,
galactosemia,
homocystinur
ia)
hypocalcemia
o traumatic (may be
rosette shaped)
o intraocular
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

43

progressive
microangiopathy,
leading to macular
edema
progressive diabetic
retinopathy -->
neovascularization -->
traction --> retinal
detachment and
vitreous hemorrhage
rubeosis iridis
(neovascularization of
the iris) leading to
neovascular glaucoma
(poor prognosis)
macular ischemia

Clinical Pearl
Macular edema is the most common
cause of visual loss in patients with
background DR.

Background:

altered vascular permeability

(loss of pericytes, breakdown
of blood-retinal barrier,
thickening of basement
membrane)
retinal vessel closure

Classification

non-proliferative: increased
vascular permeability and
retinal ischemia
o dot and blot
hemorrhages
o microaneurysms
o hard exudates (lipid
deposits)
o macular edema
advanced non-proliferative
(or pre-proliferative):
o non-proliferative
findings plus
o venous beading (in 2
of 4 retinal quadrants)
o intraretinal
microvascular
anomalies (IRMA) in
1 of 4 retinal
quadrants
IRMA:
dilated, leaky

vessels within
the retina
o cotton wool spots
(nerve fibre layer
infarcts)
proliferative
o 5% of patients with
diabetes will reach this
stage
o neovascularization:
iris, disc, retina to
vitreous
o neovascularization of
iris (rubeosis iridis)
can lead to
neovascular glaucoma
o vitreous hemorrhage
from bleeding fragile
new vessels, fibrous
tissue can contract
causing tractional
retinal detachment
o increased risk of
severe visual loss

Type 2 DM
20% at time of diagnosis
60% after 20 years

Screening Guidelines for Diabetic

Retinopathy

Type 1 DM
o screen for retinopathy
beginning annually 5
years after disease
onset
o screening not
indicated before the
onset of puberty
Type 2 DM
o initial examination
shortly after diagnosis,
then repeat annually
pregnancy
o ocular exam in 1st
trimester, close
follow-up throughout

Treatment

Clinical Pearl
Presence of DR in:
Type 1 DM
25% after 5 years
60% after 10 years
>80% after 15 years

as pregnancy can
exacerbate DR
gestational diabetics
not at risk for
retinopathy

Diabetic Control and

Complications Trial (DCCT)
o tight control of blood
sugar decreases
frequency and severity
of microvascular
complications
blood pressure control
focal laser for clinically
significant macular edema
panretinal laser
photocoagulation, for
proliferative diabetic
retinopathy, reduces
neovascularization, hence
reducing the angiogenic
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
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

44

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 = 2030 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
a.m.)

pressures >21 mmHg more

likely to be associated with
glaucoma; however, up to 50%
of patients with glaucoma do
not have IOP >21mmHg
normal C:D (cup:disc) ratio
<0.4
be suspicious of glaucoma if
C:D ratio >0.6, C:D ratio
difference between eyes >0.2 or
cup approaches disc margin
loss of peripheral vision most
commonly precedes central loss
sequence of events: gradual
pressure rise, followed by
increased C:D ratio, followed
by visual field loss
screening tests should include:
o medical and family
history
o visual acuity testing
o slit lamp exam to
assess anterior
chamber depth
o ophthalmoscopy to
assess the disc features
o tonometry by
applanation or
indentation to measure
the IOP
o visual field testing

Pink disk with blurred margins

Cribosa not visible
Flamed shaped hemorrhages

Causes of Papilledema
central retinal vein occlusion
systemic illness
HTN, vasculitis, hypercapnia
toxic/metabolic/nutritional
deficiency
infiltration
o neoplastic: leukemia,
lymphoma, glioma
o non-neoplastic:
sarcoidosis
pseudotumour cerebri
o idiopathic signs and
symptoms of increased
ICP, with a normal CT
o usually in obese young
women
compressive
o meningioma,
hemangioma, thyroid
ophthalmopathy
Optic Atrophy
Damage to the optic nerve from
many different kinds of pathologies.
Not a disease, but rather a sign of an
underlying condition
Causes:

Features of Papilledema
Engorged retinal veins
Loss of cupping

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,

45

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