Loren Warmington

Causes of Clubbing o Budd-Chiari

Respiratory Causes of Hepatomegaly Syndrome
Cancer Infection o Hepatoma
- Bronchogenic Ca Viral
-Lung Mets -Hepatitis - Causes of Splenomegaly
-Pleural Mesothelioma - EBV Infection
- Oseophageal cancer Bacterial Bacterial Subacute
COPD -Weils disease (leptospiro.) bacterial endocarditis
Tuberculosis - Syphilis Viral - CMV, EBV
Parasitic Parasite - Malaria
Suppurative Lung Disease
-Hydatid cyst Haematological
- Lung Abscess
-Schistosomiasis, Lymphoproliferative
- Empyema
-Amoebic abscess,
- Bronchiectasis - Lymphoma
- Malaria
Cystic Fibrosis - Chronic LL
- Leishmaniasis
Interstitial Lung disease Myeloproliferative disease
Malignancy
- Sarcoidosis - Myelofibrosis
Hepatocellular carcinoma
- Fibrosing alveolitis -Chronic ML
Metastases GI, Lung, breast -Polycythemia vera
- Asbestosis etc.
Pulmonary AV fistuala and melanomas -Essential thrombo.
Hematologic Thalassemia
Myeloproliferative Sickle cell
Cardiovascular
-Myelofibrosis
Congenital Cyanotic Heart Vascular congestion
-CML Cirrhosis
disease
Lymphoma
- Tetralogy of Fallot (ToF) Hepatic vein
-Hodgkins
- Coarctation of aorta obstruction
- Non-Hodgkins
- Pulmonary stenosis (critical) Connective Tissue
Leukaemia
Subacute Bacterial endocarditis RA, SLE
-ALL
Eisenmengers syndrome -AML Storage disorders
Left Atrial myxoma Sickle cell Gauchers disease
Isolated Toe clubbing -Hepatic sequestration Niemann-Pick disease
- PDA with Shunt reversal -Extramedullary Infiltrative
- Called Eisenmenger PDA haematopoiesis Amyloidosis
Abdomen Hepatic congestion Sarcoidosis
Liver Cirrhosis Cardiac failure
Hepatic vein thrombosis Causes of Massive Splenomegaly
Neoplasm
Storage disorders (>8cm)
- Colorectal Ca
Wilsons Infection
- Gastric Ca
Haemochromatosis Visceral Leishmaniasis
- GI lymphoma
- Hepatoma Gauchers (Kala-azar)
Inflammatory BD Infiltrative Malaria
- Crohns Disease Sarcoidosis Schistosomiasis
- Ulcerative colitis Amyloidosis Haematologic
Malabsorption Biliary obstruction; e.g. Pancreatic Myeloproliferative
- Celiac disease Ca - CML, Myelofibrosis
- Whipples disease Fatty Liver (NASH) Sickle cell
- Cystic Fibrosis Early cirrhosis -Splenic Sequestration in
- Intestinal Polyposis Whipples disease the young, HbSC disease
Other
Hyperthyroidism Causes of Pulsatile liver Storage Disorder
- Particularly Graves Tricuspid regurgitation o Gauchers
Idiopathic Idiopathic Tropical (Africa
Thymoma & South-East Asia)
Causes of Tender Hepatomegaly Causes of Moderate Splenomegaly
Thalassemia
Hepatitis (4 -8 cm)
Rapid liver enlargement Lymphoproliferative disorders
o Rt heart failure Hodgkins disease

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 Loren Warmington
Chronic lymphoytic RA, SLE Refeeding edema
leukemia, Drugs
Cirrhosis with portal hypertension - Phenytoin, hydrallazine, Decreased oncotic pressure
- allopurinol Hypoalbuminemia
Causes of Hepatsplenomealy Other Hormonal
List is essentially the same as - Sarcoidosis hypothyroidism
splenomegaly alone. Common exogenous steroids
causes include Localized Lynphadenopahy pregnancy
- Chronic leukemias estrogen
- Lymphoproliferative disorders Causes of Ascites
- Cirrhosis with portal HTN Portal (SAAG > 1.1g/dL)
- Myelofibrosis Exudative (Protein > Causes of Jaundice
2.5g/L) Unconjugated
Causes of Palpable Kidneys o Budd-Chiari Prehepatic
Thin individual o CCF Hemolytic anemia
AD Polycystic kidney disease Transudative (Protein < - Sickle Cell Anemia -
Maligancy 2.5g/dL) - Hereditary Spherocytosis
- Renal Cell Cancer o Cirrhosis - Hereditary Elliptocytosis
- Wilms Tumour o Hepatic failure Gilberts syndome
(Nephroblastoma) Hematoma resorption
Non-Portal (SAAG < 1.1g/dL)
Hydronephrosis (Can be
Exudative (Protein >
bilateral rarely) Conjugated
2.5g/dL)
Renal Cyst / Abscess o Intra-abdominal Hepatic
Amyloidosis (Can be bilateral Viral Hepatits A B, C
malignancy
rarely) o Intra-abdominal Leptospirosis
Hypertrophy of a single infection e.g. Tb Hepatic Abscess
functioning kidney o Pancreatitis Post Hepatic
Nephropathy Choledocholithiasis
Transudative (Protein <
o HIV Ascending Cholangitis
2.5g/dL)
o Sickle cell o Nephrotic Sclerosing cholangitis
o Diabetes Pancreatits
Syndrome
o Protein-losing Cancer at head of Pancreas or
Iliac Fossa Ampule
Renal Transplant (May have enteropathy
o Severe Methastatic cancer
cushinoid features 2nd to steroids Foreign body in CBD eg. worm
malnutrition with
Generalized Lymphadenopathy anasarca Causes of Tachpnea/SOB
Infection Cardiovascular
Viral Causes of Local Edema
acute MI
-HIV, Ebstein Barr virus, inflammation /infection
venous or lymphatic obstruction CHF/LV failure
CMV, Measles, Mumps,
Rubella, Viral Hepatitis, thrombophlebitis aortic stenosis
Bacterial chronic lymphangitis mitral stenosis
- IE, Tb, Syphilis resection of regional lymph elevated pulmonary venous
Fungal nodes pressure
- Histoplasmosis filariasis
Protozoal Respiratory
-Toxoplasmosis, Airway disease
Some Causes of Generalized Edema
- Filariasis Increased hydrostatic pressure asthma
- Leishmaniasis Increased fluid retention COPD exacerbation
Malignancy Cardiac causes e.g. CHF upper airway obstruction
o Leukaemia Hepatic causes e.g. (foreign body, mucus
-ALL, CLL cirrhosis plugging, anaphylaxis)
o Lymphoma Parenchymal lung disease
Renal causes e.g. acute
-Hodgkins, Non-Hodgkins
and ARDS
Metastatic Solid Tumour pneumonia
chronic renal failure
Connective Tissue Disease interstitial lung disease
Vasodilators (especially CCBs)
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 Loren Warmington
Pulmonary vascular dis. Vascular Disease symptomatic, 50% are
PE PE malignant
pulmonary HTN Elevated pulmonary venous chest pain, cough, dyspnea,
pulmonary vasculitis pressure: recurrent respiratory infections
Pleural disease LVF hoarseness, dysphagia,
pneumothorax Mitral stenosis Horners syndrome,
pleural effusion Vascular malformation facial/upper extremity edema
Miscellaneous (SVC compression)
Neuromuscular and chest wall disorders Impaired coagulation paraneoplastic syndromes (e.g.
C-spine injury Pulmonary endometriosis myasthenia gravis (thymomas))
polymyositis, myasthenia gravis,
Guillain-Barri syndrome Mediastinal Mass Investigations
kyphoscoliosis

Anxiety/psychosomatic Etiology and Pathophysiology CXR (compare to previous)

Severe anemia CT with contrast (provides
diagnosis is made by location information regarding anatomic
Causes of Cough and patients age location, density, relation to
Airway Irritants anterior compartment mediastinal vascular structures)
Inhaled smoke, dusts, fumes (sternum to anterior border of MRI specifically indicated
Aspiration astric contents pericardium) - more likely to be in the evaluation of neurogenic
(GERD) malignant tumours
Oral secretion o 5 Ts Thymoma ultrasound (best for assessment
Foreign body Thyroid enlargement of structures in close proximity
(goiter) to the heart and pericardium)
Postnasal drip
Teratoma radionuclide scanning 131I
Airway Disease
Thoracic aortic (for thyroid), Gallium (for
URTI including postnasal drip
aneurysm lymphoma)
and sinusitis Tumours (lymphoma, biochemical studies thyroid
Acute or chronic bronchitis parathyroid, function, serum calcium,
Bronchiectasis esophageal, phosphate, parathyroid
Neoplasm angiomatous) hormones, AFP, beta-hCG
External compression by node o lymphoma, lipoma, biopsy (mediastinoscopy,
or mass lesion pericardial cyst percutaneous needle aspiration)
Asthma middle compartment (anterior
COPD to posterior pericardium) Management
Parenchymal Disease o pericardial cyst,
Pneumonia bronchogenic
depends on the diagnosis
Lung abscess cyst/tumour,
lymphoma, lymph decide if the lesion should be
Interstitial lung disease excised (most isolated benign
node enlargement,
CHF aortic aneurysm masses should be removed)
Drug-induced (e.g. ACE inhibitor) posterior compartment needle aspiration of suspected
(posterior pericardium to benign cystic lesion
Differentials of Hemoptysis resection via minimally
vertebral column)
Airway Disease invasive video assisted
o neurogenic tumours,
Acute or chronic bronchitis procedures (bronchogenic
meningocele, enteric
Bronchiectasis cysts, lymphomas, cysts, localized neurogenic
Bronchogenic CA diaphragmatic hernias, tumours)
Bronchial carcinoid tumour esophageal tumour, exploration via sternotomy or
Parenchymal Disease aortic aneurysm thoracotomy
Pneumonia diagnostic biopsy rather than
TB major operation if mass is
Lung abscess likely to be a lymphoma, germ
Miscellaneous: cell tumour, or unresectable
Signs and Symptoms
Goodpastures syndrome invasive malignancy
Idiopathic pulmonary 50% asymptomatic (most of
hemosiderosis these are benign); when
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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 non-
SCLC (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
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
Signs and Symptoms
cough (75%); beware of
chronic cough that changes in
character
dyspnea (60%)
Loren Warmington
chest pain (45%) o most often associated
hemoptysis (35%) with SCLC
other pain (25%)
clubbing (21%) Investigations
constitutional signs: anorexia,
weight loss, fever, anemia initial diagnosis
o imaging: CXR, CT
Presentation by Location of chest + upper
Tumour Extension abdomen, PET scan,
bone scan
o cytology: sputum
lung, hilum, mediastinum,
o biopsy: bronchoscopy,
pleura: pleural effusion,
atelectasis, wheezing percutaneous,
mediastinoscopy
pericardium: pericarditis,
staging work-up
pericardial tamponade
o blood work: LFTs,
esophageal compression:
calcium, ALP
dysphagia
o imaging: CXR, CT
phrenic nerve: paralyzed
thorax and abdomen,
diaphragm
bone scan,
recurrent laryngeal nerve: neuroimaging
hoarseness o invasive:
superior vena cava syndrome: bronchoscopy,
obstruction of SVC causing mediastinoscopy,
neck and facial swelling, as mediastinotomy,
well as dyspnea and cough thoracotomy
o other symptoms
associated with SVC Therapy for Bronchogenic
compression: Cancer
hoarseness, tongue
swelling, epistaxis,
chemotherapy (no role for
and hemoptysis
o physical findings chemo alone, only in
include dilated neck combination with other
veins, increased treatments)
number of collateral o cisplatin and etoposide
veins covering the o paclitaxel, vinorelbine,
anterior chest wall, and gemcitabine are
cyanosis, edema of the new NSCLC therapies
face, arms, and chest, o new biologics, e.g.
Pembertons sign epidermal growth
o milder symptoms if factor inhibitor
obstruction is above (Gefitinib)
the azygos vein o complications:
lung apex (Pancoast tumour): acute: tumour
Horners syndrome, brachial lysis
plexus palsy, most commonly syndrome,
infection,
C8 and T1 nerve roots
bleeding,
rib and vertebrae: erosion
myelosuppres
distant metastasis to brain,
sion,
bone, liver, adrenals
hemorrhagic
paraneoplastic syndromes
cystitis
o a group of disorders
(cyclophosph
associated with amide),
malignant disease, not
cardiotoxicity
related to the physical (doxorubicin)
effects of the tumour , renal
itself
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 Loren Warmington
toxicity Transudative Pleural Effusions o esophageal perforation
(cisplatin), Pathophysiology: alteration of (elevated pleural fluid
peripheral systemic factors that affect the amylase)
neuropathy formation and absorption of pleural o pancreatic disease
(vincristine) fluid (i.e. increased capillary (elevated pleural fluid
chronic: hydrostatic pressure, decreased amylase)
neurologic plasma oncotic pressure) o Meigs syndrome
damage, (ascites and
leukemia, etiology hydrothorax
second associated with an
primary congestive heart failure ovarian fibroma or
neoplasms other pelvic tumour
cirrhosis
radiotherapy trauma
nephrotic syndrome
surgery o chylothorax: occurs
pulmonary embolism (may
o only chance for cure is when the thoracic duct
cause transudative or exudative
resection when tumour is disrupted and chyle
effusion)
is still localized accumulates in the
o contraindications if peritoneal dialysis, pleural space, due to
any evidence of local hypothyroidism, CF, trauma, tumour
extension or urinothorax o hemothorax: due to
metastases rupture of a blood
patients with Exudative Pleural Effusions vessel, commonly by
surgically trauma or tumours
resectable Pathophysiology: increased other
disease must permeability of pleural capillaries or o pneumothorax
undergo medi lymphatic dysfunction (spontaneous,
astinal node traumatic, tension)
sampling etiology o pleural thickening
since CT (chronic infection,
thorax is not neoplasm,
infectious
accurate inflammatory)
o parapneumonic
in 20-40% of
cases effusion (associated
with bacterial Appearance of Fluid
poor
pneumonia, lung
pulmonary
abscess Bloody - trauma, malignancy
status (i.e.
o empyema (bacterial, White - chylothorax, empyema
unable to
fungal, TB), TB Black - aspergillosis, amoebic liver
tolerate
pleuritis, viral abscess
resection of
infection Yellow-green - rheumatoid pleurisy
lung)
Viscous - malignant mesothelioma
palliative care for end-stage
malignancy Ammonia odour - urinothorax
disease Food particles - esophageal rupture
o lung carcinoma (35%)
Analysis of Pleural Effusion
o lymphoma (10%)
Protein, LDH - transudate vs.
Pleural Effusion o metastases: breast
exudate
Light's criteria - a pleural effusion is (25%), ovary, kidney
likely exudative if at least one of the mesothelioma Gram stain, Ziehl-Nielsen stain
following exists: (TB), culture - looking for
vascular/cardiac
1. The ratio of pleural fluid specific organisms
o collagen vascular
protein to serum protein is Cell count differential -
diseases: RA, SLE
greater than 0.5 neutrophils vs. lymphocytes
o pulmonary embolism,
2. The ratio of pleural fluid LDH (lymphocytic TB, lymphoma)
after coronary artery
and serum LDH is greater than Cytology - malignancy,
bypass surgery
0.6 infection
intra-abdominal
3. Pleural fluid LDH is greater Glucose (low) RA, TB,
o subphrenic abscess
than 2/3 times the normal upper empyema, malignancy,
limit for serum esophageal rupture

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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
dyspnea: varies with size of
effusion and underlying lung
function
pleuritic chest pain
often asymptomatic
inspection: trachea deviates
away from effusion, ipsilateral
decreased expansion
percussion: decreased tactile
fremitus, dullness
auscultation: decreased breath
sounds, bronchial breathing and
egophony at upper level,
pleural friction rub
Investigations
CXR
o must have >250 ml of
pleural fluid for
visualization
o lateral: small effusion
leads to blunting of
posterior costophrenic
angle
o PA: blunting of lateral
costophrenic angle
o dense opacification of
lung fields with
concave meniscus
o decubitus: fluid will
shift unless it is
loculated
o supine: fluid will
appear as general
haziness
Loren Warmington
thoracentesis: indicated if
pleural effusion is a new
finding
o risk of re-expansion
pulmonary edema if 2
L of fluid is removed
o inspect for colour,
character, and odour of
fluid
o analyze fluid
pleural biopsy: indicated if
suspect TB, mesothelioma, or
other malignancy (and if
cytology negative)
U/S: detects small effusions
and can guide thoracentesis
treatment depends on cause,
drainage if symptomatic
CT can be helpful in
differentiating parenchymal
from pleural abnormalities
Treatment
thoracentesis
treat underlying cause
Obstructive Lung Disease
Characterized by obstructed
airflow, decreased (decreased
FEV1 ) flow rates (most marked
during expiration), air trapping
(increased RV/TLC), and
hyperinflation (increased FRC,
TLC)
Differential diagnosis includes
asthma, chronic obstructive
pulmonary disease (COPD),
cystic fibrosis (CF), and
bronchiectasis
Flow rate
FEV1 - decreased
FVC - decreased
FEV1/FVC - decreased
FEF25-75 - decreased
Lung Volumes
TLC - decreased
FRC - decreased
VC - decreased
RV - decreased
RV/TLC - N
Restrictive Lung Disease
6
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
Emphysema (Pink Puffer)
Symptoms
Loren Warmington
dyspnea ( exertion)
minimal cough
tachypnea
decreased exercise tolerance
Signs
pink skin
pursed-lip breathing
accessory muscle use
cachectic appearance due to
anorexia + increased work of
breathing
hyperinflation/barrel chest,
hyperresonant percusion
decreased breath sounds
decreased diaphragmatic
excursion
Investigations
PFT:
decreased FEV1, decreased
FEV1/FVC
increased lung volume
decreased DCO
CXR:
increased AP diameter
flat hemidiaphragm (on
lateral CXR)
decreased heart shadow
increased retrosternal space
bullae
decreased peripheral
vascular markings
Bronchitis (Blue Bloater)
Symptoms
chronic productive cough
purulent sputum
hemoptysis
Signs
mild dyspnea initially
cyanotic (2o to hypoxemia and
hypercapnia)
peripheral edema from RVF (cor
pulmonale)
crackles, wheezes
prolonged expiration if
obstructive
frequently obese
Investigations
PFT: decreased FEV1, decreased
FEV1/FVC, N TLC,
increased or N DCO
CXR: AP diameter normal
increased bronchovascular
markings enlarged heart
with cor pulmonale
Treatment of Stable COPD
Prolong survival
7
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
 Loren Warmington
ventilatory function, associated nodular, or organic antigens
with higher mortality in certain reticulonodular pattern (hypersensitivity
risk groups (FEV1 <20%) (nodular <3 mm), pneumonitis)
o lung transplant Kerley B lines,
hilar/mediastinal
Others adenopathy
o diffuse ground-glass
appearance early in
patient education, eliminate
disease progresses to
respiratory irritants/allergens honey-combing late in
(occupational/environmental), disease DIFFERENTIAL DIAGNOSIS OF
exercise rehabilitation to o DDx: pulmonary RESPIRATORY ALKALOSIS
improve physical endurance Characterized by decreased PaCO2
fibrosis, interstitial
secondary to hyperventilation
pulmonary edema
Causes of interstitial Lung (CHF), PCP, TB
Disease Hypoxemia
(miliary), sarcoidosis,
Upper Lung Disease pneumoconiosis, pulmonary disease (pneumonia,
Farmer's lung lymphangitic edema, PE, interstitial fibrosis)
Ankylosing spondylitis carcinomatosis severe anemia
Sarcoidosis o DDx of cystic lesions: heart failure
Silicosis end-stage emphysema, high altitude
Neurofibromatosis PCP, histiocytosis X, Respiratory centre stimulation
TB (miliary) lymphangiomyomatosi CNS disorders
s hepatic failure
Eosinophilic granuloma
PFTs Gram-negative sepsis
(histiocytosis)
o restrictive pattern: drugs (ASA, progesterone,
Lower Lung Disease
decreased lung theophylline, catecholamines,
Bronchiolitis obliterans with
volumes (VC and psychotropics)
organizing pneumonia (BOOP)
TLC) and compliance pregnancy
Asbestosis o normal or increased
Drugs (nitrofurantoin, anxiety
FEV1/FVC (>70-
hydralazine, INH, amiodarone, 80%), i.e. flow rates pain
many chemo drugs) are actually normal or mechanical hyperventilation
Aspiration supernormal when (excessive mechanical
Scleroderma corrected for absolute ventilation)
Hamman Rich (interstitial lung volume
o DCO decreased due to DIFFERENTIAL DIAGNOSIS OF
pulmonary fibrosis)
less surface area for RESPIRATORY ACIDOSIS
Rheumatologic disease
gas exchange Characterized by increased PaCO2
pulmonary vascular secondary to hypoventilation
Signs and Symptoms
disease
respiratory centre depression
ABGs
SOB, especially on exertion (decreased RR)
o initially may be
dry crackles drugs (anesthesia, sedatives,
normal
dry cough narcotics)
o with progression of
cyanosis trauma
disease, hypoxemia
clubbing (only in IPF and and decreased PaCO2 increased ICP
asbestosis) may be present encephalitis
features of cor pulmonale Other stroke
note that signs and symptoms o bronchoscopy, central apnea
vary with underlying disease bronchoalveolar supplemental O2 in chronic
process lavage, lung biopsy CO2 retainers (i.e. COPD)
o c-ANCA (Wegners), Neuromuscular disorders (decreased
Investigations anti-GBM TV)
(Goodpastures), ESR, myasthenia gravis
ANA (lupus), RF Guillain-Barr syndrome
CXR/high resolution CT
(RA), serum- poliomyelitis
o decreased lung precipitating
volumes, reticular, muscular dystrophies
antibodies to inhaled
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 Loren Warmington
ALS Maintenance factors (2[Na] + glucose + urea);
myopathies volume depletion: increased normal = 10
chest wall disease (obesity, proximal reabsorption of
kyphoscoliosis) NaHCO3 and increased 5. If anion gap is increased, is the
Airway obstruction (asthma, foreign aldosterone change in bicarbonate the same as
body) (decreased FEV) hyperaldosteronism (1o or 2o): the change in anion gap?
Parenchymal disease distal Na reabsorption in
COPD exchange for K and H excretion if not, consider a mixed picture
pulmonary edema leads to HCO3 generation,
aldosterone also promotes
pneumothorax Ventilatory Failure
hypokalemia
pneumonia Wont Breathe
hypokalemia: transcellular K/H
pneumoconiosis respiratory centre depression
exchange, stimulus for hypothyroid
acute respiratory distress ammoniagenesis and HCO3
syndrome (ARDS) sleep apnea
generation Cant Breathe
Mechanical hypoventilation
(inadequate mechanical ventilation) neuromuscular disorders
airway obstruction
Anion Gap Metabolic Acidosis parenchymal disease
MUDPILES Approach to Acid-Base Status
Methanol
Uremia 1. What is the pH acidemic (pH
Diabetic ketoacidosis Causes of Tachcardia/Palpitations
<7.35), alkalemic (pH >7.45), or Cardiac
Paraldehyde normal (pH 7.35-7.45)
Isopropyl alcohol / Iron / INH arrhythmias (PAB, PVB, SVT,
Lactic acidosis VT)
2. What is the primary disturbance? mitral valve prolapse
Ethylene glycol
Salicylates valvular heart disease
metabolic: change in HCO3 and hypertrophic cardiomyopathy
Causes of Non-Anion Gap pH in same direction Endocrine
Metabolic Acidosis: HARDUP respiratory: change in HCO3 thyrotoxicosis
Hyperalimentation and pH in opposite direction pheochromocytoma
Acetazolamide
hypoglycemia
RTA 3. Has there been appropriate Systemic
Diarrhea compensation? (Table 7 below)
Ureteroenteric fistula fever
Pancreaticoduodenal fistula anemia
metabolic compensation occurs Drugs
over 2-3 days reflecting altered tobacco,
Metabolic Alkalosis
renal HCO3
Requires initiating event and caffeine,
production/excretion
maintenance factors alcohol,
Initiating event respiratory compensation
through ventilation control of epinephrine,
GI (vomiting, NG) or renal loss ephedrine,
PaCO2 occurs immediately
of H aminophylline, atropine
inadequate compensation may
exogenous alkali (oral or Psychiatric
indicate a second acid-base
parenteral administration), milk panic attack
disorder
alkali syndrome
diuretics (contraction
4. If there is metabolic acidosis, Causes of Bradycardia
alkalosis): decreased excretion
of HCO3, decreased ECF what is the anion gap and osmolar Physiologic
volume, therefore increased gap? Athlete
[ HCO3] Elderly
posthypercapnia: renal anion gap = [Na] - [Cl] - Pathologic
compensation for respiratory [ HCO3]; normal = 10-15 Heart block
acidosis is HCO3 retention, mmol/L Hypothermia
rapid correction of respiratory osmolar gap = measured
Hypothyroidism
disorder results in transient osmolarity calculated
osmolarity = measured Sick sinus syndrome
excess of HCO3

9
 Loren Warmington
Raised intracranial obesity Rheumatic mitral disease
pressure male, (esp Mitral Stenosis)
Drugs postmenopausal female Aortic Stenosis
-blockers sedentary lifestyle HTN
Ca2+-channel blockers hyperhomocysteinemia Thyrotoxicosis
(Verapamil, Diltiazem) Ischemic heart disease
Digoxin toxicity Sym. & Signs of Left Heart Failure Drugs
dyspnea, orthopnea, PND peripheral o Alcohol
Differentials of Chest Pain fatigue , syncope, systemic CCF, Cardiomyopathy
*can be fatal acutely hypotension, cool extremities Atrial Flutter
Pulmonary slow capillary refill, peripheral
cyanosis, pulsus alternans
pneumonia Causes of Collapsing Pulse
mitral regurgitation, S3
pulmonary embolism (PE)* edema, cough and crackles
pneumothorax/hemothorax* Fever
empyema Sym. & Signs of Left Heart Failure Anemia
pulmonary neoplasm Right heart failure can mimic most Thyrotoxicosis
bronchiectasis of the symptoms of forward left Aortic regurgitation
TB heart failure if decreased RV output Pregnancy
Cardiac leads to LV underfilling). Exercise
MI/angina* Elevated JVP with Abdinal JR and
Kussmauls sign, hepatomegaly Left Parasternal Heave
myocarditis L Atrial enlargement (2nd to severe
tricuspid regurgitation, S3 (right-
pericarditis/Dresslers sided),pulsatile liver MR)
syndrome* RV Enlargement w/ Pulmon. HTN
cardiac tamponade* Complicatons of MI
Severe LV Enlargement
Gastrointestinal ACT RAPID
esophageal: spasm, GERD, Apex beat (location & character)
Arrhythmias (SVT, VT, VF)
esophagitis, ulceration, Tapping Palpable S1 (Think MS)
Congestive cardiac failure
achalasia, neoplasm Thrusting LV Hypertrophy
Thromboembolic disorders eg.
PUD Displaced Dilatation from volume
stroke, (DVT, PE later on)
overload eg. AR, MR R to L shunt
gastritis Rupture (ventricle - Tampanade,
or Cardiomyopathy
pancreatitis septum - VSD, papillary muscle -
Impalpable Obesity, effusion and
biliary colic Regurgitation)
Hyperinflation
Mediastinal Aneurysm (ventricle)
lymphoma Pericarditis
Palpable P2
Infaction (a second one)
thymoma Pulmonary hypertension
Death/ Dressler's syndrome
Vascular Shock
dissecting aortic aneurysm Features of First heart sound
Surface structures Loud: mitral stenosis,
Precipitants of Heart Failure
costochondritis HTN (common)
Soft: mitral incompetence
rib fracture Endocarditis/environment (e.g. heat
wave) Features of Second heart sound
skin (bruising, shingles)
Anemia
breast Soft: Aortic or pulmonary stenosis
Rheumatic heart disease and other
valvular disease
Loud: Systemic(A2) or P. HTN (P2)
Risk Factors for Atherosclerosis Thyrotoxicosis Wide Fixed split: ASD
Failure to take meds (very common) Paradoxical Fixed Split: Delayed
Major Arrhythmia (common) LV or early RV emptying
smoking Infection/ischemia/infarction (common)
family history (FHx) of MI Lung problems (PE, pneumonia,
(first degree male relative <55 COPD)
Endocrine (pheochromocytoma, Causes of Mitral regurgitation
or first degree female relative
hyperaldosteronism)
<60) Ring
Dietary indiscretions (common)
diabetes mellitus (DM) Dilated cardiomyopathy
hypertension (HTN Hypertensive heart disease
Cause Irregularly irregular pulse Ischemic cardiomyopathy
Minor
Atrial Fibrillation Leaflet
hyperlipidemia
10

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.
Loren Warmington
Severity gauged by LVD, S3,
diastolic flow rumble.
Investigations
ECG: LAE, left atrial delay
seronegative arthritides
(bifid P waves), +/- LVH
CXR: LVH, LAE, pulmonary
venous HTN
Echo: severity of MR, (LV
Aortic Incompetence
function - EF, LA/LV),
(leaflets flail, vegetations
etc.)
Card. Cath: Assess coronaries,
assess flow and contours in
LA, Prominent LA V
wave on Swan-Ganz
Treatment
Asymptomatic: serial Echos, IE
prophylaxis.
Symptomatic: decrease preload
(diuretics)and decrease afterload
(ACEIs) for severe MR & poor
surgical candidate; stabilize
acute MR with vasodilators b/f
surgery
Surgery if: acute MR with CHF,
papillary muscle rupture, NYHA
class III-IV CHF, AFib, LVEF
<60%, increasing LV size,
earlier surgery if valve
repairable
Surgical Options
Valve repair: >75% of pts with
MR & myxomatous MV disease
(MVP). Annuloplasty rings,
leaflet repair, chordae
transfers/shorten/replacement
Valve replacement: failure of
repair, heavily calcified annulus
Advantage of Repair: low rate of
endocarditis, no anticoagulation,
less chance of re-operation
Causes of Aortic Incompetence
Ring
Left ventricular dilatation
HTN
Valve
RHD
IE
Bicuspid aortic valve
Root
Marfans
11
Syphilitic Aortitis
Aortic dissection
Takayasus aortitis
Ankylosing spondylitis,
RA, SLE
Trauma
Etiology
Supravalvular:
Aortic root disease (Marfans,
atherosclerosis & dissecting
aneurysm, connective tissue
disease)
Valvular:
Congenital (bicuspid AV, large
VSD), IE
Acute Onset: IE, aortic dissection,
trauma, failed prosthetic valve
Pathophysiology
Volume overload => LV
dilatation => increased SV, high
sBP & low dBP => increased
wall tension => pressure
overload => LVH (low dBP =>
decreased coronary perfusion)
Symptoms
(Usually only becomes
symptomatic late in disease
when LV failure develops)
Dyspnea, orthopnea, PND,
syncope, angina.
Physical Exam
Waterhammer pulse, bisferiens
pulse, Difference in femoral-
brachial systolic BP > 20 (Hills
test wide pulse pressure)
hyperdynamic apex, displaced
PMI, heaving apex
Auscultation: early
decrescendo diastolic murmur
at LLSB (cusp See this more
due to RHD) or RLSB (aortic
root), best heard sitting,
leaning forward, on full

expiration. Soft S1, absent S2,
S3 (late)
Investigations
ECG: LVH, LAE
CXR: LVH, LAE, aortic root
dilatation
Echo/TTE: Gold standard.
Quantify AR, leaflet or aortic
root anomalies. Visualize
regurge into LV.
Radionuclide scan: Sensitive to
decreased LV function (EF
doesnt increase w/ exercise
Cath: if >40 yrs and surgical
candidate - to assess for
ischemic heart disease
Exercise testing: hypotension
with exercise
Treatment
Asymptomatic: serial Echos,
afterload reduction (ACEIs if
normal LV function)
Symptomatic: avoid exertion,
treat CHF
Surgery if: NYHA class III-IV
CHF, LVEF < 50% with/without
symptoms, increasing LV size
Surgical Options
Valve replacement:Most Cases.
Valve types include mechanical,
bioprosthetic, homograph and
sometimes pulmonary autograph
Valve repair: limited role. repair
of valves to improve coaptation
Aortic root replace (Bentall
proced.):when ascending aortic
aneurysm present, valved
conduit used
Other Signs in Aortic Regurge
Large-volume, 'collapsing' pulse
also known as:
Watson's water hammer pulse
Corrigan's pulse (rapid upstroke
and collapse of the carotid artery
pulse) low diastolic and
increased pulse pressure
de Musset's sign (head nodding in
time with the heart beat)
Quincke's sign (pulsation of the
capillary bed in the nail)
Traube's sign (systolic and diastolic
murmurs described as 'pistol shots'
Loren Warmington
heard over the femoral artery when
it is gradually compressed)
Duroziez's sign (a double sound
heard over the femoral artery when
it is compressed distally)
Mller's sign (pulsations of uvula)
Austin Flint murmur, a soft mid-
diastolic rumble heard at the apical
area. It appears when regurgitant jet
from the severe aortic insufficiency
renders partial closure of the
anterior mitral leaflet.
Mitral Stenosis
Etiology
Rheumatic disease most
common cause; Lung carcinoid,
Mitral annular calcification,
Lupus. Congenital rarely
Pathophysiology
MS => fixed CO & Left atiral
enlargement => increased LA
pressure => pulmonary vascular
resistance & CHF; worse with
Afib (no atrial kick), tachycardia
(decreased atrial emptying time)
& pregnancy (increased
preload)
Symptoms
SOBOE, orthopnea, fatigue,
palpitations, peripheral edema,
malar flush (Pulm. Htn), pinched
and blue facies (severe MS).
Hemoptysis (late). If TR or RVF
then hepatic enlargement/pulsatility,
ascites, peripheral edema.
Physical Exam
Irregular pulse if AFib ( no A
wave on JVP), left parasternal
lift, palpable diastolic thrill at
apex (tapping apex not
displaced)
Auscultation: mid-diastolic
rumble at apex, best with bell
in LLD position following
exertion, No radiation. Loud S1
12
(valves not pliable), OS
following loud P2 (heard best
during expiration). Crackles. If
pulm. Htn present look for
loud /palpable P2, Pulmonary
Regurge (Graham Steell
murmur). It may also be
associated with MR and TR.
Long murmur & short A2-
Opening snap interval correlate
with worse MS
Investigations
ECG: Normal S rhythm/AFib,
LAE (P mitrale), RVH,
RAD
CXR: L atrial enlargement (LA
appendage, double
contour, carina splaying)
Pulmonary Congestion
(Kerley B lines), MV
calcification, Flattened
left heart border.
Echo/TTE: Thickened calcified
valve, fused leaflets, LAE,
PAP, TR
Cath: concurrent CAD if >40
yrs (male) or >50 yrs (female)
Treatment
Avoid exertion, fever (increased
LA pressure), treat AFib (rate
control, cardioversion) and CHF,
increase diastolic filling time
(beta-blockers, digitalis). IE
prophylaxis? Anticoagulation
previous embolus.
Surgery if: NYHA class III-IV
CHF, failure of medical therapy
(usually MVA <1.2 cm2),
Worstening P Htn, systemic
embolization, IE, severe life
style limitations
Surgical Options
Percutaneous balloon
valvuloplasty: young rheumatic
pts & good leaflet morphology,
asymptom pts with mod-sev
MS, new-onset AFib, pulmon
HTN
Contraindication: Left atrial
thrombus, mod-sev MR
Open Mitral Commissurotomy:
If mild calcif +leaflet/chordal
thickening. Best if valve
repairable
Open Mitral Commissurotomy:
Rarely done in North A.
Above steps have Restenosis in

50% pts in 8yrs
Valve replacement: immobile
leaflets/mod-sev calcification &
severe scarred leaflets, MR
Aortic stenosis
Causes:
Congenital (bicuspid >
unicuspid valve), calcification
(wear and tear), rheumatic
disease
Pathophysiology
Outflow obstruction =>
increased EDP => concentric
LVH => LV failure =>
concentric CHF, subendocardial
ischemia
Symptoms
Triad of Exertional angina,
syncope (fixed CO or
arrythmias) and dyspnea. PND,
orthopnea, peripheral edema
Physical Exam
Narrow pulse pressure, brachial-
radial delay, pulsus parvus et
tardus, sustained PMI
Auscultation: crescendo-
decrescendo Systolic ejection
murmur radiating to R
clavicle & carotid (may have
thrill at neck), musical quality at
apex (Gallavardin phenomenon),
thrill in 2nd RICS, S4 (early in
disease), soft S2 w/paradoxical
splitting, S3 (late)
Complications:
Recurrent PE, pulmonary
infections pneumonia and
bronchitis, LA thrombus
(Systemic embolic to kidney,
brain, spleen, arm)
Investigations
ECG: LVH & strain, LBBB,
LAE, AFib
CXR: post-stenotic aortic root
dilatation, calcified valve,
Loren Warmington
LVH, LAE, CHF (later)
ECHO:
Test of choice. Reduced
valve area (RVA) pressure
gradient (PG), LVH,
reduced LV function
Card Cath:
Rule out CAD before
surgery esp. with cases of
angina. Also in inconclusive
ECHO - PG, RVA
Treatment
Asymptomatic:
Serial Echos, avoid exertion
?IE prophylaxis
Symptomatic: avoid
nitrates/arterial dilators &
ACEIs in severe AS
Surgery if: symptomatic, LV
dysfunction or in moderate AS
when other cardiac surgery is
done
Surgical Options
Valve replacement : Procedure of
choice. aortic rheumatic valve
disease & trileaflet valve
Open/Balloon valvuloplasty:
Repair may be possible in children.
Rarely done in adults Temporizing
in Pregnancy, patient stabilization
or as palliative if people with
comordities.
Tricuspid Regurg
RHD
I.E. (esp in IV drug abuse)
Pulm HTN
Carcinoid syndrome
Rt ventricular failure
Tricuspid Regurge
Etiology
RV dilatation, IE (IV drug use),
rheumatic disease,
congenital (Ebstein anomaly),
carcinoid
13
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
 Loren Warmington
rumble 4th left intercostals Percutaneous or open balloon MV displaced into LA during
space valvuloplasty systole; no causal mechanisms
found for symptoms
Investigations Pulmonary Regurge
ECG: RAE Symptoms
CXR: dilatation of RA without Prolonged, stabbing chest pain,
pulmonary artery enlargement dyspnea, anxiety/panic,
Echo: diagnostic palpitations, fatigue, presyncope

Treatment Physical Exam

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
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,
pulmonary ejection click, right-
sided S4
Investigations
ECG: RVH
CXR: prominent pulmonary
arteries enlarged RV
echo: diagnostic
Treatment
Balloon valvuloplasty if severe
symptoms
Surgical Options
Etiology
Pulmonary HTN, IE, rheumatic
disease, tetrology of Fallot, post-
repair
Pathophysiology
Increased RV volume =>
increased wall tension => RV
hypertrophy => right heart
failure
Symptoms
Chest pain, syncope, fatigue,
peripheral edema
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
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
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

14

infants may initially have a
L>R shunt and therefore are not
cyanotic but the RVOTO is
progressive, resulting in
increasing R>L shunting with
hypoxemia and cyanosis
history: hypoxic spells
primary pathophysiology is
hypoxia, leading to increased
pulmonary vascular resistance
(PVR) and decreased systemic
resistance, occurring in
exertional states (e.g. crying,
exercise)
paroxysm of rapid and deep
breathing, irritability and crying
hyperpnea, increasing cyanosis
often leading to deep sleep and
decreased intensity of murmur
(decreased flow across
RVOTO)
peak incidence at 2-4 months of
age
o if severe may lead to
seizures, loss of
consciousness, death
(rare)
o management: O2,
knee-chest position,
fluid bolus, morphine
sulfate, propanolol
physical exam:
single loud S2 due to severe
pulmonary stenosis (i.e RVOTO)
investigations:
ECG: RAD, RVH
CXR: boot shaped heart (small
PA, RVH), decreased
pulmonary vasculature, right
aortic arch (in 20%)
treatment: surgical repair within
first two years of life, or earlier if
marked cyanosis, spells, or severe
RV outflow tract obstruction
Ventricular Septal Defect (VSD)
most common congenital heart
defect (30-50% of CHD)
Small VSD (majority)
history: asymptomatic, normal
growth and development
Loren Warmington
physical exam: early systolic to
holosystolic murmur, best
heard at left lower sternal
border (LLSB)
investigations: ECG and CXR
are normal
treatment: most close
spontaneously, do not need
surgical closure even if remains
patent
Moderate-to-large VSD
natural history: secondary
pulmonary hypertension, CHF
by 2 months of age
history: delayed growth and
development, decreased
exercise tolerance, recurrent
URTIs or asthma
episodes, CHF
physical exam: holosystolic
murmur at LLSB with thrill,
mid-diastolic rumble at apex,
size of VSD is inversely related
to intensity of murmur
investigations:
o ECG: left ventricular
hypertrophy (LVH),
left atrial hypertrophy
(LAH), RVH
o CXR: increased
pulmonary
vasculature,
cardiomegaly, CHF
treatment: treatment of CHF
and surgical closure by 1 year
of age
Patent Ductus Arteriosus (PDA)
patent vessel between
descending aorta and left
pulmonary artery
epidemiology
o functional closure
within first 15 hours of
life, anatomical
closure within first
days of life
o 5-10% of all
congenital heart
defects
o common in premature
infants (1/3 of infants
<1750 grams)
15
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
investigations:
ECG-RVH early in infancy, LVH
later in childhood
prognosis and treatment
o if associated with
other lesions (e.g.
PDA, VSD) can cause
CHF
o complications:
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,
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
Pulmonary Stenosis (Children)
Loren Warmington
valvular (90%), subvalvular, or y descent opening of
supravalvular tricuspid valve
usually part of other congenital ventricular filling
heart lesions (e.g. Tetralogy of
Fallot) or in association with Raised JVP with normal
other syndromes (e.g. waveform Rt heart
congenital rubella, Noonan failure; fluid overload
syndrome) Raised JVP with absent
critical pulmonic stenosis: pulsation SVC
inadequate pulmonary blood obstruction
flow, dependent on ductus for Absent a wave A. Fib
oxygenation, progressive Large a wave pulm HTN
hypoxia and cyanosis pulm stenosis, tricuspid
history: spectrum from stenosis
asymptomatic to CHF Cannon a wave complete
physical exam: wide split S2 on heart block
expiration, SEM at ULSB, CV wave tricuspid
pulmonary ejection click regurgitation
investigations:
o ECG: RVH
o CXR: dilated post- Lower Motor Exam Check
stenotic pulmonary List
artery Look at attitude of limb,
treatment: surgical repair if Neurocutaneous lesion,
critically ill or severe PS, or if Spontaneous or induced
presence of symptoms in older fasciculations.
infants/children Do clonus at knees as well
systemic venous return re-
enters systemic circulation
Causes of Proximal Myopathy
directly
Congenital
most prominent feature is
Muscle dystrophy
cyanosis (O2 sat <75%)
Inflammatory
differentiate between cardiac
Polymyositis
and other causes of cyanosis
Dermatomyositis
with hyperoxic test
o obtain preductal, right Polymyalgia rheumatica
Endocrine
radial ABG in room
air, repeat ABG after Cushings Syndrome
the child inspires (including iatrogenic)
100% oxygen Diabetes Mellitus
o if PaO2 improves to Hypothyroidism /
greater than 150 Hyperthyroidism
mmHg, cyanosis less Acromegaly
likely cardiac in origin Addisons disease
survival depends on mixing via Conns syndrome
shunts (e.g. ASD, VSD, PDA) Hyperparathyroidism /
hypoparathyroidism
JVP Metabolic
A Rt atrial contraction Osteomalacia
C bulging of tricuspid Hypokalemia
Hypercalcemia
valve into Rt atrium on
Toxic
ventricular contraction
Alcohol
x descent lowering Rt
Vitamin E
atrial pressure as tricuspid
ring moves down Organophosphate
V atrial filling Drugs
Corticosteroids
16
 Loren Warmington
Amiodarone Causes of a Sensory Level Rheumatoid & vasculitides (SLE,
Vincristine (Sensation is lost below a RA, Polyarteritis nodosa, Sjogrens,
Paraneoplastic particular level) Churg-Strauss)
Carcinomatous Alcohol
Transverse myelitis Paraproteinemia (Multiple
neuromyopathy Spinal cord compression myeloma) / Paraneoplastic (non-
Dermatomyositis Spinal cord tumour metastatic manifestation)
Infectious (HIV, Leprosy, Lyme
Cervical spondylosis
Causes of Spastic Paraparesis disease, diphtheria, tetanus,
Traumatic injury to spinal cord
botulism)
HAM/TSP Sarcoidosis
Spinal cord compression Causes of Peripheral Neuropathy Thyroid (hypothyroidism)
Multiple Sclerosis
Renal failure
Subacute Combined Oculomotor Nerve
Infection
Degeneration of the cord
HIV CN 3 motor nucleus at level of
(Vit B12 def) superior colliculus + Edinger-
Transverse Myelitis Leprosy
Lyme disease Westphal (parasympathetic
Parasagittal Meningioma peripheral fibres) passes b/w
Infiltrative
HIV-associated posterior cerebral & superior
Sarcoidosis
myelopathy cerebellar arteries superior
Amyloidosis
Tabes dorsalis orbital fissure
Inflammatory Ischemia (e.g. Diabetic
Guillain-Barre mononeuropathy)
Causes of Spastic Hemiplegia RA o Pupillary sparing
SLE Compression (e.g. post
CVA Nutritional communication artery
Tumour Vit B1 Deficiency aneurysm)
Brown-Sequard Vit B6 Deficiency
Abducens Nerve
Causes of Flaccid paraparesis Vit B12 deficiency
Vit E Deficiency DM
Poliomyelitis Endocrine HTN
Guillain-Barre Diabetes Mellitus Vasculitis
Motor Neuron Disease Acromegaly
Spina bifida Causes of Facial Weakness
Heavy metal upper motor neuron
Botulism Lead TIA/stroke
Cauda equina syndrome Mercury post-ictal hemiparesis
Drugs
tumour
Isoniazid
Flaccid Hemiplegia infection: otitis media,
Phenytoin
mastoiditis, Epstein-Barr
Acute CVA Metronidazole virus (EBV), herpes zoster
Plexopathy Methotrexate virus (HZV), Lyme
disease, HIV
Sensory Exam Check List Peripheral Neuropathy (DANG
THE RAPIST) lower motor neuron
Look for Ulcers, U. Cath or Diaper
Do light touch, sharp touch, DM, Uremia
Amyloidosis infection: otitis media,
Proprioception (toe and ankle) mastoiditis, Epstein-Barr
Nutritional (Vit B1, 6, 12 def)
Guillain-Barre virus (EBV), herpes zoster
Causes of Sensory Disturbance virus (HZV), Lyme
Toxins & drugs (lead, mercury,
stroke organophosphate, metronidazole, disease, HIV
tumour isoniazid, ethambutol, vincristine, idiopathic (Bells
multiple sclerosis amiodarone) palsy)
peripheral neuropathies Hereditary (Friedrichs ataxia, sarcoid
B12 deficiency porphyria, Charcot-marie-tooth) neuropathy (DM)
Endocrine (acromegaly) parotid gland

17

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 Mechanical
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
Loren Warmington
Causes of Diplopia
Neuromuscular:
cranial nerve III/IV/VI
palsies (DM, tumour,
trauma, aneurysm)
brainstem pathology
(stroke, tumour, MS)
myasthenia gravis
Wernicke's encephalopathy
leptomeningeal disease
(e.g. meningitis)
Guillain-Barr
syndrome (e.g. Miller-
Fisher Variant)
thyroid ophthalmopathy
cavernous sinus pathology
trauma (e.g. orbital
fracture)
General Approach to Neuro Exam
State of Consciousness/Arousal
Glasgow Coma Scale
(EVM = 456)
reflexes: responses to pain
may include decerebrate
and decorticate posturing
Mental Status Exam
appearance, behaviour,
mood, affect, speech,
thought process, thought
content, perceptions,
insight, judgement
assess as is appropriate
throughout the interview
Cognition
Mini-Mental Status Exam
(MMSE), clock drawing,
Baycrest Neurocognitive
Assessment, MOCA
frontal lobe testing for
perseveration
Cranial Nerve Examination
Cranial Nerve Interpretation
CN1:
Unilateral loss of smell suggests
interior frontal lobe lesion
(avoid irritative stimuli which
stimulate CN5)
CN2:
Look at optic discs for edema
and optic atrophy
18
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)
Symmetrical weakness of proximal
muscles suggests myopathy; of
distal muscles suggests
polyneuropathy
Reflexes Interpretation
Increased in upper motor neuron
disease
Decreased/absent in lower motor
neuron disease, myopathies or
neuromuscular junction disorders
Slow relaxation of knee or ankle
reflex is seen in hypothyroidism
Babinski sign suggests an upper
motor neuron lesion but may be
seen following a seizure
Loren Warmington
Sensory Examination Where is the Lesion ?
posterior columns Cortex and internal Capsule
vibration, Contralateral sensory & motor
proprioception, deficits
light touch)
Spinothalamic Cortical lesions:
Associated with aphasia,
pain
neglect, extinction,
temperature graphaesthesia, visual loss
Cortical sensation (higher level dysfunctions) and
graphesthesia, astereognosia
stereognosis, Internal capsule lesions:
extinction, Associated with pure motor,
2-point discrimination pure sensory losses,
incoordination, absence of
cortical features
Co-ordination
finger to nose, Common causes:
Seizure disorder (cortex only)
heel to shin,
Coma
rapid alternating
Stroke
movements
Cerebellum and Basal Ganglia
Stance & Gait Coordination Problems
Romberg, Cerebellar Lesions:
tandem gait Abnormal intentional
Movements. Clumsiness,
Sensory Exam Interpretation unsteadiness, vertigo.
Hemisensory loss - with sensory Tandem gait impairment,
level or dissociation loss suggests nysatagmus, abnormal heel
spinal cord lesion to shin, dysdiadockinesis,
abnormal finger to nose and
Symmetrical distal sensory loss rapid alternating movements
suggests polyneuropathy
Basal Ganglia:
Loss of vibration sense suggests Tremor, bradykinesia,
peripheral neuropathy or posterior cogwheel rigidity,
column lesion involuntary movements
Impaired graphesthesia and Common Causes:
stereognosis with intact primary Cerebellar degeneration
sensation indicates parietal lesion Parkinsons disease
Stroke
Other Stuff
Dolls movement, if absent, Brainstem (unilateral)
suggests pons or midbrain lesion or Midbrain CN 3-4
very deep coma Pons CN 6-7
Medulla CN 8-10
Loss of vestibulo-ocular reflex
with caloric stimulation suggests Bilateral motor abnormalities
brain stem lesion or drug toxicity (UMN pattern). Crossed
sensory signs (ipsilateral
Absence seizures can be face and contralateral body)
precipitated by hyperventilation
MIDBRAIN:
Characteristic skin lesions are Diplopia, ptosis, pupillary
seen in neurocutaneaous syndromes changes (large or midposition
(e.g. neurofibromatosis, tuberous and unreactive)
sclerosis complex, Sturge-Weber
syndrome) PONS:
19
 Loren Warmington
LMN facial weakness, Common Causes: Best Verbal Response
quadriparesis in bilateral pontine Myasthenia gravis 5 = Answers questions appropriately
lesions, pinpoint pupils (why?) Lambert-Eaton syndrome 4 = Confused, disoriented
Botulism 3 = Inappropriate words
MEDULLA: 2 = Incomprehensible sounds
lateral or medial medullary Muscle 1 = No verbal response
syndromes Proximal & symmetrical
muscle weakness Best Motor Response
Common Causes No sensory loss 6 = Obeys commands
Cranial nerve palsies LMN signs wasting, normal 5 = Localizes to pain
Stroke or reflexes, normal or tone 4 = Withdraws from pain
3 = Decorticate (flexion)
Unilteral Spinal Cord Common Causes: 2 = Decerebrate (extension)
Upper Motor neuron signs Muscular dystrophies 1 = No response
Ipsilateral paralysis and Myopathies including
proprioceptive loss polymyositis Acute Confusional states
Sensory level, bowel/bladder Dermatomyositis (delirium)
dysfunction paraparesis I WATCH DEATH"
Contralateral pain-temperature Altered Mental Status Infectious
loss below the level of the Coma Withdrawal from drugs
lesion in Brown-Sequard Diffuse CNS Acute metabolic disorder
syndrome head trauma Trauma
infection CNS pathology
Common Causes : inflammation/ vasculitis Hypoxia
Spinal Cord Syndromes global cerebral ischemia Deficiencies in vitamins
sublcilincal seizure/ post- Endocrinopathies
Nerve Root ictal state Acute vascular insults
Radicular pain (sharp, electric, hypertensive Toxins
radiating) + sensory loss in Heavy metals
encephalopathy
dermatome/weakness in Dementia
Metabolic
myotome or absent reflex
diabetic ketoacidosis Other psychiatric
Common Causes: hypoglycemia (e.g. depression)
Nerve root compression electrolyte disturbance
Disk herniation acid-base disturbance Mental Status Exam: ASEPTIC
thiamine deficiency Appearance and behaviour
Peripheral Nerve Systemic Speech
Ipsilateral motor and sensory liver failure Emotion (mood and affect)
deficits along a nerve Perception
renal failures
distribution. Thought content and process
sepsis Insight and judgment
LMN signs power, wasting, Focal CNS Cognition
reflexes, normal or tone) abscess
In Polyneuropathy (distal epidural/ subdural
weakness, glove and stocking hematoma
distribution of sensory loss) Rheumatology
hemorrhage/ aneurysm Demographics: name, age,
Common Causes: hydrocephalus occupation
Neuropathy stroke History
tumour SLE
Neuromuscluar Junction venous occlusion Joint pain (duration &
Proximal & symmetrical severity), swelling, redness,
muscle weakness Glascow Coma Scale warmth
No sensory loss Eyes Open Chest pain
Fatiguability (?Repeated 4 = Spontaneously Photosensitivity
strength testing) 3 = To voice Seizure
Diplopia, ptosis, bulbar 2 = To pain Change in personality
1 = No response Recurrent early pregnancy
weakness
losses

20

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
Loren Warmington
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 Signs and Symptoms of
Counselling Station
1. Introduction
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
21
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
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
81-
Absent or minimal symptoms
90
If symptoms are present, they
71- are transient and expected
80 reactions to psychosocial
stressors
Some mild symptoms or some
61-
difficulty but generally
70
functioning well
51- Moderate symptoms or
60 difficulty
41-
Serious symptoms or difficulty
50
Some impairment in reality
31-
testing/communication,
40
impairment in several areas
Behaviour is influenced by
21- delusions/hallucinations or
30 serious impairment in
communication/judgment
Some danger of hurting self or
others or occasionally fails to
11-
maintain minimal hygiene or
20
gross impairment in
communication
1- Persistent danger of severely
10 hurting self or others or
Loren Warmington
persistent inability to maintain o tangentiality - speech
minimal personal hygiene or is oblique or
serious suicidal act irrelevant; does not
come back to the
0 Inadequate information original point
o loosening of
Mental Status Exam associations - illogical
shifting between
topics
General Appearance and
o flight of ideas -
Behaviour
quickly skipping from
one idea to another
dress, grooming, posture, gait, where the ideas are
physical characteristics, body
marginally connected,
habitus, apparent vs. associated with mania
chronological age, facial o word salad - jumble of
expression (e.g. sad, words lacking
suspicious) meaning or logical
psychomotor activity (agitation, coherence
retardation), abnormal perseveration - repetition of
movements or lack thereof the same verbal or motor
(tremors, akathisia, tardive response to stimuli
dyskinesia, paralysis), attention echolalia - repetition of
level and eye contact, attitude phrases or words spoken by
toward examiner (ability to someone else
interact, level of co-operation)
thought blocking - sudden
cessation of flow of thought
Speech and speech
rate (e.g. pressured, slowed), clang associations - speech
rhythm/fluency, volume, tone, based on sound such as
articulation, quantity, rhyming or punning
spontaneity neologism - use of novel words
or of existing words in a novel
Mood and Affect fashion
mood - subjective emotional
state; in patients own words
Thought Content
affect - objective emotional
state; described in terms of
suicidal ideation/homicidal
quality (euthymic, depressed,
ideation
elevated, anxious), range (full,
o low - fleeting
restricted, flat, blunted),
thoughts, no
stability (fixed, labile), mood
formulated plan, no
congruence, appropriateness,
intensity intent
o intermediate - more
frequent ideation, well
Thought Process
formulated plan, no
coherence - coherent, active intent
incoherent o high - persistent
logic - logical, illogical ideation and profound
stream hopelessness/anger,
o goal-directed well formulated plan
o circumstantiality - and active intent,
speech that is indirect believes
and delayed in suicide/homicide is the
reaching its goal; only helpful option
eventually comes back available
to the point obsession - recurrent and
persistent thought, impulse or
22

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
Loren Warmington
level of consciousness
orientation: time, place, person
memory: immediate, recent,
remote
global evaluation of intellect
(below average, average, above
average)
intellectual functions: attention,
concentration, calculation,
abstraction (proverb
interpretation, similarities test),
language, communication
Insight
patients ability to realize that
he or she has a physical or
mental illness and to
understand its implications
Judgment
ability to understand
relationships between facts
and draw conclusions that
determine ones action
Attitude to examiner
Types of Delusions
Persecutory - belief that others are
trying to cause harm
Delusions of reference -
interpreting publicly known
events/celebrities as having direct
reference to the patient
Erotomania - belief that another is
in love with you
Grandiose - belief of an inflated
sense of self-worth or power
Religious - belief of receiving
instructions/powers from a higher
being; of being a higher being
Somatic - belief that one has a
physical disorder/defect
Nihilistic - belief that things do not
exist;a sense that everything is
unreal
Psychosis
characterized by a significant
impairment in reality testing
delusions or hallucinations
(with/without insight into their
pathological nature)
behaviour so disorganized that
it is reasonable to infer that
reality testing is disturbed
23
Differentials of Psychosis
primary psychotic disorders:
schizophrenia,
schizophreniform, brief
psychotic, schizoaffective,
delusional disorder
mood disorders: depression
with psychotic features, bipolar
disorder (manic episode with
psychotic features)
personality disorders:
schizotypal, schizoid,
borderline, paranoid, obsessive-
compulsive
general medical conditions:
tumour, head trauma, dementia,
delirium, metabolic
substance-induced psychosis:
intoxication or withdrawal
DSM-IV-TR Diagnostic Criteria
for Schizophrenia
A. characteristic symptoms (active
phase): >2 of the following, each
present for a significant portion of
time during a 1-month period (or
less if successfully treated):
delusions **
hallucinations **
disorganized speech (e.g.
frequent derailment or
incoherence)
grossly disorganized or
catatonic behaviour
negative symptoms, e.g.
affective flattening, alogia
(inability to speak), or avolition
(inability to initiate and persist
in goal-directed activities)
**Note: only 1 symptom is required
if delusions are bizarre or
hallucinations consist of a voice
keeping a running commentary on
the person's behaviour or thoughts,
or 2 or more voices conversing with
each other
B. social/occupational dysfunction:
>1 major areas of functioning
(work, interpersonal relations, self-
care) markedly below the level
achieved prior to the onset of
symptoms
 Loren Warmington
C. continuous signs of disturbance (imitative repetition of
for >6 months, including >1 month anothers
of active phase symptoms; may movements, gestures
include prodromal or residual or posture)
phases disorganized
o disorganized speech
D. schizoaffective and mood and behaviour; flat or
disorders excluded inappropriate affect
o poor premorbid
E. the disturbance is not due to the personality, early and
direct physiological effects of a insidious onset, and
substance or a general medical continuous course
condition (GMC) without significant
remissions
F. if history of pervasive undifferentiated
developmental disorder, additional o symptoms of criteria A
diagnosis of schizophrenia is made met, but does not fall
only if prominent delusions or into the 3 previous
hallucinations are also present for at subtypes
least 1 month residual
o absence of prominent
delusions,
Subtypes
hallucinations,
disorganized speech,
paranoid
grossly disorganized
o preoccupation with
or catatonic behaviour
one or more delusions o continuing evidence of
(typically persecutory
disturbance indicated
or grandiose) or
by the presence of
frequent auditory
negative symptoms or
hallucinations
two or more
o relative preservation
symptoms in criteria A
of cognitive present in attenuated
functioning and affect; form
onset tends to be later
in life; believed to
have the best Good Prognositic Factors
prognosis Acute onset
Precipitating factors
catatonic
Good cognitive functioning
o at least two of: motor
Good premorbid functioning
immobility (catalepsy No family history
or stupor); excessive
Presence of affective symptoms
motor activity Absence of structural brain
(purposeless, not
abnormalities
influenced by external
Good response to drugs
stimuli); extreme Good support system
negativism (resistance
to Etiology - multifactorial:
instructions/attempts disorder is a result of interaction
to be moved) or between both biological and
mutism; peculiar environmental factors
voluntary movement
genetic 50% concordance in
(posturing, stereotyped
monozygotic (MZ) twins; 40%
movements, prominent
if both parents have
mannerisms);
schizophrenia; 10% of
echolalia (repeating
dizygotic (DZ) twins, siblings,
words/phrases of
children affected
anothers speech)
or echopraxia
24
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
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)

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
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
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
Loren Warmington
treatment: antipsychotics,
mood stabilizers,
antidepressants
prognosis: between that of
schizophrenia and that of mood
disorder
DSM-IV-TR Diagnostic Criteria
for Delusional Disorder
A. non-bizarre delusions for at least
1 month
B. criterion A for schizophrenia
has never been met (though patient
may have tactile or olfactory
hallucinations if they are related to
the delusional theme)
C. functioning not markedly
impaired; behaviour not obviously
odd or bizarre
D. if mood episodes occur
concurrently with delusions, total
duration has been brief relative to
duration of the delusional periods
E. the disturbance is not due to the
direct physiological effects of a
substance or GMC
subtypes: erotomanic,
grandiose, jealous, persecutory,
somatic, mixed, unspecified
treatment: psychotherapy,
antipsychotics, antidepressants
prognosis: chronic, unremitting
course but high level of
functioning
Folstein Mini Mental State Exam
(MMSE) to assess Dementia:
Orientation (time and place) 5
points
Memory (immediate and delayed
recall) 5 points
Attention and Concentration
Language (comprehension, reading,
writing, repetition, naming)
Spacial ability (intersecting
pentagons)
Gross screen for cognitive
dysfunction: Total score is out of
25
30; <24 abnormal 20-24 mild, 10-19
moderate, <10 severe
See attached Form
DSM-IV-TR Diagnostic Criteria
for Dementia (Alzheimers Type)
A. the development of multiple
cognitive deficits manifested by
both
1. memory impairment
(impaired ability to learn new
information or to recall
previously learned information)
2. >1 of the following
cognitive disturbances:
o aphasia (language
disturbance)
o apraxia (impaired
ability to carry out
motor activities
despite intact motor
function)
o agnosia (failure to
recognize or identify
objects despite intact
sensory function)
o disturbance in
executive functioning
(i.e. planning,
organizing,
sequencing,
abstracting)
B. the cognitive deficits in Criteria
A1 and A2 each cause significant
impairment in social or
occupational functioning and
represent a significant decline from
a previous level of functioning
C. the course is characterized by
gradual onset and continuing
cognitive decline
D. the cognitive deficits in Criteria
A1 and A2 are not due to any of the
following:
1. other central nervous system
conditions that cause
progressive deficits in memory
and cognition
2. systemic conditions that are
known to cause dementia
3. substance-induced conditions

E. the deficits do not occur
exclusively during the course of a
delirium
F. the disturbance is not better
accounted for by another Axis I
disorder
Investigations (rule out reversible
causes)
standard: as in Delirium
as indicated: VDRL, HIV,
SPECT, CT head in dementia
indications for CT head, as in
Delirium section plus: age <60,
rapid onset (unexplained
decline in cognition or function
over 1-2 months), dementia of
relatively short duration (<2
years), recent significant head
trauma, unexplained
neurological symptoms (new
onset of severe
headache/seizures)
Management
treat medical problems and
prevent others
provide orientation cues (e.g.
clock, calendar)
provide education and support
for patient and family (day
programs, respite care, support
groups, home care)
consider long-term care plan
(nursing home) and power of
attorney/living will
inform Ministry of
Transportation about
patients inability to drive
safely
consider pharmacological
therapy
o cholinesterase
inhibitors (e.g.
donepezil (Aricept))
for mild to severe
disease
o glutamatergic NMDA
receptor antagonist
(e.g memantine) for
moderate to severe
disease
Loren Warmington
o low-dose neuroleptics Men: 2 or less/day
(haloperidol, Women: 1 or less/day
risperidone) and Elderly: 1 or less/day
antidepressants if
behavioural or Drinking Problem
emotional symptoms Drinking above the recommended
prominent - start low guidelines, associated with:
and go slow Drinking to or reduce
o reassess depression or anxiety
pharmacological Loss of interest in food
therapy every 3 Lying/hiding drinking habits
months
Drinking alone
Injuring self or others while
intoxicated
Were drunk more than three or
Substance Abuse History
four times last year
Increasing tolerance
Validatedscreeningquestionnaire
Withdrawal symptoms: feeling
(Alcohol):
irritable, resentful,
unreasonable when not
CeverfelttheneedtoCut drinking
downondrinking? Experiencing medical, social,
A ever felt Annoyed at or financial problems caused by
criticism of your drinking? drinking
G ever feel Guilty about your
drinking? Adverse Medical Conditions -
E ever need a drink first thing alcohol
in morning (Eye opener)?
formen,ascoreof>2isa GI: gastritis, dyspepsia, pancreatitis,
positivescreenandforwomen, liver disease, bleeds, diarrhea,
ascoreof>1isapositive oral/esophageal cancer
screen Cardiac: hypertension, alcoholic
ifpositiveCAGE,thenassess cardiomyopathy
furthertodistinguishbetween Neurologic: Wernicke-Korsakoff
problemdrinkingandalcohol syndrome, peripheral neuropathy
Hematologic: anemia,
dependence
coagulopathies
Other: trauma, insomnia, family
General Assessment violence, anxiety/depression,
Whenwasthelastdrink? social/family dysfunction, sexual
Doyouhavetodrinkmoreto dysfunction, fetal damage
getthesameeffect?
Doyougetshakyornauseous Investigations
whenyoustopdrinking?
Haveyouhadawithdrawal
GGT and MCV for baseline
seizure? and follow-up monitoring
Howmuchtimeandeffortdo AST, ALT (usually, AST:ALT
youputintoobtainingalcohol?
approaches 2:1 in an alcoholic)
Hasyourdrinkingaffectedyour CBC (anemia,
abilitytowork,gotoschool,or thrombocytopenia), PT
haverelationships? (decreased clotting factors
Haveyousufferedanylegal production by liver)
consequences?
Hasyourdrinkingcausedany Management
medicalproblems?
intervention should be
Moderate Drinking consistent with patients
26

motivation for change
(motivational interviewing)
regular follow-up is crucial
10% of patients in alcohol
withdrawal will have seizures
or delirium tremens
Alcoholics Anonymous/12-step
program
outpatient/day programs
for those with chronic,
resistant problems
family treatment (Al-Anon,
Alateen, screen for
spouse/child abuse)
in-patient program if:
dangerous or highly
unstable home
environment
severe medical/psychiatric
problem
addiction to drug that may
require in-patient
detoxification
refractory to other
treatment programs
Non Pharmacological
behaviourmodification: Management of Alcohol Withdrawal
hypnosis,relaxation
training,aversiontherapy, Monitor using the Clinical Institute
assertivenesstraining, Withdrawal Assessment for Alcohol
operantconditioning
supportiveservices:half assessment include
wayhouses,detoxification
centres,Alcoholics
Anonymous
psychotherapy,
motivationalinterviewing
medicationsimportantas
adjunctivetreatment:
SSRIs,ondansetron,
topiramate
pharmacologic
diazepam for withdrawal
disulfiram (Antabuse)
o blocks conversion
of acetaldehyde to
acetic acid (which
leads to flushing,
headache,
nausea/vomiting,
hypotension if
alcohol is
ingested)
naltrexone
o competitive
opioid antagonist
Loren Warmington
that reduces A <10 points; tapering
cravings and dose not required
pleasurable o observe 1-2 h after last
effects of drinking dose and re-assess on
o note: prescription CIWA-A scale
opioids become o thiamine 100 mg IM
ineffective; may then 100 mg PO OD
trigger withdrawal for 3 days
in opioid- o supportive care
dependent (hydration and
patients nutrition)
if history of withdrawal
Signs of Alcohol withdrawl seizures
(Delerium Tremens) o diazepam 20 mg q1h
Autonomic hyperactivitiy for minimum of three
(diaphoresis, tachycardia, increased doses regardless of
respiration) subsequent CIWA
Hand tremor scores
Insomnia if history of seizure disorder or
Psychomotor agitation multiple withdrawal seizures
Anxiety despite diazepam, use anti-
Nausea or vomiting seizure medication (e.g.
Grand mal seizures Dilantin)
Visual/tactile/auditory if oral diazepam not tolerated
hallucinations o diazepam 2-5 mg
Persecutory delusions
IV/min maximum
10-20 mg q1h; or
lorazepam SL
if >65 yr or severe liver
disease, severe asthma, or
respiratory failure are present,
(CIWA-A) scoring system. Areas of use short acting benzodiazepine
o lorazepam PO/SL/IM
1-4 mg q1-2h
nausea and vomiting if hallucinosis present
paroxysmal sweats o haloperidol 2-5 mg
tactile disturbances IM/PO q1-4h max
visual disturbances 5 doses/day or atypical
tremor antipsychotics
(olanzapine,
anxiety
risperidone)
auditory disturbances o diazepam 20 mg x 3
headache, fullness in head doses as seizure
agitation prophylaxis
o orientation and (haloperidol lowers
clouding of sensorium seizure threshold)
all categories are scored from admit to hospital if:
0-7 (except: o still in withdrawal
orientation/sensorium 0-4), after >80 mg of
maximum score of 67 diazepam
mild <10 o delirium tremens,
moderate 10- recurrent arrhythmias,
20 or multiple seizures
severe >20 o medically ill or unsafe
basic treatment protocol using to discharge home
CIWA-A scale
o diazepam 20 mg PO Wernicke-Korsakoff Syndrome
q1-2h prn until CIWA-
27

alcohol-induced amnestic
disorders due to thiamine
deficiency
necrotic lesions
mammillary bodies,
thalamus, brain stem
Wernickes
encephalopathy (acute and
reversible): triad of
nystagmus (CN VI palsy),
ataxia and confusion
Korsakoffs syndrome
(chronic and only 20%
reversible with treatment):
anterograde amnesia and
confabulations; cannot
occur during an acute
delirium or dementia and
must persist beyond usual
duration of
intoxication/withdrawal
management
o Wernickes:
thiamine 100 mg
PO OD x 1-2
weeks
o Korsakoffs:
thiamine 100 mg
PO bid/tid x 3-12
mon
Prognosis
relapse is common and should
not be viewed as failure
monitor regularly for signs of
relapse
25-30% of abusers exhibit
spontaneous improvement over
1 year
60-70% of individuals with
jobs and families have an
improved quality of life 1 year
post-treatment
Cocaine
Intoxication
elation, euphoria, pressured
speech, restlessness,
sympathetic stimulation (i.e.
tachycardia, mydriasis,
sweating)
prolonged use may result in
paranoia and psychosis
Overdose
Loren Warmington
medical emergency:
hypertension, tachycardia,
tonic-clonic seizures, dyspnea,
and ventricular arrhythmias
treatment with IV diazepam to
control seizures and propanolol
or labetalol to manage
hypertension and arrhythmias
Withdrawal
initial crash (1-48 hrs):
increased sleep, increased
appetite
withdrawal (1-10 wks):
dysphoric mood plus fatigue,
irritability, vivid, unpleasant
dreams, insomnia or
hypersomnia, psychomotor
agitation or retardation
complications: relapse, suicide
(significant increase in suicide
during withdrawal period)
management: supportive
management
Treatment of Chronic Abuse
optimal treatment not
established
psychotherapy, group therapy,
and behaviour modification
useful in maintaining
abstinence
studies of dopamine agonists to
block cravings show
inconsistent results
Complications
cardiovascular: arrhythmias,
MI, CVA, ruptured AA
neurologic: seizures
psychiatric: psychosis,
paranoia, delirium, suicidal
ideation
Ganja
marijuanaisthemostoftenused
illicitdrug
psychoactivesubstancedelta9
tetrahydrocannabinol(9THC)
smokingisthemostcommon
modeofselfadministration
28
intoxicationcharacterizedby
tachycardia,conjunctivalvascular
engorgement,drymouth,increased
appetite,increasedsenseofwell
being,euphoria/laughter,muscle
relaxation,impairedperformanceon
psychomotortasksincluding
driving
highdosescancause
depersonalization,paranoia,and
anxiety
maytriggerpsychosisand
schizophreniainpredisposed
individuals
chronicuseassociatedwith
toleranceandanapathetic,
amotivationalstate
cessationdoesnotproduce
significantwithdrawalphenomenon
treatmentofdependence
includesbehaviouraland
psychologicalinterventionsto
maintainanabstinentstate
Medical Uses of Ganja
Anorexia-cachexia (AIDS, cancer)
Spasticity, muscle spasms (multiple
sclerosis, spinal cord injury)
Levodopa-induced
dyskinesia (Parkinson's Disease)
Controlling tics and obsessive-
compulsive behaviour (Tourette's
syndrome)
Reducing intra-ocular pressure
(glaucoma)
Mood Disorders
Mood disorders are defined by the
presence of mood episodes
mood episodes represent a
combination of symptoms
comprising a predominant
mood state that is abnormal in
quality or duration; examples
include: major depressive,
manic, mixed, hypomanic
types of mood disorders
include:
o depressive (major
depressive disorder,
dysthymia)
o bipolar (bipolar I/II
disorder, cyclothymia)
o secondary to GMC,
substances,
medications

Secondary Causes of Mood
Disorders
infectious:
encephalitis/meningitis,
hepatitis, pneumonia, TB,
syphilis
endocrine: hypothyroidism,
hyperthyroidism,
hypopituitarism, SIADH
metabolic: porphyria,
Wilsons disease, diabetes
vitamin disorders:
Wernickes, beriberi,
pellagra, pernicious anemia
collagen vascular diseases:
SLE, polyarteritis nodosa
neoplastic: pancreatic cancer,
carcinoid, pheochromocytoma
cardiovascular:
cardiomyopathy, CHF, MI,
CVA
neurologic: Huntingtons
disease, multiple sclerosis,
tuberous sclerosis, degenerative
(vascular, Alzheimers)
drugs: antihypertensives,
antiparkinsonian, hormones,
steroids, antituberculous,
interferon, antineoplastic
medications
Medical Workup of Mood
Disorder
routine screening:
o physical examination
o complete blood count
o thyroid function test
o electrolytes
o urinalysis, urine drug
screen
addtional screening:
o neurological
consultation
o chest x-ray
o electrocardiogram
o CT scan
Risk Factors for Depression
sex:female>male
age:onsetin2550yearage
group
familyhistory:depression,
alcoholabuse,sociopathy
Loren Warmington
childhoodexperiences:lossof
parentbeforeage11,negative
homeenvironment(abuse,
neglect)
personality:insecure,
dependent,obsessional
recentstressors(illness,
financial,legal)
postpartum<6months
lackofintimate,confiding
relationshipsorsocialisolation
DSM-IV-TR Criteria for Major
Depressive Episode
A. >5 of the following
symptoms have been present
during the same 2-week period
and represent a change from
previous functioning; at least
one of the symptoms is either
1) depressed mood, or 2) loss
of interest or pleasure
(anhedonia) Note: Do not
include symptoms that are
clearly due to a general
medical condition, or mood-
incongruent delusions or
hallucinations
depressed mood most of the
day, nearly every day, as
indicated by either subjective
report or observation made by
others
markedly diminished interest or
pleasure in all, or almost all,
activities most of the day,
nearly every day
significant weight loss when
not dieting or weight gain, or
decrease or increase in
appetite nearly every day
insomnia or hypersomnia
nearly every day
psychomotor agitation or
retardation nearly every day
fatigue or loss of energy nearly
every day
feelings of worthlessness or
excessive or inappropriate guilt
(which may be delusional)
nearly every day (not merely
self-reproach or guilt about
being sick) there must be an interval of at least
diminished ability to think or
concentrate, or indecisiveness,
nearly every day
29
recurrent thoughts of death
(not just fear of dying),
recurrent suicidal ideation
without a specific plan, or a
suicide attempt or a specific
plan for committing suicide
B. the symptoms do not meet
criteria for a Mixed Episode
C. the symptoms cause
clinically significant distress or
impairment in social,
occupational, or other
important areas of functioning
D. the symptoms are not due to
the direct physiological effects
of a substance or a GMC
E. the symptoms are not better
accounted for by bereavement,
i.e. after the loss of a loved one,
the symptoms persist for longer
than 2 months or are
characterized by marked
functional impairment, morbid
preoccupation with
worthlessness, suicidal
ideation, psychotic symptoms,
or psychomotor retardation
Criteria for Depression (>5):
MSIGECAPS
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,
2 consecutive months in which
criteria are not met for a MDE)

B. the Major Depressive Episode is
not better accounted for by
Schizoaffective Disorder and is not
superimposed on Schizophrenia,
Schizophreniform Disorder,
Delusional Disorder, or Psychotic
Disorder not otherwise specified
C. there has never been a Manic
Episode, a Mixed Episode, or a
Hypomanic Episode. Note: This
exclusion does not apply if all of the
manic-like, mixed-like, or
hypomanic-like episodes are
substance- or treatment-induced or
are due to the direct physiological
effects of a general medical
condition
Features/Specifiers
psychotic with hallucinations
or delusions
chronic - lasting 2 years or
more
catatonic - at least two of:
motor immobility; excessive
motor activity; extreme
negativism or mutism;
peculiarities of voluntary
movement; echolalia or
echopraxia
melancholic - quality of mood
is distinctly depressed, mood is
worse in the morning, early
morning awakening, marked
weight loss, excessive guilt,
psychomotor retardation
atypical - increased sleep,
weight gain, leaden paralysis,
rejection hypersensitivity
postpartum
seasonal - pattern of onset at
the same time each year (most
often in the fall or winter)
Etiology
biological
genetic: 65-75% MZ twins; 14-
19% DZ twins
neurotransmitter dysfunction at
level of synapse (decreased
activity of serotonin,
norepinephrine, dopamine)
Loren Warmington
secondary to general medical
condition
psychosocial
psychodynamic (e.g. low self-
esteem)
cognitive (e.g. negative
thinking)
environmental factors (e.g. job
loss, diet (omega 3 fatty acids),
bereavement, history of abuse)
co-morbid psychiatric
diagnoses (e.g. anxiety,
substance abuse, mental
retardation, dementia, eating
disorder)
Treatment
biological: antidepressants,
lithium, antipsychotics,
anxiolytics, electroconvulsive
therapy (ECT), light therapy
psychological
o individual therapy:
psychodynamic,
interpersonal,
cognitive behavioural
therapy
o family therapy
o group therapy
social: vocational
rehabilitation, social skills
training
experimental: deep brain
stimulation, transcranial
magnetic stimulation, vagal
nerve stimulation
DSM-IV-TR Criteria for Manic
Episode
A. a distinct period of
abnormally and persistently
elevated, expansive, or irritable
mood, lasting >1 week (or any
duration if hospitalization is
necessary)
B. during the period of mood
disturbance, >3 of the
following symptoms have
persisted (4 if the mood is only
irritable) and have been present
to a significant degree:
o inflated self-esteem or
grandiosity
30
o decreased need for
sleep (e.g. feels rested
after only 3 hours of
sleep)
o more talkative than
usual or pressure to
keep talking
o flight of ideas or
subjective experience
that thoughts are
racing
o distractibility (i.e.
attention too easily
drawn to unimportant
or irrelevant external
stimuli)
o increase in goal-
directed activity
(either socially, at
work or school, or
sexually) or
psychomotor agitation
o excessive involvement
in pleasurable
activities that have a
high potential for
painful consequences
(e.g. engaging in
unrestrained buying
sprees, sexual
indiscretions, or
foolish business
investments)
C. the symptoms do not meet
criteria for a Mixed Episode
(see below)
D. the mood disturbance is
sufficiently severe to cause
marked impairment in
occupational functioning or in
usual social activities or
relationships with others, or to
necessitate hospitalization to
prevent harm to self or others,
or there are psychotic features
E. the symptoms are not due to
the direct physiological effects
of a substance (e.g. drug of
abuse, medication, or other
treatment) or a general medical
condition (e.g.
hyperthyroidism). Note:
Manic-like episodes that are
clearly caused by somatic
antidepressant treatment (e.g.
medication, electroconvulsive
therapy, light therapy) should
not count toward a diagnosis of
Bipolar I Disorder

Criteria for Mania (>3): GST PAID
Grandiosity
Sleep (decreased need)
Talkative
Pleasurable activities, Painful
consequences
Activity
Ideas (flight of)
Distractable
Mixed Episode
criterion met for both manic
episode and major depressive
episode (MDE) nearly every
day for 1 week
criteria D and E of manic
episodes are met
Hypomanic Episode
criterion A of a manic episode
is met, but duration is >4 days
criterion B and E of manic
episodes are met
episode associated with an
uncharacteristic decline in
functioning that is observable
by others
change in function is not
severe enough to cause marked
impairment in social or
occupational functioning or to
necessitate hospitalization
absence of psychotic features
BIPOLAR I / BIPOLAR II
DISORDER
Bipolar I Disorder
o disorder in which at
least one manic or
mixed episode has
occurred
o commonly
accompanied by at
least 1 MDE but not
required for diagnosis
Bipolar II Disorder
o disorder in which
there is at least 1 MDE
and at least 1
hypomanic episode
o no past manic or
mixed episode
Risk Factors
Loren Warmington
slight increase in upper
socioeconomic groups
60-65% of bipolar patients have
family history of major mood
disorders
Treatment
biological: mood stabilizers,
anticonvulsants, antipsychotics,
antidepressants, ECT (Note:
Treatment of bipolar depression
must be done extremely
cautiously, as a switch from
depression to mania can result.
Monotherapy with
antidepressants should be
avoided)
psychological: supportive and
psychodynamic psychotherapy,
cognitive or behavioural
therapy
social: vocational
rehabilitation, leave of absence
from school/work, drug and
EtOH cessation, substitute
decision maker for finances,
sleep hygiene, social skills
training, education for family
members
Anxiety Disorders
Anxiety is a universal human
characteristic involving tension,
apprehension, or even terror, which
serves as an adaptive mechanism to
warn about an external threat by
activating the sympathetic nervous
system (fight or flight)
manifestations of anxiety can
be described along a continuum
of physiology, psychology, and
behaviour
physiology - main brain
structure involved is the
amygdala; neurotransmitters
involved include serotonin,
cholecystokinin, epinephrine,
norepinephrine, dopamine
psychology ones perception of
a given situation is distorted
which causes one to believe it
is threatening in some way
behaviour - once feeling
threatened, one responds by
escaping or facing the situation,
31
thereby causing a disruption in
daily functioning
anxiety becomes pathological
when
fear is greatly out of proportion
to risk/severity of threat
response continues beyond
existence of threat or becomes
generalized to other
similar/dissimilar situations
social or occupational
functioning is impaired
Differential Diagnosis
endocrine: hyperthyroidism,
pheochromocytoma,
hypoglycemia,
hyperadrenalism,
hyperparathyroidism
CVS: congestive heart failure,
pulmonary embolus,
arrhythmia, mitral valve
prolapse
respiratory: asthma,
pneumonia, hyperventilation
metabolic: vitamin B12
deficiency, porphyria
neurologic: neoplasm,
vestibular dysfunction,
encephalitis
substance-induced: intoxication
(caffeine, amphetamines,
cocaine), withdrawal
(benzodiazepines, alcohol)
Medical Workup of Anxiety
Disorder
routine screening: physical
examination, CBC, thyroid
function test, electrolytes,
urinalysis, urine drug screening
additional screening:
neurological consultation, chest
x-ray, electrocardiogram
(ECG), CT scan
DSM-IV-TR Diagnostic
Criteria for Generalized
Anxiety Disorder
A. excessive anxiety and worry
(apprehensive expectation),
occurring more days than not for at
least 6 months, about a number of

events or activities (such as work or
school performance)
B. the person finds it difficult to
control the worry
C. the anxiety and worry are
associated with >3 of the
following 6 symptoms (with at
least some symptoms present
for more days than not for the
past 6 months). Note: Only one
item is required in children
(1) restlessness or feeling
keyed up or on edge
(2) being easily fatigued
(3) difficulty concentrating
or mind going blank
(4) irritability
(5) muscle tension
(6) sleep disturbance
(difficulty falling or
staying asleep, or restless
unsatisfying sleep)
D. the focus of the anxiety and
worry is not confined to
features of an Axis I disorder,
such as panic disorder, social
phobia, etc.
E. the anxiety, worry, or
physical symptoms cause
clinically significant distress or
impairment in social,
occupational, or other
important areas of functioning
F. the disturbance is not due to
the direct physiological effects
of a substance or a GMC and
does not occur exclusively
during a Mood Disorder, a
Psychotic Disorder, or a
Pervasive Developmental
Disorder
Treatment
psychotherapy, relaxation,
mindfulness, and CBT
caffeine and EtOH
avoidance, sleep hygiene
pharmacotherapy:
o benzodiazepines
(short term, low
Loren Warmington
dose, regular
schedule, long
half-life, no prn)
o buspirone (tid
dosing)
o others:
SSRIs/SNRI,
TCAs, beta-
blockers
combinations of above
DSM-IV-TR Diagnostic Criteria
for Post-Traumatic Stress
Disorder
associated with the trauma and
A. the person has been exposed to a
traumatic event in which both of
the following were present:
(1) the person experienced,
witnessed, or was confronted
with an event or events that
involved actual or threatened
death or serious injury, or a
threat to the physical integrity
of self or others
(2) the person's response
involved intense fear,
helplessness, or horror. Note: In
children, this may be expressed
instead by disorganized or
agitated behaviour
B. the traumatic event is
persistently re-experienced in one
(or more) of the following ways:
(1) recurrent and intrusive
distressing recollections of the
event, including images,
thoughts, or perceptions. Note:
In young children, repetitive
play may occur in which
themes or aspects of the trauma
are expressed
(2) recurrent distressing dreams
of the event. Note: In children,
there may be frightening
dreams without recognizable
content
(3) acting or feeling as if the
traumatic event were recurring
(includes a sense of reliving the
experience, illusions,
hallucinations, and dissociative
32
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
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
Loren Warmington
feeling dizzy, unsteady,
lightheaded, or faint
derealization (feelings of
unreality) or depersonalization
(being detached from oneself)
fear of losing control or going
crazy
fear of dying
paresthesias (numbness or
tingling sensations), chills or
hot flushes
(2) at least one of the attacks has
been followed by 1 month (or
more) of >1 of the following:
persistent concern about having
additional attacks
worry about the implications of
the attack or its consequences
(e.g. losing control, having a
heart attack, "going crazy")
a significant change in behavior
related to the attacks
B. absence of agoraphobia
C. the panic attacks are not due to
the direct physiological effects of a
substance or GMC
D. the panic attacks are not better
accounted for by another mental
disorder, such as Social Phobia,
Specific Phobia, Obsessive-
Compulsive Disorder, Post-
Traumatic Stress Disorder,
Separation Anxiety Disorder
Treatment
supportive psychotherapy,
relaxation techniques
(visualization, box-breathing),
cognitive behavioural therapy
(correct distorted thinking,
desensitization/exposure
therapy)
pharmacotherapy
o benzodiazepines (short
term, low dose,
regular schedule, long
half-life, no prn)
o SSRIs/SNRI (start
low, go slow, aim high
since anxiety patients
are very sensitive)
33
o other antidepressants
(Trazodone,
Remeron, MAOIs;
avoid Wellbutrina)
Panic Disorder with Agoraphobia
Agoraphobia - anxiety about being
in places or situations from which
escape might be difficult (or
embarrassing) or where help may
not be available in the event of
having an unexpected panic attack
fears commonly involve
situations: being out alone,
being in a crowd, standing in a
line, or travelling on a bus
situations are avoided, endured
with anxiety or panic, or
require companion
treatment: as per panic disorder
Criteria for Panic Disorder (>4):
"STUDENTS FEAR the 3 Cs"
Sweating
Trembling
Unsteadiness, dizziness
Depersonalization, Derealization
Excessive heart rate, palpitations
Nausea
Tingling
Shortness of breath
Fear of dying, losing control, going
crazy
3 C's: Chest pain, Chills, Choking
Suicide
Risk Factors
Epidemiologic factors
age: increases after age 14;
second most common cause of
death for ages 15-24; highest
rates in persons >65 years
sex: male
race/ethnic background: white
or native Canadians on reserves
marital status:
widowed/divorced

living situation: alone; no
children <18 years old in the
household
other: stressful life events;
access to firearms
psychiatric disorders
mood disorders (15% lifetime
risk in depression; higher in
bipolar)
anxiety disorders (especially
panic disorder)
schizophrenia (10-15% risk)
substance abuse (especially
EtOH 15% lifetime risk)
eating disorders (5% lifetime
risk)
adjustment disorder
conduct disorder
personality disorders
(borderline, antisocial)
past history
prior suicide attempt
family history of suicide
attempt/completion
Symptoms associated with suicide
hopelessness
anhedonia
insomnia
severe anxiety
impaired concentration
psychomotor agitation
panic attacks
Approach
Ideation Do you have thoughts
about ending your life,
committing suicide?
Passive would rather not be
alive but doesnt admit to idea
that involves act of initiation
o Id rather not wake up
o I wouldnt mind if a
car hit me
Active
o I think about killing
myself
Plan - Do you have a plan as to
how you would end your life?
Loren Warmington
Intent -You talk about wanting
to die, but are you planning to
do this? What has stopped you
from ending your life?
Past attempts - Highest risk if
previous attempt in past year,
ask about lethality, outcome,
medical intervention
Assessment of Suicidal
Ideation
Onsetandfrequencyof
thoughtsWhendidthisstart?
Howoftendoyouhavethese
thoughts?
Controloversuicidalideation
Canyoustopthethoughtsor
callsomeoneforhelp?
LethalityDoyouwanttoend
yourlife?Orgetareleasefrom
youremotionalpain
AccesstomeansHowwill
yougetagun?Whichbridgedo
youthinkyouwouldgoto?
TimeandplaceHaveyou
pickedadateandplace?Isitin
anisolatedlocation?
ProvocativefactorsWhat
makesyoufeelworse(e.g.
beingalone)?
ProtectivefactorsWhatkeeps
youalive(e.g.friends,family,
pets,faith,therapist)?
Final Arrangements - Have you
written a suicide note? Made a
will? Given away your
belongings?
Practised suicide or aborted
attempts - Have you put the gun
to your head? Held the
medications in your hand?
Stood at the bridge?
Ambivalence - There must be a
part of you that wants to live -
you came here for help
Assessment of Suicide Attempt
Setting isolated vs. others
present, chance of discovery
Planned vs. impulsive attempt,
triggers/stressors
Intoxication
Medical attention brought in
by another person vs. brought
in by self to ER
34
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
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
associated with personal or
family history of atopy
(asthma, hay fever,
anaphylaxis, eosinophilia)
Loren Warmington
polygenic inheritance: one
parent >60% chance for child;
two parents >80% chance for
child
frequently affects infants,
children, and young adults
females only slightly more at
risk than males (1.3:1 over the
age of 2 years)
almost 15% of children in
developed countries under the
age of 5 are affected; half of
these cases are diagnosed by 1
year of age
half of all patients with AD are
over 18 years of age
the earlier the onset, the more
severe and persistent the
disease
long-term condition with 1/3 of
patients continuing to show
signs of AD into adulthood
childhood onset and hereditary
forms are associated with a
defect in the protein filaggrin
Signs and Symptoms
inflammation, lichenification,
excoriations are secondary to
relentless scratching
atopic palms: prominent palmar
creases
associated with
o keratosis pilaris
(hyperkeratosis of hair
follicles, chicken
skin)
o xerosis
o occupational hand
dryness
patients usually suffer from
three flares per year
Distribution
infant (onset at 2-6 months
old): face, scalp, extensor
surfaces
childhood (>18 months):
flexural surfaces
adult: hands, feet, flexures,
neck, eyelids, forehead, face,
wrists
Investigations
35
no prerequisite investigations to
diagnose atopic dermatitis
may consider: skin biopsy,
immunoglobulin serum levels
(often elevated serum IgE
level), patch testing, and skin
prick tests to look for contact or
environmental allergies
Treatment
majority of cases are mild and
easily managed
goal: reduce signs and
symptoms, prevent or reduce
recurrences, and provide long-
term management to prevent
progression from early disease
to full AD flare
treatment maximized (i.e. less
flare-ups, modified course of
disease) if diagnosis made early
and treatment plan
individualized
o individualized based
on age, severity, sites
and extent of
involvement, presence
of infection, previous
responses to therapy
reassure patients that although
there is no absolute cure, the
disease can be controlled
avoid triggers of AD: irritants
(detergents and solvents,
certain clothing, water
hardness), inappropriate
bathing habits (long hot
showers), microbes (S. aureus),
stress, sweating, contact
allergens, and environmental
aeroallergens (dust mites)
enhance barrier function of the
skin
o simplest and most
important aspect of
controlling AD
o involves regular
application of
moisturizers +/-
diluted corticosteroid
wet-wrap dressings
emollients
hydrate the
skin and
reduce
pruritus
 Loren Warmington
o twice daily application (Elidel) and o oral antibiotics
is recommended even tacrolimus (i.e. cloxacillin,
in absence of (Protopic) cephalexin) for
symptoms, especially block widespread S.
after bathing or calcineurin aureus infections
swimming and inhibit
bathing inflammatory Seborrheic Dermatitis
promotes cytokine
hydration transcription
when in activated Greasy, erythematous, yellow,
followed by T-cells and non-pruritic scaling papules
the other and plaques; occurs in areas
application of inflammatory rich in sebaceous glands
moisturizers cells
to the skin o significant adverse
Etiology
consider psychological support events may include
for some patients skin burning and
transient irritation possible etiologic association
o advantages of long- with Pityrosporum ovale
Anti-inflammatory therapies (yeast)
a) topical corticosteroids: term management of
o effective, rapid AD over long-term
corticosteroid use: Epidemiology
symptomatic relief for
rapid,
acute flares
o different formulations sustained common in infants and at
effect in puberty
and potencies suitable
controlling increased incidence in
for nearly any area of
pruritus immunocompromised patients
skin
produce no e.g. HIV
o best applied
skin atrophy in adults, can cause dandruff
immediately after
safe for the (pityriasis sicca)
bathing
o control inflammation face and neck
no significant
with a potent topical Signs and Symptoms
steroid; prescribe a systemic
milder one following toxicities
associated infants - one cause of cradle
resolution of acute cap
flare with their use
children may be generalized
o systemic
Prognosis with flexural and scalp
immunosuppression
50% clear by age 13, few involvement
may be needed in
persist >30 years of age adults - diffuse in areas of scalp
severe cases
o flares may respond to margin with yellow to white
flakes, pruritus, and underlying
systemic anti-
erythema
staphylococcal therapy
sites: scalp, eyebrows,
side effects:
eyelashes, beard, face, trunk,
skin atrophy,
body folds, genitalia
purpura, Complications face: eyebrows, sides of nose,
striae, steroid
posterior ears, glabella
acne, perioral
infections are common: chest: over sternum
dermatitis,
and glaucoma diagnose early and treat
when used appropriately (i.e. Treatment
around the antibiotic, antifungal,
eyes antiviral therapy);
infections must be resolved face: Nizoral cream OD + mild
b) topical immunomodulators steroid cream OD or bid
before applying anti-
o long-term scalp: salicylic acid in olive oil
inflammatory treatments
management o topical mupirocin or Derma-Smoothe FS lotion
o calcineurin inhibitors (peanut oil, mineral oil,
or fusidic acid is
such as pimecrolimus often sufficient fluocinolone acetonide 0.01%)
36

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
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
Epidemiology
association with hepatitis C
may be triggered by severe
emotional stress
Signs and Symptoms
small, polygonal, flat-topped,
shiny, violet papules; resolves
with hyperpigmented macules
Wickhams striae: greyish lines
over surface; pathognomonic
Loren Warmington
sites: wrists, ankles, mucous precedes other lesions by
membranes in 60% (mouth, 1-2 weeks
vulva, glans), nails, scalp
mucous membrane lesions: Etiology
lacy, whitish reticular network,
milky-white plaques/papules; suspected human herpes virus 7
increased risk of SCC in
erosions and ulcers
Treatment
nails: longitudinal ridging;
dystrophic
scalp: scarring alopecia no treatment needed; clears
spontaneously in 6-12 weeks,
spontaneously resolves in
reassurance
weeks or lasts for years (mouth
topical corticosteroids when
and shin lesions)
post-inflammatory
Koebner phenomenon:
pigmentation is a concern
develops in areas of trauma
Clinical Pearl
Treatment
Secondary syphilis can present with
a non-pruritic papulosquamous
topical corticosteroids with
eruption but usually ALSO has
occlusion or intradermal steroid palmar lesions.
injections
short courses of oral prednisone
(rarely) Psoriasis
photochemotherapy for
generalized or resistant cases Mnemonic
oral retinoids for erosive lichen
planus in mouth PSORIASIS: Pathophysiology
Pink papules/Plaques/Pinpoint
Mnemonic bleeding (Auspitz sign)/Physical
The 6 Ps of Lichen Planus injury (Koebner phenomenon)
Silver scale/Sharp margins
Purple, Pruritic, Polygonal, Onycholysis/Oil spots
Peripheral, Papules, Penis (i.e. Rete Ridges with Regular elongation
mucosa) Itching
Arthritis/Abscess
(Monro)/Autoimmune
Pityriasis Rosea
Stratum corneum with nuclei
Immunologic
Definition and Clinical Features
Stratum granulosum absent
acute, self-limiting,
erythematous eruption
characterized by red, oval
plaques/patches with Classification
central scales that do not
extend to edge of lesion
plaque psoriasis
sites: trunk, proximal
guttate psoriasis
aspects of arms and legs
erythrodermic psoriasis
long axis of lesions follows
pustular psoriasis
parallel to ribs producing
Christmas tree psoriatic arthritis
pattern on back
varied degree of pruritus Differential Diagnosis
most start with a
herald patch which atopic dermatitis, mycosis
fungoides (cutaneous T-cell
37

lymphoma), seborrheic
dermatitis, tinea
PLAQUE PSORIASIS
a common chronic and recurrent
disease characterized by well-
circumscribed erythematous
papules/plaques with silvery-white
scales, mostly at sites of repeated
trauma
Pathophysiology
decreased epidermal transit
time from basal to horny layers
shortened cell cycle of psoriatic
and normal skin --> excess
keratinization with scales
Epidemiology
multifactorial inheritance
Clinical Pearl
Woronoffs Ring
Woronoffs ring: blanched halo that
surrounds psoriatic lesions after
topical or phototherapy treatments
Signs and Symptoms
worse in winter (lack of sun
and humidity)
Koebner phenomenon
(isomorphic response):
induction of new lesion by
injury
Auspitz sign: bleeds from
minute points when scale is
removed
sites: scalp, extensor surfaces
of elbows and knees, trunk,
nails, pressure areas
usually non-pruritic
exacerbating factors: drugs
(lithium, ethanol, chloroquine,
beta-blockers), sunlight, stress,
obesity
Treatment
preventative measures: avoid
sunburns, avoid drugs that
exacerbate the condition (beta-
blockers, lithium, corticosteroid
Loren Warmington
rebound phenomenon,
interferon, etc.)
first-line treatment mainly
involves topical treatments,
usually prescribed if less than
5-10% of the body surfaces are
involved. If the affected area is
>10%, use topical medications
as adjuncts to phototherapy or
systemic drugs
systemic treatments should be
considered if:
o psoriatic lesions cover
>10% of the body
surface area
o unsuccessful topical
therapies
o disease is causing
psychological distress
GUTTATE PSORIASIS ("DROP-
LIKE")
Definition and Clinical Features
discrete, scattered salmon-pink
scaling papules
sites: generalized, sparing
palms and soles
often antecedent streptococcal
pharyngitis
Treatment
UVB phototherapy, sunlight,
lubricants
penicillin V or erythromycin if
Group A beta-hemolytic
Streptococcus on throat culture
ERYTHRODERMIC
PSORIASIS
Definition and Clinical Features
generalized erythema with fine
desquamative scale on surface
associated symptoms:
arthralgia, severe pruritus
may present in patient with
previous mild plaque psoriasis
aggravating factors: lithium,
beta-blockers, NSAIDs,
38
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
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)
Loren Warmington
Etiology and Pathophysiology
autoimmune disorder, unknown
etiology
hallmark of RA is hypertrophy
of the synovial membrane
o outgrowth of activated
rheumatoid synovium
(pannus) into and over
the articular surface
results in destruction
of articular cartilage
and subchondral bone
two theories attempt to explain
chronic remissions and
exacerbations seen in RA
o sequestered Ag
o molecular
Common sites of joint
involvement in mimicry RA
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

Criteria Definition
1. Morning Joint stiffness >1
stiffness hour for >6 weeks
Investigations
At least 3 active
joints for >6 weeks;
2. Arthritis of RF positive in 80% of patients
commonly involved
three or more o non-specific, also seen
joints are PIP, MCP,
joint areas in other rheumatic
wrist, elbow, knee,
ankle, MTP diseases (e.g. SLE,
Sjogrens), chronic
At least one active inflammation (e.g.
3. Arthritis of
joint in wrist, MCP SBE, hepatitis, TB)
hand joints
or PIP for >6 weeks and 5% of healthy
Bilateral population
4. Symmetric involvement of PIP, anti-CCP (cyclic citrullinated
arthritis MCP, or MTP for >6 peptide): sensitivity (~80%)
weeks increased disease activity is
Subcutaneous associated with decrease Hb
Signs and Symptoms
nodules over bony (anemia of chronic disease),
5. Rheumatoid prominences, increased platelets, elevated
nodules extensor surfaces or variable course of ESR, CRP, and RF
in juxta-articular exacerbations and
regions remissions Classification of Global
morning stiffness >1 hr, Functional Status in RA
Found in 60-80% of
6. Serum RF improves with use, (American College of
RA patients
aggravated by rest Rheumatology, 1991)
Erosions or symmetric joint
periarticular involvement
7. osteopenia, likely to Class I: able to perform usual
signs of disease activity: ADLs (self-care, vocational,
Radiographic see earliest changes synovitis (assessed by
changes at ulnar styloid, 2nd avocational)
tender and swollen joint Class II: able to perform self-
and 3rd MCP and count), elevated serum
PIP joints care and vocational activities,
markers of inflammation
such as ESR or CRP,
39

restriction of avocational
activities
Class III: able to perform self-
care, restriction of vocational
and avocational activities
Class IV: limited in ability to
perform self-care, vocational,
avocational activities
Complications of Chronic
Synovitis
joint deformities (see Figure 8
below)
o swan neck deformity,
boutonnire deformity
o ulnar deviation of
MCP; radial deviation
of wrist joint
o hammer toe, mallet
toe, claw toe
o flexion contractures
atlanto-axial and subaxial
subluxation
o C-spine instability
o neurological
impingement (long
tract signs)
o difficult intubation
limited shoulder mobility,
spontaneous tears of the rotator
cuff leading to chronic spasm
tenosynovitis => may cause
rupture of tendons
Carpal Tunnel Syndrome
ruptured Bakers cyst
(outpouching of synovium
behind the knee); presentation
similar to acute DVT
decreased functional capacity
and early mortality
Loren Warmington
Treatment
goals of therapy
o control disease activity
o relieve pain and
stiffness
o maintain function and
lifestyle
o prevent or control
joint damage
o key is early diagnosis
and early intervention
with disease
modifying anti-
rheumatic drugs
(DMARDs)
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.
Clinical Pearl
Common Syndromes in RA
1. Sjogrens syndrome (sicca
complex, dry eyes and mouth)
40
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
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
corticosteroids
local
o intra-articular
injections to
control symptoms
in a specific joint
o eye drops for eye
involvement
systemic (prednisone)

o 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
o moderate to high
dose (20-60+
mg/day) for
cardiopulmonary
disease
o high dose (1
mg/kg/day) for
vasculitis
o do baseline
DEXA bone
density scan and
start
bisphosphonate,
calcium, and
vitamin D therapy
if using
corticosteroids >3
months at >7.5
mg/day
side effects: osteoporosis,
avascular necrosis (AVN),
hypertension, cataracts,
glaucoma, peptic ulcer
disease (PUD),
susceptibility to
infection, hypokalemia,
hyperglycemia,
hyperlipidemia, weight
gain, acne
Clinical Pearl
cautions/contraindications:
active infection, Only DMARDs (not analgesics or
osteoporosis, hypertension, NSAIDs) alter the course of RA!
gastric ulcer, diabetes, TB
C) Surgical Therapy
2. Disease Modifying
Antirheumatic Drugs (DMARDs)
combination DMARDs are the
standard of care
start DMARDs within 3 months
of diagnosis to decrease disease
progression, symptoms and
signs
DMARDs reduce or prevent
joint damage, and are
Loren Warmington
associated with better long- reconstruction (tendon
term disability index repair)
delayed onset of action (may surgery indicated for
take 8-12 weeks) structural joint damage
many DMARDs have potential
toxicities that require periodic SLE
monitoring Diagnostic Criteria of SLE: MD
if repetitive flares, progressive SOAP BRAIN
joint damage, or ongoing Malar rash Blood
disease activity after 3 months Discoid rash Renal
of maximal therapy > change or Serositis Arthritis
add other DMARDs Oral ulcers Immune
mild and early stages: ANA Neurologic
o hydroxychloroquine or Photosensitivity
sulfasalazine
monotherapy preferred Signs and Symptoms
moderate to severe disease
(especially if unfavourable characterized by periods of
prognostic factors): exacerbation and remission
o methotrexate is the systemic
gold standard o fever, malaise, fatigue,
o single regimen with
lymphadenopathy,
methotrexate or weight loss
leflunomide
vascular
o combination therapy:
o Raynauds
methotrexate +
phenomenon,
sulfasalazine +
thrombosis, vasculitis,
hydroxychloroquine;
livedo reticularis
methotrexate +
(mottled
cyclosporine;
discolouration of skin
methotrexate +
leflunomide
due to narrowing of
blood
biologics: indicated if persistent
vessels, characteristic
disease activity lacy or net-like
o commonly used after appearance)
failure of other dermatologic
DMARDs; however,
o maculopapular rash,
evidence suggests
photosensitivity,
benefit from use in
panniculitis
early RA as well
(inflammation of
subcutaneous fat and
muscle tissue),
alopecia (hair loss),
urticaria, purpura,
oral, nasal, genital
ulcers
ophthalmic
o conjunctivitis,
synovectomy: debridement episcleritis,
and/or removal of inflamed keratoconjunctivitis,
synovium from individual cytoid bodies (cotton
joints (surgical or wool
radioactive) exudates on
joint replacement (hip, fundoscopy =
shoulder, knee) infarction of nerve cell
joint fusion (wrist, thumb, layer of retina)
ankle, C-spine) gastrointestinal
41

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
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 anti-
Sm 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
venous clotting and increased
PTT
Treatment
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
Loren Warmington
and taper when Contact dermatitis
possible Tachyphylaxis (tolerance)
o treatment is tailored to
organ system involved Systemic:
and severity of disease Dermatological
o all medications used to Thin, fragile skin
treat SLE require Mild hirsutism
periodic monitoring
Bruising
for potential toxicites
Facial erythema
dermatologic
o preventative: use Increased sweating
sunscreen, avoid UV Impaired wound healing,
light and estrogens Striae
o topical steroids for Acne
rash, antimalarials Growth suppression in children
musculoskeletal Hypertension
o bisphosphonates, Hyperlipidemia
calcium, vitamin D to Hyperglycemia
combat osteoporosis Cushingoid Faces and buffalo
o antimalarials hump
(hydroxychloroquine Adrenal suppression and
if no serious internal atrophy
organ involvement => Weight gain, Na and water
retention, K depletion
improves long term
Infections, especially viral, TB
control and prevents
and fungal
flares)
o NSAIDs Osteoporosis, aseptic bone
gastroprotective agent necrosis, ruptured Achilles
for arthritis (also Gastrointestinal
beneficial for pleuritis Despespsia, Peptic ulcer
and pericarditis and perforation
organ threatening disease Pancreatitis
o systemic steroids to CNS
euphoria
minimize end organ
Psychosis, increased
damage secondary to
inflammation high- intracranial pressure,
dose oral increased tendency to
prednisone/IV epilepsy
methylprednisolone in Cataracts, increased intra ocular
severe disease pressure
o steroid sparing agents: Amenorrhea, premature
azathioprine, menopause
methotrexate, Teratongenity (fetal cleft
mycophenolate palate)
o IV cyclophosphamide Rebound disease on reducing
for serious organ dosage
involvement (e.g. Myopathy or muscle atrophy
cerebritis or SLE
nephritis) Cataracts
any opacity of the lens
Side Effects of Steroids most common cause of
reversible blindness worldwide
Local: types: nuclear sclerosis,
Atrophy cortical, posterior subcapsular
(see Figure 16 below)
Perioral dermatitis
Steroid acne
Etiology
Rosacea
42

acquired
o age-related (over 90%
of all cataracts) Clinical Pearl
o cataract associated
with systemic disease
Macular edema is the most common
(may have juvenile
cause of visual loss in patients with
onset)
background DR.
diabetes
mellitus
metabolic Background:
disorders
(e.g. Wilsons
disease,
galactosemia,
homocystinur
ia)
hypocalcemia
o traumatic (may be
rosette shaped)
o intraocular Classification
inflammation (e.g.
uveitis)
o toxic (steroids,
phenothiazines)
o radiation
congenital
o present with altered
red reflex or
leukocoria
o treat promptly to
prevent amblyopia
Diabetic Retinopathy
most common cause of
blindness in young people in
North America
blurring of distance vision with
rise of blood sugar
consider DM if unexplained
retinopathy, cataract, EOM
palsy, optic neuropathy, sudden
change in refractive error
loss of vision due to
o progressive
microangiopathy,
leading to macular
edema
o progressive diabetic
retinopathy -->
neovascularization -->
traction --> retinal
detachment and
vitreous hemorrhage
o rubeosis iridis
(neovascularization of
the iris) leading to
neovascular glaucoma
(poor prognosis)
Loren Warmington
o macular ischemia
altered vascular permeability
(loss of pericytes, breakdown
of blood-retinal barrier,
thickening of basement
membrane)
retinal vessel closure
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)
43
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
Clinical Pearl
Presence of DR in:
Type 1 DM
25% after 5 years
60% after 10 years
>80% after 15 years
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
as pregnancy can
exacerbate DR
o gestational diabetics
not at risk for
retinopathy
Treatment
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
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
Loren Warmington
Group Mild to moderate narrowing o medical and family
1 or sclerosis of the arterioles history
o visual acuity testing
Group Moderate to marked o slit lamp exam to
2 narrowing of the arterioles
assess anterior
Local and/or generalized
chamber depth
narrowing of arterioles
o ophthalmoscopy to
Exaggeration of the light
assess the disc features
reflex
o tonometry by
Arteriovenous crossing
changes (AV nipping) applanation or
indentation to measure
Group Retinal arteriolar narrowing the IOP
3 and focal constriction o visual field testing
Retinal edema
Cotton-wool patches
Hemorrhage
Group Same as group 3, plus
4 papilledema
Glaucoma
aqueous is produced by the
ciliary body and flows from the
posterior chamber to the
anterior chamber through the
pupil, and drains into the
episcleral veins via the
trabecular meshwork and the
canal of Schlemm
an isolated increase in IOP is
termed ocular hypertension (or
glaucoma suspect) and these
patients should be followed for
increased risk of developing
glaucoma (~10% if IOP = 20-
30 mmHg; 40% if IOP = 30-40
mmHg; and most if IOP >40
mm Hg) Features of Papilledema
Engorged retinal veins
average IOP is 15 3 mm
Hg (diurnal variation, higher in Loss of cupping
a.m.) Pink disk with blurred margins
pressures >21 mmHg more Cribosa not visible
likely to be associated with Flamed shaped hemorrhages
glaucoma; however, up to 50%
of patients with glaucoma do Causes of Papilledema
not have IOP >21mmHg central retinal vein occlusion
normal C:D (cup:disc) ratio systemic illness
<0.4
HTN, vasculitis, hypercapnia
be suspicious of glaucoma if
toxic/metabolic/nutritional
C:D ratio >0.6, C:D ratio
deficiency
difference between eyes >0.2 or
infiltration
cup approaches disc margin
o neoplastic: leukemia,
loss of peripheral vision most
lymphoma, glioma
commonly precedes central loss
o non-neoplastic:
sequence of events: gradual
sarcoidosis
pressure rise, followed by
pseudotumour cerebri
increased C:D ratio, followed
by visual field loss
screening tests should include:
44
 Loren Warmington
o idiopathic signs and Acute Loss of Vision (occurring in cataract
symptoms of increased seconds to days) glaucoma
ICP, with a normal CT
o usually in obese young Clinical Pearl Vitreous/Fundus/Optic Nerve:
women Top 3 in DDx of Acute Loss of age-related macular
compressive Vision degeneration (ARMD)
o meningioma, diabetic retinopathy
hemangioma, thyroid 1. trauma/foreign body
2. retinal artery/vein occlusion retinal vascular
ophthalmopathy
3. retinal detachment insufficiency
compressive optic
Optic Atrophy
neuropathy (intracranial
Cornea/Anterior Segment:
mass, orbital mass)
Damage to the optic nerve from intraocular neoplasm
many different kinds of pathologies. corneal edema
retinitis pigmentosa (RP)
Not a disease, but rather a sign of an hyphema
underlying condition acute angle-closure glaucoma
Cortical/Other
trauma/foreign body pituitary adenoma
Causes:
medication-induced
Vitreous/Retina/Optic Nerve: (sildenafil, amiodarone)
glaucoma, vitreous hemorrhage nutritional deficiency
anterior ischemic optic retinal detachment
neuropathy, retinal artery/vein occlusion
retinal lesions eg. Causes of Red Eye
acute macular lesion
chorioretinitis, intraocular
optic neuritis lids/orbit/lacrimal system
bleed
temporal arteritis o hordeolum/chalazion
tumour, aneurism or pagets
disease pressing on the optic anterior ischemic optic o blepharitis
nerve, neuropathy (AION) o foreign
optic neuritis (retrobulbar body/laceration
neuritis) Cortical/Other: o dacryocystitis/dacryoa
Lebers hereditary optic occipital infarction/hemorrhage denitis
neuropathy, cortical blindness Conjunctiva/sclera
Congenital functional (non-organic, o subconjunctival
Division of optic nerve diagnosis of exclusion) hemorrhage
surgeryor trauma o conjunctivitis
Chronic Loss of Vision (occurring o dry eyes
Signs and symptoms: over weeks to months) o pterygium/pinguecula
low visual acuity, o episcleritis/scleritis
Clinical Pearl o preseptal/orbital
peripheral vision impairment,
cellulitis
difficulty with colour vision, Top 3 in DDx of Chronic Loss of
Vision cornea
pallor of the optic disc on
o foreign body
fundoscopy
o keratitis
Reversible Irreversible o abrasion, laceration
Management:
optic nerve atrophy is an 1.Cataract 1. age-related macular o ulcer
irreversible condition, management 2.Refractive degeneration anterior chamber
of the underlying condition is error 2. glaucoma o uveitis (iritis,
crucial to prevent exacerbation 3. corneal 3. diabetic retinopathy iridocyclitis)
dystrophy o acute angle-closure
glaucoma
Transient Loss of Vision (lasting o hyphema
seconds to hours) o hypopyon
Cornea/Anterior Segment: endophthalmitis
transient ischemic attack (TIA) corneal dystrophy,
migraine with aura scarring, edema Polcystic Kidey Disease
papilledema refractive error
45
 Loren Warmington
PKD1 (1:400), PKD2 polycystic changes are always monitor blood pressure and
(1:1,000), accounts for about bilateral and can present at any treat hypertension with ACEI
10% of cases of renal failure age dialysis or transplant for ESRD
autosomal dominant; at least 3 clinical manifestations rare (disease does not recur in
genes: PKD1 (chr 16p), PKD2 before age 20-25 transplanted kidney)
(chr 4q), PKD3 (location not kidneys are normal at birth but may require nephrectomy to
yet determined) may enlarge to 10 times normal create room for renal transplant
polycystin protein from PKD1 volume
responsible for cell-cell and variable progression to renal Chronic Renal Disease
cell-matrix interaction functional impairment (ESRD
defect can lead to abnormal cell
abnormal markers (Cr, urea)
in up to 50% by age 60)
GFR <60 ml/min for >3 months
growth and cyst formation investigations
or
extrarenal manifestations: most radiographic diagnosis best
kidney pathology seen on
common; multiple accomplished by renal U/S
asymptomatic hepatic cysts (enlarged kidneys, multiple biopsy or
(33%) cerebral aneurysm cysts throughout renal decreased renal size on U/S
(10%), diverticulosis and mitral parenchyma, increased cortical
valve prolapse (25%) thickness, splaying of renal Stages of Chronic Kidney Disease
polycystic liver disease rarely calyces) (K/DOQI, 2002)
causes liver failure CT abdo with contrast (for GFR
o less common: cysts in equivocal cases, occasionally Definition
(mL/min/1.73m2)
pancreas, spleen, reveals more cystic
Normal or
thyroid, ovary, seminal involvement) Stage
increased >90
vesicles, and aorta gene linkage analysis for PKD1 1
GFR
for asymptomatic carriers
Signs and Symptoms o Cr, BUN, urine R&M Mild
Stage
(to assess for decrease in 60-89
2
hematuria) GFR
often asymptomatic; discovered
incidentally on imaging or by Moderate
Stage
screening those with FHx Treatment decrease in 30-59
3
acute abdominal flank pain/dull GFR
lumbar back pain goal: to preserve renal function Severe
Stage
hematuria (microscopic by prevention and treatment of decrease in 15-29
4
frequently initial sign, gross) complications GFR
nocturia (urinary concentrating educate patient and family End stage
defect) about disease, its Stage
renal <15 (or dialysis)
manifestations and inheritance 5
rarely extra-renal presentation disease
(e.g. ruptured berry aneurysm, pattern
Etiology and Incidence of Chronic
diverticulitis) genetic counselling:
Kidney Disease (CKD)
HTN (increased renin due to transmission rate 50% from
affected parent Diabetes 42.9%
focal compression of intrarenal
arteries by cysts) (60-75%) prevention and early treatment Hypertension 26.4%
palpable kidneys of urinary tract and cyst Glomerulonephritis
infections (avoid 9.9%
instrumentation of GU tract)
TMP/SMX, ciprofloxacin: able Other/Unknown 7.7%
to penetrate cyst walls, achieve Interstitial
4.0%
therapeutic levels nephritis/Pyelonephritis
adequate hydration to prevent Cystic/Hereditary/Congenital
Common Complications stone formation 3.1%
avoid contact sports due to
urinary tract and cyst Secondary GN/Vasculitis 2.4%
greater risk of injury to
infections, HTN, CRF, enlarged kidneys
nephrolithiasis (5-15%), flank screen for cerebral aneurysms if Management
and chronic back pain strong family history of
aneurysmal hemorrhages diet
Clinical Course

46
 Loren Warmington
protein restriction with R - RBCs: manage anemia with [Na] <10-
adequate caloric intake limits erythropoietin 20
endogenous protein catabolism O - Osteodystrophy: give mmol/L
K restriction (40 mmol/day) calcium between meals (to increase - urine
Na and water restriction Ca) and calcium with meals (to bind osmolalit
PO4 restriction (1 g/d) and decrease PO4) y > 500
avoid extradietary Mg (i.e. N - Nephrotoxins: avoid mOsm/kg
antacids) nephrotoxic drugs (ASA, -
gentamicin) and adjust doses of fractional
renally excreted medications excretion
medical of Na <
1%
cinacalcet for
hyperparathyroidism (sensitizes Acute Renal Injury
parathyroid to calcium --> Clinical Pearl
decreased PTH) Definition
calcium supplements (e.g. Differentiating Pre-renal from
TUMS) treats hypocalcemia abrupt decline in renal function ATN
when given between meals and leading to increased Pre-
binds phosphate when given nitrogenous waste products ATN
renal
with meals formerly known as Acute Renal
consider calcitriol if RBC, pigmented
Failure (ARF) Urinalysis normal
granular casts
hypocalcemic (despite normal
phosphate levels) Clinical Features Urine [Na] <20 >40 mEq/L
sevelamer (phosphate binder) if Urine [Cr]/
both hypercalcemic and >40 <20
azotemia (increased BUN, Cr) [Na]
hyperphosphatemic
abnormal urine volume (anuria, Urine <350
vitamin D analogues are being >500
oliguria, polyuria) osmolality mOsm/kgH2O
introduced in the near future
erythropoietin injections (Hct FeNa <1 >1
<30%) for anemia Clinical Pearl
DDAVP for prolonged bleeding The 2 most common causes of acute Investigations
time kidney injury in hospitalized patients blood: CBC, electrolytes, Cr,
ACEI for hypertension (target are prerenal azotemia and acute BUN (think prerenal if increase
130/80 or less), loop diuretics tubular necrosis. Remember that in BUN is relatively greater
when GFR <25 mL/min prerenal failure can lead to ATN. than increase in Cr), Ca, PO4
o statins for urine volume, C&S, R&M:
dyslipidemia Clinical Pearl sediment, casts, crystals
o adjust dosages for Clues to Clues to Clues to Post- urinary indices
renally excreted Pre- Renal Renal foley catheterization (rule out
medications (avoid Renal Etiology Etiology bladder outlet obstruction)
nephrotoxic Etiology - - known fluid challenge (i.e. fluid bolus
medications) - clinical: appropriat solitary kidney to rule out most prerenal
decreased e clinical - older man causes)
Dialysis (hemodialysis, peritoneal BP, context - recent imaging: abdo U/S (assess
dialysis) increased - retroperitoneal
kidney size, hydronephrosis,
HR, urinalysis surgery
post-renal obstruction)
Renal transplantation positive positive - anuria
indications for renal biopsy:
orthostati for casts: - palpable
c HR & - bladder o diagnosis is not certain
BP pigmented - ultrasound o prerenal azotemia or
Mneumonic ATN is unlikely
changes granular indicates
Management of Complications of - in ATN hydronephrosi o oliguria persists >4
CKD increased - WBC in s weeks
N - low-nitrogen diet [urea] >> AIN
E - Electrolytes: monitor K increased - RBC in Red Flag
P - pH: metabolic acidosis [Cr] GN Indications for Dialysis in AKI
H - Hypertension - urine

47
 Loren Warmington

Hyperkalemia (refractory) high morbidity with multi-

organ failure, most commonly Digitalis
Acidosis (refractory)
overdose
Volume overload (refractory) in prerenal azotemia (ischemic (blocks
Elevated BUN (>35 mM) insult) Na-K
Pericarditis ATPase)

Encephalopathy Treatment of Hyperkalemia Succinylch
Edema (pulmonary) oline
serum K >5.0 mEq/L
Treatment Figure 12. EKG Changes in
Approach to Hyperkalemia Hyperkalemia
1) preliminary measures
1. emergency measures: obtain
pre-renal ECG, if life threatening begin
o correct prerenal treatment immediately
factors: optimize 2. rule out factitious
volume status and hyperkalemia; repeat blood test
cardiac performance 3. hold exogenous K, and any
renal K retaining medications Signs and Symptoms
o exclude reversible 4. assess potential causes of
renal causes: d/c transcellular shift
usually asymptomatic but may
nephrotoxic drugs, 5. estimate GFR (calculate
develop nausea, palpitations,
treat infection, CrCl/use Cockcroft-Gault) muscle weakness, muscle
optimize electrolytes 6. if normal GFR, calculate stiffness, paresthesias,
and hold ACEI/ARB TTKG = (Uk/Pk)/(Uosm/Posm) areflexia, ascending paralysis,
post-renal o TTKG <7 = decreased and hypoventilation
o consider obstruction: effective aldosterone impaired renal ammoniagenesis
structural (stones, function and metabolic acidosis
strictures) vs. o TTKG >7 = normal ECG changes and
functional aldosterone function
(neuropathy) cardiotoxicity (do not correlate
o treat with foley well with K concentration)
Causes of Hyperkalemia o peaked and narrow T
catheter, indwelling
bladder catheter, waves
nephrostomy, stenting Incre o decreased amplitude
Factitio ased Cellular Decreased and eventual loss of P
us Intak Release Excretion waves
2) treat complications
e o prolonged PR interval
Prolonged Diet Intravascul
o widening of QRS and
fluid overload Decreased
use of KCl ar eventual merging with
o NaCl restriction GFR
tourniquet tabs hemolysis T wave (sine-wave
o high dose loop Sample IV KCl Rhabdomy renal
pattern)
taken olysis failure
diuretics from vein Insulin o AV block
low
o hyperkalemia (refer to where IV deficiency o ventricular fibrillation,
effective
Treatment of KCl is asystole
Hyperkalemia) running Hyperosmo circulating
Sample lar states volume
o adjust dosages of hemolysis (e.g. Clinical Pearl

medications cleared by Leukocyt hyperglyce
NSAIDs in
kidney osis mia) In patients with diabetes, increased K
(extreme) Metabolic renal and hyperglycemia, often just giving
3) definitive therapy depends Thrombo acidosis insufficienc insulin to restore euglycemia is
on etiology cytosis (except for y
sufficient to correct the
Note: Renal transplant is not a (extreme) keto- and
Normal
lactic hyperkalemia.
therapy for AKI (unlike other acidosis) GFR but
organs eg: liver) Tumour hypoaldost
lysis Mnemonic
eronism
syndrome Treatment of Hyperkalemia
Prognosis (see Table 7
Drugs
beta- below) SEE BIG K DROP
blockers

48

SEE - Calcium gluconate
BIG - B-agonist, Bicarb, Insulin,
Glucose
K - KayexalateTM
DROP - Diuretics, Dialysis
Treatment
acute therapy is warranted if
ECG changes present, K high,
symptoms present
tailor therapy to severity of
increase in K and ECG changes
o K <6.5 and normal
ECG
treat
underlying
cause, stop K
intake,
increase the
loss of K via
urine and/or
GI tract (see
below)
o K between 6.5 and
7.0, no ECG changes:
add insulin to above
regimen
o K >7.0 and/or ECG
changes: first priority
is to protect the heart:
add Ca gluconate to
above
1. Protect the Heart
Ca gluconate 1-2 amps (10 mL
of 10% solution) IV
antagonizes cardiac toxicity of
hyperkalemia, protects cardiac
conduction system, no effect on
serum K
onset within minutes, lasts 30-
60 minutes
2. Shift K into Cells
regular insulin (Insulin R) 10-
20 units IV, with 1-2 amp
D50W
o onset of action 15-30
min, lasts 1-2 h
o monitor blood glucose
q1h
Loren Warmington
o can repeat every 4-6 nephrotic
hours, or give infusion rapidly progressive
of 1 unit/hour glomerulonephritis
NaHCO3 1-3 amps (given as 3 asymptomatic urinary
amps of 7.5% or 8.4% NaHCO3 abnormalities
in 1L D5W)
o onset of action 15-30 each glomerulonephropathy can be
min, transient effect, caused by a primary disease OR can
drives K into cells in occur secondary to a systemic
exchange for H disease
beta2-agonist (Ventolin) in
nebulized form (dose = 2 cc or
some glomerulonephropathies
10 mg inhaled) or 0.5 mg IV
can present as more than one
o onset of action 30-90
syndrome at different times
min, stimulates Na-K
ATPase
o caution if patient has 1) ACUTE NEPHRITIC
SYNDROME
heart disease as
tachycardia may result
from this high dose of Clinical/Lab Features
beta2-agonist
proteinuria (<3.5
3. Enhance K Removal from Body g/day/1.73m2/day)
abrupt onset hematuria
A. via urine (microscopic or macroscopic)
o furosemide (>40 mg azotemia (increased Cr and
IV), may need IV NS urea)
to avoid hypovolemia RBC casts and/or dysmorphic
o fludrocortisone RBCs in urine
(synthetic oliguria
mineralocorticoid) if HTN (due to salt and water
suspect aldosterone retention)
deficiency
B. via gut
Etiology
o cation-exchange
resins: calcium
etiology can be divided into
resonium or
low and normal complement
Kayexalate (less
levels (Table 8 below)
preferred because it
binds Na in exchange frequently immune-mediated,
for K) plus sorbitol PO with Ig and C3 deposits found
to avoid constipation in GBM
o Kayexalate enemas outcome dependent on etiology
with tap water (not
sorbitol) Mnemonic
C. dialysis (renal failure, life Features of Nephritic Syndrome
threatening hyperkalemia
P - Proteinuria
unresponsive to therapy)
H - Hematuria
A - Azotemia
Presentation of Glomerular R - RBC casts
Disease O - Oliguria
H - Hypertension
Each glomerulonephropathy
presents as one of 4 major
glomerular syndromes NEPHROTIC SYNDROME
acute nephritic Clinical Pearl
49

Presentation of Nephrotic
Syndrome
1) severe proteinuria (>3.5 g/d)
2) hypoalbuminemia
3) edema
4) hyperlipidemia, lipiduria
5) oval fat bodies (microscopy)
6) hypercoagulable state (protein C
and protein S lost in urine)
Clinical/Lab Features
heavy proteinuria (>3.5
g/1.73m2/d)
hypoalbuminemia
edema
hyperlipidemia, lipiduria, fatty
casts and oval fat bodies on
microscopy
hypercoagulable state (i.e.
Protein C and Protein S urinary
losses)
glomerular pathology on renal
biopsy:
o minimal change
disease (or minimal
lesion disease or nil
disease) i.e.
glomeruli appear
normal on light
microscopy
o membranous
glomerulopathy
o focal segmental
glomerulosclerosis
(FSGS)
o membranoproliferative
glomerulonephritis
each can be idiopathic or
secondary to a systemic disease
or drug
Investigaton of Glomerular disease
Blood work
first presentation: electrolytes,
Cr, urea, albumin, fasting lipids
determining etiology: CBC,
ESR, serum immune
electrophoresis, C3, C4,
ANA, p-ANCA, c-ANCA,
cryoglobulins, HBV, HCV
serology, ASOT (anti-
streptolysin - O titres), VDRL,
HIV
Loren Warmington
urinalysis: RBCs, WBCs, casts,
protein
24 hr urine for protein and CrCl
radiology
CXR (infiltrates, CHF,
pleural effusion)
renal ultrasound
renal biopsy (percutaneous or
open)
urine immunoelectrophoresis
for Bence Jones protein if
proteinuria present
Systemic Lupus Erythematosus
lupus nephritis can present as
any of the glomerular
syndromes
nephrotic syndrome with an
active sediment is most
common presentation
glomerulonephritis caused by
immune complex deposition in
capillary loops and mesangium
with resulting renal injury
serum complement levels are
usually low during periods of
active renal disease
children and males with SLE
are more likely to develop
nephritis
HIV-Associated Renal Disease
1) direct nephrotoxic effect of
HIV infection, antiretroviral
drugs (e.g. tenofovir, indinavir)
and other drugs used to treat
HIV-associated infections
2) HIV-associated nephropathy
o histology: focal and
segmental glomerular
collapse with
mesangial sclerosis,
collapsing
FSGS
o tubular cystic dilation
and tubulo-reticular
inclusions
o clinical features:
predominant in black
men, heavy
proteinuria,
progressive renal
insufficiency
50
o prognosis: kidney
failure within one year
without treatment
o therapy: short-term,
high dose steroids,
ACEI, HAART
Amyloidosis
nodular deposits of amyloid
in mesangium, usually
related to AL amyloid
presents as nephritic range
proteinuria with progressive
renal insufficiency
can be primary or secondary
secondary causes: multiple
myeloma, TB, rheumatoid
arthritis, malignancy
Sickle Cell Disease
sickling disorders due to a
mutant beta globin chain, most
commonly caused by a
Glu --> Val substitution at
position 6 resulting in HbS
rather than HbA
Sickle cell anemia occurs when
an individual has two HbS
genes (homozygous) or one
HbS gene + another mutant
beta globin gene (compound
heterozygote)
Pathophysiology
at low pO2, deoxy HbS
polymerizes, leading to rigid
crystal-like rods that distort
membranes --> sickles
the pO2 level at which sickling
occurs is related to the
percentage of HbS present
o in heterozygotes
(HbAS), sickling
occurs at a pO2 of 40
mmHg
o in homozygotes
(HbSS), sickling
occurs at a pO2 of 80
mmHg
sickling is aggravated
by increased H+, increased
CO2, increased 2,3-
DPG, increased temperature
and osmolality

sickle cells are fragile and
hemolyze; they also block
small vessels
Clinical Features
HbAS (heterozygous): patient will
appear normal except at times of
extreme hypoxia and infection
(sickle cell trait)
HbSC (most common compound
heterozygote)
milder anemia
similar clinical features to
HbSS although milder
spleen not always atrophic in
adult
HbSS (homozygous)
chronic hemolytic anemia
jaundice in the first year of life
may have retarded growth and
development +/- skeletal
changes
spleen enlarged in child and
atrophic in adult
types of crises:
o I. Aplastic crises
o toxins and infections
(especially parvovirus
B19) transiently
suppress bone marrow
activity
o II. Splenic
sequestration crises
o usually in children,
with significant
pooling of blood in
spleen, resulting in
acute decreased Hb
and shock
o uncommon in adults
because of functional
asplenia from repeated
infarction (adults with
HbSC may not have
functional asplenia)
o III. Vaso-occlusive
crises (infarction)
o may affect many
different organs
causing pain
(especially in back,
chest, abdomen and
Loren Warmington
extremities), fever, and o presence of HbF in the
leukocytosis (e.g. SS cells decreased
acute chest syndrome) polymerization and
o precipitated by precipitation of HbS
infections, o note: hydroxyurea is
dehydration, rapid cytotoxic and may
change in temperature, cause bone marrow
pregnancy, menses suppression
and alcohol treatment of vaso-occlusive
o crisis
o oxygen (only if
Table 5. Investigations for Sickle hypoxic)
Cell Disease o hydration (reduces
viscosity)
o antimicrobials
HbAS HbSS
o correct acidosis
increased o analgesics/narcotics
reticulocyte (give enough)
, decreased o magnesium (inhibits
CBC normal
Hb, potassium and water
decreased efflux from RBCs
Hct thereby preventing
normal; dehydration)
Peripheral possibly a sickled o indication for
blood few target cells exchange transfusion:
cells acute chest syndrome,
stroke, bone marrow
HbA
necrosis, priapism, and
fraction No HbA,
CNS crisis
of 0.65 Only HbS
Hb prevention of crises is key
(65%); and HbF.
electrophoresi o establish diagnosis
HbS Proportions
s o avoid conditions that
fraction change with
of 0.35 age. favour sickling
(35%) (hypoxia, acidosis,
dehydration, fever)
+ve o vaccination in
sickle cell childhood (e.g.
Other prep pneumococcus
(screenin (heptavalent and 23-
g test) valent),
meningococcus, Hib)
o prophylactic penicillin
Hb electrophoresis from 3 months until 5
distinguishes HbAS, HbSS and years of age
other variants o good hygiene,
nutrition, and social
Treatment support
screening for potential
genetic counseling complications
folic acid to prevent folate o regular bloodwork
deficiency (CBC, retic, iron
indices, BUN, LFTs,
hydroxyurea to enhance
creatinine)
production of HbF
o urinalysis annually
o stops repression of the
o transcranial doppler
gene for HbF or
annually until 16 years
initiates differentiation
old
of stem cells in which
this gene is active
51
 Loren Warmington
o retinal examinations hematuria; loss of renal o hepatic vein
annually from 8 years kidney thrombosis (Budd-
concentrating ability
old Chiari)
o echocardiography intestines acute abdomen idiopathic
every two years from placenta stillbirths rare - Wilsons disease,
10 years old (to screen penis priapism Gauchers
for pulmonary
hypertension) digits dactylitis
Mnemonic
femoral
avascular necrosis
head
Cirrhosis Complications:
bone infarction, infection VARICES
ankle leg ulcers Varices
Anemia
Clinical Pearl Clinical Pearl Renal failure
Functional asplenism increased Acute Chest Syndrome Infection
susceptibility to infection by Coagulopathy
Affects 30% of patients with sickle Encephalopathy
encapsulated organisms cell disease and may be life
S. pneumoniae Sepsis
threatening. Presentation includes
N. meningitidis dyspnea, chest pain, fever,
H. influenzae tachypnea, leukocytosis, and Diagnosis
Salmonella (osteomyelitis) pulmonary infiltrate on CXR.
Caused by vaso-occlusion, infection definitive diagnosis is
Figure 8. Pathophysiology of or pulmonary fat embolus from histologic (liver biopsy)
Sickling infarcted marrow. other tests may be suggestive:
o blood work: liver
Cirrhosis enzymes, bilirubin,
PT/PTT, increased
diffuse, irreversible fibrosis gamma globulin,
plus hepatocellular nodular decreased albumin
regeneration o imaging: U/S is the
decompensated cirrhosis: primary imaging
modality, then CT
means development of ascites
+/- increased bilirubin +/-
encephalopathy +/- increased Management
INR
treat underlying disorder
Etiology alcohol cessation
follow patient for
Organs Affected by Vaso- alcohol (85%) complications (see below)
Occlusive Crisis prognostic factors include
chronic viral hepatitis (B, B+D,
Organ Problem C but not A nor E) o nutrition (EtOH
brain seizures, stroke autoimmune consumption)
hemochromatosis o ascites
eye hemorrhage, blindness
alpha-1-antitrypsin deficiency o varices
liver infarcts, RUQ syndrome o encephalopathy
drugs and toxins
chest syndrome, long- o labs: albumin, INR,
o methotrexate
lung term pulmonary bilirubin, creatinine
biliary cirrhosis
hypertension liver transplantation for end-
o primary
gall stage disease if no alcohold for
stones o secondary
bladder >6 months
chronic hepatic congestion
hyperdynamic flow o cardiac cirrhosis
heart Complications
murmurs (chronic right heart
enlarged (child); atrophic failure, constrictive
spleen pericarditis) hematologic changes in cirrhosis
(adult)

52

pancytopenia from
hypersplenism
decreased clotting factors
o fibrin, thrombin, I, II,
V, VII, IX, X
renal failure in cirrhosis
classifications
o pre-renal (usually due
to overdiuresis)
o acute tubular necrosis
(ATN)
o hepatorenal syndrome
o hepatorenal syndrome
can occur at any time
in severe liver disease,
especially after:
overaggressiv
e diuresis or
large volume
paracentesis
GI bleeding
sepsis
differentiate hepatorenal
syndrome from pre-renal
failure
o prerenal azotemia =
hepatorenal lab
findings
o clinical (very difficult)
o intravenous fluid
challenge (giving
volume expanders
improves
o prerenal failure but not
hepatorenal syndrome)
o pulmonary capillary
wedge pressure
measurements
(PCWP) (preferable)
differentiate hepatorenal
syndrome from ATN
o treatment for
hepatorenal syndrome
is generally
unsuccessful
vasopressin,
octreotide,
midodrine
(increased
renal blood
flow by
Loren Warmington
increased diagnosis via contrast-enhanced
systemic echocardiography; demonstrate
vascular s intrapulmonary shunting
resistance) only proven treatment is liver
definitive transplantation
treatment is
liver Hepatic Encephalopathy
transplant
hepatopulmonary syndrome
acute neuropsychiatric syndrome
(HPS)
secondary to liver disease
o present in patients
with the triad of
1) liver Pathophysiology
disease
2) increased porto-systemic shunt around
alveolar- hepatocytes and decreased
arterial hepatocelular function increases
gradient toxins (believed to be ammonia
while from gut, mercaptans, fatty acids,
breathing amino acids) to brain
room air, and
3) evidence Precipitating Factors
for
intrapulmona nitrogen load (GI bleed, protein
ry vascular load from food intake, renal
abnormalities failure, constipation)
o majority of cases due drugs (narcotics + CNS
to cirrhosis, though depressants)
can be due to other electrolyte disturbance
chronic liver diseases, (hypokalemia, alkalosis,
such as noncirrhotic hypoxia, hypovolemia)
portal hypertension
infection (spontaneous bacterial
o thought to arise from
peritonitis)
ventilation-perfusion
deterioration in hepatic
mismatch,
intrapulmonary function or superimposed liver
disease
shunting and
limitation of oxygen
diffusion failure of Stages
damaged liver to clear
circulating pulmonary I: apathy, restlessness, reversal
vasodilators, versus of sleep-wake cycle, slowed
the production of a intellect, impaired
vasodilating substance computational abilities,
by the liver) impaired handwriting
clinical features: II: asterixis, lethargy,
hyperdynamic circulation with drowsiness, disorientation
cardiac output >7 L at rest and III: stupor (rousable),
decreased pulmonary + hyperactive reflexes, extensor
systemic resistance plantar responses
dyspnea, platypnea (increase in IV: coma (response to painful
dyspnea in upright position, stimuli only)
improved by recumbency) and
orthodeoxia (desaturation in the
Investigations
upright position, improved by
recumbency)
distinguish from non-liver-
related neuropsychiatric disease
in a patient with liver problems
53
 Loren Warmington
(e.g. alcohol withdrawal or minimal o sinusoidal (e.g.
intoxication, sedatives, ammonia cirrhosis, alcoholic
subdural hematoma, metabolic also acts as a hepatitis)
encephalopathy) laxative to o post-sinusoidal (e.g.
also distinguish from the causes eliminate right-sided heart
of metabolic encephalopathy nitrogen- failure, hepatic vein
(e.g. renal failure, respiratory producing thrombosis, veno-
failure, severe hyponatremia, bacteria from occlusive disease,
hypoglycemia); all easy to colon constrictive
exclude/confirm if inadequate response with pericarditis)
diagnosis chiefly clinical, lactulose, may try antibiotics signs of portal hypertension:
supported by laboratory broad-spectrum antibiotics
findings, exclusion of other (metronidazole, neomycin, Clinical Pearl
neuropsychiatric diseases rifaximin) eliminate ammonia
Portal Hypertension
only pathognomonic finding is producing bacteria from bowel
Cause = increase flow AND increase
fetor hepaticus lumen
resistance
characteristic EEG findings: neomycin is less effective than
diffuse (non-focal), slow, high lactulose plus more side effects Signs
amplitude waves (ototoxicity, nephrotoxicity) Esophageal varices
combination of the two may be Melena
more effective for resistant Splenomegaly
cases only Ascites
Hemorrhoids
Treatment avoid causing severe diarrhea
with lactulose to decrease Management
fluid/electrolyte problems beta-blockers
treat underlying liver disease Nitrates
best acute treatment in
and precipitating factors Shunts [e.g. Transjugular
comatose patient is tap water
decrease generation of intrahepatic
enemas until clear
nitrogenous compounds portosystemic shunt (TIPS)]
o decreased dietary
protein to 50 g/day; Mnemonic
vegetable protein is Precipitating Factors for Hepatic Management
better tolerated than Encephalopathy
animal protein Hemorrhage in GI beta-blockers (propanolol,
o lactulose tract/Hyperkalemia nadolol) and nitrates decreases
prevents Excess dietary protein risk of bleeding from varices
diffusion of Paracentesis shunts
NH3 Acidosis/Anemia o goal: decrease portal
(ammonia) Trauma venous pressure
from the Infection o transjugular
colon into Colon surgery intrahepatic
blood Sedatives portosystemic shunt
by lowering (TIPS): interventional
pH and radiologist creates a
forming non- Portal Hypertension shunt between portal
diffusible and hepatic vein via a
NH4+ Pathophysiology catheter placed in the
(ammonium) pressure = flow x resistance liver
serves as a unlikely that increased flow o can be used to stop
substrate for alone can cause portal acute bleeding or
incorporation hypertension (although prevent rebleeding
of ammonia described in AV-fistula or o shunt usually remains
by bacteria, massive splenomegaly) open for no longer
promotes 3 sites of increased resistance than up to one year
growth in o pre-sinusoidal (e.g. o other (rare):
bowel lumen portal vein portocaval, distal
of bacteria thrombosis, spleno-renal (Warren
which schistosomiasis, shunt)
produce sarcoidosis)
54
 Loren Warmington
Child-Pugh Classification extravascular fluid o secondary urinary Na
*Note: Childs classification is rarely into peritoneal space and water retention
used for shunting, but is still useful in cirrhosis, HP and OP balance
to quantitate the severity of cirrhosis is disrupted, precipitating Diagnosis
ascites by one or more of the
following mechanisms:
Score: 5-6 (Childs A), 7-9 (Childs clinically detectable when >500
B), 10-15 (Childs C) o fibrotic constriction of
mL
sinusoids resulting in
portal HTN and
Ascites increased HP --> Investigations
increased HP drives
accumulation of excess free fluid lymphatic diagnostic paracentesis - should
fluid in the peritoneal cavity drainage into the be done on most patients:
abdomen o cells and differential
across hepatic capsule o chemistry (albumin,
Clinical Pearl
and mesentery protein, amylase, TG)
Secondary bacterial peritonitis (as o renal hypoperfusion o C&S, gram stain
opposed to primary bacterial --> Na and H2O o cytology (usually
peritonitis) usually results from a retention positive in peritoneal
perforated viscus or surgical o PGE opposes sodium carcinomatosis)
manipulation. retention (NSAIDs
may precipitate renal
failure)
Etiology o less important fact is
Treatment
hypoalbuminemia -->
decreased OP
Table 18. Serum-Ascites Albumin therapeutic paracentesis safe,
underfill theory
Gradient as an Indicator of the especially if albumin infusion
Causes of Ascites o portal hypertension
and hypoalbuminemia given concomitantly
* in nephrotic syndrome: decreased medical
serum [Alb] to begin with therefore lead to transudation of
Na and water into o Na restriction
gradient not helpful
peritoneum causing o diuretics
decreased (spironolactone,
serum [Alb] - serum [Alb] - intravascular volume furosemide)
ascitic [Alb] >11 ascitic [Alb] <11 and secondary o aim for 0.5 kg loss per
g/L g/L renal sodium and day to prevent ARF
Cirrhosis/severe water retention via (this is maximum rate
Peritoneal renin-angiotensin- of ascitic fluid)
hepatitis
carcinomatosis aldosterone system o 1 kg loss per day if
Chronic hepatic
TB
congestion (right overflow theory peripheral edema
Pancreatic
heart failure, Budd- o liver disease primarily surgical
disease
Chiari) causes renal retention o TIPS, liver
Serositis
Massive liver of Na and water which transplantation
Nephrotic
metastases then "overflows" into (reserved for
syndrome*
Myxedema peritoneal cavity medically refractory
combined theory (incorporating cases)
Pathogenesis of Ascites in both above theories) is most
Cirrhosis popular Complication: Bacterial
o liver disease causes Peritonitis
vasodilation via nitric
normal physiology
oxide, increasing primary/spontaneous bacterial
o intravascular vascular capacitance
hydrostatic pressure peritonitis (SBP)
o decreased effective
(HP) and oncotic o complicates ascites,
intravascular volume
pressure (OP) are does not cause it
(i.e. volume to
balanced (Starling (occurs in 10% of
capacitance ratio
forces) --> preventing cirrhotic ascites)
low, but absolute
accumulation of o 1/3 of patients are
volume is high)
asymptomatic, thus do
55
 Loren Warmington
not hesitate to do a detects prolonged (weeks) disease
diagnostic paracentesi hepatic dysfunction ALT > AST = viral hepatitis
s must exclude malnutrition and
o fever, chills, renal or GI losses, acute illness
abdominal pain, ileus, Clinical Pearl
hypotension, Risk of developing infection from
Clinical Pearl
worsening needle puncture
encephalopathy All clotting factors except factor VIII HBV 30%
o gram negatives are exclusively synthesized in the HCV 3%
compose 70% of liver. HIV 0.3%
pathogens: E. coli
(most common Clinical Pearl
Figure 14. TimeCourse of
pathogen), Streptococ Order of deterioration of Liver
cus, Klebsiella Acute Hepatitis B Infection
Function Tests:
diagnosis: 1. increased PT/INR
o absolute neutrophil 2. increased bilirubin
count in peritoneal 3. decreased albumin
fluid >0.25x109 cells/L
increased AST, ALT =
(250 cells/mm3) or
hepatocellular damage
WBC count >0.5x109
ALT more specific to liver;
cells/L (500
cells/mm3) AST from multiple sources
o gram stain is positive o elevation of both
in only 10-50% of highly suggestive of
patients liver injury
o culture is positive in implies hepatitis
only 80% of patients (inflammation) or vascular
(not needed for injury (ischemia)
diagnosis) if AST, ALT >1000, think of
treatment common bile duct stone, virus, Chronic Hepatitis
o IV antibiotics drugs, ischemia, autoimmune
(cefotaxime is the hepatitis an increase in serum
treatment of choice transaminases for >6 months;
until C&S is available) increased ALP with increased requires a liver biopsy to
for 5-10 days; GGT = cholestatic disease determine severity/need of
prophylaxis with daily biochemical cholestasis treatment
norfloxacin (drugs)
systemic disease (e.g. Etiology
Tests of Liver Function sepsis), pregnancy
infiltrative disease (tumour, viral (B, B+D, C, not A or E)
Prothrombin Time (PT) fat, lymphoma) drugs (methyldopa, INH,
mass lesions (stone, nitrofurantoin, amiodarone)
daily marker of hepatic protein tumour, abscess) autoimmune
synthesis genetic (Wilsons disease,
must exclude co-existing Inflammatory (PBC, PSC) alpha1-antitrypsin deficiency)
vitamin K deficiency metabolic (nonalcoholic
Clinical Pearl steatohepatitis: NASH)
Serum Bilirubin Serum transaminases >1000 due to
viral hepatitis Clinical Features
product of heme metabolism in drugs
common bile duct stone
the RES of liver and spleen often asymptomatic, detected
hepatic ischemia
must exclude extrahepatic incidentally
rarely immune hepatitis
causes of hyperbilirubinemia constitutional symptoms
fatigue, malaise, anorexia,
Serum Albumin Level Clinical Pearl
weight loss
AST > ALT (usually AST/ALT >2 signs of chronic liver disease
and AST <300) = alcoholic liver

56

hepatomegaly (firm) and
splenomegaly
increased AST, ALT therapy
Drug induced Liver Disease
Specific Drugs
acetaminophen
o metabolized by
hepatic cytochrome
P450 system
o can cause fulminant
hepatic failure
(transaminases >1,000
U/L)
o requires 10-15 g in
normals, 4-6 g in
alcoholics/anticonvuls
ant users
o recent studies have chlorpromazine
emphasized liver
disease in chronic
users >4 g/day
o mechanism: high
acetaminophen dose
saturates
glucuronidation and
sulfation elimination
pathway --> reactive
metabolite is formed --
> covalently binds
to hepatocyte
membrane
presentation
methotrexate
o first 24 hrs: nausea
and vomiting usually
within 4-12 hours
o next 24-48 hrs: hepatic
necrosis resulting
in increased
aminotransferases,
jaundice, possibly
hepatic
encephalopathy, acute
renal failure, death
o after 48 hrs: continued
hepatic
amiodarone
necrosis/resolution
o note: potential delay in
presentation in
sustained-release
products
o blood levels of others
acetaminophen
correlate with the
severity of hepatic
injury, particularly if
Loren Warmington
time of ingestion sulfonamides,
known tetracyclines
herbs
o gastric lavage/emesis o chaparral, chinese
(if <2 hrs after herbs (e.g. germander,
ingestion) comfrey, bush tea)
o oral charcoal
o N-acetylcysteine Facial Nerve Palsy
(Mucomyst) can be
given PO or IV, most
Clinical Features
effective within 8-
10 hours of ingestion,
but should be given no the entire face on ipsilateral
matter when time of side is weak
ingestion; promotes taste dysfunction to ant 2/3 of
hepatic glutathione tongue
synthesis both voluntary and involuntary
o no recorded fatal movements are affected
outcomes if NAC impaired lacrimation, decreased
given before increase salivation, numbness behind
in transaminases auricle, hyperacusis
UMN weakness
o cholestasis in 1% after o weakness of
4 weeks; often with contralateral lower
fever, rash, jaundice, face; frontalis is
pruritus and spared
eosinophilia
INH Clinical Pearl
o 20% develop elevated
Forehead is spared in a UMN CN
transaminases but VII lesion.
<1% develop
clinically
significant disease Investigations
o susceptibility to injury
look for associated
increases with age
brainstem or cortical
symptoms and signs to
o may rarely cause
help localize lesion
cirrhosis, especially in
the presence of
obesity, Differential Diagnosis
diabetes, alcoholism
o scarring develops
idiopathic = Bells Palsy,
without symptoms or 80-90% of cases
changes in liver trauma: temporal bone fracture-
enzymes, 90% longitudina, 10%
therefore biopsy may transverse
be needed in long-
infection: (otitis media,
term treatment
mastoiditis, Ebstein-Barr virus
(EBV), Ramsay-Hunt
o can cause same Syndrome (herpes zoster oticus,
histology and clinical HSV)
outcome as alcoholic other
hepatitis
o sarcoidosis, Group B
Streptococcus, DM
o azoles, statins, mononeuropathy,
methyldopa, parotid gland
phenytoin, PTU, pathology
rifampin,
57

Bells Palsy
see Otolaryngology
Definition
an idiopathic facial nerve palsy
Clinical Features
acute onset of unilateral (rarely
bilateral) LMN facial weakness
diagnosis of exclusion
o must rule out
brainstem lesion
etiology
o unknown: thought to
be due to swelling and
inflammation of facial
nerve in its canal
within the temporal
bone, may be due to
HSV infection of CN
VII
associated features which may
be present
o pain behind ipsilateral
ear (often precedes
weakness)
o prodromal viral upper
respiratory tract
infection (URTI)
o hyperacusis
o decreased taste
sensation
o abnormal tearing
(decreased
lacrimation)
Treatment
patient education and
reassurance
eye protection (because of
inability to close eye)
o artificial tears,
lubricating ointment
o patch eye at night
steroids (weigh risks and
benefits)
o start early after onset
of symptoms (within
12 hours)
o typical regime is
prednisone 40-60 mg
tapered over 7-10 days
Loren Warmington
acyclovir o compressive lesions -
o controversial but some tumor, AV
evidence to support its malformation
use o non-compressive
lesions - MS, stroke
Clinical Pearl
An isolated cranial nerve defect, Investigations
especially of CN VI or VII, is most
likely the result of a peripheral, and EMG - observe high frequency
not a brainstem, lesion. discharges of motor unit
potentials that correlate with
clinically observed facial
Prognosis movements
MRI - detailed analysis of
spontaneous recovery in 85% posterior fossa (especially with
over weeks to months FIESTA sequence) to obeserve
poor outcome aberrant blood vessels
o if complete paralysis overlying the facial nerve
lasts 2-3 weeks
o if elderly or HTN Treatment
o if symptoms of
hyperacusis, abnormal carbamazapine and
tearing benzodiazepines (i.e.
clonazepam) very useful in
Hemifacial Spasm early/mild stages
botox injections - latency 3 - 5
Definition days; duration 6 months
surgery - useful when
segmental myoclonus of facial idiopathic or compressive -
muscles innervated by CN VII treat with decompression of the
aberrant blood vessels - usually
Clinical Features very favourable results
usually presents in the 5th or
6th decade of life
almost always presents
unilaterally, beginning as
myoclonus of orbicularis
oculi and can spread to other
muscles after a few years
clonic movements eventually
progress to tonic contractions
of involved muscles
Etiology
majority of cases due to chronic
irritation of facial nerve nucleus
or nerve (causing aberrant
transmission within the nerve)
most common cause is
idiopathic, caused by aberrant
AICA artery compressing facial
nerve within the
cerebellopontine angle
other causes
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