MRCP PACES – Zhemin’s Notes

Cardiology
Respiratory
Abdomen
Neurology
Station 5
Conditions
Communications
Memory List
CARDIOLOGY
Physical Examination
• Inspection
o Scars: Median sternotomy (CABG, valve surgery, aortic surgery), lateral thoracotomy (BT shunt, mitral
valvotomy/commisurotomy, aortic procedure, PDA ligation, coarctation repair), saphenous venous
graft, radial graft
o Syndromes: Marfan’s/Ehlers-Danlos, Ankylosing Spondylitis, Down’s, Turner’s
o Devices (usually upper left chest): ICD (young patient with ICD think HOCM), pacemakers
o Neck pulsation: JVP elevation, pulsations (TR – Giant V waves, AR- Corrigan’s sign; differentiate by
assessing if can be occluded and if pulsatile)
o Listen for bedside clicks
• Hand
o Dorsum: Clubbing, splinter hemorrhages
o Palmar: Osler’s nodes, Janeway lesions
• Pulse:
o Regularity, collapsing, rate, volume
o Radio-radial delay
• Forearm: Bruising
• Eyes: Conjunctival pallor, scleral icterus
• Mouth: Central cyanosis, high arched palate
• Neck: As above
• Precordium Palpation:
o Apex, parasternum, pulmonary area, aortic area
o Consider feeling for dextrocardia if not well felt
• Auscultation
o 4 point auscultation
o Heart sounds (presence, loudness, quality, splitting), murmurs (diastolic, systolic)
o Accentuation maneuvers: Left lateral, lean forward held in fixed expiration
o Carotid radiation
o CONSIDER ADDITIONAL ESPECIALLY YOUNG
§ Infraclavicular: BT shunts
§ Back (Coarctation of aorta, PS can radiate to back)
• Bases of lungs
• Check for pedal edema
• Offer to check other features if syndromic/associated diseases
• Wish list: Review blood pressure and temperature, urine dipstick for microscopic haematuria, fundoscopy for
Roth spots

Complications
• Pulmonary Hypertension
• Infective Endocarditis
• Congestive Cardiac Failure
• Atrial Fibrillation

Approach
• Scar
o Valve replacement
o Corrective or palliative surgery for congenital or acquired heart disease
o Previous CABG
• Cyanotic
o Eisenmenger’s
§ Will invariably have pulmonary HTN (Loud P2, parasternal heave)
§ Differential Clubbing: PDA (LL +/- L UL involvement)
§ Symmetrical Clubbing: VSD, ASD
§ May have PR or TR
o Congenital cyanotic heart disease – untreated or palliative surgery
§ BT shunt: Listen for infraclavicular murmur, appreciate reduced volume of radial pulse
§ Check for dextrocardia
§ Describe murmurs and offer possible causes
• Young: Avoid early commitment to diagnosis especially if possible corrective surgery or cyanotic heart disease –
Comment on the following: Young, presence of syndromic features, cyanotic vs acyanotic, scars, murmurs heard
Murmurs
Murmur Differentials
Apex Diastolic Mitral Stenosis
Apex Systolic Mitral Regurgitation, VSD, TOF (has VSD), HOCM
LLSE Diastolic AR, PR (can be due to pulmonary HTN, corrected ToF)
LLSE Systolic TR, VSD, HOCM, MR
ULSE Diastolic PR, AR
ULSE Systolic PS (supravalvular, valvular), ToF (has RVOT Obstruction), ASD, Coarctation of Aorta, PDA,
HOCM
URSE Diastolic AR
URSE Systolic AS (stenosis or sclerosis), HOCM
Continuous BT shunt, PDA
Systolic + Diastolic Mixed aortic valve disease (or AR with flow murmur), PDA, Mixed mitral valve disease,
pulmonary HTN resulting in Graham steel murmur (PR) and TR, MS with TR
Loud S1 MS, bioprosthetic mitral valve
Loud S2 Pulmonary HTN, bioprosthetic aortic valve (especially if there is a median sternotomy scar)

Standard Valve Pathologies

Etiology** Associated Features/ Severity Markers Surgical Indications***
MR A: Ischemic degeneration Apex: Thrusting EF 30-60%
C: MVP (mid systolic click, HS: Soft S1, presence of S3, short mid LVESD > 40mm
mid to late systolic diastolic murmur PASP > 50mmHg
murmur, accentuated by
standing/valsalva) Repair or replace, percutaneous
(Mitraclip) or open
MS A: Rheumatic heart disease, Apex: Tapping MV area < 1cm2
severe mitral annular HS: Loud S1 (increased force in closing of Gradient > 10mmHg
calcification, LA myxoma stenosed mitral valve), opening snap Recurrent embolic events while on
C: Congenital parachute (shortly after P2) anticoagulation
valve Long murmur more severe
Options: Percutnaeous balloon
A/w Ortner’s syndrome (hoarseness of valvotomy/PTMC
voice 2’ compression of RLN by enlarged
LA)
AR Acute: Dissection, infective Pulse: Collapsing (pulse pressure > EF < 50%
endocarditis diastolic pressure) LVESD > 50mm
Corrigan’s Sign Regurgitation fraction > 50%
Chronic: Apex: Thrusting Significant aortic root dilation
-Congenital: BAV HS: Soft S2, presence of S3 (>45mm in Marfan’s, >55mm in
-Acquired: Rheum Short murmur more severe others)
(Marfan’s, Ank spond),
Vasculitic (Takayasu), De Musset’s (head bob), Durozier’s Generally valve replacement
Infective (treponemal) (femoral art murmur), Quincke’s (nail bed
pulsation)
AS A: Calcific degeneration Pulse: Slow rising and low volume EF < 50%
C: Bicuspid aortic valve, Apex: Heaving Gradient > 40mmHg
William’s syndrome HS: Soft S2 (valve stiff) AV area < 0.6cm2
(supravalvular) Exercise test demonstrating
A/w Heyde Syndrome (angiodysplasia decreased exercise tolerance or fall
causing anemia, coagulopathy from VWF in SBP
shearing, AS), coarctation VT, syncope
Options: TAVI (transapical or
transfemoral)
TR A: Pulmonary HTN Giant V waves
(commonest cause), Pulsatile liver
Functional, Carcinoid
C: Ebstein’s Anomaly
* A: Acquired C: Congenital
** Infective endocarditis and rheumatic heart disease can affect any valve
*** Surgical indications for all include symptomatic despite maximal medical therapy, concomitant open heart surgery for
other reason
Prosthetic Valve
• Additional Complications
o Valve thrombosis: Metallic heart sounds not crisp
o Valve leak: Regurgitant murmur
o Hemolysis: Jaundice, pallor
• INR Targets
o Aortic Valve: 2-3
o Mitral Valve: 2.5-3.5
o Ball in Cage Valve (Starr Edwards): 3.5-4.5
o Generally need bridging (except for bileaflet tilting disc in aortic position with no other
thromboembolic RF): Stop warfarin 48H pre op, start IV heparin when INR <2, heparin stopped 4-6
hours pre-op and restarted after op until INR >2.5
• Types
o Bioprosthetic (don’t need anticoagulation, shorter longevity – 30-60% failure rate over 10-15 years)
o Metallic (need anticoagulation, longer longevity): Starr Edwards (Ball in cage), Bjork-Shiley (Single tilting
disc), St Jude’s (Double-tilting disc)

Rarer Conditions
• ASD: ESM over ULSE (flow murmur across pulmonary valve), fixed splitting of second heart sounds (constant
volume back flow to R heart hence P2 delayed), severity characterized by (pulm HTN, AF), surgically repair if:
paradoxical emboli/symptomatic/hemodynamically significant; but pulm HTN cannot be too severe,
Lutembacher syndrome (secundum ASD with rheumatic MS)
• VSD: PSM with no respiratory variation, causes (congenital vs acquired – ischemic rupture)
• PDA: Machinery continuous murmur (With increasing severity, diastole component reduces), collapsing pulse
• Coarctation of Aorta: ESM (can be due to associated bicuspid aortic valve or due to coarctation itself – thoracic
spine, back), AR murmur due to congenital bicuspid aortic valve, radio-radial/femoral delay, relatively
underdeveloped lower body, associated syndromes (Turner’s)
• HOCM: ESM (LVOT obstruction) – accentuated by standing/valsalva, PSM (MR from anterior systolic motion of
MV), double apical impulse, jerky/bifid pulse, ICD, management (betablocker/verapamil, ICD, alcohol septal
ablation, surgical myomectomy, genetic counseling – AD inheritance)
• PS: ESM with radiation to suprasternal notch and back, associated syndromes (Noonan’s, congenital Rubella)
• ToF: 1) RVOT Obstruction 2) Overriding aorta 3) VSD 4) RV hypertrophy
o May be a/w syndromes like DiGeorge
o Palliated: BT shunt (infraclavicular murmur, lateral thoracotomy scar, low volume radial pulse),
remnant cyanosis with clubbing
o Corrected: EDM (PR murmur), ESM (RVOT obstruction may remain)
o Murmur ddx:
§ Systolic: VSD (either remnant, or patch dehiscence), TR (from pulm HTN), PS/RVOT
§ Diastolic: PR, AR (complication during repair or aortic root disease)

Investigations
• General
o Electrocardiogram: Arrhythmias, chamber enlargement
o Plain Chest Radiograph: Features of fluid overload such as Kerley B lines and congested lung fields
o Echocardiogram: Confirm diagnosis, evaluate severity and etiology, assess for complications
• Prosthetic Valve
o PT/INR (or AF on anticoagulation)
o FBC, LDH, bilirubin, haptoglobin, peripheral blood film, – Hemolytic anemia
o Fluoroscopy to evaluate valve function

Management
• Multidisciplinary, involving cardiologist and allied health staff, anchored in patient education
• Smoking cessation and control of CVS RF, cardiopulmonary rehabilitation
• Generally limited role of medical therapy for valvular pathology, but heart failure treated with GDMT and
diuretics
• Should patient remain symptomatic despite maximal medical therapy to consider surgery
o Replacement vs repair
o Open vs minimally invasive approaches (e.g. percutaneous, transapical)
• Anticoagulation if atrial fibrillation
• Metallic Valve in Pregnancy
o Either Clexane first trimester then warfarin or clexane throughout; warfarin has early teratogenicity risk
and late fetal loss risk but clexane has higher risk of thromboembolism
 o Add on aspirin

Infective Endocarditis
• Modified Duke’s Criteria
o 2 major, or 1 major 3 minor, or 5 minor
o Major: Microbiological (Strep viridans, Strep Bovis, Staph aureus, HACEK), Echocardiogram (intracardiac
mass, abscess, new valvular regurgitation)
o Minor: Clinical (fever, predisposing heart condition, IVDA), Vascular phenomena (emboli, Janeway
lesions, ICH), Immunologic phenomena (GN, Osler’s nodes, Roth spots, Rheumatoid factor)
• Empirical Therapy
o Native Valve: Cloxacillin IV 2g Q4H + Ampicillin IV 2g Q4H + Gentamicin IV 1mg/kg Q8H
o Prosthetic Valve: Vancomycin IV 1g Q12H + Gentamicin IV 1mg/kg Q8H + Rifampicin PO 600mg Q12H
• Prophylaxis
o Indications
§ Predisposing Condition
• Uncorrected cyanotic heart disease
• Previous infective endocarditis
• Prosthetic valve replacement/repair
• Transplanted heart with valve regurgitation
• Repaired congenital heart disease
o Within 6 months
o Residual regurgitation or shunts
§ Procedures: Dental (with gingival manipulation), respiratory tract (disrupt respiratory
mucosa), GI/GU (if ongoing infection)
o Antibiotics: Amoxicillin 2g or Clindamycin 600mg 1 hour before procedure
RESPIRATORY
Physical Examination
• Inspection:
o General: Associated conditions (Cushing’s – from steroid treatment, Scleroderma, Dermatomyositis,
RA, SLE, Ank Spond, Psoriasis)
o Chest: Scars (chest tube scars/biopsy/VATS scars may be small, lateral thoracotomy scars may be
relatively posterior hence important to inspect carefully; causes of lateral thoracotomy scar include
lobectomy/pneumonectomy, single lung transplant, lung volume reduction surgery, open biopsy), RT
marks, symmetry of chest expansion
o Bedside: Sputum mug (bronchiectasis), inhalers (COPD, bronchiectasis), incentive spirometry
(bronchiectasis)
• Hands:
o Dorsum: Clubbing, nicotine staining, wasting of dorsal interossei, rheumatological sigsn (arthritis,
sclerodactaly, gottron’s papules)
o Palmar: Palmar erythema, wasting of thenar or hypothenar eminence
o Asterexis
• Pulse, respiratory rate
• Eyes: Conjunctival pallor, Horner’s
• Mouth: Central cyanosis, oral thrush (if on steroids), microstomia
• Tracheal deviation
• Feel for apex, parasternal heave – CONSIDER DEXTROCARDIA FOR KARTEGENER’S
• Chest expansion, percussion, auscultation, vocal resonance
• Cervical lymphadenopathy, pedal edema
• Offer to check other features if syndromic/associated diseases
• Wish list: Temperature, pulse oximetery, sputum mug, drug and occupational history (especially for ILD)
• Can present diagnosis if ILD/bronchiectasis, lobectomy/pneumonectomy – else present findings if
fibrothorax/collapse/consolidation/effusion

Complications
• Cor Pulmonale
• Pulmonary Hypertension
• Polycthemia
• Respiratory Failure
• Respiratory Distress

Types of Cases
• Bilateral Disease: ILD, Bronchiectasis, COPD
• Unilateral Disease: Lobectomy/pneumonectomy, collapse/consolidation/fibrothorax
• Others: Extraparenchymal disease like kyphoscoliosis and morbid obesity (causing restrictive lung disease),
pulmonary hypertension

Investigations
• Plain chest radiograph
• HRCT
• Pulmonary function test
• Invasive: Bronchoscopy (with BAL, TBLB), percutaneous biopsy

General Treatment
• Multidisciplinary, involving respiratory physician and allied health staff, anchored in patient education
• Smoking cessation, Vaccination (Influenza, Pneumococcal), Chest Physiotherapy
• Symptomatic relief: Mucolytics, bronchodilators
• Treatment of infective exacerbations with antibiotics
• LTOT (at least 18 hours)
o PaO2</=55mmHg or SpO2 </=88%
o PaO2</=59mmgHg or SpO2 </=89% if 1) Cor pulmonale 2) RH failure 3) Erythrocytosis
• Surgical: Pneumonectomy/lobectomy (usually for complications), Lung transplant

Bronchiectasis
• Features: Coarse pan/early inspiratory crepitations that change on coughing, chesty cough, clubbing, rmb to
check for dextrocardia
 • Causes:
o Congenital: Cystic fibrosis, Kartegener’s Syndrome (dextrocardia, situs inversus, primary ciliary
dyskinesia), Hypogammaglobulinemia
o Acquired:
§ Focal: Extraluminal (lymph nodes), luminal (tumour, previous TB), intraluminal (mucus
plugging)
§ Diffused: Post infectious (bronchiolitis obliterans), Rheumatological disorders (RA, SLE,
Sjogren’s), Yellow Nail Syndrome (Yellow nails, pleural effusion, lymphedema), ABPA
• Investigations
o Plain Chest Radiograph: Tram tracks, ring shadows
o High Resolution Computed Tomography: Signet ring sign, dilated bronchi
o Pulmonary Function Test: Often obstructive picture (FEV1/FVC < 70%)
o Etiological Evaluation: Sputum culture, ciliary motility testing, genetic testing and sweat test for CF
• Treatment: General treatment (as above), bronchodilators, treat underlying cause
• Complications: Recurrent infection, hemoptysis, empyema, disseminated infection
• Cystic Fibrosis
o Genetics: AR disorder, defect in CFTR gene on Chr 7 – Prevents chloride moving out of cells
o Organs: Pancreatic insufficiency, diabetes, meconium ileus with distal IO (previous surgery), subfertility,
osteoporosis
o Infections: Besides common haemophilus, staph aureus, pseudomonas, also a/w burkholderia cepacia

Interstitial Lung Disease

• Features: Fine end inspiratory crepitations that do not change with coughing, dry cough, clubbing
• Causes
o Types:
§ Known cause: Drug, rheumatic, occupational radiation
§ Idiopathic: Chronic Fibrosing (IPF, Idiopathic NSIP), Acute Fibrosing (AIP, COP), Smoking
Related (Desquamative Interstitial Pneumonia)
§ Granulomatous: Sarcoidosis
§ Others: PLCH/histiocytosis X, LAM
o Idiopathic, Rheumatological, Occupational Exposure, Drug, Radiotherapy
o Apical vs Basal
§ Apical: Rheum (Ankylosing spondylitis, Psoriasis, Sarcoidosis), Most pneumoconiosis except
asbestosis (silicosis, coal worker pneumoconiosis, berrylosis), RT, TB, ABPA
§ Basal: Idiopathic, Most rheumatological disorders (scleroderma, dermatomyositis, RA),
asbestosis, drug induced (amiodarone, bleomycin, MTX, isoniazid)
• Additional Information
Histology Idiopathic Clinical Associated Conditions Features
Syndrome
Usual Interstitial IPF - >50yo CTD, drugs, asbestosis Subpleural and basilar predom retic,
Pneumonia – Prognosis traction bronchiect
poor, most common Honeycombing in 70% of cases
GGO – less significant
Nonspecific Intertitial Idiopathic NSIP CTD, drugs, hypersen Subpleural and basilar predom retic,
Pneumonia (NSIP) – pneumonitis traction bronchiect
Younger pts, prognosis >Cellular: GGO predominant
better, second most >Fibrotic: Traction bronchiect, retic
common predominant
Two types: Cellular, No or minimal honeycombing
fibrotic Sparing of immediate subpleural lung is
specific, not sensitive
Organising Pneumonia Cryptogenic OP Drugs, infections, toxic Focal areas of consolidation (nodular, mass
inhalations, CTD like)
Peribronchovascular and subpleural
May have some GOO
Atoll or reversed halo sign
Desquamative Idiopathic DIP Smoking related
Interstitial Pneumonia
(DIP)/Respiratory
Bronchiolitis ILD
 Diffuse alveolar damage Acute Interstitial Presents as ARDS without ARDS features
Pneumonia an identifiable cause Extensive GOO and consolidation
(Hamman-Rich
Syndrome)
• Investigations
o Plain Chest radiograph: Reticular-nodular shadowing
o High Resolution Computed Tomography: Ground glass changes, honey combing
o Pulmonary Function Test: Restrictive picture (FEV1/FVC > 70%, FVC < 80%, TLC < 80%) with reduced
transfer factor (DLCO < 80%)
o Lung Biopsy
o Etiological Evaluation:
§ Drug and occupational history
§ RA: RF, anti-cyclic citrullinated peptide antibody
§ SLE: ANA, anti-dsDNA, complements
§ DM: Anti-Jo1 for antisynthetase
§ Systemic sclerosis: Anti-centromere antibody (localized), anti-topoisomerase (ILD), anti-RNA
polymerase (renal crisis)
o Complications: Echocardiogram (evaluate for pulmonary HTN – PASP > 25)
• Treatment
o General treatment (as above), stop offending drug/occupational exposure, immunosuppression
(steroid, immunomodulators), consider Perfenidone (antifibrotic) /Nintedanib (TKI) for IPF

Lobectomy/Pneumonectomy
• Clinical Features
o Tracheal Deviation: Pneumonectomy or Upper Lobectomy
o Lobectomy: Findings are generally normal because rest of lung fills up
o Pneumonectomy: Tracheal deviation, bronchial breath sounds adjacent to trachea, rest of lung reduced
chest expansion, dullness to percussion, absent breath sounds, decreased vocal resonance
• Causes: Cancer (Early NSCLC), Abscess, Bronchiectasis with hemoptysis, Tuberculosis, Lung volume reduction
surgery, Trauma
• Preoperative Evaluation for Pneumonectomy
o FEV1 > 2L: Low risk
o FEV1 < 2L: High risk
• Types of Pneumonectomy: Simple (removal of affected lung) vs Extrapleural (additional removal of diaphragm,
parietal pleura and pericardium – for malignant mesothelioma
• Post Pneumonectomy Syndrome
o Extrinsic compression of distal trachea and mainstem bronchus due to mediastinal shifting and
compensatory hyperinflation that occurs in remaining lung; usually approx. 6 months post op
o Presents as progressive dyspnea, cough, inspiratory stridor and pneumonia
o Treat with surgical repositioning of mediastinum and filling of post pneumonectomy space with non-
absorbable material +/- bronchial stenting

Fibrothorax/Collapse/Consolidation/Effusion
• Features
Trachea Percussion Auscultation Vocal Resonance Causes
Collapse Towards Dull Reduced BS Reduced Extra-luminal: LN
Mural: Tumour
Luminal: FB, mucus
Consolidation - Dull Bronchial BS Increased Infection,
malignancy,
infarction (PE)
Effusion Away Stony Dull Reduced Reduced Exudative
Transudative
Fibrothorax Towards Dull Reduced BS Reduced TB
• Pleural Effusion
o Light’s Criteria (1 out of 3 – exudative)
§ Pleural protein : serum protein > 0.5
§ Pleural LDH : serum LDH > 0.6
§ Pleural LDH > 2/3 upper limit of normal serum LDH level
o Other pleural fluid tests:
§ Microscopy: Cell count, cytology
§ Microbiological: Gram stain, cultures, AFB
 § Biochemistry: pH (<7.2 suggestive of empyema), glucose (low: malignancy, empyema, RA,
TB), ADA, protein, LDH, haematocrit (haemothorax)
o Causes
§ Transudative: Fluid overload (heart failure, renal failure), hypoalbuminemia (nephrotic
syndrome, chronic liver disease, hypothyroidism),
§ Exudative: Parapneumonic effusion, empyema, TB, malignancy, connected tissue disorders
§ Others: Chylothorax, haemothorax
ABDOMEN
Physical Examination
• Inspection
o Liver: Jaundice, pedal edema
o Renal: AVF/AVG, Catheter scars, parathyroidectomy scar, deltoid implant scar
o Haematology: Pallor, catheter (for chemotherapy), bony features of extramedullary haematopoiesis
o Scars

§ Mercedes Benz: Liver transplant

§ Kocher’s Scar (Cholecystectomy): Think chronic haemolytic anemia
§ Lumbar/Loin Incision: Nephrectomy – although nephrectomy is sometimes done via an
laparotomy especially if kidneys are big
§ Left sided scars: Splenectomy – Think chronic haemolytic anemia
§ Oblique iliac fossa scar: Kidney transplant
§ Laparotomy scar: Splenectomy, kidney + pancreatic transplant, bowel sugery (IBD)

Types of Cases
• Chronic Liver Disease +/- Portal Hypertension
• Liver Transplant
• Ballotable Kidneys
• Kidney Transplant
• Haematological Malignancy
• Chronic Haemolytic Anemia
• Solid Organ Mitosis

Liver
• Causes of Chronic Liver Disease: A Very MAD Cow – Alcoholic, Viral hepatitis, Metabolic (NASH, Wilson’s disease,
haemochromatosis), Autoimmune (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing
cholangitis), Drug induced, Congestive hepatopathy
• Portal Hypertension
o Serum Ascites Albumin Gradient – Determination of ascites etiology
§ High (>1.1g/dL): Portal Hypertension (‘Transudative’ equivalent)
§ Low (<1.1g/dL): Non Portal Hypertension (‘Exudative’ equivalent): Infection, malignancy, TB,
rheumatological disorders
o Causes
§ Pre Sinusoidal: Biliary disease (PBC, PSC), portal vein thrombosis
§ Sinusoidal: Causes of chronic liver disease as above
§ Post Sinusoidal: Budd Chiari Syndrome (hepatic vein thrombosis; presents with abdominal
pain, ascites, liver enlargement), cardiac disease
• Child’s Pugh Scoring: Anemia, Bilirubin, Coagulopathy, Distension (Ascites), Encephalopathy
1 point 2 points 3 points
Albumin (g/L) >35 28-35 <28
Bilirubin (umol/L) <34 34-50 >50
Coagulopathy (INR) <1.7 1.7-2.3 >2.3
 Coagulopathy (PT) – <4 4-6 >6
seconds over control
Distension Absent Moderate (shifting dullness) Severe (fluid thrill)
Encephalopathy None Grade I-II Grade III-IV
Child’s A: 5-6 points
Child’s B: 7-9 points
Child’s C: 10-15 points
• Investigations – Direct according to stem’s presenting complaint (e.g. abdominal distension)
o Imaging
§ Characterise organomegaly
§ Evaluate for mitotic lesions
§ Evaluate for portal hypertension
o Diagnostic paracentesis – If ascites present
§ Tests: Cell count/cytospin, gram stain/cultures, cytology
§ >250 PMN suggestive of SBP, treat with ceftriaxone
o Etiology Work Up for Chronic Liver Disease
§ Drug history, ethanol ingestion history
§ Viral: Anti HCV antibodies, HBsAg and anti-HBc serology
§ Autoimmune
• Autoimmune hepatitis: Anti-nuclear antibody, anti-smooth muscle antibody, IgG,
anti liver kidney microsomal antibody, soluble liver antigen
• PBC: Anti-mitochondrial antibody
§ Metabolic
• NASH: Fasting glucose/lipids, Hba1c
• Wilson’s Disease: Serum ceruloplasmin and urinary copper
• Haemochromatosis: Iron panel (ferritin, iron saturation)
§ Liver biopsy
o Evaluation of Severity of Liver disease: Liver function test (albumin, bilirubin), coagulation profile
o Complications
§ Renal Panel: Hepatorenal Syndrome
§ AFP: Malignancy
• Management
o Multidisciplinary, involving hepatologist and allied health staff, anchored in patient education
o Ethanol avoidance, hepatitis virus vaccinations, education on food hygiene, avoid hepatotoxic drugs
o Treatment of underlying disease
o Screening: OGD (varices), AFP/imaging (HCC)
o Treat Complications
§ Ascites: Salt restriction, diuretics, therapeutic paracentesis
§ SBP Prophylaxis [With fluoroquinolone (Ciprofloxacin)]: Primary (cirrhosis + BGIT, cirrhosis +
ascites with fluid protein < 1.5g/dL w renal/hepatic failure), Secondary (previous SBP)
§ Varices: Non selective beta blockers (propranolol), variceal band ligation

Renal
• Complications
o Anemia
o Tertiary hyperparathyroidism: Parathyroidectomy +/-deltoid implantation
o Fluid overload
o Uremia: Pruritus, pericardial rub, uremic flap, bruising
• Examine for previous access sites: Neck, groin, PD catheter, AVF/AVG (check arms and thigh too!)
• APKD
o Inheritance: AD, PKD 1 on Chr 16, PKD 2 on Chr 4
o Associations/Complications
§ Hypertension, Polycythemia
§ Extrarenal: Abdomen (diverticular disease, abdo wall hernia), Brain (berry aneurysms at
MCA/ICA – CN3, hemiparesis), Cardiac (MVP, MR, AR), Cysts involving other sites (liver,
pancreas)
§ Renal: Infection, bleeding, malignant transformation
o Diagnosis: Family History + Supportive Sonographic Findings
o Screening
§ US Kidneys: Ravine’s Diagnostic Criteria
• <30yo: 2 cysts in either 1 or both kidneys
• 30-59yo: At least 2 cysts in each kidney
 • >60yo: At least 4 renal cysts in each kidney
§ CNS Screening
• Indications: Family history of ICH/known aneurysm – rescreen 5 yearly (if normal)
o Indications for nephrectomy: Complications (bleeding, infection), space constraints for kidney
transplant
• Other Syndromes a/w Renal Neoplasms: Tuberous sclerosis (Angiomyolipomatosis), Von Hippel Lindau (RCC)
• Ballotable Kidneys
o Unilateral: Neoplasm, Asymmetrical APKD, Hydronephrosis
o Bilateral: APKD, Syndromic Neoplasms (Tuberous Sclerosis, VHL), Bilateral Hydronephrosis, Acromegaly,
Amyloidosis
• Renal Allograft
o Questions to answer: Etiology, Prev RRT, Graft function, immunosuppression, complications of ESRF
o RIF mass ddx: Caecal carcinoma, crohn’s disease, ovarian tumour, ileocaecal/appendiceal abscess
o Transplant Complications
§ Acute: Surgical complications (anastomotic leak), Acute rejection
§ Chronic:
• Immunosuppression related: OI, derm/haemato malignancy
• Rejection, delayed function
• Disease recurrence

Haematology
• Myelo/Lymphoproliferative Disorder
o Additional Examination: Lymphadenopathy (Cervical, axillary, inguinal), BMA scar
o Types of Myeloproliferative Disorders: Polycythemia Rubra Vera, Essential Thrombocytosis, Chronic
Myeloid Leukemia, Myelofibrosis
o Investigations
§ FBC: Quantitative abnormalities of cell lines
§ Peripheral blood film: Blast cells, leukoerythroblastic picture (marrow disruption – seen in
MF)
§ Imaging: Evaluation of organomegaly, lymphadenopathy, complications (e.g. thrombosis)
§ Bone marrow aspirate: Cytology, histology, immunohistochemistry, cytogenetics
§ Specific Tests: JAK2 (ET, PRV), Philadelphia Chromosome (CML)
o Treatment
§ PRV: Phlebotomy, hydroxyurea, aspirin
§ ET: Hydroxyurea, aspirin
§ CML: TKI (e.g. Imatinib), stem cell transplant
§ MF: Hydroyxyurea, stem cell transplant
• Chronic Haemolytic Anemia
o Examples: Thalassemia, hereditary spherocytosis
o Additional Examination
§ Bony features of extramedullary haematopoiesis: Frontal bossing, maxillary hyperplasia
§ Abdominal Scars: Cholecystectomy, Splenectomy
§ Complications of Iron Overload: Hepatomegaly, fluid overload from heart failure, diabetic
prick marks
o Investigations
§ FBC: Anemia
§ Hemolysis: LFT, Haptoglobin, Peripheral Blood Film (anisocytosis/poikilocytosis, fragments
from hemolysis)
§ Hb Electrophoresis: Elevated HbA2 in beta-thal
§ Genotyping/Mutation Analysis
o Management
§ Transfusions, folate supplement, iron chelation
§ Splenectomy (to reduce splenic sequestration and RBC consumption) – will need vaccination
against encapsulated bacteria (pneumococcus, meningococcus, haemophilus influenzae
§ Bone marrow transplant
§ Treat complications (iron overload – DM, hormonal insufficiency, CLD, heart failure,
osteoporosis)
§ Genetic counseling
o Clinical Considerations
§ Lethargy: Anemia, hypopituitarism (adrenal insufficiency, hypothyroidism), heart failure
§ Jaundice: Hemolysis, Chronic Liver Disease, Biliary Pathology

Immunosuppression
• General:
o Generally lower doses of immunosuppression required in liver transplant
o In kidney transplant, usually require steroids + calcineurin inhibitor + antimetabolite (e.g MMF)
• Steroids: Habitus (rounded countenance, truncal obesity, supraclavicular fat pads), skin thinning/easy
bruisability, proximal myopathy, cataract, oral thrush, abdominal striae, spinal tenderness (compression fracture)
• Calcineurin Inhibitors
o Cyclosporine: Gingival hypertrophy, hypertrichosis, hypertension
o Tacrolimus: Tremors, DM (NODAT)
• Generally also look out for rash/skin lesions (increased risk of dermatological malignancy)
NEUROLOGY
Common Conditions
• CN: Isolated 3/6/7, groups, tumour (NPC, parotid etc), systemic (Myasthenia Gravis, Miller Fisher, Multiple
Sclerosis, Progressive Supranuclear Palsy), Horner’s
• Upper Limb: Parkinsonism, myotonic dystrophy, FSHD, myasthesia gravis, motor neuron disease, cerebellar,
cervical myelopathy
• Lower Limb: Peripheral neuropathy, spastic paraparesis

Overview of Neurology Management

• Multidisciplinary, involving neurologist and allied health staff, anchored in patient education
• Aim to prevent disease flares, optimize function and quality of life
• Rehab, physio, prescription of mobility aids, special footwear, nutritional assistance (NGT/PEG), respiratory
support
• Specific treatment
• Symptom directed treatment: Spasticity (baclofen), incontinence (oxybutynin), pain (analgesia)
• Surgical correction of deformities

General
• Peripheral neuropathy can cause have more proximal involvement because roots can be involved – E.g. GBS
• Root lesions may not cause sensory loss because of overlap (esp if only single nerve root affected)
• Muscle atrophy ++: LMN, axonal; ALS, Myotonic dystrophy
• Fasciculations suggest denervation =/= MND
• Rmb that no sensory CAN STILL BE NEUROPATHY – AIN, MMN, GBS (motor prominence, proximal weakness
because ROOT IS AFFECTED – polyradiculoneuropathy)
• Dermatomes

Cranial Nerves
General
• Inspection:
o Voice
o SCARS (lift hair line), neck, nose
o Dysconjugate gaze, ptosis, facial nerve, NGT
• Feel for lymph nodes!
• CN rules of 4: Brainstem origin, clubs, meningeal/subarachnoid space/base of skull, peripheral nerve (MF, GBS,
Mononeuritis Multiplex)

Complex Ophthalmoplegia
• Etiology
 o Central: MS (INO, one and a half), NMO, PSP, Parinaud (midbrain)
o Nerve: MF, GBS, Mononeritis Multiplex
o NMJ: MG
o Muscle: Thyroid, CPEO (mitochondrial myopathy), MD, inflammatory myopathy
o Meningeal
o Melanoma with glass eye
• Predominant Upgaze: PSP, Parinaud syndrome (upward gaze palsy, sun setting eyes, pupillary light-near
dissociation - pupils respond to near stimuli, but not light, bilateral lid retraction, convergence retraction
nystagmus)

Ptosis
• Muscle: CPEO, myotonic dystrophy
• NMJ: MG
• Nerve: CN3
• Others: Horner’s
• Ptosis + Ophthalmoplegia: Muscle (MD, mitochondrial myopathy, CPEO), NMJ disorder, CN3 pathology

Bulbar Pathology
• Muscle: Occulopharyngeal muscular dystrophy, inflammatory myopathy (DM, PM)
• NMJ: MG
• Nerves: Lower CN
• AHC: MND

Clubs
• Orbital apex/SOF (if 2 involved then orbital apex): 2, 3, 4, 5i, 6
o Tumours, vasculitis (Wegeners/churg strauss), infiltrative (sarcoid), infectious (abscesses), trauma
• Cavernous sinus: 3, 4, 5 i and ii, 6; can have horner’s
• Cerebellopontine angle: 5/6/7/8, cerebellum
o Acoustic neuroma
• Jugular foramen: 9-11
o Tumours (Glomus tumour, meningioma, NF), infiltrative (lymphoma, sarcoid)
• Lateral medullary syndrome (post commonly affected is the posterior inferior cerebellar artery)
o Ipsilateral: Sympathetic (Horner’s), Cerebellar, Sensory nucleus of V, 8/9/10 also involved
o Contralateral: Spinothalamic

Horner’s Syndrome
• Features: Ptosis, Miosis, Anhidrosis (proximal lesions)
• Examine
o Hands: Clubbing, wasting
o Face: Other CNs – LMS, syringobulbia, cavernous sinus
o Neck: Thryoid, LN, bruit, scars
o Lung: Apex
• Localisation
o First order: Brain/spinal cord: Anhidrosis to face and arm; MRI brain/spine
§ MS, LMS, syringomyelia
o Second order: C8-T12, sympathetic chain, apex of lung: Anhidrosis to face; CT thorax, MRI/MRA of
head/neck, carotid doppler
§ Pancoast tumour
§ Neck pathology: Lymph node, masses, neck surgery
o Third order: Carotid artery, cavernous sinus: No anhidrosis; MRI/MRA of head/neck, carotid Doppler,
MRI cavernous sinus/orbits
§ Internal carotid dissection, cavernous sinus tumour
• Diagnosis
o Diagnose Horner’s: 10% cocaine solution test blocks presynaptic reuptake of norE at NMJ in dilator
muscle (absence of dilation confirms diagnosis of horners)
o Distinguish between pre and post ganglionic: Hydroxyamphetamine/Paradrine test causes norE
release into synpatic cleft, presence of dilation suggests preganglionic

CN3
• Features: Down and out eye with ptosis
• Other things to evaluate for
o Pupillary dilation: Suggest compressive causes as the pupillary fibers run superficially
 o Contralat pyramimidal: Weber’s (basal midbrain)
o Contralat ataxia: Benedikt’s (paramedian midbrain); cerebellar signs could also suggest MS
o CN2, CN4 (look down and in; if involved may be an ‘out’ rather than ‘down and out’ pupil), CN5 –
Orbital apex, SOF, cavernous sinus
• Compressive: Posterior communicating artery aneurysm

CN 7
• Check parotids, check tongue/ear for vesicles
• Other Innvervation
o Taste (anterior 2/3 of tongue carried by corda tympani)
o Hyperacuisis (motor branch to stapedius)
• Causes of LMN 7
o Unilateral: Commonest is Bell’s. Anatomy specific consider Ramsay Hunt (ears), parotid pathology
(parotid gland), brainstem stroke, demyelination, SOL (E.g. CPA), infection (Lyme disease, TB),
infiltration (sarcoid, lymphoma), vasculitis
o Bilateral: Bilateral Bell’s, Sarcoidosis/amyloidosis, GBS, Dystrophies (FSHD, MD), Mobius syndrome
(congenital facial weakness a/w bilat 6th nerve palsies)
• Treatment
o Bell’s Palsy: Pred 60mg OM x 1 week, Acyclovir 400mg 5x/day x 10 days (or valacyclovir 100mg TDS x 1
week)
o Ramsay Hunt: Acyclovir 800mg 5x/day x 7 days; no steroids

Bulbar Palsy
• Cervical LN, scars, RT marks
• Proximal myopathy, percussion myotonia
• Fatigueability
• Long track signs, reflexes (UMN – NMD, LMN – GBS/MF)
• PEG!

Upper Limbs
General
• May want to screen: Check scapula (FSHD), grip myotonia, scrutinize for fasciculations
• Conditions
o Myopathies:
§ Proximal: Rmb to check for dermatological feature of DM
§ Distal: MD, mitochondrial myopathy/inclusion body myositis (distal UL and proximal LL
involvement: wrist and finger flexors, quadriceps; usually asymmetrical)
o NMJ: MG (but more commonly eye)
o Nerve/Root: Screen median, ulnar, radial nerve distributions; if minimal sensory loss, more likely root
because of cross innervation (or motor neuropathy – affected AIN/PIN)
o Extrapyramidal: Parkinsonian – IF YOUNG THINK WILSONS!
o Cerebellar
o Cervical Myelopathy
• Some LMN Specific Considerations
o Don’t forget spinal shock!

Hand Nerve Exams

Assessing APB and dorsal interossei differentiate median (APB weak), ulnar (interosseous weak) and T1 radiculopathy (both
weak)
• Median
o Inspection: Scars (wrist), wasting of thenar eminence
o Motor:
§ Hand: Thumb abduction (APB), FDP index and middle finger
§ Proximal: Forearm pronation
o Sensory: Radial 3.5 fingers, thenar eminence (spared in CTS)
o Special tests: Phalen’s, Tinel’s, O sign (suggestive of AIN, rather than CTS pathology)
o Level of injury: Usually carpal tunnel, proximal rare
• Ulnar
o Inspection: Wasting of hypothenar eminence, dorsal guttering, ulnar claw (ulnar paradox: proximal
lesions less pronounced claw)
o Motor:
§ Hand: Finger abduction, FDP ring and little finger
 o Sensory: Ulnar 1.5 fingers, dorsum sparing for guyons canal lesion
o Special Tests: Froment’s
o Level of injury: Guyon canal, elbow (pressure/trauma at medial epicondyle)
• Radial
o Inspection: Wrist drop, finger drop
o Motor: Finger extension (specifically MCPJ, extension can still occur at IPJ because supplied by intrinsic
muscles), wrist extension (spared for PIN pathology), elbow extension, supination, test triceps jerk too
o Sensation: Anatomical snuffbox (spared in PIN pathology)
o Level of injury: Axilla (crutches, Saturday night palsy), humeral shaft, elbow (fracture, dislocation)
o Differential would be C7 radiculopathy which has additional features of weak shoulder adduction and
wrist flexion

Lower Limbs
Conditions
• Spastic paraparesis
o Spinal cord usually (offer parasagittal lesion)
o Check for sensory level, and check back for scars
o Etiology
§ Young: Hereditary spastic paraparesis, inflammatory (transverse myelitis, INO, MS) – CHECK
EYES!
§ Old: Degenerative
§ Compressive:
• Extra dural
• Intadural
o Intamed: Syringomyelia
o Extramed
§ Non compressive: Demyelinating, Infective, Vascular, Infiltrative, Toxic B12, Hereditary
• Flaccid paraparesis
o NMJ (less likely)
o Muscle: Myopathy (DMD, BMD)
o Peripheral neuropathy: CMT
o AHC: MND, Polio
• Foot drop: Common peroneal vs sciatic vs L5/S1
• Cerebellar

Upgoing plantar and absent ankle jerks

• Friedrich’s Ataxia
• Tabes dorsalis
• SADC
• Dual pathology

Foot Drop
• Motor
o Foot inversion: Affected suggests L4/5 or sciatic nerve
o Hip abduction and internal rotation: Affected suggests L4/5
• Reflexes: Ankle jerks lost in sciatic nerve or S1 radiculopathy
• Sensory
o Deep br of common peroneal: only 1st webspace
o Common peroneal: 1st webspace, dorsum of foot, lateral calf
o Sciatic (L4/5/S1 dermatomes): whole leg
o L4/5: sensation of foot dorsum and lateral calf, extending to lateral side of leg
• Etiology: Check for scars, palpate peroneal nerve, SLR/check spine

Cerebellar
• Cerebellar alone
o Unilateral: CVA, SOL, Demyelinating, Trauma
o Bilateral:
§ Common: CVA
§ Young: MS, congenital (SCA, friedrichs)
§ Specific
• Phenytoin (gum hypertrophy)
• Alcohol (parotidomegaly)
 • Wilson’s (KF rings)
§ Others: Paraneoplastic, infection (HIV), hypothyroidism, wilsons disease
• Cerebellar plus
o CN: Brainstem, groups (CPA, LMS, syringobulbia), MS
o Motor
§ UMN: Hemiparesis (Ataxic hemiparesis), quadriparesis (MS, friedrichs, spinocerebellar
degeneration)
§ LMN: Miller fisher
o Sensory: LMS
o Extrapyramidal: MSA
• Additional Examination Steps:
o Mouth: Gum hypertrophy, parotidomegaly
o Neruo: Pronator drift (ataxic hemiparesis), reflexes (UMN – MS, ataxic hemiparesis, spinocerebellar
ataxia, LMN – MF, Friedrich’s), check tone and bradykinesia (MSA), ophthalmoplegia (MS, MF)

Parkinsonism
• UK Brain Bank Criteria: Bradykinesia with at least 2 of rigidity, resting tremor, postural instability
• TRAP: Tremor, Rigidity (Cogwheel, lead pipe), Akinesia (Finger, palm, wrist, foot tapping), Postural instability
• Plus
o Cerebellar
o Corticospinal: Pronator drift, reflexes
o Autonomic: Postural BP
o PSP: Eye movements
o Corticobasal Degen: Comb hair (+/- recognize number on hand, hold object in hand)
• Function: Open bottle, write (micrographia)
• Treatment: Comment about presence or absence of dyskinesias
• Offer: MMSE, postural BP, drug history, screen mood
• Staging: Hoehn and Yahn Stage (5 stages)
o 1: unilateral involvement
o 2: bilateral involvement, balance OK
o 3: balance affected, physically independent
o 4: dependent but able to walk or stand unassisted
o 5: need wheelchair or bedridden unless assisted
• Non-motor symptoms: Dementia, depression, REM sleep disorders
• Treatment (generally targets motor symptoms)
o Old: Levodopa
o Young: MAOi (selegeline), Dopamine agonist (pramipexole, ropinirole)
o Surgery: Deep brain stimulation, thalmotomy/pallidotomy

Gait
• Causes of Unsteady Gait
o Cerebellum
o Vestibulopathy
o Sensory Ataxia
o Extrapyramidal
§ Hypokinesia: Parkinsonism
§ Hyperkinsesia: Dystonia, Myoclonus, Chorea, Athetosis, Ballismus
• Types of gait
o Apraxic: Parkinsonian
o Spastic (Circumduction)
o Parkinsonian: Festinating, reduced arm swing
o Ataxic: Cerebellar
o Sensory ataxia (stamping)
o High steppage: Foot drop
o Waddling/Myopathic: Proximal myopathy (or hip pathology)

Conditions

Neurological Syndromes
• Peripheral Neuropathy
 o Causes: (D, A-J): Diabetes, Alcohol, B12/folate, Cancer, Drugs (isoniazid, cisplatin, amiodarone,
phenytoin, dapsone), Environmental (Lead), Familial (CMT), GBS/CIDP, Hypothyroid, Infections (HIV,
Lyme), sJogrens
o Motor Predominant: AIDP/CIDP, MMN, Lead toxicity, Diabetic amyotrophy, drugs (dapsone), critical
care neuropathy, porphyria
o Sensory Neuronopathy (dysasthesiae, asymmetrical sensory loss, ataxia, absent reflexes, no motor
loss): Paraneoplastic, Sjogren’s, Drugs (chemotherapy)
o Thickened Nerves: HSMN, leprosy, CIDP, infiltrative disorders (lymphoma, amylod), acromegaly
o Specific Antibodies
§ Multifocal Motor Neuropathy: Anti GM1 antibody
§ Paraneoplastic: Anti Hu and Yo
• Spinal Cord Disorders
o Types
§ Anterior Cord
• Causes: Anterior spinal artery infarction
§ Posterior Cord (Dorsal column): Loss of proprioception and vibration sense
• Causes: B12/folate (check for conjunctival pallor, glossitis, vitiligo), tabes dorsalis,
MS, Friedrich’s ataxia, HIV associated vacuolar myelopathy
§ Central Cord (Syringomyelia, intramedullary tumour)
• Features
o Dissociated sensory loss: Loss of pain/temp at level (suspended sensory
level), preserved proprioception, upper limbs more involved than lower
limbs
o UMN signs in LL: Hyper reflexia, extensor plantars
o Check for Horner’s (may have sympathetic C8/T1 involvement)
§ Brown Sequard: Ipsilateral motor and proprioception loss, contralateral pin prick/hot-cold
loss
o Features
§ Predominantly motor: Compression
§ Asymmetry: Myelitis, compression
§ Marked spasticity: Hereditary spastic paraparesis, MND
§ Other associated features: Cerebellar (MS, spinocerebellar ataxias), eye movements (MS,
spinocerebellar ataxia), reduced visual acuity (NMO, spinocerebellar ataxia)
o Mixed UMN/LMN: Dual pathology (cervical myelopathy with peripheral neuropathy), cervical
radiculomyelopathy, MND, Syringomyelia, SCD, Tabes dorsalis, Friedrich’s ataxia

Specific Conditions
• Multiple Sclerosis
o Types: Relapsing remitting (commonest at onset), secondary progressive, primary progressive,
progressive relapsing, clinical isolated syndrome (CIS)
o Clinical Isolated Syndrome
§ Definition: Single first clinical episode reflecting a demyelinating event in the CNS (usually
followed by at least partial resolution)
§ Investigations
• Contrast-enhanced MRI
• If MRI does not meet McDonald criteria for dissemination in time/space, consider
CSF fluid examination for oligoclonal bands
§ Progression risk
• MRI shows demyelinating lesions: 60%
• MRI normal: 20%
§ Management: Close follow up/reimage if new symptoms, possible role for DMT if significant
radiological lesions
o Clinical Features
§ Neurological Deficits: Eyes (INO, one and a half syndrome, optic neuritis), cerebellar, spastic
paraparesis
§ Lhermitte’s (electric shock radiating during neck flexion), Uhthoff phenomenon (Worsening
of symptoms with rise in temperature)
o Investigations
§ MRI brain and spine with contrast looking for lesions disseminated in space and time –
Suggestive sites (periventricular, corpus callosum, centrum semiovale)
§ CSF analysis: Fluid specific oligoclonal bands
§ Evoked potentials (sensory, visual): Delayed conduction
§ Inflammatory markers: ESR, CRP
 § Specific Serologies: NMO (aquaporin 4), Myelin Oligodendrocyte Glycoprotein (MOG)
antibodies
o Diagnosis: Modified McDonald Criteria – Proving CNS lesions disseminated in space and time
o Treatment
§ Acute flares: Steroids (KIV PLEX)
§ Disease modifying treatment:
• Injectables: Interferon beta
• Infusions: Monoclonal antibodies
• Oral therapy: Fingolimod
§ Complications: Spasticity (baclofen), incontinence (oxybutynin)
o Other Associated Demyelinating Disorders
§ Acute Disseminated Encephalomyelitis: Follows viral illness, fever, stiff neck, encephalopathy
§ Neuromyelitis Optica: Transverse myelitis (3 or more contiguous segments), optic neuritis,
Aquaporin 4
§ MOG Encephalomyelitis
• Myasthenia Gravis
o Clinical Features
§ Fatigueability
§ Involvement: Occular (complex opthalmoplegia, ptosis), bulbar, limb weakness, respiratory
§ Additional examination steps
• Repetitive ab/adduction of one arm to compare fatigueability
• Curtain sign: Manually raise lid of less affected side, shine torch, count 1-20
• Neck flexion
• Check neck for scar, thymomas
o Investigations
§ Serology: Acetylcholine Receptor or Muscle Specific Kinase (MuSK) antibodies; New abs Agrin
and LRP4; LEMS – voltage gated calcium channel abs
§ Bedside Tests: Tensilon test (short acting Ach-esterase inhibitor), ice-pack test
§ Electrophysiologic studies
• Repetitive Nerve Stimulation: Decremental pattern
• Single Fiber EMG: Jitter pattern
§ CT Thorax: Associated thymoma
o Treatment
§ ABCs, respiratory assessment with NIF – If < 20cmH2O consider intubation
§ Acute: Plasmapheresis, IVIG
§ Chronic: Pyridostigmine, Immunosuppression (steroids, immunomodulators)
§ Thymoma: Thymectomy
o Drugs to avoid: Antibiotics (fluoroquinolone, aminoglycosides), antirheumatics (hydroxychloroquine),
cardiac drugs (MgSO4, beta bockers, procainamide)
o Lambert Eaton Myasthenic Syndrome: Improved with repetitive movement, a/w small cell lung cancer,
affected pre-synaptic voltage gated ion channels
• Motor Neuron Disease
o Types: Mixed (Amyotrophic lateral sclerosis), UMN (Primary lateral sclerosis), LMN (Progressive
muscular atrophy, Kennedy’s Disease)
o Clinical Features:
§ Only motor involvement – Limbs, bulbar
§ No eye, sensory, autonomic, extrapyramidal involvement
o Investigations primarily to exclude other pathologies – imaging, electrophysiologic studies, lumbar
puncture
o Treatment: Largely supportive, role for Riluzole (antiglutamatergic drug) in ALS
o Kennedy’s Disease: Perioral fascicualtions (quivering chin), tongue scalloping/midline furrow, sensory
neuronopathy, calf pseudohypertrophy
• Gullain Barre Syndrome
o Types
§ Acute Inflammatory Demyelinating Polyneuropathy (AIDP): Commonest
§ Acute Motor Axonal Neuropathy (AMAN): Preceded by campylobacter jejuni infection
§ Acute Motor Sensory Axonal Neuropathy (AMSAN): AMAN + sensory involvement
o Clinical Features: Peripheral neuropathy, proximal involvement may be > distal involvement, bulbar,
external ophthalmoplegia, facial, autonomic, respiratory failure
o Investigations
§ Neurophysiologic Studies
 • NCS: Demyelinating (conduction slowing and blocks) vs axonal pattern (conduction
amplitude reduction)
• EMG: Reduced recruitment
§ Lumbar puncture: Albuminocytologic dissociation (raised protein with normal WBC)
§ Blood tests: GQ1B for Miller Fisher
o Treatment: PLEX, IVIG
o Miller Fisher Syndrome
§ Triad: 1) Ophthalmoplegia 2) Ataxia 3) Areflexia
§ Descending paralysis
§ A/w GQ1B antibodies
• FSHD
o Clinical Features: Scapular winging, proximal myopathy, facial nerve palsy, distal LL weakness
o Associations: Cardiac conduction defects, hearing loss, retinal telangiectasia, epilepsy, cognitive
impairment
o Genetics: FSHD1 is AD, inappropriate expression of DUX4 gene
o Investigations: EMG, muscle biopsy, genetic testing
o Management: Supportive
• Myotonic Dystrophy
o Autosomal dominant with anticipation and expansion
o Symptoms: Syncope (cardiomyopathy), SOB (heart failure), Weakness
o Clinical Features
§ Key features: Percussion myotonia, grip myotonia, difficulty opening eyes after firm closure
§ Face: Male frontal balding pattern, temporalis and masseter wasting
§ Trunk: Gynaecomastia, testicular atrophy, goiter, AICD
§ Hands: DM prick marks
§ Legs: Foot drop, foot orthoses
o Complications: Diabetes mellitus, hypogonadism, thyroid goiter, cardiomyopathy with conduction
defects, cataracts, sensorineural hearing loss
o Investigations: EMG (dive bomb pattern on stimulation), genetic testing, endocrine/DM evaluation
o Treatment: Multi dip, functional optimization, mexiletine for myotonia (but can cause weakness)
• Hereditary Spastic Paraparesis
o Genetics: Variable (AD, AR, X-linked)
o Clinical features: Spastic paraparesis, subtle proprioception loss, pes cavus/hammer toes, bladder
involvement
• Friedrich’s Ataxia
o Genetics: AR
o Clinical features: Pes cavus, mixed LL signs (hyporeflexia but upgoing plantars), distal sensory loss,
cerebellar signs
o Associated features: Hearing loss, optic atrophy, hypertrophic cardiomyopathy, kyphoscoliosis, urinary
incont
• Spinocerebellar Ataxia
o Genetics: AD
o Clinical features: Ataxia
o Associations: Ophthalmoplegia, optic atrophy, extrapyramidal features
• Ataxia Telangiectasia
o Genetics: AR
o Associations: Telangiectasia, IgA def with reccurent chest infections, lymphoreticular malignancy
• HSMN
o Clinical Features: Inverted champagne bottle appearance of legs, pes cavus and clawed toes, foot drop
with high steppage gait, predominantly lower limb and motor involvement
o Demyelinating more common than axonal
o Inheritance: 3 types – different inheritance patterns, AD most common
o Treatment: Supportive, genetic counseling
• Huntington’s Chorea
o Autosomal Dominant CAG trinucleotide repeat disorder affecting Chr 4 with 100% penetrance –
Demonstrates expansion and anticipation
o Presents with all forms of dyskinesis (dystonia, myclonus, rigidity), cognitive impairment, psychiatric
disturbance
o Treatment: Largely supportive, genetic counseling, chorea (tetrabenazine, anti-psychotics)
• Benign Intracranial Hypertension
o Clinical Significance: Can cause visual loss
o Symptoms: Headache with raised ICP features, may have visual symptoms/pulsatile tinnitus/diplopia,
risk factors (fat, female, fertile, OCP use)
 o Signs: False localizing CN6, papilloedema
o Investigation: CT/MRI brain TRO SOL, LP to prove high pressures (>25cm H2O)
o Treatment: Non-pharm (stop OCP, lose weight), Pharm (CAI like acetazolamide, loop diuretics), Surgical
(Frequent LP, Optic nerve sheath fenestration, VP shunt), Early ophthalmo referral if vision impaired
• Normal Pressure Hydrocephalus
o Classic triad of cognitive impairment, urinary incontinence and magnetic gait
o Investigations
§ Imaging: Dilated ventricles – ventriculomegaly (Evans ratio > 0.31)
§ Lumbar puncture: Normal pressure, normal CSF constituents
§ High volume LP: Assess for improvement of gait and cognition
o Management: CSF shunting (e.g. VP shunt)
STATION 5
OVERVIEW
• Approach based history
• Pick up on clues in stem – which clinic was the patient referred from, subtle abnormalities in vitals
• Inspect patient carefully
• Consider multiple layers of consult
o Basic requirements: Address presenting complaint, assess severity
o Multiple issues
o Multiple approaches (e.g. lower limb swelling 2’ nephrotic syndrome – nephrotic syndrome etiology
needs to be identified)
o Consider social aspect: Work issues, care concerns, driving etc
• General Screening: Infection (fever), malignancy (LOW/LOA, bone pain, change in bowel habits), females (OCP,
pregnancy/pregnancy losses, menstrual history)
• Don’t know what is going on/Multi Systemic:
o LA SHIT (Lupus, Amyloidosis, Sarcoidosis, HIV, Infective Endocarditis, TB)
o I IN EMD CVS
§ Infective: SHIT (Syphilis, HIV, IE, TB)
§ Inflammatory: SLE, Sarcoid, Amyloid, Vasculitis
§ Neoplastic/Paraneoplastic – Rmb common mets (bone, lung)
§ Endocrine: Cushings, Thyroid, Addisons, Calcium
§ Metabolic: B12/Folate Others: Haemocrhomatosis, Wilsons
§ Drugs: OCP, Steroids/TCM, ALCOHOL
§ Congenital
§ Vascular: Remember that vasculitis or dissection can cause hypoperfusion to virtually any
organ
§ Systemic: Renal, Liver, Cardiac
• Counseling: Diagnosis, diagnostics, disposition, RX/referrals, return advice

• Approach Cases
1 Headache Headache with monocular BOV: GCA
Headache with transient BOV and diplopia, taking OCP: BIH
Thunderclap headache with homonymous hemianopia, taking OCP: CVT
Headache + glucosuria. Further hx yields palpitations, sweating secondary to
Pheochromocytoma.
Headache with bitemporal hemianopia 2’ Acromegaly
2 Giddiness/Dizziness Postural giddiness secondary to Parkinson’s disease
Postural giddiness secondary to newly initiated thiazide diuretic and poor oral intake
3 Loss of Syncope from ankylosing spondylitis with resultant arrhythmias
Consciousness Recurrent LOC from seizures, on b/g Tuberous Sclerosis
LOC which was actually falling asleep 2’ OSA (has HTN, poorly controlled)
Syncope from CMP on b/g MD
4 Weakness/Lethargy Proximal weakness secondary to valproate dose adjustment with impact on statin toxicity
Lethargy, clarified to be weakness, in patient with dermatomyositis, with possible underlying
malignancy
Weakness secondary to hypokalemic periodic paralysis
Lethargy 2’ symptomatic anemia from UBGIT from gastric harmatoma b/g Peutz Jegher
Tiredness from symp anemia – further hx haematochezia, arthropathy – IBD with enteropathic
arthritis
Weakness from Cushing’s
Lethargy from adrenal insufficiency on b/g iatrogenic cushing’s (TCM stopped)
Panhypopituitarism from previous pit surgery – medication non compliance, ddx is disease
recurrence
5 Visual Disturbance Diplopia secondary to thyroid eye disease
Chronic BOV 2’ RP
Ptosis causing visual problems, from Horner’s syndrome 2’ post op complications
Monocular BOV 2’ CRAO on b/g APS
Monocular BOV 2’ CRVO 2’ hyperviscosity from CML
6 Tremors Tremors from Parkinson’s Disease – Main point to assess non motor complications of PD
Tremors from Wilson’s disease
7 Hyperkinesis Choreoathetosis 2’ hyperglycemia from steroid use
8 Amnesia Amnesia 2’ CNS involvement of Wilson’s Disease (also got liver invovlement)
9 Parasthesia Parasthesia from HSMN
Parasthesia with further history yielding late onset poorly controlled asthma – Churg Strauss
Parasthesia 2’ hypocalcemia from pseudohypoparathyroidism
10 Recurrent Falls Recurrent falls due to foot drop from peroneal nerve palsy from mononeuritis multiplex from
Churg Strauss
11 Chest Pain Odynophagia from candida esophagitis likely AIDS with high risk sexual practices
Chest pain from aortic dissection on b/g Marfan’s
12 Palpitations Palpitations from pheochromocytoma on b/g NF1
Palpitations from amiodarone induced thyroiditis
13 Hypertension Young HTN on b/g Neurofibromatosis – RAS, pheo, coarctation of aorta
Poorly controlled hypertension, further history yields leg pain and kidney autotransplantation
surgery from takayasu arteritis
14 Shortness of Breath SOB secondary to symptomatic hemolytic anemia secondary to stenosed aortic valve; ddx
include bleeding from overwarfarinsation, fluid overload from HF
SOB secondary to symptomatic anemia from BGIT, secondary to HHT
Poorly controlled asthma due to medication non-compliance from recent NS enlistment
SOB secondary to amyloidosis causing nephrotic syndrome and cardiomyopathy on b/g RA
SOB 2’ ILD in a patient with psoriasis on MTX and works in a shipyard: impt Ddx lung OIs,
cancers
SOBOE from symptomatic anemia from SLE
SOBOE from ILD in patient with ankylosing spondylitis
15 Hemoptysis Hemoptysis from goodpastures syndrome
Hemoptysis from mitral stenosis 2’ rheumatic heart disease
16 Cough Station 2: Cough on b/g smoking hx, with shipyard occupation exposure. Ddx COPD, ILD,
Malignancy
17 Lower Limb Swelling LL swelling secondary to nephrotic syndrome from amyloidosis on b/g bronchiectasis
LL swelling from pretibial myxedema – Grave’s s/p thyroidectomy, now hypothyroid
Station 2: LL swelling with urine dipstick + protein, b/g RA with frequent NSAID use, recent
commencement of CCB. Ddx: 1. 2’ amyloid 2. NSAID 3. CCB
LL swelling from nephrotic syndrome from NPC with membranous nephropathy
Unilateral swelling from DVT 2’ epo producing RCC causing hyperviscosity syndrome
18 Abdominal Pain Abdominal pain and fever in returning traveler, associated splenomegaly: Typhoid fever
Abdominal pain secondary to ischemic gut, examination yielded AF
Kidney stones from urate ppt on b/g gout with recent uptitration of thiazide diuretics
Abdo pain 2’ porphyria
19 Dysphagia Dysphagia secondary to MND
Station 2: Dysphagia on b/g GERD symptoms – Ddx stricture, hiatal hernia, cancer
Dysphagia 2’ myasthenia gravis
20 Diarrhea Station 2: Diarrhea from IBD. Ddx infective. Also had joint pains
21 Constipation Constipation 2’ hypercalcemia in men syndrome (mum had thyroid op), with polyuria 2’ DI
22 Vomiting Vomiting 2’ Adrenal Insufficiency
23 Jaundice Jaundice 2’ Haemochromatosis. Also has DM, hypogonadism symptoms
24 BGIT Acromegaly with BGIT from ? CRC
25 Acute Kidney AKI from arcoxia in b/g patient with known IBD; ddx HUS/TTP from infective colitis,
Injury/Renal dehydration
Impairment
26 Urinary Frequency Polyuria from DI from hypercalcemia from MEN1/2a (has family history of uncertain surgeries)
Polyuria from DI from hypercalcemia from malignany from prostate mets – ddx LUTS from
prostate ca, cauda equine from mets to bone
27 Haematuria Haematuria from RCC, history yield concomitant pheochromcytoma symps: VHL
Incidental microscopic haematuria on routine test, further hx low grade fever: IE
28 Anemia Anemia in young female with Grave’s Disease, oral ulcers found – B12/folate deficiency
Station 2: Referral for anemia/thrombocytopenia for pregnant patient (with GDM, hx of
pregnancy related HTN) – Ddx HUS/TTP, HELLP, viral infection related cytopenia, HTN TMA
29 Easy Incidental thrombocytopenia from APS
Bruisability/Bleeding
30 Young Stroke Young stroke with APS
31 Raynaud’s Raynaud’s 2’ scleroderma and OCP use
32 Back Pain Back pain secondary to metastases from prostatic ca
Back pain (and fever) from discitis from foot wound with concomitant IE
33 Osteoporosis
34 Joint Pain Oligoarthritis with rash 2’ psoriatic arthropathy, ppt by HIV
 Gout flare ppt by psoriasis
35 Hand Hand pain 2’ Raynaud’s on b/g Scleroderma
Pain/Clumsiness Hand pain 2’ subclavian steal syndrome from artherosclerosis (CVS RF)
36 Epistaxis
37 Weight Weight gain from Cushing’s
Gain/Obesity
38 Excessive Pheochromocytoma on b/g NF
Sweating/Night
Sweats
39 Pituitary Axis
40 Gynaecomastia
41 Fever 2 week fever on b/g kidney transplant, likely myeloproliferative disease
Fever with no localising symptoms, only finding is that of a murmur: IE
Station 2: Fever. a/w odynophagia, ulcers, swollen glands. Significant travel hx! Ddx: HIV,
haemato malignancies, TB, travel infections
42 LOW/LOA Station 2: LOW/LOA with LFT derangement – NASH, Alochol, cancer
43 Itch Itch secondary to obstructive jaundice from primary biliary cirrhosis
Itch secondary to PRV
44 Oral Ulcers
45 Hyponatremia Station 2: Hyponatremia on b/g psychiatric history with subacute pulmonary symptoms
(cancer vs drugs vs poor oral intake)
46 Hypernatremia
47 Hypokalemia Hypokalemia with NAGMA 2’ Sjogrens
48 Hyperkalemia
49 Hypercalcemia
50 Hypocalcemia Hypocalcemia 2’ pseudohypoparathyroidism (Albright’s Hereditary Osteodystrophy)
51 Acidosis Hypokalemia with NAGMA 2’ Sjogrens
52 Alkalosis
53 Flushing Flushing 2’ carcinoid, also has diarrhea and hepatomegaly on examination
54 Red Eyes Bilateral eye redness 2’ Grave’s disease
55 Polycythemia
56 Periorbital Swelling Periorbital swelling 2’ hereditary angioedema
57 Rash Bullous/vesicular rash 2’ cutaneous porphyria
Livedo reticularis 2’ cryoglobinemia from hepatitis C

HEADACHE
Approach
Impt features: Thunderclap, Raised ICP, BOV
Primary Headaches Secondary Headaches
Migraine Preceding light flashes, Red Flags: Progressive, thunderclap (sudden onset, worst ever
abnormal smells headache), raised ICP (cough, lying down), neurological symptoms,
Prefer dark room meningism (neck stiffness, photophobia, rash), constitutional symps
(fever, LOW/LOA), extremities of age
Cluster Unilateral tearing, Intracranial Vascular (sudden): SAH (APKD), venous sinus
rhinorrhea, droopy eyelid thrombosis, pituitary apoplexy, carotid/vertebral
artery dissection
Tension Band like Infection: Meningitis, encephalitis, abscess
Stressors Tumour: Primary, haematological malignancy,
metastasis, pituitary (acromegaly)
Others: Benign intracranial hypertension
Extracranial GCA, sinusitis, glaucoma, dental
Systemic Hypertension (pheochromocytoma, OSA)
medication induced (analgesia, CCB, nitrates),
hyperviscosity (polycythemia, haem malig)

Important
Venous Sinus Thrombosis, Benign Intracranial Hypertension, GCA, Pituitary Apoplexy, Pheochromocytoma, Acromegaly,
APKD with SAH

Specifics
• SAH: Kidney disease (APKD), bleeding disorders
 • Venous sinus thrombosis: OCP, clotting disorders, pregnancy
• GCA: Pain worse on chewing, combing hair, BOV, muscle weakness, RAPD, tender pulsatile temporal artery
• Pituitary pathology: VF reduced, bumping into objects, hormonal related questions
• Pheochromocytoma: Episodic headaches, palpitations, family history (MEN)

Patterns
• Headache + Hypertension: Pheochromocytoma, Hypertension causing HA, CCB use, Raised ICP with Cushing’s
reflex, Pituitary tumours with 2’ endocrinopathy (acromegaly, cushing’s)
• Headache + BOV: GCA, glaucoma, BIH, SOL with visual tract compromise (pituitary tumour, cerebral SOL)
• Thunderclap Headache: SAH, cerebral venous sinus thrombosis, cervical artery dissection, reversible cerebral
vasoconstriction syndromes
• Headache with raised ICP features: SOL (rmb pituitary tumour), BIH, thrombosis/hemorrhage

GIDDINESS/DIZZINESS
Approach
Impt features: Spinning, postural association, near black out
Vertiginous: Peripheral Acute vs chronic? Episodic vs first episode?
Spinning -BPPV, Vestibular neuronitis, Labyrinthitis, Ear symptoms: Ringing in ears? Deafness?
sensation Meniere’s, migrainous vertigo Fullness of ear?
-Ear: Otitis media, ototoxic drugs (aminoglycosides) Neurological symptoms: Especially
cerebellar (coordination)
Central
-Cerebellar: All causes, CPA, MS Acoustic neuroma (ask hearing loss,
-Brainstem: VBI, posterior fossa infarction consider NF2)
Presyncope: Cardiac Chest pain, SOB, diaphoresis, palpitations
Near black out? -Aortic stenosis, AMI, HOCM, arrhythmias (brady,
Improve with sick sinus, heart block, VT, QT prolong) – PACES
sitting/lying? conditions that cause CMP/arrhythmia problems Sudden head movements, wearing tight
Preceding include muscle pathology (MD, DMD), Ank spond collar?
cardio/neuro
symptoms? Vascular: Subclavian steal syndrome
Postural
association? Neuro: Oral intake. Polyuria/polydipsia?
-Carotid sinus hypersensitivity Tremors/slowing of movements?
-Vasovagal, situational (cough, micturition, Hot environment, prolonged standing?
defecation) TCM use
Blood loss
Orthostatic / Postural Hypotension
Dehydration
Drugs
Autonomic: DM, PD/MSA, LEM, GBS/CIDP
Adrenal insufficiency
Anemia
Light- Hypoglycemia (adrenal insufficiency, insulinoma in Missed meals?
headedness MEN) Do you have any fever? LOW/LOA
Any form of acute illness (electrolytes, sepsis)

Important
HOCM, aortic stenosis, ank spond with conduction defects, DM/PM with CMP, postural hypotension (secondary to
neurological cause), adrenal insufficiency (from steroid withdrawal on b/g Cushing’s), NF2 with acoustic neuroma,
cerebellar pathology, hypoglycemia (adrenal insuff, insulinoma in MEN1)

LOSS OF CONSCIOUSNESS
Approach
Remember to incorporate driving/high risk activity counseling
Seizures: Aura, jerking/tensing, up- Syndromes: Sturge Weber, Tuberous
rolling of eyes, frothing around sclerosis, Down’s syndrome
mouth, tongue biting loss of Acute: Infection, inflammation (SLE),
bowel/urinary continence, post-ictal electrolyte disturbances, drug overdose,
confusion, Todd’s paralysis vascular, uremic/hepatic encephalopathy,
alcohol withdrawal
Chronic: Any CNS insult
 Syncope: Quick resolution following Cardiac: Valve (aortic stenosis), arrhythmia Cardiac: Chest pain, palpitations
recumbency (HOCM), underlying myopathy (Myotonic
dystrophy, DMD/BMD, ank spond), Postural Hypotension:
Exertion association (general arrhythmics (heart failure, congenital Precipitated by postural
exertion, upper limb exertion) pathology like WPW, Brugada) changes, fluid losses, medication
Postural association Postural Hypotension: Hypovolemia,
drugs, neurological disorder (DM,
Parkinson’s, GBS), adrenal insufficiency
Vasosagal: Prolonged standing, emotion
(fear), situational (micturition)
Steal Syndrome: Triggered by upper limb
activity
Others: Drop attacks, fell asleep Drop Attack: Meniere’s, Cataplexy
Fell Asleep: OSA
Drowsiness CNS pathology: Infection, mets, vascular
event
Hypoglycemia
Electrolytes: Hypercalcemia,
Hypo/hypernatremia
Drugs – Opioids
Uremia, hepatic encephalopathy,
hypoxia/CO2 narcosis

WEAKNESS/LETHARGY
Approach
Impt Features: Lethargy vs weakness, distribution, distal vs proximal, sensory involvement, tempo of disease, episodic?
Fatigue/ Specific: OSA, anemia, heart failure, panhypopit, hypothyroidism, adrenal insufficiency, drugs (beta
Lethargy blockers), depression, chronic fatigue syndrome, fibromyalgia
General: Cancer, chronic infections (HIV, TB), systemic diseases (liver, kidney dysfunction),
autoimmune disorders (polymyalgia rheumatica, fibromyalgia)
Weakness By Distribution:
-Onset -Hemiparesis Pattern: Usually brain pathology (unless traumatic brown sequard)
-Which limbs? -Paraparesis Pattern: Usually spinal cord pathology (ask for bowel/urinary incont)
-Proximal vs -Quadri/Tetraparesis Pattern: Tends to be more non specific – cord (neck pain/sensory level) vs LMN
distal vs >Proximal Weakness
global • Myopathy: Metabolic, Congenital, Rheum (Dermatomyositis, polymyositis), Endocrine
-Sensation (Grave’s, Hypothyroidism, Cushing’s, Acromegaly, Adrenal insufficiency), Neoplastic, Drugs
-Neck/ • NMJ: Myasthemia, Lambert Eaton (small cell lung ca)
brainstem • Anterior horn cell: MND
symptoms • GBS
>Distal Weakness
• Peripheral neuropathies

Episodic Weakness: Hypokalemic periodic paralysis, hemiplegia migraine, TIA, hypoglycemia

Important
• Fatigue: Panhypopituitarism, hypothyroidism, adrenal insufficiency, OSA
• Weakness: Dermatomyositis, Cushing’s, Myasthenia
• Muscle aches: Fibromyalgia (normal inflammatory markers), PMR (raised inflammatory markers), myositis
(statins, DM/PM)h

VISUAL DISTURBANCE
Approach
Diplopia: Muscle: Thyroid eye disease, CPEO Thyroid symptoms
Double vision, usually improves with NMJ: MG Drooping eyelid, fatigueability
closing one eye Nerves: CN 3,4,6, CN rules Other CN or neuro symptoms
Central: INO, wernicke’s
encephalopathy, brainstem lesion,
club lesions

Visual Field: Bitemporal hemianopia: Pituitary Endocrine symptoms

tumor (acromegaly, prolactin) Neurological symptoms
 Side vs central, bumping into things, Homonymous hemianopia: Optic
difficulty reading, difficulty seeing tract, temporo/parietal lobe (with
things at one side cortical signs), Occipital lobe (macular
sparing) – vascular, SOL
Ocular Vision Reduction ACUTE GCA Symptoms: Headache, jaw
Painful vs painless Optic neuritis and RD usually not claudication; swollen pallid optic disc
Transient vs permanent sudden
Eye redness, discharge, Optic Nerve Optic Neuritis: Pain on eye
floaters/flashers -Ischemic Optic Neuropathy movement, optic disc swollen or
Colour vision, night vision >Arteritic: GCA normal
>Non-arteritic: Idiopathic
Optic nerve and retinal pathology can -Optic Neuritis: Multiple sclerosis Papilloedema: Optic disc swollen
give rise to -Papilloedema: Raised ICP (SOL, BIH)
-Reduced VA CRAO/BRAO: Pale retina with cherry
-Reduced pupillary reflex Retina red spot at fovea
-RAPD -CRAO/BRAO (similar to a stroke):
Thrombosis (artherosclerosis), CRVO/BRVO: Flame hemorrhages,
embolus (cardioembolic, cotton wool spots
hypercoaguable state), arteritis
(vasculitis) Retinal Detachment: Elevated retina
-CRVO/BRVO: CVS risk factors, with folds
hypercoagulable state
-Retinal Detachment: High myopia,
preceding floaters

Eye: Glaucoma, vitreous hemorrhage

(loss of red reflex), uveitis,
endophthalmitis

CHRONIC
>Congenital: RP, Lebers
>DM/HTN retinopathy
>Infective: CMV retinitis
>Inflammatory: Wegeners, sarcoid
>Neoplasm: Compressive
>Drugs: Ethambutol, methanol
>Metabolic: Mitochondrial disease,
B12 deficiency

Patterns
• Transient BOV: Amaurosis fugax, migraine, seizures
• Painful vision loss: Glaucoma, Optic Neuritis (MS)
• Gradual onset visual loss
o Ocular: Retinitis pigmentosa, DM/HTN/Cataract, Open angle glaucoma, Macular degeneration
o Neuro: optic nerve compression, nutritional/toxic optic neuropathies
o Papilledema of any cause

Important
Thyroid eye disease, pituitary pathology with VF defect, amaurosis fugax in TIA, Retinitis Pigmentosa, RAO/RVO with
underlying thromboembolic predisposition (APS, haemato malignancy)

TREMORS
Approach
Congenital Conditions:
Wilsons Disease Liver symptoms, anemia, family history
Friedrich’s, Spinocerebellar Ataxia
Acquired Neurological Conditions: Secondary Parkinsonism: Drugs (psychiatric, antiemetics),
-Parkinson’s (Primary vs Secondary, Parkinson’s Plus – Strokes, Trauma (Pugilistic), Infections (JE, CJD)
Vision, unsteady gait, self control, alien limb, speech Cerebellar Pathology: Stroke, neoplastic/paraneoplastic,
difficulties) MS
-Cerebellar Pathology: Refer above
 Systemic:
-Essential Tremors: Family Hx
-Endocrine: Thyroid disease, Pheochromocytoma,
Hypoglycemia
-Drugs: Beta agonists, phenytoin, lithium, Pmhx: Seizure, psychiatric, immunosuppression, alcohol
tacrolimus/cyclosporine, theophylline, caffeine, alcohol
withdrawal
-CLD, CKD, CO2 retention

Characterisation
• Young vs Recent (acute, subacute, chronic)
• Resting (Parkinsons) vs Postural (Essential, systemic) vs Intentional (Cerebellar)
• Bilateral vs Unilateral
• Involvement: Hand, mouth/voice, lower limbs
• Associated parkinsonian, cerebellar features
• For parkinsonian: Look for parkinson’s plus, secondary parkinsons (drugs, ischemic, SOL), complications (TRAP,
freezing, autonomic, cognition, mood, sleep, function)

HYPERKINESIS
Approach
• Congenital: Wilson’s Disease, Huntington’s Disease
• CNS Pathology: Basal ganglia pathology (CVA, tumour)
• Infection: Syndenham’s Chorea (Rheumatic Fever)
• Inflammatory: SLE
• Neoplastic: PRV
• Endocrine: Thyrotoxicosis, hyperglycemic hemichorea
• Metabolic: Electrolyte disturbances
• Drugs: Anti-convulsant/OCP, L-dopa/neuroleptics/metoclopramide, steroids
• Pregnancy
Characterisation
• Chorea: Unpredictable jerky movements affecting diff body parts in random fashion
• Athetosis: Writhing movements of limbs
• Dystonia: Sustained involuntary contractions causing abnormal posture

Treatment
• Dopamine receptor blockers
• Atypical neuroleptics (olanzapine, risperidone)

AMNESIA
Approach
‘Primary’ Dementias
-Alzheimers
-Frontotemporal: Behaviour and speech problems, apathy
-Lewy Body: Parkinsonian features, fluactuating consciousness, visual hallucinations
-Vascular Dementia: Stroke episodes, stepwise decline
Delirium: Acute fluctuating course of AMS with inattention
Neurological Others
-Transient: TGA, Seizures, ?Migraine, TIA
-NPH: Gait problems, urinary incontinence
-Huntington’s disease
-Any CNS Pathology: Neoplastic, Infective, Inflammatory, Vascular
Systemic
-Wilson’s Disease
-Uremia, hepatic encephalopathy
-Inflammatory: SLE
-Infective: HIV, Syphilis, CJD
-Endocrine: Hypothyroidism, Hypercalcemia, Hypoglycemia, Panhypopituitary
-Metabolic: B12/folate
-Drugs: Steroid, Psychotropic, Alcohol (Korsakoff’s Psychosis – Retrograde and anterograde amnesia, confabulation)
Psychological: Depression
Characterisation
• Establish Dementia: Other A’s: Agnosia, aphasia, apraxia, executive dysfunction
• Ensure not delirium
• Progressive vs transient/episodic, STML vs LTML, retrograde vs anterograde amnesia

PARASTHESIA
Neurological Refer to memory list section
-Peripheral Neuropathy
-Nerve compression/irritation
-Plexus/nerve root pathology
Systemic
-Electrolyte disturbances
-Endocrine: Thyroid, hypocalcemia

RECURRENT FALLS
• Unsteadiness (Cerebellar, Vestibular, Sensory Ataxia, Extrapyramidal, NPH)
• Weakness (any neurological disorder)
• LOC/Presyncope (refer to approach)
• Perceptual disturbances: Vision/hearing problems
• Pain: Joint pains, leg pains
• Systemic: Infections, electrolyte/metabolic disturbances, drugs

CHEST PAIN
Approach
Cardiac/Vascular: Heart – IHD, valve, Is it worse with exertion, better with rest/GTN?
Exertional, better CMP, arrhythmia, Tearing pain radiating to the back?
with rest pericarditis Is it better on sitting up, leaning forward? Worse with
SLE inspiration/coughing?
Aortic dissection Marfan’s Any hair loss, joint pain, oral ulcers?
Vasculitis
Anemia
Blood loss, hemolysis symptoms
Respiratory: Upper, lower Marfan’s Cough, fever
Worse with deep airway Coagulopathy
inspiration/cough Pneumonia, Any leg swelling? Any recent travel? Any use of OCP?
Cancer Any LOW or LOA?
Bronchiect, ILD Pneumothorax risk factors? (Marfans, COPD)
PE, vasculitis
Pneumothorax

GIT: Esophagitis Any pain on swallowing?

Meal associations GERD/ulcer Scleroderma Pain worse on lying down? Related to food?
Pain with swallowing Esophageal Candidiasis NSAIDs/steroids?
rupture (HIV)
MSK/Cutaneous: Trauma Did you recently fall or hurt your chest? Any back/joint
Worse with Costochondritis pains?
movement/palpation, Zoster
rash Secondary tumor

Important
Pericarditis (post infectious, SLE), aortic dissection, pneumothorax (b/g Marfan’s), PE (with coagulopathy risk factors),
esophagitis (with scleroderma/HIV)

PALPITATIONS
Approach
Impt features: Exertional (anemia, HOCM) vs non-exertional (thyroid, pheochromocytoma), regular vs irregular
Cardiac Young: Prolonged QTc, brugada, WPW Family history of SCD
Other cardiac conditions: IHD, valvular Previous cardiac disease
pathology, HOCM
Extra-Cardiac AF: Thyroid disease, hypertension, OSA Endocrine: Thyroid, pheochromocytoma
symptoms
Anemia: Bleeding, hemolysis
 Sinus Tachycardia: PE, anemia, Drug History
pheochromocytoma, thyroid disease, infection, OSA: Snoring, sleep, daytime somnolence
drugs (sympathomimetics, beta agonist)

HYPERTENSION
Approach
Renal RAS, Glomerulonephritis, Scleroderma Haematuria, frothy urine, urine output
renal crisis
Endocrine Grave’s, Cushing’s, Acromegaly, Conn’s, Grave’s: Diarrhea, LOW, heat intolerance, anxious
Pheochromocytoma (a/w MEN syndrome, Cushing’s: Weight gain, change in appearance, easy
NF, VHL) bruising
Acromegaly: Change in appearance, hand larger and
sweatier, vision problems
Conn’s, Liddle’s syndrome (AD channelopathy)
Phemochromocytoma: Headache, palpitations
Neurogenic Cushing’s reflex: Any cause of raised ICP Headache, neurological symptoms
Aortic Coarctation of aorta: A/w NF, Marfan’s Coarctation: Asymmetry in limb development
Vasculitis (E.g. Takayasu Arteritis): Vasculitis: Claudication symptoms, rash, neurological
Claudication – hand, leg, gut deficits
Labile White coat hypertension
Pregnancy Eclampsia, Pre-Eclampsia
OSA Associated with acromegaly, Snoring, daytime somnolence
hypothyroidism, down’s syndrome
Drugs Sympathomimetics, cyclosporine, OCP, Epo
Rmb to assess age of onset of HTN, medication/dietary compliance, complications (eye, kidney, HTN heart disease, AF)

Important
Neurofibromatosis (Pheochromocytoma, renal artery stenosis, coarctation of aorta), scleroderma renal crisis, endocrine
disorders above, vasculitis (listen for bruits and feel for differential pulses), OSA

Guidelines
http://tusk.tufts.edu/mobi/view/content/M3052C/2641554
1. ACC/AHA 2017: Stricter approach (130/80), SPRINT Trial
2. JNC 8 (2014): More permissive approach (140/90), ACCORD BP Trial
3. SPRINT Trial
a. Significant benefit: Heart failure and all cause cardiovascular mortality
b. No difference in rates of stroke, myocardial infarction, and acute coronary syndrome.
4. Singapore Guidelines
http://www.smj.org.sg/sites/default/files/07_CPG-298122017_Hypertension.pdf

Targets: <80yo 140/90, >80yo 150/90

5. Evidence Reconciliation
a. Stricter: High-risk (ASCVD>10%, DM, heart-failure) but not too frail
b. Permissive: Healthy, frail

SHORTNESS OF BREATH
Approach
Exertional (cardiac, anemia, respiratory), Lying down (fluid overload), cough/noisy breathing
Occupational history, drug history and smoking history paramount
Respi Wheeze: COPD, Asthma, Churg Strauss Chronic: Asthma, COPD, ILD,
Dry Cough: ILD, cancer Bronchiectasis
Chesty Cough: Bronchiectasis, Cystic Fibrosis Serious: Cancer, TB, PE,
Hemoptysis: Cancer, TB pneumothorax (Marfan’s)
 Pulmonary hypertension Common: Pneumonia
-Group 1: Pulmonary arterial HTN (Idiopathic, heritable, PACES: Pulmonary-renal syndromes,
drug/toxins, CTD/HIV/portal HTN/congenital heart disease sarcoidosis
-Group 2: PH 2’ LH disease
-Group 3: PH 2’ Chronic lung disease
-Group 4: PH 2’ Pulmonary Art Obstruction
-Group 5: PH 2’ Multifactorial mechanisms

Don’’ forget upper airway pathologies – anaphylaxis,

epiglottitis, compressive pathology
Cardiac Symptoms: Chest pain, diaphoresis, palpitations CMP Causes
Causes of heart failure: IHD, arrhythmias, valve pathology, -Ischemic
amyloid, iron deposition, alcohol -Valvular
-Myocardium (congenital, infection,
CTD, drugs like alcohol, doxorubicin,
zidovudine, metabolic like
hemochromatosis/amyloid,
endocrine like thyroid)
Neuromuscular Acute: Myasthenia Gravis, GBS/MF
Chronic: Muscle dystrophies, Motor neuron disease
Anemia Other associated exertional symptoms: SOB, giddiness,
lethargy, palpitations
Blood loss, hemolysis, marrow problem, haematinic
deficiency
Fluid Overload Other non cardiac causes of fluid overload: Renal,
hypoalbuminemia causing effusions (nephrotic syndrome,
liver disease, protein losing enteropathies)
Systemic Acidosis (DKA, lactic acidosis), Thyrotoxicosis, Anxiety

HEMOPTYSIS
Approach
Important to exclude epistaxis, haematemesis
• Coagulopathy (refer to coagulopathy approach – important to consider HHT)
• Respiratory
o Common: Bronchiectasis, Lung Cancer, Tuberculosis, PE
o Vasculitis/Pulmonary Renal Syndromes (ask about haematuria/oliguria and other vasculitis symptoms):
Wegener’s, MPA, Churg Strauss, Goodpasture’s Syndrome
• Cardiac: Pulmonary edema, mitral stenosis

COUGH
Approach
Respi: Sputum, hemoptysis Infections (pneumonia, TB, OIs in HIV!), Malignancy, PE
Chronic Conditions: COPD, asthma, bronchiectasis, ILD
Autoimmune: Wegener’s, Churg Strauss, autoimmune conditions with ILD
Occupational
Sarcoidosis, Kartegener’s Syndrome
Upper Airway: PND URTI, sinusitis (think wegener’s), UACS/AR, laryngitis, malignancy of upper airway
component worse lying
Cardiac: Cardiac symptoms Heart failure
GI: Food association, reflux GERD (with resultant laryngopharyngeal reflux) – think scleroderma
Others Drugs: ACE inhibitors, bronchospasm meds (NSAIDs, beta blockers)
Smoker’s Cough
Functional

LOWER LIMB SWELLING

Approach
• Fluid overload vs localised
• Whole leg swelling vs focal swelling (e.g. joint)
• Acute vs chronic: Acute (cellulitis, DVT, arthritis)
• Unilateral vs bilateral
 Fluid Overload Cardiac: Chest pain, palpitations, diaphoresis
-Intravascular overload: Orthopnea, Renal (think scleroderma renal crisis): Frothy urine, haematuria, oliguria,
PND, HTN polyuria, uremia
-Extravascular overload Liver: Jaundice, RHC pain
(hypoalbuminemia): Anasarca GI: Diarrhea, haematochezia, dietary restrictions
(swelling elsewhere), BP lowish
Localised Bilateral: Chronic venous insufficiency, Pelvic mass (LOW/LOA, gynae
symptoms), Lymphedema (lymph node removal, RT, parasites)
Unilateral: DVT (immobility, clotting problems), soft tissue infection, acute limb
ischemia, arthritis, bone tumours, haematoma
Others Pretibial myxedema
Edema from hypothyroidism
Drug Induced: Calcium channel blockers

Important
Nephrotic syndrome, scleroderma renal crisis, calcium channel blockers, thyroid disease

Nephrotic Syndrome
• Primary (MCD, Membranous nephropathy, FSGS) vs Secondary
• Secondary causes
o By etiology: DM, Infective (Hep B/C, HIV), Inflammatory (SLE, amyloidosis), Neoplastic (Myeloma,
Hodgkin’s, solid organ malignancy/NPC associated membranous nephropathy), Drugs (NSAIDs,
penicillamine, gold, captopril)
o By histology: MCD (NSAIDs, Hodgkin’s), FSGS (HIV, reflux nephropathy, obesity), Membranous
nephropathy (Hep B, autoimmune disease, cancer, thyroiditis, drugs like
NSAIDs/penicillamine/gold/captopril

ABDOMINAL PAIN
Approach
Hepatobiliary/ Jaundice, dark urine, Biliary colic, cholecystitis, cholangitis, pancreatitis
Pancreatic pale stools, fever
Gastrointestinal Meal associations, PUD, gastric perforation, appendicitis, diverticulitis, IBD, constipation
bloating, dysphagia/ colic
odynophagia, vomiting,
diarrhea,
Peritoneum Peritonitis
Urological Haematuria, frothy Ureteric colic, pyelonephritis, APKD with cyst rupture
urine
Gynaecological PV discharge, PID, endometriosis, pregnancy complications
dyspareunia
Vascular Meal associations, hx of Aortic aneurysm/dissection, vasculitis, mesenteric ischemia, lupus gut
afib, claudication
elsewhere
Spleen Splenic infarct/rupture
Referred Pain Cardiac, Respi, Testicular
Systemic Hypercalcemia, porphyria, DKA, adrenal insufficiency, familial
Mediterranean fever, sickle cell anemia, hereditary angioedema

Characterisation
• Intermittent: Biliary colic, renal colic, constipation colic, gut claudication, acute intermittent porphyria, hereditry
angioedema
• Dark urine: Ureteric colic, biliary obstruction, acute intermittent porphyria
• Site, associated symptoms

DYSPHAGIA
Remember to examine abdomen for presence of PEG
Approach
• Oropharyngeal (initiation problem) vs esophageal (food stuck problem)
• Esophageal: Mechanical (more food) vs functional (more liquids)
• Associations: Choking, regurgitation, pain (esophagitis), dryness (sjogren’s)
• Complications: Aspiration, malnutrition
Causes
• Oropharyneal
o Mechanical: RT, head and neck tumours/goiters/lymph nodes
o Functional: Almost any neurological disorder (remember dermato/polymyositis as a muscular cause of
dysphagia; stroke, PD, MG, GBS)
• Esophageal
o Mechanical: Malignancy, stricture (reflux, radiation, eosinophilic esophagitis, crohn’s), hiatal hernia,
webs/rings (Plummer Vinson a/w IDA)
o Functional: Achalasia, esophageal dysmotility (scleroderma), dryness (sjogren’s)
• Esophagitis (pain): Candida (HIV/immunocompromised), GERD, Barrett’s, drugs (bisphosphonates, doxycycline),
RT, caustic ingestion

DIARRHEA
Approach
Acute vs chronic, bloody vs non-bloody, important risk factors (travel, immunocompromised)
Make sure it is not incontinence!
Gastrointestinal (non- Infectious – GE, SIBO (scleroderma), C diff (recent antibiotics), OI in HIV
inflammatory) (microsporidia, cryptosporidia, CMV colitis)
Secretory – Villous adenoma, VIPoma
Malabsorption – Lactose intolerance, celiac, pancreatitis, short bowel
Malignant – Overflow, lymphoma
Functional - IBS
Gastrointestinal (inflammatory) IBD, Lupus gut, Ischemic, RT, Infections – bacterial (shigella, e coli), viral (CMV
colitis), fungal
Systemic Hyperthyroidism, drugs (antibiotics, laxatives, metformin, colchicine), carcinoid,
VIPoma/Gastrinoma (think MEN1), DM autonomic neuropathy

CONSTIPATION
Approach
• Gastrointestinal: Malignancy (a/w LOW/LOA, tenesmus, overflow diarrhea), Stricture (IBD, diverticular disease)
previous instrumentation), Intestinal Obstruction (A/w vomiting/abdominal distension, 2’ tumour, adhesions,
volvulus, hernia), IBS
• Systemic: Hypothyroidism, Hypercalcemia (MEN syndrome), Drugs (Opioids, iron supplements), Ileus,
Neurological disorders (spinal cord, cauda equina, autonomic dysfunction)
Complications
• Diverticular disease, hemorrhoids, anal fissures, prolapse

VOMITING
Important associated symptoms: Abdominal pain, giddiness/headache, other GI symptoms (diarrhea, constipation)
Approach
• Gastrointestinal: Infective (GE, acute appendicitis), Inflammatory (IBS, systemic sclerosis – but more dysphagia,
DM/PM, SLE), Neoplastic (Gastric/esophageal malignancy), Intestinal Obstruction
• Hepatobiliary: Cholecystitis, pancreatitis, cholangitis, hepatitis
• Genitourinary: Pyelonephritis, ureteric colic, testicular torsion, PID, pregnancy!
• CNS:
o Central: Bleed, Tumour, Meningitis/Abscess
o Vertigo: BPPV, Vestibular neuronitis
• Systemic: DKA, Addisonian Crisis (postural giddiness, TCM use), Drugs (chemotherapeutic agents, digoxin toxicity
– recent klacid use), Pain

Complications
• Electrolyte disturbances
• Hypotension/postural hypotension

JAUNDICE
Approach
Pre-Hepatic Hemolysis (refer to anemia approach) Symptoms of anemia
Portal vein thrombosis Hypercoagulant risk factors
Hepatic A Very MAD Cow Viral hepatitis: Blood transfusion, tattoos, sexual
Alcoholic Hepatitis history, family history
Viral hepatitis NASH: Metabolic syndrome
Wilson’s: Movement disorders, family history
 Metabolic: NASH, Wilson’s, Haemochromatosis: Secondary causes such as
Haemochromatosis, Alpha-1 Antitrypsin transfusions, other disease manifestations (DM,
Autoimmune: AIH, PBC, PSC hypogonadism)
Drugs: DILI (paracetamol, augmentin, TCM) Autoimmune: Other autoimmune features, PSC
Cardiac a/w ulcerative colitis
Drugs: OTC drugs, TCM
Others: HCC, Gilbert Syndrome, Ischemic Cardiac: Orthopnea, PND, cardiac pathologies
(sepsis, hypotension), Infiltrative (Sarcoid,
Amyloid, TB, Lymphoma), Infections (liver
abscess, CMV/EBV)
Post-Hepatic Cancer: Pancreatic (other periampullary Tea coloured urine, pale stools
malignancy), cholangiocarcinoma Previous instrumentation to biliary tree
Stones: Cholangitis Constitutional symptoms
Stricture: Previous instrumentation
Budd Chiari (hepatic vein thrombosis) Hypercoagulant risk factors

BGIT
Approach
• Upper BGIT:
o Variceal – CLD history
o Common: Gastric ca, PUD (think MEN1 with Zollinger Ellison, NSAID use), mallory weiss tear (alcoholc
hx), dieulafoy lesions
o Syndromes: HHT, Peutz Jegher
• Lower BGIT
o Massive upper BGIT
o Anorectal: Piles
o Colon
§ Non inflammatory: CRC, diverticular bleed, angiodysplasia
§ Inflammatory: IBD, ischemic colitis (a/w gut claudication, check for AF), infective colitis (think
HIV with OIs)
o Associations with CRC: Acromegaly, FAP/HNPCC
• Coagulopathy: Refer to coagulopathy approach

ACUTE KIDNEY INJURY/RENAL IMPAIRMENT

Approach
Pre-Renal Hypotension, sepsis
Systemic disease: Cardio renal, hepatorenal
Renal artery stenosis
Drugs: ACEi/ARB
Renal Tubular: ATN ATN: Sepsis, hypotension, drugs
Interstitium: AIN (Fever, eosinophilia, granular casts) (iodinated contrast, aminoglycosides,
vancomycin)
Other tubulointerstitial insults: Drugs (acyclovir, AIN: Drugs (penicillin, cephalosporins,
chemotherapy), Urate nephropathy (tumour lysis, gout), NSAIDs), Infections, CTD (SLE, Sarcoid,
phosphate (bowel prep), pigment injury (rhabdomyolysis) Sjogren’s)

Glomerular: GN:
-Primary: MCD, membranous nephropathy (a/w malignancy, -Pulmonary symptoms: SOB,
PLA2R) hemoptysis, sinusitis (Wegeners),
-Secondary: asthma (Churg Strauss)
>Nephritic (haematuria, hypertension, AKI): Goodpasture’s, -Infections: Hep B/C, HIV
SLE, infective endocarditis, IgA nephropathy/post infective -SLE screen: Rash, hair loss, ulcers,
GN cytopenias
>Nephrotic (anasarca, hypotension): DM,
Myeloma/amyloidosis, Hep B/C, HIV, SLE, IgA
nephropathy/post infective GN

Vasculitis: Wegener’s, MPA, Churg Strauss

Microvascular disease: MAHA (HUS/TTP), Scleroderma,
thromboembolic disease

Structural: APKD cx, RCC

 Post-Renal Bilateral obstruction or unilateral obstruction in single
functioning kidney: Malignancy, stones, stricture (previous
instrumentation/TB), prostatic enlargement

Differentials by Etiologies
• Infective: HUS/TTP, IgA nephropathy (synpharyngitic), post infective GN, infective endocarditis
• Inflammatory: SLE, Vasculitis, Pulmonary-Renal syndromes, Scleroderma, Sjogren’s
• Neoplastic: Cancers a/w membranous glomerulopathy, myeloma, tumour lysis syndrome, urological malignancies
• Endocrine: -
• Metabolic: Urate nephropathy, pigment (rhabdomyolysis), phosphate nephropathy
• Drugs: NSAIDs, antibiotics, contrast, chemotherapy
• Congenital: -
• Systemic: Cardio-renal, hepato-renal, pulmonary-renal syndromes

Investigations
• Basic: U/E/Cr, FBC (eosinophilia for AIN, thrombocytopenia for HUS/TTP, SLE), LFT (hepatorenal), CK (rhabodo)
• UFEME, urine PCR
• US KUB (CT KUB if concerned about calculi), PVRU/bladder scan
• GN work up: ANCA, ANA, Hep B/C, HIV, myeloma screen
• Thorough drug history
• Renal biopsy
Complications
• Uremia: Lethargy, confusion, gastritis, bruising, gastritis
• Fluid overload: Orthopnea, PND, pedal edema, reduction in urine output
• Electrolyte disturbances
• Anemia

URINARY FREQUENCY
Approach
• Lower Urinary Tract Symptoms (Frequency, incontinence, nocturia, hesitancy, terminal dribbling, double voiding)
o Urological (check for haematuria too): BPH, stones, UTI (dysuria), bladder/urothelial cancer
o Neurological: Spinal cord, autonomic dysfunction, Parkinson’s disease, congenital disorders
(spinocerebellar ataxia, spina bifida)
o Drugs: Anticholinergics
• Polyuria (>3L per day)
o Polydipsia: Mouth dryness (Sjogren’s, anticholinergic medications), Psychogenic
o Diabetes mellitus (other causes of solute diuresis)
o Diabetes insipidus
§ Nephrogenic: Hypercalcemia (MEN, sarcoid, malignancy), Lithium
§ Cranial (important to screen other pituitary symptoms): Trauma, ICH, surgery, neoplasm,
vascular event
o Drugs: Diuretics
Investigations
• General: Urea/Electrolyte/Cr (in particular looking for hypernatremia which is a/w DI, solute diuresis),
Hba1c/FPG, adjusted calcium
• DI Work-Up:
Key principles: Osomotic diuresis urine osm higher, urine in polydipsia driven polyuria is appropriately dilute, urine
in DI driven polyuria is inappropriately dilute
o Water Deprivation Test/Hypertonic Saline Test (DI vs polydipsia): Urine would become concentrated in
polydipsia but not DI (remains <600mOsm/kg at 8hour mark)
o DDAVP Challenge:
§ Nephrogenic: No response to DDAVP
§ Cranial: Responds to DDAVP (urine becomes concentrated) - >600 mOsm/kg; hence can treat
with intranasal desmopressin

HAEMATURIA
Approach
Mimics: Menses, myoglobinuria, beet
root, drugs (rifampicin)
Systemic: Coagulopathy,
cyclophosphamide (hemorrhagic
cystitis)
 Urology Malignancy: APKD, VHL (clear cell RCC),
-Malignancy: RCC, urothelial ca Malignancy: LOW/LOA, family Tuberous Sclerosis (angiomyolipomatosis)
(bladder, ureter), prostate ca history, risk factors (smoking, dye Stones:
-Stones: Painful, loin to groin pain exposure – for urothelial cancer, -Hypercalcemia (Cancer, PTH – think MEN
-Infection travel – for schistosomiasis) I/IIa, Sarcoidosis, TB)
-Other structural pathology: Cyst -Uric acid: Gout flares (think secondary
events (APKD), AVM (HHT) causes for gout – haematological
malignancy, CKD, diuretics
-Drugs: Indinavir (HIV), Acyclovir
Renal
-Glomerulonephritis (GN): Hep B/C, -GN: Reduced urine output, -GN: Recent infective symptoms,
HIV, IgA nepropathy, post infective frothy urine, high BP autoimmune symptoms
GN, Infective Endocarditis, SLE, -Vasculitis/Pulmonary renal -Vaculitis: Rash, claudication (hand, leg,
Scleroderma, Alport syndrome syndromes: Hemoptysis, SOB, gut), weakness/numbness (mononeuritis),
(hearing, vision problems) cough family history
-Vasculitis/Pulmonary renal
syndromes: Wegener’s, PAN, HSP
Goodpasture’s

Management
IgA nephropathy -Without proteinuria, renal prognosis is good, low risk of progression. Follow up
-If proteinuria, renal function affected:
>ACE-I if Cr ok
>immunosuppression with IV methylpred/pred, immunosuppressants like cyclophosphamide,
azathioprine
>may have role for fish oil
Post-strep GN -Excellent outcomes
-Supportive treatment: manage fluid overload, hypertension. May require supportive dialysis for a
while
Alport syndrome -Hereditary disease with abnormal type 4 collagen chains that are found in kidney, cochlear and
eye. Usually X-linked.
-Supportive treatment: ACE-I for proteinuria. RRT
Wegener’s and -Mild disease (not life/organ threatening): steroids with MTX
Microscopic -Severe disease:
polyangitis >induction: IV methylprednisolone + cyclophosphamide or rituximab. May include plasma
exchange
>maintenance: azathioprine, rituximab, MTX
Goodpasture Condition where there is short-lived production of circulating antibodies against glomerular
basement membrane
-Course of steroids (oral with or without IV methylpred) + cyclophosphamide. Monitor anti-GBM
until negative then stop.
-risk of recurrence is low

ANEMIA
Approach
• Assess for symptoms of anemia: Exertional SOB/giddiness/palpitations/chest pain
• Assess for losses, followed by going down the diagnostic sieve below

Macrocytic (>95fL) -B12/Folate: Diet restrictions, GI symptoms, Pernicious anemia: A/w other
pancreatic symps, oral ulcers, ataxia, peripheral autoimmune disorders (check thyroid,
neuropathy vitiligo)
-Liver Disease
-Hypothyroidism
-Chronic ethanol ingestion
-Reticulocytosis
Normocytic Hemolytic Anemia: Yellowing of skin/eyes Hemolytic Anemia
-Immune: SLE/Sjogren’s (CTD symptoms),
Anemia of Chronic Disease: Hx of chronic drugs (penicillins, cephalosporins),
diseases haematological malignancy (B symptoms),
infections (mycoplasma, EBV, CMV)
Marrow problems: Other cell lines affected
(bruising, frequent infections)
 -Non-Immune: Mechanical heart valve,
Splenic Sequestration: Liver disease HUS/TTP, malaria, congenital (sickle cell,
G6PD, wilson’s disease), HTN TMA

Anemia of Chronic Disease: CKD, CLD, CTD

Marrow Problems: MDS, Multiple

Myeloma, Aplasias, RT, infiltrative disease
Microcytic (<85fL) -IDA: Losses (BGIT, PV bleed, haematuria, -Sideroblastic anemia: Congenital vs
epistaxis, constitutional symptoms to suggest acquired (drugs like isoniazid/linezolid,
malignancy, dysphagia might suggest plummer alcohol, copper def)
vinson syndrome), dietary (vegetarian) -Lead poisoning: Gasoline,
-Thalassemia: Family history paint/pigments, batteries, cosmetics
-Sideroblastic anemia
-Lead poisoning

Differentials by Etiologies
• Infection: HUS/TTP, malaria
• Inflammatory: SLE, Sjogren’s
• Neoplastic: GI malignancies, haematological malignancies (myeloma, MDS, LPD/MPD)
• Endocrine: Hypothyroidism
• Metabolic: B12/folate def, ethanol ingestion, iron def
• Drugs: Linezolid, isoniazid
• Systemic Disease: CKD, CLD, CTD
• Congenital: Thalassemia, red cell aplasia

Anemia with Thrombocytopenia

• Marrow Pathology: Primary vs Secondary (infections – rmb HIV, autoimmune – SLE, malignancy –
haematological, metabolic – B12/folate, alcohol, drugs)
• MAHA/TMA : HUS (Shigella, E coli O157:H7)/TTP (check ADAMTS 13), Drug induced TMA (Quinine, quetiapine),
Pre-Eclampsia/HELLP Syndrome, severe hypertension, SLE, infections (IE, HIV, CMV)
• Chronic Liver Disease

Investigations
• FBC: Evaluate extent of anemia, evaluate other cell lines, MCV, RDW (high often suggests haemetinic pathology)
• PBF: Evidence of hemolysis, megaloblasts/hyper segmented neutrophils for B12/folate def
• Hemolysis: Haptoglobin, LDH, Unconjugated Bilirubin, Reticulocyte count (assess marrow response), DCT
• Hematinics: Iron, B12/folate (consider anti IF, anti parietal cell abs)
• Systemic disease: RP, LFT, TFT, CTD (ANA, SLE screen)
• BMA for marrow specific pathologies
• Organ specific evaluation: OGD/colono/FOBT, imaging of gynae organs

EASY BRUISABILITY/BLEEDING
Approach
• Type of Bleed: Superficial, deep
• Congenital vs acquired (new problem) – FAMILY HISTORY IMPORTANT
• Other types of bleed: Menstrual, previous dental/surgical procedures, BGIT, haematuria
• Life threatening bleeds: ICH, BGIT, Retroperitoneal, Retropharyngeal

Connective Tissue Congenital: Marfan’s, Ehlers Danlos, HHT

Acquired: Cushing’s, HSP, Vasculitis
Platelet Infection: Viral infections (dengue), HUS/TTP, HIV, Hep C
Inflammatory: SLE, Sjogren’s, APS
Primary haematological disorders: Myelodysplasia
Congenital: vWD, ITP
Drugs: Antiplt/NSAIDs, heparin, quinine, sulphonylurea, sodium valproate
Function: vWD
Squestration: Splenomegaly
Consumption: DIVC (infection, malignancy, trauma, intravascular hemolysis), ITP (Can be 2’ HIV,
Hep C, SLE)
Clotting Factors Haemophilia
Liver Disease
 Vit K def
DIVC
Medication: Warfarin, NOAC
Acute Promyelocytic Leukemia (APML)

Important
Cushing’s, HHT, infections, drugs, haematological disorders, autoimmune disorders

Investigations
• FBC: Thrombocytopenia (other affected cell lines)
• PT, APTT
• DIC: Fibrinogen
• Specifics: VWF antigen assay, clotting factor assays (VIII, IX) for haemophilia/VWD, mixing studies for acquired
inhibitors (antiphospholipid syndrome, idiopathic, malignancy, CTD), LFT (liver disease)

YOUNG STROKE
• CVS RF (Screen DM/HTN/HLD/smoking): Familial hypercholesterolemia
• Cardiac (Echo, telemetry): Atrial Fibrillation, paradoxical emboli, intracardiac thrombus, infective endocarditis
• Vascular (Vessel imaging): Vasculitis (Takayasu, GCA, PAN), Moya Moya, Fibromuscular Dysplasia, Arterial
Dissection (Marfan’s, Ehler’s Danlos)
• Pro-thrombotic States (Haematology screen): PT/APTT/INR, antiphospholipid abs, factor V leiden mutation,
protein C/S deficiency, anti-thrombin III deficiency, OCP use, hyperviscosity syndrome, nephrotic syndrome,
malignancy
• Metabolic: CADASIL, Fabry’s Disease, MELAS
• Drugs: Cocaine, metamphetamine

RAYNAUD’S PHENOMENON
Causes
• Infective: Hep B, C
• Inflammatory:
o Systemic sclerosis, SLE/APLS, DM/PM, RA -- skin tightening, rashes, joint pain, muscle pain!
o Vasculitis
o Buerger’s disease (<45yo, heavy smokers, dx of exclusion)
• Neoplasm: Myeloproliferative disorders, polycythemia
• Endocrine: Hypothyroidism
• Mechanical: Vibration Injury
• Drugs (ABBCCC)
o Interferon alpha
o Betablockers, Bromocriptine
o Contraceptive pill, Chemo (cisplastin, bleomycin), Ciclosporin
PE
• Fingers: cold/cyanosed, finger pulp atrophy, gangrenous finger tips, dilated nail-fold capillaries
o Look: nails, skin, joints
o Feel: joint tenderness, sclerodactyly
o Move: and function
• Examine the toes too
• Face: Tight skin, telangiectasia, Rash (SLE, DM)
• Neck: rashes, cervical LN
• Proximal weakness
• Chest: Heart loud P2, Respi for ILD
• Abdomen: HSM, masses
• Others: pulses
• Offer complete examination for malignancy

Investigations
• Nail fold capillaroscopy
• FBC (Haem, AI), RP (renal impairment), LFT (CLD), Clotting profile (APLS)
• AI: ESR, anti-ENA, SLE (complements, dsDNA), RF, Cryoglobulinemia
• Neoplasm: PBF, serum protein electrophoresis
• Vascular: ABPI
• Endocrine: TFT
 • CXR: cervical rib

BACK PAIN
Approach
Mechanical Back Pain Osteoporosis screen!
-Trauma
-DDD
-Don’t forget pathological fractures: Osteoporosis,
malignancy
Inflammatory Back Pain Night Pain
-Infection (abscess, TB, septic emboli from IE) Inflammatory Features: Stiffness, worse after prolonged
-Inflammatory: AS, other spondyloarthropathies (Psoriatic, rest
IBD, reactive) other autoimmune diseases (RA, SLE) Screen for neoplastic disease
-Neoplastic: Metastatic, Multiple Myeloma
Systemic
-Aortic aneurysm/dissection
-Pancreatitis
-Kidney Stones/Infection
-Hypercalcemia
Complications
• Cauda equina
• Spinal stenosis with neurogenic claudication
• Radiculopathy
• Pain with functional impairment

OSTEOPOROSIS
• Risk Factors: Early menopause, smoking
• Secondary Causes
o Drugs: Steroids, alcohol
o Endocrine: Cushing’s, thyrotoxicosis, hypogonadism, hyperparathyroidism
o Liver disease
o Malignancy: Multiple myeloma

JOINT PAIN
Approach
Mechanical AVN: Steroid use, deep sea diving
-OA
-Traumatic Injury: Contusion, Haemarthrosis,
Ligamentous/Soft Tissue Injury
-Others: Avascular Necrosis, osteoporosis with fragility #
Inflammatory Psoriasis
-RA Triggers: Alcohol, smoking, steroid withdrawal, HIV
-Spondyloarthropathy:
>Psoriasis: Rash, nail changes
>Ank Spond: Back pain Gout
>IBD: Diarrhea, blood in stool, abdominal pain -2’ causes: Haematological malignancy, renal disease,
>Reactive: Recent GI/urinary infection, eye redness, pain drugs (thiazides), hemolysis
passing urine, rash -Triggers: Trauma, sugared drinks, alcohol, dehydration,
-SLE: Rash, hair loss, ulcers, renal/CNS involvement shellfish
-Behcet’s: Genital Ulcers Pseudogout
-Crystal Arthropathy: Gout, pseudogout -2’causes: Haemochromatosis, hypercalcemia
-Infective: Septic arthritis, gonococcal arthritis
(tenosynovitis, vesiculopustular lesions, polyarthralgia),
viral illness
-Others: Haemochromatosis, hypercalcemia, hemolytic
anemia, Wilson’s Disease, Sarcoidosis

Characterisation
• Abrupt vs Gradual vs Intermittent
• Articular vs Periarticular: Articular (pain, swelling, limitation of movement) vs Periarticular (localize to adjacent to
joint)
• Inflammatory vs Mechanical: Morning stiffness > 1 hour, relation to activity, night pain
 • Distribution: Rmb back pain and enthesitis (mono/oligo/polyarticular, axial vs peripheral)
• Systemic Symptoms: Eye symptoms, GI symptoms, Rash, Genital lesions/discharge, Sexual History

Physical Examination
Hand Exam Look
• Dorsum: Joints, skin, nails
• Palm: palmar erythema
• Make a fist and turn over to see if fist is fully formed
• Elbows: rheumatoid nodules, psoriatic plaques, gouty tophi/olecranon bursitis, surgical
scars
Feel
• Joints: DIPJ, PIPJ, MCPJ, wrist (piano key ulnar)
• Skin: sclerodactyly and extent
Move
• Power grip: grip my fingers tightly
• Wrists, Elbow
• Are you able to undo a button on your shirt? Are you able to pick up this coin?
Others
• Any relevant systemic examination
Treatment
• Complications of steroid use
Knee Exam Look
• Front, side, back
Feel
• Warmth
• Effusion: patella ballotment, cross fluctuant, bulge test (milk, empty medial, swipe lat, look
for bulge)
• Palpate: quadriceps, patella, tibial tuberosity. MCL and LCL. Medial and lat joint lines
Move
• Fixed flexion deformity/ extensor lag
• Flex fully and also feel for crepitus
• Screen for hip pathology
Special tests
• PCL: posterior sag, posterior drawer
• ACL: anterior drawer. Lachmanns test (done at 20deg)
• Valgus and varus stress test (extension and 10deg flexion)
• Mcmurray’s test: flex fully. Medial meniscus: ext rotate and apply valgus force and extend.
Lat meniscus the opposite
Foot Exam Look
• Ulcers, callosities, deformities, scar
• Vascular: Trophic changes
• CVI: skin pigmentation
Feel
• Ulcer
• Vascular: temperature, cap refill, pulses
• Neuropathy: Semmes Weinstein monofilament test (8 or more sites to be normal). Pin prick,
Proprioception
Move: ankle, subtalar (inversion, eversion)
Stand: look for collapsed arches
Gait / Shoes

Important side effects of rheum drugs

• Avoid pregnancy on all immunosuppressants except azathioprine, sulfasalazine and hydroxychloroquine
• Methotrexate, sulphasalazine, azathioprine, leflunomide: all cause nausea, neutropenia and thrombocytopenia,
deranged LFT
o MTX: also pneumonitis
o Azathioprine: check thiopurine methyltransferase level before starting. Predicts BM toxicity
• Hydroxychloroquine: nausea, retinopathy, skin rash
• Cyclophosphamide:
o Infection: issues of reactivation of latent infections, and BM suppression
§ Screen for TB, Hep B, Hep C, HIV prior to starting
 § Stop other immunosuppressants, tail down steroids
§ Prophylaxis against PCP
o Hemorrhagic cystitis: Oral mesna before and after each infusion
o Infertility: Sperm banking
o Malignancy: LT surveillance for malignancy of all forms. Risk dependent on cumulative doses
o Nausea, vomiting, reversible alopecia, teratogenicity

HAND PAIN/CLUMSINESS
• Parasthesia: Refer to paresthesia approach (can also be other neurological symptoms such as stiffness, tremors,
myelopathy etc)
• Raynaud’s: Refer to Raynaud’s approach
• Claudication: Vasculitis (Takayasu), artherosclerosis, cervical rib compression at thoracic outlet, surgery
(coarctation repair, ToF repair)
• Joint pain: Refer to joint pain approach

EPISTAXIS
Approach
Easy bleeding Coagulopathy – congenital or acquired
Platelet – production, destruction, dysfunction, organ
Connective tissue – HHT
ENT Infection
Inflammation: Wegener’s, Churg strauss, allergic rhinitis
Neoplasm – NPC
Trauma

WEIGHT GAIN/OBESITY
Approach
Fluid:
Cardiac/Hepatic/Renal/Gastro causes of fluid overload
Physiological:
-Excessive intake
-Reduced physical activity
-Genetics
Systemic:
-Endocrine: Cushing’s, Hypothyroidism, PCOS, Insulinoma, Acromegaly
-Neuro: CNS lesions with hypothalamus involvement
-Drugs: Antidepressants/antipsychotic, sulphonylurea, OCP, valproate
-Genetics: Prader Willi, Leptin Deficiency

EXCESSIVE SWEATING/NIGHT SWEATS

• Infection: TB, sub-acute/chronic infections (IE, abscess, HIV)
• Inflammatory: Less likely
• Neoplasm: Haematological malignancies
• Endocrine: Pheochromocytoma, hyperthyroidism, acromegaly, carcinoid, hypoglycemia
• Others: Autonomic neuropathy

PITUITARY AXIS
When to Screen: Headache, visual field defect, when one of the axis affected (especially when suspecting central cause)
Features
Thyroid Low: Dry skin, hair loss, Low: Peaches and cream TSH, T4/3
weight gain, appearance, bradycardia,
constipation, cold coarse hair, delayed tendon
intolerance, lethargy, reflex, edema
peripheral edema,
menorrhagia.
Complications include
CTS, OSA
Corticosteroids Low: Lethargy, postural Low: Postural hypotension Low: 8am cortisol, synacthen test
giddiness High: Low dose dexamethasone
High: Cushing’s suppression
 Sex Hormones Low: Decreased libido, Low: Gynaecomastia, Testosterone, estradiol, FSH, LH
gynaecomastia, absent testicular atrophy
morning erections
Growth Hormone High: Acromegaly Refer below High: IGF1, OGTT for non suppression
features of GH
Prolactin High: Gynaecomastia, Prolactin
galactorrhea
Desmopressin High: DI U/E/Cr, urine osm, water
deprivation/salt suppression, DDAVP

Causes of hypopituitarism: Tumour (primary pituitary, metastatic), hemorrhage (pituitary apoplexy), ischemic (Sheehan
syndrome), infiltrative (sarcoidosis, haemochromatosis/iron overload)
Causes of decreased libido: Vascular (Leriche’s syndrome), Neurological (spinal cord/brain/autonomic disorders), Hormonal
(hypogonadism, hyper/hypothyroidism, hyper/hypocortisolism), drug induced (beta blockers, anti depressants/psychotics),
psychogenic (depression, anxiety)
Causes of hypothyroidism: Central (similar to hypopituitarism) vs Thyroid related (autoimmune, iatrogenic –
RAI/thyroidectomy, drugs – amoidarone/lithium, infiltrative – leukemia, haemochromatosis)

GYNAECOMASTIA
Approach
• Hypogonadism: Pituitary tumour, testicular tumour
• Hyperthyroidism
• CLD, CKD
• Drugs: Spironolactone, anti-androgens (dutasteride)
• Breast cancer: BRCA
• Congenital: Klinefelter syndrome

FEVER
Approach
Travel, Immunosuppression on b/g autoimmune dz/transplant, HIV (seroconversion, OIs)
• Infection:
o Bacterial, viral, fungal, parasitic
o Prolonged: TB, IE, abscess, HIV (with OI), Malaria
o Localising questions: CNS (headache, neck stiffness, photophobia), Upper respi (RN, blocked nose, ear
pain/discharge), dental (gum pain, tooth pain), respi (cough, SOB), cardiac (fluid overload, embolic
phenomenon), GI (jaundice, odynophagia, diarrhea, vomiting), GU (dysuria, back pain, discharge), soft
tissue (rash, skin redness), bone/joint pain
o Travel history important – soil/water exposure, animal exposure, food exposure, vaccinations, malaria
prophylaxis
§ Malaria – CNS involvement, hemolytic anemia, liver dysfunction. Giemsa microscopy,
antigen/molecular based tests. Treatment depends on resistance epidemiology, usually
chloroquine, if res can give malarone/mefloquine/quinine based therapy
§ Typhoid – GI (constipation/diarrhea), relative bradycardia, rose spots, hepatosplenomegaly,
BGIT. Blood and stool cultures. Treat with ceftriaxone.
§ Leptospirosis – A/w freshwater swimming. Conjunctival suffusion, Weil’s disease (jaundice,
renal impairment), other involvement (aseptic meningitis, ARDS/pulmonary hemorrhage).
Labs can have cytopenias, hyponatremia, transaminitis, renal impairment. Diagnosed with
serology, molecular tests, cultures. Treat with doxycycline or azithromycin.
§ Rickettsia – Rat exposure. Non specific, non localizing symptoms. Labs can have
thrombocytopenia, transaminitis, normal white cell/neutrophil count. Diagnosed on serology.
Treat with doxycycline
o Sexual history: Married? Number of partners? Gender? Oral/anal/vaginal? Receptive vs penetrative?
o Transfusions, tattoos, IVDA
• Haematological malignancies – with B symptoms
• CTD/Autoimmune disorders – inclusive of sarcoidosis
• Hyperthyroidism (especially if storm)
• Drug fever
• In context of immunosuppression, common infections like CAP still commonest, but must consider OIs and
haematological malignancies
• Fever with LN: HIV, TB, lymphoma, sarcoidosis, autoimmune, viruses (CMV, EBV)

LOW/LOA
Approach
Establish intentionality of weight loss, appetite (appetite ok in malabsorption/thyroid disorders)
• Malignancy: Solid organ, haematological
• Endocrine: Hyperthyroidism, DM, Addison’s, Pheochromocytoma
• Chronic infections: TB, HIV
• Malabsorption: GI pathology (chronic pancreatitis, SIBO – carbohydrate breath test, celiac – IgA anti tissue
transglutaminase ab/SI biopsy, lactose intol)
• Chronic Disease: CKD, CLD, Heart Failure, COPD
• Psychogenic: Depression, anorexia, dementia

ITCH
• Localised Rash: Eczema, urticaria, scabies, fungal rash
• Systemic disease: Cholestasis, ESRF with uremia, PRV (erythromelalgia – hands pain with
erythema/pallor/cyanosis), mastocytosis, hyper/hypothyroidism
• Drugs (opioids, alcohol withdrawal)
• Psychogenic

ORAL ULCERS
• Aphthous ulcers
• Infective: HIV with oral thrush, STIs (syphilis, herpes), viral (HFMD, herpangina)
• Inflammatory: SLE, behcet’s, IBD, pemphigus/pemphigoid
• Neoplastic: Tongue SCC
• Metabolic: B12/folate deficiency (B12 more glossitis, folate more mouth ulcers)
• Drugs: Inhaled corticosteroids, SJS/TENS, methotrexate, thionamides (causing agranulocytosis)

HYPONATREMIA
Approach
• Pseudo/Translocational: Hyperlipidemia, hyperglycemia
• Hypovolemic:
o Losses: Vomiting, diarrhea, urinary losses (diuretics)
o Poor intake
• Euvolemic
o Adrenal insufficiency, hypothyroidism
o Polydipsia (Psychogenic, Response to dry mouth)
o SIADH
§ Drugs: Psychiatric medications, anti-epileptics (CBZ, sodium valproate)
§ Lung: Malignancies (small cell lung ca)
§ CNS: Trauma, tumour, surgery
§ Others: Pain, HIV
• Hypervolemic:
Hypervolemia either due to back damming (CCF) or third spacing (CLD)
o Cardiac disease
o Liver disease
o Kidney disease

Evaluation
• Ascertain hyponatremia
• Assess serum osm: Normal osm is 275-290 mosmol/kg
• Assess ADH action (urinary osm): >100 mosmol/kg
• Assess appropriateness of ADH action (urinary sodium): >40meq/L (inappropriate)

HYPERNATREMIA
Usually due to excessive fluid losses/poor intake
• DI, solute diuresis (Hyperglycemia in DM)
• Vomiting/Diarrhea/insensible losses in patient who cannot respond to thirst mechanism

HYPOKALEMIA
• Shifts: Nebs, insulin, beta-agonist
• Others: Periodic paralysis (a/w Grave’s)
• GI losses: Vomiting/diarrhea
• Urinary Losses
 o Hypertensive:
§ Aldo high, renin low: 1’ Hyperaldosteronism (Conn’s)
§ Aldo high, renin high: 2’ Hyperaldosteronism (Renin producing tumour, RAS)
§ Aldo low, renin low (non aldosterone mineralocorticoid excess): Cushing’s, Liquorice, Liddle’s
o Normotensive/Hypotensive:
§ Acidemia: RTA, DKA
§ Alkalemia:
• Diuretics
• Bartter’s (loop diuretic like, more serious, a/w growth retardation)/Gittelman’s
(thiazide like diuretic, less serious); both generally AR inheritance

HYPERKALEMIA
Common: Renal impairment, drugs (K sparing diuretics); exclude tumour lysis, hypoaldosteronism, rhabdomyolysis
• Cellular release: Breakdown (tumour lysis, rhabdomyolysis, hemolysis), shifts (hyperglycemia, insulin def, beta
blockers)
• Impaired excretion: Renal impairment, hypoaldosteronism, K sparing diuretics
• Excessive intake: Rare
Treatment
• Protect Heart: 10mls of 10% calcium gluconate over 10mins (may require multiple doses)
o Stabilises cardiac membrane
o Used in 1.ECG changes, 2.K more than 6mmol/L
• Shift K+ Into Cells
o Insulin + glucose (10U IV actrapid dilute in 40mls of D50%)
• Potassium removal
o Calcium resonium (cation resin)
§ Given PO or via NGT 15g TDS for 3 days (takes days to work)
§ If cant take orally, give PR 30mg
• Dialysis (if intractable)

HYPERCALCEMIA
Calcium adjustment: Ca + 0.02 x (40-albumin)
• PTH Mediated: Primary hyperparathyroidism (think MEN1/2a), tertiary hyperparathyroidism (in CKD)
• PTH related peptide: Malignancy (lung ca, RCC, multiple myeloma)
• 1,25 Vit D mediated: Granulomatous disease (TB, sarcoid, lymphoma)

HYPOCALCEMIA
• Hypoparathyroidism: Surgical, autoimmune (polyglandular autoimmune syndromes), radiation, infiltrative
(haemochromatosis, Wilson’s, granuloma, metastatic disease)
• PTH resistance: Type 1a a/w Albright’s hereditary osteodystrophy (short stature, brachydactyly, rounded facies,
mild intellectual disability; AD inheritance)
• Vit D def/resistance: Low UV exposure, malabsorption (celiac, crohn’s), renal/liver disease
• CKD
• Extravascular Deposition: Pancreatitis, osteoblastic metastases, hyperphosphatemia
• Drugs: Bisphosphonates, calcimemetics
• Hypomagnesemia

ACIDOSIS
AG = Na – Cl – Bicarb (normal 10-14)
• Metabolic Acidosis
o HAGMA: Lactate, Renal Impairment, DKA, toxins (salicylate, methanol, ethylene glycol)
o NAGMA: RTA, diarrhea, others (Adisson’s, CAI, ureterostomy, pancreastomy)
o Winter’s formula: PCO2 = 1.5 x bicarb + 8 +/- 2
• Respiratory Acidosis (CO2 retention)
o Won’t Breathe (Central – Respiratory Depression): Opioids, brainstem lesions, OSA/OHS
o Can’t Breathe
§ Neuromuscular: MG, GBS, MND, spinal cord disorders
§ Thoracic wall: Kyphoscoliosis, ank spond, fibrothorax
o Can’t Breathe Enough (Respiratory): COPD, asthma. PE/endstage ILD/bronchiectasis

ALKALOSIS
• Respiratory: Causes of hyperventilation (pain, anxiety, respiratory distress)
• Metabolic
 o Volume Contraction: Diuretics, Barter’s/Gittelmans’s
o Aldosterone related
§ Primary hyperaldosteronism
§ Cushing’s, Liddle’s, Licorice

FLUSHING
• Physiological: Menopause, emotional flushing
• Neurological: Autonomic dysfunction
• Neoplastic: RCC, PRV
• Inflammatory: SLE
• Endocrine: Carcinoid, pheochromocytoma, VIPoma, hyperthyroidism, mastocytosis
• Drugs: Alcohol, serotonin syndrome, food ingestion (spicy foods)
• Others: Mitral stenosis, anaphylaxis, SVCO
• Dermatological: Rosacea

EYE REDNESS
Systemic diseases: RA, SLE, Sjogren’s, Ank spond, Grave’s disease
Associated symptoms: Pain, BOV, ophthalmoplegia, discharge, floaters
• Bilateral: Uveitis (ank spond), scleritis/episcleritis (RA), ketatoconjunctivitis sicca (Sjogren’s), thyroid eye disease
with chemosis (Grave’s)
• Unilateral: Trauma, glaucoma, conjunctivitis, blepharitis

POLYCYTHEMIA
• Primary: PRV, congenital methemoglobinemia
• Secondary:
o Hypoxia related (Chronic pulmonary disease, R>L shunts, OA/OHS, high altitude, CO poisoning
o Autonomous EPO Production: RCC, HCC, Pheochromocytoma

EYE SWELLING
• Nephrotic Syndrome
• Allergy: Anaphylaxis, Urticaria, contact dermatitis
• Drugs: ACEi, NSAIDs
• Thyroid eye disease
• Hereditary angioedema
• Autoimmune disorders: Dermatomyositis (heliotrope rash)
• Pressure effect: SVCO, retroorbital tumour

RASH
• Nodular Facial: Lupus pernio (sarcoid), adenoma sebaceum, acne (Cushing’s), discoid lupus
• Bullous/Vesicular
o Infective: Viral (herpes), bacterial (Staph scalded skin syndrome)
o Inflammatory: SLE, pemphigus, pemphigoid, vasculitis
o Neoplastic: Paraneoplastic pemphigus
o Metabolic: Cutaneous porphyria (photosen, worsened by alcohol), celiac
o Drugs: SJS/TENS, FDE
o Others: Contact dermatitis
• Livedo Reticularis
o Infective: Hep C - Cryoglobulinemia
o Inflammatory: SLE, APS, Vasculitis
o Neoplastic: Hematological malignancies (PRV, ET), Multiple Myeloma
o Others: Hypercoagulable states, embolic disease (cholesterol, septic)
• Erythema Nodosum
o Idiopathic
o Infection: TB, streptococcal, mycoplasma
o Inflammatory: IBD, Behcet’s, Sarcoid
o Neoplastic: NHL, pancreatic, carcinoid
o Endocrine: Pregnancy
o Drugs: OCP
• Pyoderma Gangrenosum
o Inflammatory: IBD (UC>Crohn’s), RA
o Neoplastic: Haematological malignancies
• Hyperigmentation: Addison’s, Haemochromatosis, Amiodarone
• Hypopigmentation: Vitiligo, Ashleaf macule (tuberous sclerosis), leprosy, sarcoidosis, tinea versicolor
CONDITIONS
Rheum: Scleroderma, Dermatomyositis, Ankylosing Spondylitis, Psoriasis, Rheumatoid Arthritis, SLE, GCA, Wegener’s
Granulomatosis, Takayasu Arteritis, Churg Strauss, Polyarteritis Nodosa, HSP, Sjogren’s, Behcet’s, Marfan’s
Infective Diseases: HIV and HIV associated complications, Rheumatic fever
Endocrine: Grave’s Disease, Acromegaly, Cushing’s, Adrenal Insufficiency, DI, SIADH, Autoimmune Polyglandular
Syndrome, MEN, Hypokalemia, Hyponatremia, Hypercalcemia, Hypernatremia
Neurological
• Neurocutaneous: NF, Tuberous Sclerosis, Sturge Weber
• NPH, Wernickes’, Benign Intracranial HTN, Hungtington’s
Gastro: Peutz Jegher
Liver: Wilson’s, Haemochromatosis, PBC, PSC
Others: Amyloidosis, Sarcoidosis, HHT, Subclavian Steal, Hereditary Angioedema, Retinitis Pigmentosa, Osteogenesis
Imperfecta, Porphyria
Cancer: VHL, FAP, HNPCC, Carcinoid
Endocrine: Cushing’s, Grave’s, Acromegaly, Panhypopituitarism

Marfan’s Syndrome
• Genetics: AD, fibrillin 1 mutation on chromosome 15
• Symptoms: Chest pain (aortic dissection, pneumothorax, valve pathology), shortness of breath (valve pathology),
vision problems (ectopia lentis)
• Clinical Features
o Key features (based on Ghent’s nosology): Ectopia lentis, aortic valve pathology, aortic dissection
(radio-radial delay), fibrillin 1 mutation, family history, systemic features
o Hands: Thumb sign, wrist sign, arachnodactyly
o Head: Face (Dolicocephaly, retrognathia), Eyes (Ectopia lentis, iridodonesis, enophthalmos), Mouth
(high arched palate)
o Increased arm span to height ratio, reduced upper segment to lower segment ratio
o Chest:
§ Aortic dissection, aortic regurgitation (aortic root dilation), MVP, pneumothorax
§ Pectus carinatum
o Foot: Pes planus
o Beighton score (4 or more positive): Thumb (touch forearm), little finger (>90 degrees), knee
hyperextension, elbow hyperextension, touch floor with palms
• Investigations: Slit lamp examination (ectopia lentis), Echocardiogram (aortic root evaluation, MVP), Chest
Radiograph (pneumothorax), MRI spine (dural ectasia), Genetic testing

Gout
• Clinical features
o Asymmetrical distribution
o Tophi: digits, extensor surface of forearm, elbow, Achilles tendon, Pinna
o Olecranon bursitis
o Abdo: hepatosplenomegaly
o LL edema
o BP: HTN from renal impairment. Fever
• Precipitants: Drugs (diuretics, initiation of uric lowering therapy, cyclosporine), high turnover states (psoriasis,
haemato malignancy, tumour lysis), renal impairment, intake (alcohol, red meat, carbonated drinks, seafood)
• Complications: Urate nephropathy, urolithiasis
• Inx
o Radiograph: punched out lateral erosions with sclerotic margins and overhanging edges. Joint space
preserved till late. No periarticular osteopenia
o Diagnostic arthrocentesis: Negatively birefringent needle shaped urate crystals
• Management
o Acute treatment: Rest, ice, leg elevation, NSAIDS, Colchicine, Others: IA steroid injection, prednisolone
o Chronic treatment: if 2 or more attacks/year, chronic tophaceous, urate nephropathy. Started 2 weeks
after acute flare, cover with colchicine/NSAIDs; targets - < 360umol/L for most, <300umol/L if tophi
§ Diet: low alcohol, seafood, red meat, soft drinks
§ Xanthine oxidase inhibitor: allopurinol, febuxostat
§ Uricosuric agent: probenecid

Rheumatoid Arthritis
• Symptoms:
o Joint pain (small joints, swelling and warmth, early morning stiffness > 1 hour, generally > 6wks)
 o Systemic: Fever, malaise, lymphadenopathy
o Extra-articular manifestations: Eye (scleritis, episcleritis, keratitis), sicca (Sjogren’s association),
bronchiectasis/ILD, felty syndrome (neutropenia, splenomegaly, RA), kidneys (amyloidosis),
neurological (CTS, mononeuritis multiplex), vasculitis (raynaud’s), neuropathy
• SOB in RA
o Respiratory: ILD/bronchiectasis, MTX induced ILD
o Fluid: Amyloidosis causing cardiomyopathy and nephrotic syndrome
o Infections: Due to immune suppression – CAP, Tuberculosis, PCP
• Clinical Features
o Affected joints: Symmetrical deforming polyarthropathy, active vs quiescent, characteristic features
(swan neck, boutonniere’s, Z-thumb, ulnar deviation at MCPJ, piano key sign), ROM, function, surgical
evidence (if see scar, ask if patient able to move – arthrodesis vs arthroplasty)
o Rheumatoid nodules
o Hands (telangiectasia, raynaud’s, intrinsic muscle wasting), Eyes (redness), lungs (ILD/bronchiectasis),
abdomen (organomegaly for felty’s or amyloidosis)
• Investigations
o FBC: Infection, neutropenia (felty’s)
o Inflammatory markers: ESR, CRP
o Antibodies: Rheumatoid factor, anti cyclic citrullinated peptide (CCP), other markers if considering
other differentials
o Radiological imaging: Soft tissue swelling, peri-articular osteopenia, juxta-articular erosions, loss of joint
space, joint subluxation/deformities
o Pre immunosuppression tests: RP/LFT, Hep B/C, Ophthalmic testing, latent TB screening
• Management
o Multidisciplinary: Rheumatologist, PT/OT
o Flares: NSAIDs, steroids
o DMARDs: Steroid, steroid sparing immunomodulators (MTX, Leflunomide, Hydroxychloroquine,
Sulfasalazine), biologics (TNFalpha: etanercept/infliximab/adalimumab, IL-1: Anakinra, IL-6:
tocilizumab, CD20 B cell: Rituximab, T-cell costimulation blocker: Abatacept)
o Others: Vaccinations, bone health (Vit D, osteoporosis)

Systemic Lupus Erythematosus

• Symptoms: Rash, hair loss, neurological symptoms, nephrotic/nephritic syndrome, recurrent clotting problems
• Clinical Features
o Mucocutaneous: Photosensitive rash (malar rash, discoid lupus – check ears, generalized rash), ulcers,
hair loss
o Arthritis (may be non-deforming: Jaccoud’s arthropathy), serositis
o Neurological: Seizures, encephalitis, myelitis, mononeuritis multiplex
o Nephrologic: Haematuria, frothy urine, pedal edema
o Haematological: Bruising, symptoms of anemia, frequent infections
o Antiphospholipid syndrome: Recurrent pregnancy losses, arterial/venous clotting, on examination look
for livedo reticularis
o Others: GI (lupus gut), MSK (myositis, myalgia), eye (keratoconjunctivits sicca), cardiac (libman-sacks
aseptic endocarditis causing valvular insufficiency), raynaud’s
• Investigations
o FBC (cytopenias), RP/UFEME/uPCR (renal involvement), PBF (hemolytic anemia)
o Anitbodies: ANA, anti dsDNA, anti Smith, DCT, antiphospholipid abs (Lupus anticoagulant, anti
cardiolipin, anti beta2 glycoprotein 1), complements
o Organ involvement targeted investigations: Kidney (biopsy), CNS (imaging, LP), skin (biopsy), respi
(CXR), joint (joint XR)
• Management
o Non-Pharmacological: Sunlight protection, smoking cessation
o Hydroxychloroquine (backbone), steroids, steroid sparing immunomodulators (MTX,
cyclophosphamide, MMF) – depending on organ involvement, biologics (rituximab)
o Organ specific treatment: Joints (NSAIDs), rash (topicals – steroid, tacrolimus), kidney (ACEi/ARB)
• Drug induced lupus: Hydralazine, Procainamide, Isoniazid

Antiphospholipid Syndrome
• Features (Sapporo criteria)
o Clinical: Vascular thrombosis (superficial venous thrombosis does not count), Pregnancy morbidity (loss
> 10 weeks gestation, death before 34 weeks gestation due to eclampsia/preeclampsia/placental
insufficiency, 3 or more losses < 10 weeks gestation)
 o Laboratory: Ab positivity at least 12 weeks apart, anti-cardiolipin/lupus anticoagulant/anti beta2
glycoprotein I
o Others: Cardiac valve disease, CNS involvement, renal disease, thrombocytopenia, hemolytic anemia
• Secondary causes: Autoimmune (commonly SLE), infections, drugs, malignancy (solid organ, haemato)
• Management: Anticoagulation with warfarin (rather than DOAC), LMWH in pregnancy

Sjogren’s
• Symptoms
o Dry eyes, dry mouth (dental caries, difficulty swallowing food because dry, polydipsia with resulting
polyuria that can affect sleep)
o General: Arthralgia, fibromyalgia
o Vasculitis: Raynaud’s, vasculitic rash
o Thyroid (autoimmune thyroid disease), lungs (ILD), neurology (various PNS and CNS manifestations e.g.
mononeuritis multiplex), haematology (cytopenias, increased risk of lymphoma), renal tubular acidosis
• Clinical Features
o Parotid gland enlargement
o Absence of salivary pooling in mouth, dental caries
o Lungs: ILD
• Investigations
o Antibodies: Anti Ro and La
o Functional studies to evaluate for dry eyes and salivary hypofunction
§ Eyes: Schirmer’s test: <5mm in 5 minutes
§ Salivary Hypofunction: Salivary scintigraphy or sialometry (measure amt of salivary prod)
o Imaging: MRI/ultrasound salivary glands
o Biopsy: Labial salivary gland biopsy
• Treatment
o Non-pharmacological: Smoking cessation
o Pharmacological:
§ Mild: Secretagogues (e.g. pilocarpine), moisturizing eyedrops
§ Severe: Immunomodulators

Ankylosing Spondylitis
• Symptoms: Back/neck/hip pain/stiffness
• Clinical Features:
o Description: Stooped posture with cervical hyperextension, thoracic kyphosis and loss of lumbar
lordosis with protuberant abdomen
o Neck and lumbar ROM, Faber’s test
o Occipital wall distance, schober’s test (from PSIS extend 10cm above and 5cm below, excursion should
at least be 5cm bending forward), chest expansion (<2.5cm), finger floor distance
• Extra-articular manifestations: Anterior uveitis, atlantoaxial subluxation, apical fibrosis, aortic regurgitation, AV
node dysfunction, amyloidosis, Achilles tendonitis
• Investigations:
o Imaging of spine and SI joint (XR then MRI) looking for: Spine (syndesmophytes, squaring of vertebral
bodies, romanus lesions), SI joint (sacroilitis)
o Laboratory: ESR/CRP, HLA B27
o Complications directed investigations
• Management
o Multidisciplinary: Rheumatologist, PT/OT
o Acute flares: NSAIDs
o Biologics: TNF alpha inhibitors

Psoriasis
• Symptoms: Joint pain, rash, SOB
• Triggers: HIV infection, medication (steroid withdrawal; lithium, beta blockers, NSAIDs, antimalarials)
• Clinical Features
o Rash: Papulo squamous rash with silvery scales. Patterns include extensor (chronic plaque psoriasis;
also scalp, ears), flexural, guttate, pustular, erythroderma
o Nails: Pitting, onycholysis, subungual hyperketatosis
o Joints: RA pattern, OA pattern, spondyloarthropathy pattern, arthritis mutilans; also ask for
enthesitis/dactylitis
o Others: ILD
• Investigations
 Diagnosis is clinical
o Imaging: Joint (pencil in cup appearance, periostitis), CXR (ILD changes)
• Management
o Topical: Emmoilents, kerotolytic, steroids, coal tar, vit D analogues, vit A antagonist
o Phototherapy: UVA, UVB
o Systemic: AVOID STEROIDS. Immunomodulators (MTX, ciclosporin), biologics (TNFalpha antagonists)

Scleroderma
• Symptoms: SOB (ILD, pulmonary HTN), dysphagia, hand pain/discomfort (Raynaud’s), hypertension with
proteinuria (scleroderma renal crisis)
• Clinical Features
Important to comment whether limited or diffused
o Hands: Sclerodactyly, nailfold telangiectasia, raynaud’s, digital ulcers/pitting
o Face: Pinched nose, microstomia, tight skin
o Chest: ILD, pulmonary hypertension, salt and pepper appearance
o Abdomen: Esophageal dysmotility, SIBO
• Investigations
Diagnosis is largely clinical, abs mainly for disease prognostication
o Antibodies: ANA, Anti-centromere (limited, pulmonary HTN, CREST), Anti-topoisomerase/SCL70
(diffused, ILD), Anti RNA polymerase III: Renal Crisis, Cancer
o Endoscopic/functional luminal evaluation
o Lung Function Test, HRCT, Echocardiogram
o Renal panel, UFEME, Urine PCR
• Treatment: NOT STEROIDS – steroids can precipitate renal crisis
o Raynaud’s: Gloves/smoking cessation, calcium channel blockers/nitrates/PDE5 inhibitor, sympatectomy
o Scleroderma renal crisis: Ace inhibitors, ARBs
o Esophageal dysmotility: Proton pump inhibitors, prokinetics
o ILD: Immunosuppresants (cyclophosphamide)
o Pulmonary hypertension: Diuretics, Phosphodiesterase 5 inhibitor
• Others
o Diffused: Cut off is knees and elbow
o CREST: Calcinosis cutis, Raynaud’s, Esophageal hypomotility, Sclerodactyly, Telangiectasia

Dermatomyositis/Polymyositis
• Symptoms: Rash, weakness, dysphagia, SOB
• Clinical Features
o Upper Limbs: Gottron’s papules/sign, mechanic’s hands, Raynaud's, nailfold telangiectasia, proximal
myopathy
o Face: Heliotrope rash (request patients to close eyes – rash might be hidden within lid folds)
o Trunk: Shawl sign
o Other clinical features: ILD, cardiomyopathy, dysphagia, associated malignancies
• Investigations: CK/Aldolase, EMG, MRI muscle, muscle biopsy (DM: Perifascicular atrophy and fibrosis, PM:
Intrafascicular cellular infiltrate and inflammation), skin biopsy (for DM), antibodies for prognostication
(Antisynthetase ab (Anti Jo-1 – a/w ILD, Raynaud, arthritis, mechanic’s hands), age appropriate screening for
malignancy
• Treatment: Steroid, steroid sparing immunomodulators

Fibromyalgia
• Clinical Features: Characterised by widespread MSK pain accompanied by somatic symps (fatigue, sleep
disturbances), cognitive and psychiatric disturbances
• Tender points

• Invx: Laboratory testing normal – Check FBC, ESR/CRP, CK, TSH

 • Management: Exercise, Antidepressants, Pregabalin/Gabapentin

Behcet’s
• Clinical Features: Recurrent oral aphthae, recurrent genital aphthae, eye lesions (uveitis, retinal vasculitis), skin
lesions (erythema nodosum, aceneiform lesions, papulopustular lesions), vasculitic manifestations
• Invx: Pathergy test
• Treatment
o First line: Topical steroids, topical anesthetics – for ulcers
o Second line: Prevention of ulcers with colchicine
o Systemic involvement, consider steroid and steroid sparing immunomodulators (decided based on
organ involvement)

Familial Mediterranean Fever

• Genetics: Autosomal recessive
• Clinical Features:
o Episodic attacks lasting 1-3 days
o Fever, serositis (chest, abdomen), synovitis, erysipelas skin lesions
o Family history
o Others: Pericarditis, acute scrotum
o Complications: AA Amyloidosis, small bowel IO, infertility
• Invx: Raised acute phase reactants, genetic testing
• Treatment: Colchicine mainstay

Takayasu Arteritis
• Symptoms: Limb claudication/pain/cyanosis, subclavian steal syndrome, angina (coronary artery narrowing), gut
claudication, constitutional symptoms
• Clinical Features: Differential pulses and BP, bruit, hypertension, aortic regurgitation
• Investigations: ESR/CRP, CT/MR aortogram
• Treatment: Acute flares vs maintenance, steroids vs steroid sparing immunomodulators, stenting/bypass grafting
for affected vessel segments

Giant Cell Arteritis

• Symptoms: Headache, jaw claudication, vision problems (can be transient/persistent, AION), lethargy, body
aches (polymyalgia rheumatica)
• Clinical Features: Diminished/differential pulses and bruits, Eye (RAPD, reduced VA, ophthalmoplegia,
fundoscopy – swollen and pale disc in AION), thickened and tender temporal artery, AR murmur (may be 2’ aortic
aneurysm), MSK screen for synovitis/limited ROM in polymyalgia rheumatica
• Investigations: ESR, temporal artery biopsy looking for multinucleated giant cells, can consider vessel imaging if
diagnosis uncertain (Doppler sonography of temporal artery, imaging of other vessels if clinically involved)
• Treatment: Steroids mainstay (especially essential for sight preservation), steroid sparing immunomodulators

Churg Strauss
• Symptoms: Chronic rhinosinusitis, Asthma (late onset, poorly controlled, severe episodes),
neuropathy/mononeuritis multiplex (patchy weakness and numbness), rash
• Investigations: FBC (Eosinophilia), ESR/CRP, P-ANCA, pulmonary imaging (transient pulmonary opacities), biopsy
(lung, skin, nerve)

Polyarteritis Nodosa
• Associations: NOT associated with ANCA, maybe secondarily caused by Hep B/C, hairy cell leukemia
• Symptoms
o General: Fatigue, weight loss, fever, arthralgia
o Organ specific: Skin lesions, hypertension, renal insufficiency, neurologic dysfunction (mononeuritis
multiplex), abdominal pain (mesenteric arteritis)
• Investigations
o Initial investigations based on suspected organ involvement: Creatinine, troponin, lactate, nerve
conduction studies
o Exclude differentials: ANCA, ANA
o Disease supportive features: Arteriography (mesenteric or renal, looking for microaneurysms, irregular
constrictions), cross sectional imaging (areas of infarction), biopsy

Wegener’s Granulomatosis
 • Symptoms: ENT involvement, pulmonary symptoms, renal involvement (haematuria, frothy urine, oliguria), rash
(livedo reticularis, nodules), ophthalmic manifestations (pain, diplopia, proptosis)
• Investigations: ANCA, U/E/Creat, UFEME, Urine PCR, Lung imaging, biopsy

Henoch Schonlein Purpura

• Clinical Features: Vasculitic rash (painless palpable purpura), abdominal pain (due to bowel wall vasculitis, can
cause intussusception), renal impairment (nephritis), arthritis
• Investigations: FBC, ESR/CRP, U/E/Creat, urine PCR/FEME, consider renal biopsy
• Management: Generally supportive. Role for steroids and immunosuppression if renal involvement

Inflammatory Bowel Disease

• Ask for symptoms pertaining to whole GIT: Oral ulcers, dysphagia/odynophagia, vomiting, diarrhea, perianal
lesions
• Extra-articular manifestations: Constitutional (fever, LOW) Primary sclerosing cholangitis (more UC), Uveitis,
arthritis, pyoderma gangrenosum, erythema nodosum, clubbing, nutritional deficiency (more Crohn’s because of
SB involvement)
• Investigations
o FBC (anemia), inflammatory markers
o Facecal calprotectin
o Imaging: TRO toxic megacolon
o Endoscopy: UC (continuous mucosal lesions, crypt abscess), Crohn’s (skipped transmural lesions,
granulomas)
o MRCP: To diagnose PSC
• Disease severity (Truelove and Witt’s Criteria – UC):
o Mild: <4 stools, no systemic disturbance, normal ESR
o Moderate: >4 stools, minimal systemic disturbance
o Severe: >6 stools with blood, systemic disturbance (fever, tachycardia, anemia, ESR >30)
• Treatment
o Acute flares (induction): Crohn’s (steroids, antibiotics, immunomodulators, biologics), UC (topicals and
systemic; steroids, aminosalicylates like mesalazine, immunomodulators, biologics)
o Long term (maintenance): Crohn’s (immunomodulators like aza/MTX), UC (aminosalicylate,
immunomodulators)
o Surgery: Toxic megacolon
o CRC screening

Liver Conditions
• Hepatitis B
o Diagnosis: HBsAg, HBV DNA
o Indications for Treatment:
§ Chronic hepatitis – Tx delayed for 3-6 months in newly dx HbeAg+ patients with compensated
liver disease to see if HBeAg ab seroconversion takes place
• Treat if 2 out of 3 fulfilled:
o Fibroscan: fibrotic liver
o ALT: >2X UL of normal
o HBV DNA >2000 if Hbe neg, >20000 if Hbe postive
§ Liver complications
• Acute liver failure
• Decompensated cirrhosis
• Compensated cirrhosis + HBV DNA > 2000 IU/ml
o Treatment: Nucleoside analogues like entacavir and tenofovir usually first line. Alternatives include PEG
interferon
• Hepatitis C
o Indications for Treatment: All with hepatitis C should be treated
o Treatment: Present gold standard is genotype directed interferon free, direct acting antiviral (DAA)
therapy
• Autoimmune Hepatitis
o Antibodies: ANA, Anti Smooth Muscle, IgG, Anti Liver Kidney Microsomal, Soluble Liver Antigen
o Treatment: Steroids, steroid sparing immunomodulators
• Alcoholic Hepatitis
o Maddrey’s Coefficient: Based on PT/Bil
o If > 32 to start steroids or pentoxifylline
• Primary Biliary Cirrhosis
 o Autoimmune disease of intrahepatic bile ducts
o Clinical Features: Cholestatic jaundice, pruritus, xanthoma/xanthelesma
o Invx: LFT, lipid panel, Antimitochondrial Ab. Biopsy gold standard but may not require
o Management: Mainstay is Ursodeoxycholic acid. Treatment of hypercholesterolemia with statins,
pruritus with cholesytramine. Liver transplant is definitive.
• Primary Sclerosing Cholangitis
o Inflammation of intra and extrahepatic bile ducts
o A/w ulcerative colitis
o Invx: LFT, biliary tree imaging/visualization (MRCP/ERCP) looking for biliary duct dilatation, thickening
and stricturing
o Management: Stenting, treat underlying IBD, transplant
• Wilson’s Disease
o Features: Hepatic, neuro-psychiatric, hemolysis, others (RTA type 2
with fanconi, hypoparathyroidism, arthropathy)
o Mutation in ATP7B gene on Chr 13 – Autosomal Recessive Disorder, results in impaired excretion of
copper and resulting accumulation in organs
o Diagnosis: Slit lamp for KF rings, low serum ceruloplasmin, high 24 urinary copper (>100ug/day), liver
biopsy when doubtful
o Treatment: Chelating agent (trientine, penicillamine); zinc (interfere with copper absorption) as an alt
for maintenance therapy
• Haemochromatosis
o Causes: Congenital (mutations in HFE causing increased intestinal iron absorption; AR inheritance),
Acquired (iatrogenic iron overload from transfusion)
o Clinical Features: Liver, cardiac, pancreas (diabetes), pituitary, arthropathy, skin (bronze coloured)
o Investigations
§ Iron Panel: TSAT >/= 45%, Ferritin >200ng/ml (men) and >150ng/ml (women)
§ Imaging: Liver, heart
§ Genetic testing
o Management: Phlebotomy (for congenital hemochromatosis), iron chelation (blood transfusion related
iron overload)

Grave’s disease
• Symptoms: Tremors, palpitations, increased appetite, weight loss, diarrhea, heat intolerance, oligomenorrhea,
anxiety/hypervigilance, eye symptoms
• Clinical Features
o UL: Palmar erythema, sweaty palms, tremors, thyroid acropachy, feel pulse, proximal myopathy
o Eyes: Look from top and side, test EOM
o Goiter: Diffusedly enlarged, bruit, check retrosternal extension
o CVS: Heart failure
o LL: Hyperreflexia, pretibial myxedema
• Investigations: TSH/Free T4, TSH receptor antibody
• Treatment
o Pharmacological
§ Thionamides mainstay (treatment at least 1.5 years), can give propranolol for control of
hyperthyroid symptoms
§ Carbimazole usually first line because lower hepatotoxicity
§ PTU first line during first trimester of pregnancy because lower risk of teratogenicity (aplasia
cutis, tracheoesophageal fistula, choanal atresia); carbimazole first line during second/third
trimester
§ Carbimazole preferred if breastfeeding
§ Need to counsel about agranulocytosis, hepatotoxicity
o Next lines of treatment include radioactive iodine (avoid children or pregnant women for 2 weeks,
cannot conceive for 6 months, worsens thyroid eye disease), total thyroidectomy
o Thyroid eye disease: Avoid radioactive iodine. Treatment involves ophthalmology referral, smoking
cessation, use of eyedrops, prism glasses, steroids, orbital radiation and decompression surgery
o Pretibial myxedema: Compression stockings, steroids
o Hypokalemic Periodic Paralysis
§ Acute: Potassium replacement
§ Chronic: Prevent triggers (high carb meals, vigorous exercise), CAI (acetazolamide)/K sparing
diuretics (spironolactone), potassium replacement
• Associations: Hypokalemic periodic paralysis, other autoimmune disorders (pernicious anemia, vitiligo, T1DM,
adrenal insufficiency)
• Thyroid storm:
 o Burch-Wartofsky (Fever, CVS, CNS, GIT parameters), >45 thyroid storm likely
o Treatment: IV thionamide, iodide, dexamethasone, propranolol, rate control/HF treatment drugs
• Other causes of hyperthyroidism: Hyperfunctioning nodule, thyroiditis, pregnancy (post partum), drugs
(amoidarone)
• Amiodarone induced thyroid dysfunction
o Mechanism: Direct effect on thyroxine metabolism and high iodine content
o Amiodarone induced thyrotoxicosis
Can attempt to differentiate with sestamibi imaging/color flow Doppler sonography
§ Type I: Idodine load in context of patient with nodular goiter > Results in enhanced thyroid
hormone synthesis; treat with thionamides
§ Type II: Destructive thyroiditis; treat with steroids

Adrenal Insufficiency
• Causes: Autoimmune, infective (TB adrenalitis), metastatic disease, infiltrative (sarcoid, haemochromatosis),
congenital (CAH), iatrogenic (bilateral adrenalectomy – can cause Nelson’s syndrome), hemorrhage (Water-
hosue Friderichsen syndrome – bleeding into adrenal glands 2’ meningococcemia)
• Sites of hyperpigmentation: Palms, lips, pressure areas (belt, bra lines)
• Primary adrenal insufficiency unique features: Hyperpigmentation, hyperkalemia, salt wasting (dehydration,
hypotension)

Cushing’s
• Causes: 90% iatrogenic, 90% of remaining ACTH dependent, 90% of ACTH dependent due to Cushing’s disease,
90% of Cushing’s disease due to pituitary microadenomas
• Clinical Features
o Rounded countenance, truncal obesity, supraclavicular and dorsal fat pads, virilisation (females), acne
o Thin skin, easy bruising, proximal myopathy
o Cataracts, visual fields (macroadenoma rare), mouth for thrush
o Abdominal striae, spinal tenderness for osteoporotic fractures, hip pain (AVN)
o Offer to check BP
• Cx: DM/HLD, Cataracts, Infections, AVN/osteoporosis, neuropsychiatric cx
• Investigations
o Screening: 24H urinary cortisol, overnight or low dose dexamethasone suppression test, late night
salivary cortisol
o ACTH Dependence: ACTH + Cortisol measurement
o Pituitary vs ectopic: High dose dexamethasone suppression test, CRH stimulation test, inferior petrosal
sinus sampling
• Treatment:
o Usually surgical except if due to exogenous steroids
o Medical Treatment: Pituitary (somatostatin analogue), adrenal suppressant (ketoconazole, etomidate)

Acromegaly
• Symptoms: Headache (mass effect, OSA), vision problems, poorly controlled hypertension, tiredness (from OSA),
weakness, hand numbness (CTS), BGIT (increased risk of GI malignancy), DM
• Features
o Hands: Large hands and feet, sweaty hands, CTS
o Head and Neck: Coarse facial features, prominent supraorbital ridge, prognathism, increased inter-
dental separation, macroglossia, bitemporal hemianopia
o Chest and Abdomen: Gynaecomastia (associated raised prolactin), acanthosis nigricans
o Organomegaly: Thyroid, heart, liver, spleen, kidneys
o Hypertension, colorectal cancer
• Investigations
o Acromegaly: IGF1 (screen), OGTT looking non-suppression of GH (confirm), MRI pituitary
o Assess other hormones: Prolactin, T4, LH/FSH/testosterone/oestradiol, Short syncathen test/cortisol
levels
o Cx: OSA (polysomnogram), HTN, BGIT (endoscopic evaluation), cardiomyopathy (ECG, echo), CTS (NCS),
DM (FPG, Hba1c)
• Treatment: Surgery (mainstay), radiotherapy (adjunct or monotherapy if unfit for surgery), medication
(somatostatin analogues like octreotide, dopamine agonists like bromocriptine, GH antagonists like Pegvisomont)
• Most physical features do not regress with treatment, however features of active disease (sweating, peripheral
edema) do

Pheochromocytoma
 • Associated Syndromes: MEN2, VHL, NF1
• Clinical Features: Hypertension, palpitations, headache, sweating, tachycardia, tremors
• Investigations: Urinary and plasma fractionated metanephrines and catecholamines, cross sectional imaging
(CT/MRI)
• Management: Alpha ablock with phenoxybenzamine then beta block, surgery after

Polyglandular Autoimmune Syndrome

• Type I: Mucocutaneous candidiasis, hypoparathyroidism, Addison’s disease
• Type II: Addison’s disease, Type 1 DM, Thyroid disease

Multiple Endocrine Neoplasia (MEN)

• MEN 1: Pituitary, Parathyroid, Pancreas (Insulinoma, gastrinoma, glucagonoma, VIPoma)
• MEN 2a: Parathyroid, Pheochromocytoma (can have glycosuria!), Thyroid (Medullary)
• MEN 2b: Pheochromocytoma, Thyroid (Medullary), mucosal neuromas/marfanoid body habitus

Amyloidosis
• Deposition of abnormal protein (amyloid) in organs (heart, kidney, liver, spleen, CNS, GIT) – nephrotic syndrome,
heart failure, cutaneous amyloidosis
• Diagnosis: Fat pad aspiration or biopsy (Congo red staining under polarizing microscopy – apple green
birefringence) - DEFINITIVE
o Supportive: bone marrow biopsy, imaging (echo/MRI)
• Types: AL (primary), AA (a/w chronic infection/inflammation, RA, IBD, bronchiectasis), Hereditary Amyloidosis,
Dialysis related Amyloidosis
• Treatment: AL– Chemo for MM, ASCT, AA – Treat underlying condition, Hereditary – Liver transplantation an
option (amyloid protein made in liver), dialysis (changing mode of dialysis or kidney transplant)

Sarcoidosis
• Multisystemic inflammatory condition: (Lung + LN) + Skin nodules (lupus pernio) + joint + eye. Granulomas
• Other organs: Kidney stones, liver, cardiac, CNS (cause of bilat LMN facial nerve palsy), joint, anterior uveitis
• Invx:
o Chest imaging: Bilat hilar LN, reticular parenchymal opacities
o Pulmonary function test: ILD picture
o Biopsy (preferably from peripheral sites like palpable LN, cutaneous lesions; if not then
bronch/mediastinal LN biopsy): Histology for granuloma
• Treatment: Most patients with asymp/non progressive sarcoid do not need rx. Immunosuppresion. Steroid
mainstay. Others: MTX, Hydroxychloroquine
• Lofgren’s Syndrome: Acute EN, bilat hilar lymphadenopathy, polyarthritis/arthralgia

Retinitis Pigmentosa
• Inheritance: AD most common. But patterns variable
• Clinical Features:
o Peripheral vision and night vision first affected, family history
o Associated features: Hearing, unsteadiness (cerebellar)
• Fundoscopy Findings: 1) Bone spicules 2) Arteriolar attenuation 3) Optic disc pallor
• Associated Syndromes
o Kearns-Sayre (mitochondrial): CPEO, deafness, heart block
o Usher (AR): Deafness
o Refsum (AR): Deafness, cerebellum, peripheral neuropathy, cardiomyopathy
o Lawrence-moon-bardet-biedl (AR): Deafness, learning disability, short stature, hypogonadism, renal
disease, DM, polydactyly
• Treatment: Supportive, genetic counseling

Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu)

• General: AD disorder, Onset often begins in childhood
• Clinical Features: Epistaxis, mucocutaneous telangiectasia, visceral involvement (pulmonary/hepatic – hepatic
bruit! /CNS AVMs)
• Diagnosis: Consensus Criteria (Curacao Diagnostic Criteria)
o Spontaneous and recurrent epistaxis
o Multiple mucocutaneous telangiectasia at characteristic sites
o Visceral involvement (GI, pulmonary, cerebral, hepatic)
o First degree relative with HHT
• Complications: Heart failure, portal HTN, abscesses
 • Treatment:
o Non-pharm: Humidification, local ointments
o Pharmacological: Tamoxifen, tanexemic acid, bevacizumab
o Address iron deficiency anemia - Transfusion
o Interventional therapy/surgery: Organ targeted

Idiopathic Thrombocytopenic Purpura

• Symptoms: Bleeding from various sites (must exclude serious bleeds – ICH, BGIT)
• Etiology: Primary vs Secondary (HIV/Hep B/C, CTD, haematological malignancies)
• Investigations: FBC (thrombocytopenia), PBF (excluded other pathologies), Secondary work up (Hep B/C screen,
ANA)
• Treatment:
o Non-Pharmacological: Avoid trauma, avoid drugs that interfere with plt function
o Pharmacological (depends on severity): Transfusion (threatening bleed), Steroids, immunomodulators,
tranexemic acid, IVIG
o Surgical: Splenectomy

Von Willebrand’s Disease

• Symptoms: Bleeding
• Genetics: Mainly AD (can be AR also) – Family history
• Investigations: Prolonged aPTT, slightly reduced factor VIII, vWF antigen and activity (ristocetin cofactor activity)
• Treatment: Tranexemic acid, DDAVP (promotes release of vWF), factor VIII/vWF concentrate

Haemophilia
• Symptoms: Bleeding
• Genetics: X-linked
• Investigations: Prolonged aPTT, factor VIII/IX deficiency, correction with mixing study
• Treatment:
o Non-Pharmacological: Avoid contact sports/motorbike riding, genetic counseling, avoid IM injections
o Pharmacological: Tranexemic acid, DDAVP, Factor replacement

Multiple Myeloma
• Clinical Features
o CRAB: Hypercalcemia, Renal Impairment, Anemia, Bony Disease
o Others: Hyperviscosity, immunodeficiency
• Investigations:
o Diagnostic: Serum and urine electrophoresis for monoclonal bands, bone marrow aspiration biopsy
o Supportive: PBF for rouleau, urine for bence jones protein
o Complications: Adjusted calcium, renal panel, FBC, Xrays/bone scans
• Treatment
o Underlying: Chemo, HSCT
o Complications: Hypercalcemia (hydrate, steroids, bisphosphonates, calcitonin), anemia (transfusion)

Renal Tubular Acidosis

Type 1:
• Problem with distal H+ secretion
• Worse in these sense that serum is more acidic and urine more alkalemic (cos the problem is right at the end
hence little room for remediation)
• Associated with AUTOIMMUNE DISORERS (Sjogren’s, RA), Drugs (Lithium)
Type 2:
• Problem with proximal HCO3 reclamation
• Associated with
o Monoclonal gammopathies (like myeloma), Drugs (tenofovir, CAI)
o Other losses (FANCONI): Lose amino acid, phosphate, uric acid, glucose in the urine
Investigations
• Urea/electrolytes/creat
• Urinary pH - >5.5 in Type 1, variable for Type 2
• Sodium bicarbonate load – urinary pH rises for Type 2 once bicarb resorptive capacity is exceeded
• Etiological evaluation

Chronic Ethanol Ingestion

• Liver Disease
 • Neurological Disease: Cerebellar dysfunction, peripheral neuropathy, wernicke’s encephalopathy (ataxia,
confusion, opthalmoplegia), korsakoff psychosis (retrograde and anterograde amnesia, confabulation), delirium
tremens
• Gastro: Peptic ulcer disease, pancreatitis, malnutrition
• Anemia
• Alcoholic cardiomyopathy
• Psycho-social: Mood, cognition, social support and set-up

HIV
https://flowvella.com/s/2tye/68D26E82-E56B-45F8-95B4-2233E72680CA
• AIDS Defining
o CD4< 200 OR
o Fungal: candidiasis, coccidioidomycosis, cryptococcosis, histoplasmosis, isosporiasis, PCP
o Viral: CMV, HSV
o Parasite: toxoplasmosis, cryptosporidiosis
o Neoplasm: invasive cervical ca, kaposi’s sarcoma, lymphoma
o Bacterial: MAC, TB, salmonella septicemia (non-typhoidal)
o Others: encephalopathy, recurrent pneumonia, progressive multifocal leukoencephalopathy, wasting
syndrome
• Systems: CNS (toxoplasmosis, cryptococcal), GI (ulcers, odynophagia, diarrhea), Respi (cough, SOB), Rash
• Treatment
o Principles: Counseling (notification implications), Treat HIV, Treat OI, OI Prophylaxis
o Highly Active Anti Retroviral Therapy (HAART) comprising 2 NRTI (tenofovir, lamivudine) + 1 PI or 1
NNRTI (efavirenz)
o OI Prophylaxis
§ CD4<200: PCP prophylaxis –Bactrim, Dapsone, Neb pentamidine, atovaquone
§ CD4<100: toxoplasmosis prophylaxis –Bactrim
§ CD4<50: MAC –Azithromycin
o Refer to HIV notes for OI dx and treatment

Acute Rheumatic Fever

• Non suppurative sequel of group A strep – 2-4 weeks after infection
• Clinical Features
o Joint: Migratory arthritis
o Carditis: Valvulitis commonest, others included pan/peri/epi/myocardiits
o Nodules
o Erythema Marginatum: Erythematous rash with pale centers and rounded margins
o Sydenham Chorea
• Most common sequel of ARF is Rheumatic Heart Disease – 10-20 years after original illness

Neurofibromatosis
• Genetics: AD inheritance, NF1 (Chr 17), NF2 (Chr 22)
• Clinical Features:
o NF1: (FIBROMA) Fibroma, Iris harmatomas, Bony lesions, Relative, Optic glioma, Macules, Axillary
Freckling
o NF2: Acoustic neuroma (check hearing important!), other tumours (neurofibroma, meningioma,
glioma, schwanoma)
• Physical Examination: Inspection, radioradial delay, eyes, hearing, axilla, abdomen (scars from pheo surgery)
inspect long bones
• Management: Genetic counseling, analgesia, surgery for compressive lesions
• Hypertension: Pheochromocytoma, renal artery stenosis, coarctation of aorta

Tuberous Sclerosis
• Genetics: AD
• Clinical Features
o Face: Adenoma sebaceum (papular lesions)
o Body: Ash leaf macule, shagreen pataches, café-au-lait spots
o Tumours: Angiomyolipomas (kidneys), lymphangiomyomatosis (lungs), periorbital/retinal harmatomas
(eyes), rhabdomyoma (heart)
o A/w seizures (tuberous masses in cerebral cortex)
• Management: Genetic counseling, treat epilepsy
Sturge Weber
• Genetics: Not clearly demonstrated
• Clinical Features: Ipsilateral port wine stain (V1), ipsilateral vascular abnormalities (leptomeningeal angioma),
contralateral neurological manifestations (hemiparesis, seizures)
• Invx: Skull XR (Tram track), CT/MRI Brain (Leptomeningeal angioma)
• Management: Treat epilepsy

Acute Intermittent Porphyria

• Genetics: AD, low penetrance
• Triggers: Medications, smoking, sex hormones, reduced caloric intake, stress
• Clinical Features
o Neurology: Extremity weakness and pain
o Gastro: Abdominal pain, vomiting, constipation
• Investigations
o Main test: Urinary porphobilinogen
o Second line: Urinary ALA, PBG, porphyrins, plasma, stool porphyrins
o Confirmatory: Decrease erythrocyte PBG deaminase, genetic testing
• Management: IV hemin, analgesia, avoid triggers

Osteogenesis Imperfecta
• Genetics: Most commonly autosomal dominant
• Clinical features
o Multiple, minimally or atraumatic fractures
o Others: Short stature, scoliosis, blue sclerae, hearing loss, opalescent teeth, skin and ligamentous laxity,
easy bruisability
• Ddx: Rickets/Osteomalacia
• Investigations: Skin biopsy (analysis of type I collagen genes), genetic testing

Von Hippel Lindau

• Genetics: AD
• Associated Cancers:
o PACES Relevant: Pheochromocytoma, Clear Cell RCC, Neuroendocrine Tumours of Pancreas
o Others: Retinal hemangioblastomas, papillary cystadenomas of epididymis/broad ligament, middle ear
endolymphatic sac tumours
• Management: Genetic counseling, guideline based surveillance screening, surgery

Peutz-Jeghers Syndrome
• Genetics: AD – STK 11 gene
• Clinical Features: Multiple hamartomatous polyps, mucocutaneous pigmentation (lips, perioral, buccal mucosa,
palms, soles), increased risk of GI (colon, pancreas) /non-GI (breast) cancer
• Investigations: Genetic testing

Carcinoid
• Causes: Usually small bowel neuroendocrine tumours; but can be gastric and lung too. Usually by the time
carcinoid syndrome presents, there is liver metastases; symptoms are due to secretion of hormonal products like
serotonin/prostaglandin/histamine
• Clinical Features: Flushing, diarrhea, bronchospasm, right sided cardiac valve disease
• Invx: 24H urinary collection of 5-HIAA (hydroxyindoleacetic acid), diagnostic imaging (with radiolabeled
somatostatin analogs)
• Mangement: Treatment of underlying cancer in consult with oncologist, somatostatin analogues like octreotide
for cardinoid syndrome

Hereditary Angioedema
• Due to deficiency or dysfunction of C1 inhibitor, AD inheritance – swelling is bradykinin mediated
• Clinical Features: Recurrent episodes of angioedema (skin, bowel, upper airway) w/o hives or pruritus, no
response to antihistamine therapy
• Triggers: Trauma, dental work, ace-I, stress, menstruation
• Invx: C4 (low), C1NH protein level and function, genetic testing
• Management
o Acute: C1INH concentrate or bradykin B2 receptor antagonist (Icatibant)
o Long term: Can give C1INH injectables
COMMUNICATIONS
Ethical Principles
• ABCDJ, Professionalism, Right to information
• Autonomy
o Individuals have a right to self-determination free from coercion or coaxing
o Principles for making decision for someone who lacks capacity:
§ Every patient has capacity until proven otherwise
§ Unwise decision does not mean lack of capacity
§ Any decision made for patient who lacks capacity must be in best interest
§ Formal assessment of mental capacity can only be done by practitioners who have
undergone training and whose names are registered with the Office of Public Guardian
• Beneficence: Promoting what’s best for the patient
• Confidentiality: Trust between doctor and patient
• Do no harm/ non-maleficence: Balance risk of harm against benefit
• Equitable care/ Justice: Resources are limited. Fair allocation of resources
• Professionalism
• Patients have a right to information about their condition and treatment options available
• Negligence: Duty of care, breach of duty, harm as a result of breach
o Bolam Test (applicable for diagnosis and treatment): a doctor is not negligent if the act is supported by
other respected doctors, as long as those doctors’ opinion is internally consistent and logical.
o Montgomery Test (for advice): 3 stages
§ 1) Relevant and material info withheld from patient?
§ 2) Was the doctor in possession of the information? –if not in possession, use Bolam’s test to
determine if doctor was negligent in diagnosis/ investigations
§ 3) Was the doctor justified in withholding the info from patient?

Breaking Bad News

• Setting: Greet, confirm patient, request if would like anyone else around
• Perception: Find out understanding of test, were there specific concerns/ideas/expectations
• Invite: Warning shots – unfortunately I do not have good news… one of your tests actually returned abnormal…
are you alright with me proceeding to tell you about it? …
• Knowledge: Provide information in jargon free fashion. Diagnosis, further tests, treatment, prognosis. Pay
attention to patient’s reaction, if they appear in shock, pause and identify emotion/difficulty of situation, slow
pace and allow patient space and time.
• Empathy: Empathic statements/responses as appropriate
• Summary/Strategise/Send off: Summarise what has been discussed, express recognition of difficulties for
patient, lay out follow up plans/referrals, enquire if anyone is accompanying patient back
• Scenarios: Cancer, other serious medical conditions, sudden death of a relative
• Content
o For sudden death, must remember to mention coroner’s case; but does not = post mortem

HIV
• SPIKES – But do not ask if anyone else wanted around
• Find out context of testing
• Ascertain risk factors: Blood transfusions, tattoos, IVDA, sexual practices
• HIV vs AIDs – Relay concept of compromised immune system predisposing to serious infections
• Focus on treatability of disease
• Obligation to tell partner, reportable disease – focus on the importance of partner getting diagnosed early so
that treatment can be initiated, offer to aid with the conversation
• Avoidance of intercourse (will need to inform potential partners)
• ROWID
o Risk factors – As above
o Offspring
o Work – If medical profession/CSW, may be unable to continue
o Insurance – Will have to speak to insurance company
o Driving – Nil issues
• Treatment
 o Avoid (live vaccines, raw food, untreated water)
o Start rx when CD4 <500, or AIDS defining illness
• Side effects of treatment
o Nucleoside reverse transcriptase inhibitors [eg. Zidovudine, Stavudine, Didanosine, Abacavir]- Weight
loss, N/V, hepatotoxicity with RUQ pain, abdominal bloating, peripheral neuropathy, (abacavir) drug
sensitivity for first 6/52 i.e. fever, rash, myalgia
o Non nucleoside reverse transcriptase inhibitors [eg. Efavirenz, Nevirapine] - hepatotoxicity,
hypersensitivity, (efavirenz- dizziness, nightmares, depression)
o Protease inhibitors eg. Indinavir, Ritonavir, Darunavir-GI effects, hyperlipidemia, HTN
• HIV and Pregnancy
o Teratogenic drugs like Efavirenz: So need to use contraception when on that drug
o Small chance of preterm delivery and IUGR especially with use of protease inhibitors
o Risks of transmission: 20% if not on medication, 1% if taking 3-drug combination (independent of CD4
count)
o Non-detectable viral load can still be transmitted to foetus
o Preventing transmission
§ Must attain a stable and sustainable viral load prior to conception
§ C-section
§ Baby should receive post-exposure prophylaxis x 6 weeks (Zidovudine)
§ Cannot breastfeed after birth
• Common Questions
o What if I don’t inform my wife?
§ Focus on wife’s wellbeing – risk to her, treatability
§ Also may have implications on children – if she was HIV +, possibility for transmission
§ Explain that HIV is a notifiable disease, contact tracing would be carried out by MOH. Hence
would be better for wife to hear from patient himself.
o Does that mean I cannot have sex anymore?
§ Legal to inform any sexual partner if HIV positive
§ To use barrier protection, but risk remains
• Principles: Confidentiality vs public good

Genetic Counseling
• SPIKES
• Find out purpose behind desire for genetic testing
• Find out about symptoms, family tree
• Explanation
o Involvement of other family members – most effective and accurate outcomes
§ If mutation known, can test specifically
§ Broad based testing has problems of – increase cost, variants of unknown significance (VUS)
o Limitations
§ False positives/negatives, indeterminate results
§ + test does not equate to definite disease, nor prediction of disease onset/progression
o Implications
§ To self: Anxiety, insurance
§ To offspring: Likelihood of acquiring disease, preimplantation genetics
§ To family members
• Take time to decide on whether to proceed with testing
• Refer to genetics team/geneticist
• Common Questions
o Am I obliged to tell my family? No. But as there may be implications, encourage to tell.
• Content
o AD: Neuro (MD, FSHD, Huntington’s Disease, Spinocerebellar Ataxia), Neurocut (NF1/2, Tuberous
Sclerosis), Cancer (VHL, MEN1/2, Peutz Jegher, BRCA, FAP, HNPCC), Others (APKD, Marfan’s, HHT,
HOCM, Acute Intermittent Porphyria – but low penetrance)
o AR: Neuro (Friedrich’s Ataxia, Ataxia Telangiectasia, Wilson’s Disease, Haemochromatosis), Others
(Cystic fibrosis, Beta Thalassemia)
o X-Linked: Neuro (DMD, BMD), Others (Haemophilia)
o Variable: Neuro (Hereditary Spastic Paraparesis, HSMN (AD most common)), Others (Osteogenesis
imperfect (AD most common), Retinitis Pigmentosa (AD most common))

Brain death and Organ Donation

• SPIKES
 • Explain brainstem death – the point that the patient is actually dead has to be conveyed in no uncertain terms
• Can attempt attempt to transit to organ donation by enquiring about patient’s nature, and whether he was
someone who liked to help others
• Explain process: Organs will be removed by a competent surgical team, will be closed up in a dignified manner,
body returned to the family
• Content
o HOTA: Cornea/Heart/Liver/Kidneys, opt out scheme applying to all Singaporeans 21yo and above
o MTERA: Opt in system to pledge any organ for treatment, education, research by anyone at 18yo and
above or family members of deceased
o Brainstem death: Certified by 2 doctors not involved in care of patient nor in the transplant
proceedings

EOL matters: DNR, care withdrawal, PEG/tube feeding

• SPIKES – Seek perception and understanding of condition
• Care decisions ultimately based upon collective assessment of medical status, functional status, patient’s wishes,
family’s wishes
• Explain about patient’s condition – possible impending demise, irreversibility of condition
• Focus on goals of care (tying in with patient’s expressed/surrogate wishes with patient’s current medical status
and anticipated disease trajectory) – Link specific interventions to these goals (whether they are in keeping or
not)
• Explain that the focus of the discussion is not about withdrawing treatment, but instead effecting the
appropriate treatment that would serve the patient’s best interest in this juncture
• Reiterate that you will be walking alongside this journey with the patient and the family
• Specific Questions
o Feeding/IV fluids: Patients in this state often do not perceive thirst or hunger, just like how when
you’re having a very bad flu, you generally won’t have the desire to eat, likewise the patient is going to
feel the same
o Starve to death?: Loss of appetite is part of the underlying disease trajectory. While the lack of
nutrition does contribute to the process of death, it is unlikely that the will experience hunger. We will
be monitoring closely for symptoms and signs of hunger, and comfort feeding can always be initiated.
o Conflict wrt DNR: Your views are definitely valued and heard. However, as the doctor looking after your
dad, I would be unable to provide treatment that I feel would bring more harm than good to him. I am
happy to arrange for a second opinion consult to get a different perspective on this matter. Is that
alright with you?
• If relatives remain insistent on full active care, offer to arrange a discussion with the consultant in charge
• Content
o ACP: Voluntary discussion to find out patient’s EOL/care references, documented to act as a guide if
patient becomes incapacitated, non legally binding
o AMD: Legally binding document against artificial life support in context of terminal illness (certified by 3
docotrs); made at least 21yo, 2 witnesses (one medical practictioner); medical team will need to check
with registrar of advance medical directives if patient is terminally ill and incapacitated to decide
o LPA: Empowerment to a donee to make decisions on behalf when the individual has lost capacity to do
so wrt personal welfare and property & affairs; not applicable to life sustaining or saving treatment

Medical Error/Complication
• SPIKES
• Explain medical error
• Apologise for the occurrence of the error
• Allow patient/relative to vent/rant
• Identify and empathise and validate the reasons for anger, apologise once again for its occurrence, and attempt
to steer conversation to the subsequent management of the patient
• Mitigating measures: Thorough investigation, rectifying measures to patient’s condition, systematic
improvements
• Specific Questions
o Demanding name/details of a colleague: I am sorry that it is not in my capacity to divulge this piece of
information. I recognize that a serious mistake has taken place, and as the medical team looking after
your mum, we collectively take responsibility for what has happened. A thorough investigation will be
carried out to get to the bottom of what happened. We will put you in touch with our patient relations
officers who will follow up with you on this matter.

Communication with Colleague: Misconduct, Poor Performance

• Find out colleague’s perception and understanding of his issues
 • Show concern, find out if there are any difficulties faced by the colleague
• Reflect issues objectively and find out how colleague feels about it
• Strategise to help colleague

Consent Taking
• Explain procedure/treatment
• Explain indication (and implications of not proceeding with treatment)
• Explain alternatives
• Explain risks

Capacity Assessment
• Comprehend
• Retain
• Process and weigh up
• Communicate decision

Explaining a Condition/Diagnosis
• Find out understanding and concerns first!
• Explain disease/diagnosis
• Explain treatment: Non-pharm, pharm, surgery
• Explain monitoring, complications, symptoms to pay attention to
• If relevant, offspring/work/insurance/driving impact
• Provide information about support groups, other relevant resources
Driving
Disorder Group 1 (Class 1, 2, 3 licenses) Group 2 (Class 3, 4 & vocational licenses)
Angina Not fit until angina controlled Not fit until symptom-free, must also
complete exercise stress test
ACS/CABG Not fit for 1 month Not fit for at least 2 months. After must be
symptom-free, must also complete exercise
stress test
Angioplasty Not fit for 1 week Not fit for at least 2 weeks. If stented at least
2 months. Thereafter as above.
Arrhythmia Not fit if arrhythmia liable to cause LOC. Not fit if arrhythmia caused LOC in past 2
Resume only after satisfactory control. years. If not will need to establish no
structural cardiac abnormality, must also
complete exercise stress test
Aortic Aneurysm Fit if BP controlled Unfit. Fit only after repair
Pacemaker Insertion Fit Generally unfit
Provoked Single Seizure free 1 year while off AEDs. No Seizure free 1 year while off AEDs. No
Seizure cerebral abnormality, EEG normal. cerebral abnormality, EEG normal.
Unprovoked/Epilepsy Seizure free for 3 years and off all AEDs at Seizure free for 10 years and off all AEDs. No
least 1 year. No cerebral abnormality, EEG cerebral abnormality, EEG normal
normal
Stroke No deficits – Not fit for 1 month Not fit for 1 year – Must have fully recovered,
If mild deficits, need to go through Driving and go through DARP
Assessment and Rehab Programme (DARP)
after 1 month
TIA Single: Fit if TIA free for 1 month Single: Fit if TIA free for 6 months
Multiple: Fit if TIA free for 6 months Multiple: Fit if TIA free for 1 year
Bleeds/Aneurysms Case by case by neurosurgeon Case by case by neurosurgeon
Unexplained LOC Fit if LOC free for 1 year Fit if LOC free for 1 year

Medication Counseling
• Warfarin
o Indications: AF, thrombo/embolic disease, metallic valve, APS
o Alternatives: DOAC (VTE, AF – not used in metallic valves, APS)
o Frequent monitoring, bleeding risk, dietary/medication impact on coagulation status
o Teratogenicity: Especially during first trimester
o Pregnancy: Can consider switching to heparin
• TB Medication
o 6month regimen (4 for 2 months and 2 for 4 months à RH). DOTS short course.
§ 2 months of: Rifampicin, Isoniazid, Pyrizinamide, Ethambutol
 § 4 months of: Rifampicin, Isoniazid
o Latent TB: Isoniazid for 6months
Rifampicin • Hepatotoxicity
• Thrombocytopenia
• Red-orange discoloration of urine, tears, sweat, stools
Isoniazid • Hepatotoxicity
• Polyneuropathy at high dosages hence prescribe pyridoxine vitamin B6
Pyrazinamide • Hepatotoxicity
• Gouty flaresà reduces renal excretion of Urate
Ethambutol • Dose related optic retrobulbar neuritis
• Methotrexate
o Usually dosed 1-2x/week, with folic acid
o Common Side Effects
§ Mouth ulcers
§ GI symptoms, headaches
§ Hair loss
§ ILD, pneumonitis
§ Bone marrow suppression: Infections, thrombocytopenia (bleeding risk), anemia
§ Liver impairment
o Not recommended for pregnancy or breast feeding
o Medication that can increase MTX toxicity: Bactrim, tetracycline
• Cyclophosphamide
o Infection: issues of reactivation of latent infections, and BM suppression
§ Screen for TB, Hep B, Hep C, HIV prior to starting
§ Stop other immunosuppressants, tail down steroids
§ Prophylaxis against PCP
o Hemorrhagic cystitis: Oral mesna before and after each infusion
o Infertility: Sperm banking
o Malignancy: LT surveillance for malignancy of all forms. Risk dependent on cumulative doses
o Nausea, vomiting, reversible alopecia, teratogenicity
MEMORY LIST
Interstitial Lung Disease
• Causes
o Idiopathic
o Autoimmune/Rheum: Scleroderma, DM/PM, Ank Spond, SLE, Sarcoidosis
o Iatrogenic: Drugs (Amiodarone, MTX, azathioprine), Radiotherapy
o Occupational
o Congenital: NF, tuberous sclerosis
• Location
o Apical
§ Ankylosing Spondylitis, ABPA
§ Most occupational exposures (Silicosis, Pneumoconiosis) except Asbestosis
§ TB
§ RT
o Basal
§ Most autoimmune conditions (except ank spond)
§ Asbestosis
§ Drug
• Investigations
o CXR: Reticular-nodular shadowing, honey combing (advanced)
o HRCT: Reticular abnormalities, ground glass changes, honey combing, volume loss
o PFT: Restrictive picture (reduced TLC and VC, preserved FEV1/FVC - >80%) and impaired gas exchange
(reduced transfer factor)

Bronchiectasis
• Focal
o Extra luminal: Enlarged LN
o Luminal: Mitotic lesions
o Intra luminal: FB, broncholith
• Diffused
o Post Infective: TB, bronchiolitis obliterans, ABPA
o Autoimmune: SLE, RA, Sjogren’s
o Congenital: Kartegener’s, Cystic Fibrosis
o Others: Yellow nail syndrome
• Investigations
o CXR: Ring shadows, dilated thickened airways, tram lines
o HRCT: Signet ring sign, dilated airway lumen
o PFT: Obstructive picture (FEV1/FVC<70%), degree of reversibility

Glomerulonephritis
• Primary
• Secondary
o DM/HTN
o Infection: Post Strep, IgA Nephropathy, Hep B/C, HIV
o Inflammatory: SLE, Scleroderma, Vasculitis (Wegeners, PAN), Amyloid
o Neoplastic: Multiple Myeloma, membranous nephropathy may be associated with malignancy

Erythema Nodosum
• Idiopathic
• Infection: TB, streptococcal, mycoplasma
• Inflammatory: IBD, Behcet’s, Sarcoid
• Neoplastic: NHL, pancreatic, carcinoid
• Endocrine: Pregnancy
• Metabolic
• Drugs: OCP
Pyoderma Gangrenosum
• Inflammatory: IBD (UC>Crohn’s), RA
• Neoplastic: Haematological malignancies

Raynaud’s Phenomenon
Ddx erythromelalgia (PRV/ET, small fiber neuropathy, hypercholesterolemia, verapamil/nifedipine), acrocyanosis
• Idiopathic
• Infection: Hep B, C
• Inflammatory: Scleroderma, RA, SLE, Vasculitis, Beurgers – Ask SMOKING!
• Neoplastic: Paraproteinemia, cryoglobinemia
• Endocrine: Hypothyroidism
• Metabolic: Artherosclerosis
• Drugs: ABBCCC
o Interferon alpha
o Betablockers, Bromocriptine
o Contraceptive pill, Chemo (cisplastin, bleomycin), Ciclosporin

Cushing’s: IM MEAN
● Infection
● Metabolic: DM, Lipids, Osteoporosis
● Muscle/Myopathy
● Eyes: Cataract
● Appearance: Truncal obesity, skin thinning, easy bruisability, striae
● Neurology: Mood/neuropsych symps

Mononeuritis Multiplex: WARDS PLCC

● Wegeners
● Amyloidosis
● RA
● DM
● Sarcoidosis
● PAN
● Leprosy
● Churg strauss
● Carcinomatosis

Myopathy (MCREND)
• Metabolic: Periodic paralysis, osteomalacia
• Congenital: DMD, BMD
• Rheum: DM, PM, SLE
• Endocrine: Cushing’s, hypo/hyperthyroid, acromegaly
• Neoplasm: Paraneoplastic
• Drugs: Statins, steroids, colchicine

Carpal Tunnel Syndrome: THAD RRAP

● Trauma: fracture, vibration
● Hypothyroidism
● Acromegaly
● DM
● RA
● Renal failure
● Amyloidosis
● Pregnancy

Peripheral Neuropathy
 ● Alcohol, AIDP
● B12 deficiency
● Cancer, CKD
● DM
● Drugs: TB drugs,cardiac, anitbiotics
● Environment: lead, porphyria
● Familial: HSMN
● GBS/ CIDP
● Hypothyroid
● Infections: HIV, Lyme
● J: Sjogrens

Antibodies
● Scleroderma
○ ANA: Sensitive
○ Anti Centromere: Limited scleroderma, pulmonary HTN
○ Anti Topoisomerase: Diffused scleroderma, ILD
○ Anti RNA polymerase III: Renal Crisis, Cancer
● Dermatomyositis/Polymyositis
○ ANA: ? Sensitive
○ Myositis Associated Antibodies (MSAs)
■ Antisynthetase Ab (e.g. Anti Jo1) - A/w antisynthetase syndrome (Myopathy, ILD, mechanics
hands, non erosive arthritis), worse LT prognosis
○ DM specific Abs
■ E.g. Anti Mi 2: More severe rash, decrease malignancy risk
● SLE
○ ANA, Anti ds DNA (for disease activity), Anti Smith (Sm) Antibody, DCT, Complement, anti phospholipid
antibody (lupus anticoagulant, anticardiolipin antibody, anti beta2 glycoprotein 1 antibody)
● Rheumatoid Arthritis
○ Rheumatoid Factor
○ Anti cyclic citrulinated peptide antibody
● PBC: Antimitochondrial Antibody, ANA can be raised too
● PSC: ANCA - non diagnostic (Cholangiography to demonstrate bile duct thickening with segmental dilations and
strictures in bile ducts is gold standard)
● Autoimmune Hepatitis: ANA, Anti-smooth muscle antibody, anti-liver kidney microsomal antibody (ALKM-1),
soluble liver antigen