IM2-CS-sec

Collection from previous batches, made by Abdulmalik Abdulghani, Dania AbuObaid, Faisal Alkharji, Haneen H. Alsultan, Husna Merza, Lina Serhan, Maha Alasmari, Mujahid N Al-muhaydib, Yousef Edress

اللهم يا معلّم موسى علّمني، ويا مفهم سليمان فهّمني، ويا مؤتي لقمان الحكمة وفصل الخطاب آتني الحكمة وفصل الخطاب اللهم اجعل ألستنا عامرة بذكرك، وقلوبنا بخشيتك، وأسرارنا بطاعتك، إنك على كل شيء قدير، حسبنا الله ونعم الوكيل

Any updates of this file would be within https://medatlax.com/Clinical/Level-12/IM-2/Internal-Medicine-2 OSCE & OSPE-CS link.

Contents

• Cardiovascular Disease — ischaemic heart disease · ACS · heart failure

  • Ischaemic Heart Diseases-2 — chronic stable angina · MI and its complications
  • ACS — STEMI · NSTEMI · unstable angina
  • Heart Failure-3 — chronic heart failure · acute pulmonary oedema

• Respiratory Disease (Pulmonology) — asthma

  • Asthma-2 — chronic asthma · acute severe exacerbation

• Gastroenterology and Hepatology — hepatitis · liver cancer · hepatomegaly

• Nephrology and Fluid/Electrolytes — CKD · dialysis · nephrotic syndrome

• Hematology and Oncology — sickle cell · thalassaemia · pancytopenia · lymphoma

• Rheumatology and Connective Tissue Diseases — SLE

• Neurology — stroke

  • Stroke-2 — ischaemic · intracerebral haemorrhage · SAH · subdural · CVST

• Cardiovascular Disease — cardiomyopathy · congenital · hypertension · endocarditis

  • Cardiomyopathies — dilated · hypertrophic · restrictive
  • CHD — VSD · ASD · PDA · coarctation · bicuspid valve · Eisenmenger
  • Hypertension-2 — chronic · hypertensive crisis
  • Infective Endocarditis-2 — native/prosthetic valve · acute/subacute

• Respiratory Disease — sarcoidosis · ILD · ARDS · pneumonia · COPD

  • Sarcoidosis-2 — Löfgren/Heerfordt · chronic pulmonary
  • ILD — IPF/UIP · hypersensitivity pneumonitis · silicosis · asbestosis
  • ARDS
  • Pneumonia-2 — community-acquired · hospital-acquired
  • COPD — stable · acute exacerbation

• Gastroenterology and Hepatology — GI bleeding · jaundice

  • Gastrointestinal Bleeding-2 — upper · lower
  • Jaundice-2 — prehepatic · hepatic · post-hepatic

• Nephrology and Fluid/Electrolytes — electrolyte imbalance

  • Electrolyte imbalance — Na⁺ · K⁺ · Ca²⁺

• Endocrinology and Metabolism — dyslipidaemia

  • Dyslipidemia-2 — familial hypercholesterolaemia · hypertriglyceridaemia

• Rheumatology — dermatomyositis · vasculitis

  • Dermatomyositis
  • Vasculitis — GCA · Takayasu · Kawasaki · Buerger · PAN · GPA · MPA · EGPA · HSP · Behçet · cryoglobulinaemia

• Neurology — Parkinson disease · paraplegia

  • Parkinsons disease
  • Paraplegia — compressive · intramedullary · systemic causes

• Infectious Diseases — amoebiasis · hydatid · kala-azar

  • PARASITIC INFECTIONS — amoebic colitis/abscess · hydatid disease
  • Visceral Leishmaniasis

Cardiovascular Disease

Ischemic Heart Diseases-2

A. Chronic stable angina

Scenario. Adult with exertional substernal chest pain relieved by rest or GTN, reproducible at a predictable workload, with stable observations and clear lungs — reversible myocardial ischaemia.

History — what will you ask?

• SOCRATES; pain relieved within minutes by rest or nitrate
• Risk factors — smoking, diabetes, dyslipidaemia, hypertension, family history
• No pain at rest; no crescendo pattern

Signs — what will you find?

• Usually normal between attacks
• May show LVH, S4 or a murmur of aortic stenosis
• Signs of peripheral vascular disease

Investigations — what will you order?

• ECG (often normal); exercise stress test; stress echo or myocardial perfusion scan
• CT/coronary angiography to define anatomy
• CBC, lipids, glucose, renal function

DDx — what else could it be?

• Aortic stenosis
• Anaemia
• Thyrotoxicosis
• Oesophageal spasm
• Musculoskeletal pain

Management — what will you do?

• Antiplatelet, high-dose statin, beta-blocker, nitrate, ACEI; control risk factors
• Revascularisation (PCI or CABG) for refractory symptoms or high-risk anatomy
• Secondary prevention — aspirin indefinitely after CAD

B. Myocardial infarction and its complications

Scenario. Adult with sudden persistent complete cessation of coronary flow from thrombosis on plaque: severe central chest pain lasting hours, at rest, not relieved by nitrate, with sweating and impending doom. Site: LAD anterior, circumflex lateral, RCA inferior.

History — what will you ask?

• Pain of MI (severe, prolonged, unrelieved); prior angina or MI
• Dyspnoea, palpitations, syncope
• Risk factors and complications

Signs — what will you find?

• Distressed, sweating; pulse and BP; S3, new murmur
• Basal crackles, raised JVP, muffled sounds, pericardial rub
• Signs of shock

Investigations — what will you order?

• ECG — ST elevation (LAD anterior, circumflex lateral, RCA inferior), T-wave change, ST depression
• Troponin/CK; echo; coronary angiography
• CXR, CBC, renal function, electrolytes, lipids, glucose

DDx — what else could it be?

• Angina
• Pericarditis
• Aortic dissection
• PE
• Pneumothorax
• Peptic ulcer
• Cholecystitis

Management — what will you do?

• Pre-hospital — oxygen, morphine, lidocaine for ventricular arrhythmia, atropine for block
• CCU: MONA/TASS, aspirin, dual antiplatelet + heparin, statin, beta-blocker, ACEI; reperfusion by thrombolysis or PCI
• Complications (ACT RAPID) — arrhythmia, congestive HF, tamponade/thromboembolism, rupture (ventricle, septum, papillary muscle), aneurysm, pericarditis, infection, death/Dressler

ACS

A. ST-elevation MI (STEMI)

Scenario. Adult with 20 minutes to hours of crushing central chest pain radiating to the arm, not relieved by rest or sublingual nitrate; ECG shows ST elevation with reciprocal change and troponin rises.

History — what will you ask?

• Pain — site, radiation, severity, duration, no relief with nitrate
• Sweating, nausea, dyspnoea, syncope
• Risk factors and pack-years; previous angina or PCI
• Painless MI in the elderly, diabetics, anaesthetised and transplanted hearts

Signs — what will you find?

• Distressed, pale, sweating; pulse and BP (hypotension = high risk)
• S3, new systolic murmur, basal crackles
• Signs of shock — cool clammy peripheries

Investigations — what will you order?

• 12-lead ECG immediately — ST elevation, localises the artery (LAD anterior, circumflex lateral, RCA inferior)
• Troponin; CXR; echo (EF, wall motion, complications)
• Coronary angiography — c-shaped narrowing, stent

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Pericarditis
• Aortic dissection
• Pulmonary embolism
• Pneumothorax
• Oesophageal spasm

Management — what will you do?

• ABC, MONA (no oxygen if saturation ≥94%), two IV lines, aspirin 300 mg loading then indefinitely
• Immediate reperfusion — primary PCI is the gold standard; fibrinolysis if PCI unavailable
• Dual antiplatelet + heparin, high-dose statin, beta-blocker, ACEI, nitrate, analgesia, stool softener
• Treat arrhythmia, shock, rupture; PCI/stent or CABG

B. NSTEMI

Scenario. Adult with the same ischaemic pain but ECG shows ST depression and cardiac enzymes are positive — subendocardial infarction, not for thrombolysis.

History — what will you ask?

• Same pain history; crescendo pattern, pain at rest
• Dyspnoea, palpitations, dizziness

Signs — what will you find?

• Same as STEMI — no ST elevation
• Signs of HF or mitral regurgitation if complicated

Investigations — what will you order?

• ECG — ST depression, T-wave inversion
• Troponin positive
• Echo, CXR, angiography for risk stratification

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Unstable angina (enzymes negative)
• STEMI
• Pericarditis
• PE

Management — what will you do?

• No thrombolysis
• Antiplatelet + anticoagulant, statin, beta-blocker, ACEI, nitrates
• Early invasive strategy — angiography and PCI/CABG according to risk

C. Unstable angina

Scenario. Adult with angina that is new, accelerating or occurs at rest; ECG changes are present but cardiac enzymes remain negative.

History — what will you ask?

• Pain at rest or with minimal exertion; new-onset severe angina
• Prior stable angina that changed in frequency or threshold

Signs — what will you find?

• Often normal between attacks; may show HF or new murmur

Investigations — what will you order?

• ECG — ST depression or T-wave inversion during pain
• Troponin negative (distinguishes it from NSTEMI)
• Angiography

DDx — what else could it be? (standard differential; the note gives no list of its own)

• NSTEMI
• Stable angina
• Oesophageal spasm
• Musculoskeletal pain

Management — what will you do?

• Antiplatelet + anticoagulant, statin, beta-blocker, nitrate
• Urgent angiography and revascularisation if high risk

Heart Failure-3

A. Chronic heart failure

Scenario. Adult with ischaemic heart disease, hypertension, valve disease, cardiomyopathy or AF, presenting with progressive exertional dyspnoea → orthopnoea → PND, fatigue and pitting oedema; classified ACC/AHA A–D and NYHA I–IV, decompensated by infection, ischaemia, arrhythmia, anaemia, thyroid disease, NSAIDs or non-adherence.

History — what will you ask?

• Dyspnoea (exertion, orthopnoea, PND, bendopnea), fatigue, ankle swelling
• Weight gain >2 lb/day or >5 lb/week
• Precipitant screen — infection, chest pain, palpitations, anaemia, thyroid symptoms, NSAIDs
• Adherence to drugs, salt and fluid; smoking and alcohol

Signs — what will you find?

• Raised JVP >8 cm H₂O, hepatojugular reflux
• Bibasilar crackles (may be absent if compensated)
• S3 gallop, displaced PMI
• Hepatomegaly, ascites, sacral and pedal oedema
• Cool mottled extremities in low output

Investigations — what will you order?

• BNP >100 or NT-proBNP >300 (normal excludes HF)
• Echo — LVEF, chamber size, wall motion, valves, diastolic function, RVSP
• ECG (Q waves, LVH, AF, LBBB ≥150 ms = CRT candidate); CXR (cardiomegaly, cephalisation, Kerley B lines, effusions)
• CBC, renal function and electrolytes, LFTs, TSH, iron studies, HbA1c; coronary angiography

DDx — what else could it be?

• Left vs right vs congestive; systolic vs diastolic
• Acute vs chronic vs acute-on-chronic
• Low vs high cardiac output
• Causes — IHD, hypertension, valve disease, cardiomyopathy, arrhythmia, toxins

Management — what will you do?

• General — semi-sitting rest, salt and fluid restriction, small meals, vaccination, stop smoking and alcohol, avoid NSAIDs and verapamil
• Diuretics (furosemide) and nitrates for preload; hydralazine/nitroprusside for afterload; digoxin/dobutamine/milrinone for inotropy
• ACEI/ARB + spironolactone/eplerenone + beta-blocker (bisoprolol, metoprolol); CRT, revascularisation, valve surgery, assist device, transplantation

B. Acute pulmonary oedema

Scenario. Adult with acute severe breathlessness, orthopnoea and basal crackles — fluid flooding the alveoli, most often from decompensated HF, acute MI or arrhythmia.

History — what will you ask?

• Sudden severe dyspnoea, orthopnoea, anxiety
• Chest pain or palpitations (precipitant)
• Known HF, valve disease or hypertension

Signs — what will you find?

• Distressed, sitting upright, sweating
• Tachypnoea, tachycardia, basal crackles, wheeze
• Raised JVP, S3, hypotension in cardiogenic shock

Investigations — what will you order?

• CXR — pulmonary oedema, Kerley B lines, effusions
• ABG — hypoxaemia; BNP; ECG; echo
• Look for the precipitant — MI, arrhythmia, infection

DDx — what else could it be?

• Pneumonia
• ARDS
• PE
• COPD exacerbation
• Anaphylaxis

Management — what will you do?

• Sit up, rest, oxygen; morphine with an antiemetic (anxiety and venodilation) — no longer routine
• Furosemide; nitrates
• Inotropes (dopamine, dobutamine) only for hypotension with poor perfusion — cardiogenic shock or HF with low BP
• Treat the precipitant; ventilatory support if failing

Respiratory Disease (Pulmonology)

Asthma-2

A. Chronic asthma

Scenario. Patient with cough (worse at night), wheeze, breathlessness and chest tightness recurring many times weekly and settling between attacks — reversible airflow obstruction with bronchial hyperresponsiveness.

History — what will you ask?

• Nocturnal cough, wheeze, dyspnoea, chest tightness; frequency and triggers
• Exercise, cold air, allergens, viral infection, workplace
• Atopy (eczema, hay fever), family history, aspirin sensitivity, nasal polyps
• Reliever use per week, night waking, prior ICU or intubation

Signs — what will you find?

• High-pitched wheeze, often absent between attacks
• Nasal polyps, pale nasal mucosa, pharyngeal cobblestoning, atopic dermatitis
• Prolonged expiratory phase if symptomatic

Investigations — what will you order?

• Spirometry — FEV₁/FVC <70%, ↑RV, ↑TLC
• Bronchodilator test — FEV₁ rises >12%; bronchoprovocation — FEV₁ falls ≥20%
• Peak flow for monitoring; CXR only if red flags; HRCT for atypical findings

DDx — what else could it be? (standard differential; the note gives no list of its own)

• COPD
• Cardiac failure
• Vocal cord dysfunction
• Bronchiectasis
• TB
• Anaphylaxis

Management — what will you do?

• GINA steps — 1 as-needed low-dose ICS-formoterol (exercise: 1–2 puffs pre-activity); 2 as-needed ICS-formoterol or low-dose ICS; 3–5 escalate ICS/LABA, LAMA, LTRA
• Severe — biologics (omalizumab IgE 30–700, mepolizumab, reslizumab, benralizumab, dupilumab, tezepelumab)

B. Acute severe asthma exacerbation

Scenario. Known asthmatic deteriorating over hours with inability to complete sentences, accessory muscle use, silent chest and falling peak flow — a medical emergency.

History — what will you ask?

• Speed of deterioration, reliever frequency, steroid use
• Previous ICU admission, intubation or near-fatal attack
• Trigger — viral infection, allergen, poor adherence, NSAIDs

Signs — what will you find?

• Tachypnoea, tachycardia, inability to speak in full sentences
• Accessory muscle use, prolonged expiration, reduced air entry, pulsus paradoxus
• Silent chest, cyanosis, exhaustion, altered consciousness = imminent arrest

Investigations — what will you order?

• Peak flow — <50% predicted severe, 50–70% moderate, >70% mild
• Oxygen saturation; ABG for CO₂ retention
• CXR if pneumothorax or consolidation suspected

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Anaphylaxis
• Pneumothorax
• PE
• Cardiac failure
• Vocal cord dysfunction

Management — what will you do?

• Oxygen; 3 nebulised SABA doses then every 1–4 h; ipratropium 500 µg q8h
• IV methylprednisolone 60–80 mg if not improving; magnesium sulfate 2 g IV once
• Intubate/NIV if exhausted, drowsy, worsening hypercapnia/acidosis or saturation <92%; prednisone 40–60 mg 5–7 days on discharge

Gastroenterology and Hepatology

• Hepatitis — HBV/HCV cause cirrhosis (HBsAg, HCV Ab); autoimmune hepatitis (ANA, ASMA, anti-LKM1, piecemeal necrosis); the hepatic fraction of jaundice; variceal bleeding from hepatitis-related cirrhosis.
• Liver cancer — HCC screening every 6 months with ultrasound + AFP in cirrhosis; cholangiocarcinoma as a post-hepatic jaundice cause; hydatid cyst as a liver-lesion differential.
• Abscess — liver: amoebic abscess with tender hepatomegaly, fever and RUQ pain, brownish-yellow pus aspirated for E. histolytica antigens, drained if large or the patient very sick; lung: a complication of pneumonia and a differential of cavitating TB. Causes of hepatomegaly (requested with nephrotic) — only from the notes used in these tables, each with the mechanism it gives:
• Congestive / right heart failure — hepatomegaly with hepatojugular reflux; also cor pulmonale in COPD and fibrotic ILD → Heart Failure-3 (Section 2).
• Cirrhosis — liver enlarged early, small in late stages, with splenomegaly → Cirrhosis Part 1 (Section 1).
• Amyloidosis from myeloma light chains — Bence-Jones proteins deposit as amyloid → nephrotic syndrome and organ enlargement → Multiple Myeloma (Section 1).
• Leukaemic infiltration — hepatomegaly with splenomegaly and nodes → Acute Lymphoblastic Leukemia, Chronic Lymphocytic Leukemia, Chronic Myeloid Leukemia (Section 1).
• Hepatosplenomegaly of systemic disease — visceral leishmaniasis, sarcoidosis and acromegaly all list it → Visceral Leishmaniasis (Section 3), Sarcoidosis-2 (Section 3), Acromegaly (Section 1).
• Amoebic liver abscess and hydatid cyst — tender hepatomegaly with fever and RUQ pain; smooth-walled cyst with eggshell calcification → PARASITIC INFECTIONS (Section 3).
• Acute and autoimmune hepatitis — hepatomegaly with jaundice → Jaundice-2 (Section 3), Cirrhosis Part 2 (Section 1).

Nephrology and Fluid/Electrolytes

• Chronic renal failure — anaemia of CKD → erythropoietin; normocytic anaemia of chronic disease; hyperkalaemia from reduced excretion; hypocalcaemia (↓vitamin D activation, ↑phosphate); urate nephropathy (“check urea and creatinine in gout”).
• Dialysis — for severe/refractory hyperkalaemia or life-threatening ECG change; hepatorenal syndrome → dialysis and transplant.
• Nephrotic syndrome — myeloma light chains (Bence-Jones) deposit as amyloid → nephrotic syndrome; also a secondary cause of hyperlipidaemia. For hepatomegaly see the list under Gastroenterology and Hepatology.

Hematology and Oncology

• Sickle cell — haemolytic (normocytic) anaemia: sickling test, peripheral smear, Hb electrophoresis; hydroxyurea, folic acid, transfusion/exchange transfusion; also a prehepatic cause of jaundice.
• Thalassaemia — microcytic anaemia → Hb electrophoresis; blood transfusion; the microcytic differential on the anaemia row separates it from iron deficiency.
• Pancytopenia — low reticulocytes point to marrow disease, where bone marrow biopsy is indicated; kala-azar pancytopenia; leukaemic marrow replacement.
• Lymphoma — hilar lymphadenopathy differential (TB vs lymphoma); CLL differential; Waldenström macroglobulinaemia differential; ILD differential.

Rheumatology and Connective Tissue Diseases

• SLE — Libman–Sacks endocarditis (a differential of infective endocarditis); an autoimmune cause of pericarditis; APS/SLE as a persistent thrombotic risk factor for PE; the MCTD overlap includes SLE features; CTD-associated ILD.

Neurology

Stroke-2

A. Ischaemic stroke

Scenario. Adult with sudden focal deficit — face droop, arm weakness, dysarthria — from occlusion of a cerebral artery; non-contrast CT excludes haemorrhage and the penumbra is salvageable for a few hours.

History — what will you ask?

• Last known well time; sudden onset focal deficit
• Risk factors — hypertension, AF, diabetes, smoking; previous TIA
• Symptoms of posterior circulation — vertigo, diplopia, ataxia

Signs — what will you find?

• FAST — face, arm, speech; NIHSS score
• Gaze deviation, hemianopia, neglect; no meningism
• Carotid bruit; AF on pulse

Investigations — what will you order?

• Point-of-care glucose first (hypoglycaemia mimics stroke)
• Non-contrast CT — excludes haemorrhage; early ischaemic change
• CTA head/neck for large-vessel occlusion; MRI-DWI most sensitive
• ECG/cardiac monitoring, echo, carotid imaging; thrombophilia screen if young

DDx — what else could it be?

• Intracerebral haemorrhage
• Hypoglycaemia
• Seizure with Todd’s palsy
• Migraine with aura
• Subdural haematoma

Management — what will you do?

• IV thrombolysis within 4.5 h if BP <185/110 and no contraindications
• Mechanical thrombectomy for anterior large-vessel occlusion up to 24 h in selected patients
• BP — permissive hypertension unless >220/120 (no lysis); <180/105 after lysis; early antiplatelet if no reperfusion

B. Intracerebral haemorrhage

Scenario. Adult with sudden headache, vomiting, reduced consciousness and focal deficit, often hypertensive — spontaneous bleeding into the brain parenchyma; CT shows hyperdense blood.

History — what will you ask?

• Sudden severe headache, vomiting, collapse
• Hypertension; anticoagulants/antiplatelets; cocaine or methamphetamine
• Trauma; known AVM or bleeding disorder

Signs — what will you find?

• Reduced consciousness, hypertension, bradycardia
• Focal deficit; gaze deviation; meningism may be absent
• Papilloedema; brainstem signs in cerebellar haemorrhage

Investigations — what will you order?

• Non-contrast CT — hyperdense haematoma (site, volume, intraventricular extension)
• Coagulation screen, platelets, creatinine; CT angiography if AVM suspected
• GCS and serial neurological observation

DDx — what else could it be?

• Ischaemic stroke
• SAH
• Subdural haematoma
• Tumour with haemorrhage
• Hypoglycaemia

Management — what will you do?

• Intensive BP lowering to limit haematoma expansion (INTERACT3)
• Reverse anticoagulation — warfarin (vitamin K/PCC), DOACs
• Emergent evacuation of cerebellar haemorrhage with brainstem compression or hydrocephalus; supratentorial surgery controversial

C. Subarachnoid haemorrhage

Scenario. Adult with a sudden thunderclap occipital headache — “the worst headache in my life” — often with vomiting, photophobia and neck stiffness; usually a ruptured berry aneurysm.

History — what will you ask?

• Sudden, maximal in seconds, occipital or diffuse
• Nausea, vomiting, photophobia, transient loss of consciousness
• Sentinel headache days earlier; hypertension, smoking, family history of aneurysm

Signs — what will you find?

• Neck stiffness, photophobia, Kernig’s sign
• Reduced consciousness (grade); focal deficit from vasospasm or haematoma
• Fundoscopy — subhyaloid haemorrhage

Investigations — what will you order?

• Non-contrast CT — blood in the subarachnoid space (95% sensitive in the first 24 h)
• Lumbar puncture if CT negative and suspicion remains (xanthochromia)
• MRA/CTA to define the aneurysm; echocardiography if no aneurysm found

DDx — what else could it be?

• Intracerebral haemorrhage
• Meningitis
• Migraine
• Cerebral venous thrombosis
• Pituitary apoplexy

Management — what will you do?

• Control BP and coagulopathy
• Secure the aneurysm — coiling or clipping to prevent re-bleeding
• Nimodipine to prevent vasospasm; hydrocephalus drainage; ICU care

D. Subdural haematoma

Scenario. Elderly patient with headache, fluctuating consciousness and one-sided weakness after minor trauma — blood between the dura and arachnoid, often with delayed presentation.

History — what will you ask?

• Minor head injury days to weeks earlier; may be unwitnessed
• Headache, drowsiness, confusion, fluctuating level of consciousness
• Anticoagulants, alcohol, falls

Signs — what will you find?

• Fluctuating level of consciousness
• Unilateral weakness; dilated pupil if herniation
• Bilateral signs if bilateral haematoma

Investigations — what will you order?

• CT — crescentic extra-axial collection crossing sutures
• Coagulation screen; CT angiography if acute
• Neurological observation

DDx — what else could it be?

• Ischaemic stroke
• Intracerebral haemorrhage
• Extradural haematoma
• Meningioma
• Dementia

Management — what will you do?

• Burr-hole evacuation
• Reverse anticoagulation; observe small asymptomatic collections
• Treat seizures; rehabilitation

E. Cerebral venous sinus thrombosis

Scenario. Young woman on the oral contraceptive, or postpartum, with headache of raised ICP, papilloedema and a sixth nerve palsy, sometimes seizures or focal deficit — venous infarction or haemorrhage may follow.

History — what will you ask?

• Headache of raised ICP; pregnancy/puerperium, OCP
• Dehydration, thrombophilia (protein C/S, antithrombin, factor V Leiden)
• Behçet disease, antiphospholipid syndrome, malignancy
• Seizures, reduced consciousness, focal deficit

Signs — what will you find?

• Papilloedema and 6th cranial nerve palsy
• Focal deficit if venous infarct or haemorrhage
• Signs of the underlying disease (Behçet ulcers, SLE)

Investigations — what will you order?

• MR venography / CT venography — the diagnosis
• CT may show the empty delta sign or venous infarct
• Thrombophilia screen, lupus anticoagulant, antiphospholipid antibodies
• D-dimers; fundoscopy

DDx — what else could it be?

• Arterial ischaemic stroke
• Idiopathic intracranial hypertension
• Meningitis
• Tumour with raised ICP

Management — what will you do?

• Anticoagulation — even in the presence of haemorrhage; response is often dramatic
• Endovascular thrombolysis in severe cases
• Treat the cause; manage raised ICP and seizures

Section 3

The remaining topics.

Section 3 — Cardiovascular Disease

Cardiomyopathies

A. Dilated cardiomyopathy

Scenario. Adult with exertional dyspnoea, orthopnoea, fatigue and bilateral ankle swelling — after alcohol, beriberi/malnutrition, cocaine, Chagas, doxorubicin, peripartum, takotsubo or tachycardia. All chambers dilate and walls thin; ejection fraction falls and systolic failure follows (Starling no longer applies).

History — what will you ask?

• Dyspnoea on exertion → orthopnoea → PND
• Ankle swelling, abdominal fullness, weight gain
• Palpitations (AF), syncope
• Exposure: alcohol, cocaine, chemotherapy, pregnancy, chronic parasitic infection
• Family history of cardiomyopathy or sudden death

Signs — what will you find?

• Raised JVP, tender hepatomegaly, ascites, lower-limb oedema
• Pulmonary oedema, pleural effusion
• Apex shifted left towards the axilla
• S3 gallop; pansystolic murmur of MR/TR
• Irregular pulse if AF

Investigations — what will you order?

• CXR — increased cardiac silhouette
• ECG — AF/flutter, wide QRS, VT
• Echo — dilated lumen, thin walls, low EF, increased compliance, MR/TR with S3
• Exclude the cause: alcohol history, serology, iron/thyroid, pregnancy

DDx — what else could it be?

• Hypertrophic or restrictive cardiomyopathy
• Ischaemic cardiomyopathy
• Valvular regurgitation
• Cor pulmonale

Management — what will you do?

• Treat HF — diuretics for preload, vasodilators/ACEI or ARB (best in Africans), SGLT2 inhibitor, spironolactone, beta-blocker
• Digoxin for contraction; anticoagulate AF; cardiovert arrhythmias, defibrillate VF
• Cardiac transplantation is definitive

B. Hypertrophic cardiomyopathy

Scenario. Young adult with a family history of sudden death, anginal chest pain and exertional syncope. Autosomal dominant; the septum hypertrophies while the cavity shrinks (banana shape), giving diastolic failure plus outflow obstruction — dangerous to vasodilate.

History — what will you ask?

• Anginal pain, exertional dyspnoea, syncope
• Family history of sudden death; Friedreich ataxia association
• Symptoms worse with exercise or dehydration

Signs — what will you find?

• Double apical impulse
• Ejection systolic murmur at the aortic area; pansystolic MR murmur radiating to the axilla (systolic anterior leaflet motion)
• S4 from atrial contraction against a stiff ventricle

Investigations — what will you order?

• Echo — thick wall, small cavity, high EF, reduced compliance, outflow obstruction
• ECG — deep S in V1–V3, tall R in V5–V6, pseudo-Q in II/III/aVF
• CXR — normal heart size
• Post-mortem — myofibrillary disarray

DDx — what else could it be?

• Aortic stenosis
• Hypertensive LVH
• Athlete’s heart
• Amyloid

Management — what will you do?

• Avoid digoxin; beta-blocker or calcium channel blocker
• Keep preload and afterload up — give fluid, avoid dehydration and vasodilators
• ICD if family history of sudden death
• Septal ablation with alcohol or myomectomy; transplant in end-stage disease

C. Restrictive cardiomyopathy

Scenario. Adult with diastolic heart failure and a normal-sized ventricle that cannot relax — cardiac amyloidosis (myeloma), sarcoidosis, haemochromatosis, radiation or endomyocardial fibroelastosis in African children.

History — what will you ask?

• Dyspnoea and oedema of diastolic failure
• Syncope or slow pulse (heart block)
• Systemic clues — myeloma, sarcoidosis, bronze skin and diabetes, radiotherapy

Signs — what will you find?

• S3 (maximal relaxation is early diastole)
• Raised JVP with Kussmaul’s sign
• Hepatomegaly, ascites, oedema
• Pansystolic murmur of MR

Investigations — what will you order?

• Echo — normal ventricular size, low compliance, MR, variable wall thickness and EF
• ECG — AF, VT/VF, heart block
• CXR — signs of heart failure
• Biopsy of the affected organ (amyloid)

DDx — what else could it be?

• Constrictive pericarditis
• Hypertrophic cardiomyopathy
• Cardiac amyloidosis
• Haemochromatosis

Management — what will you do?

• Same as dilated cardiomyopathy; beta-blocker preferred to lengthen diastole
• Cautious reduction of preload and afterload; pacemaker and ICD
• Cardiac transplantation definitive

CHD

A. Ventricular septal defect (VSD)

Scenario. Child or adult with a harsh holosystolic murmur at the lower left sternal border — the commonest congenital heart disease; small (≤3 mm) defects are asymptomatic and often close by age 6, large (6–10 mm) need repair before age 2.

History — what will you ask?

• Exertional dyspnoea, easy fatigue, palpitations
• Fainting, repeated lung infections
• Failure to thrive in infants

Signs — what will you find?

• Loud harsh holosystolic murmur at the lower left sternal border
• Pulmonary plethora; LA and LV enlargement
• Signs of Eisenmenger if late

Investigations — what will you order?

• ECG, CXR, echo (TTE/TOE)
• Cardiac catheterisation, MRI, CT

DDx — what else could it be?

• ASD
• PDA
• Mitral regurgitation
• Tetralogy of Fallot

Management — what will you do?

• Follow-up; symptomatic medication
• Catheter device closure or surgical repair
• Complications — Eisenmenger, endocarditis, HF, arrhythmia, pulmonary hypertension

B. Atrial septal defect (ASD)

Scenario. Often asymptomatic child or adult with recurrent chest infections or mild fatigue; a large shunt gives a left precordial bulge and a wide, fixed split S2.

History — what will you ask?

• Asymptomatic; recurrent respiratory infections, failure to thrive
• Older children — mild fatigue, dyspnoea worsening with age

Signs — what will you find?

• Left precordial bulge; prominent RV impulse at the lower left sternal border
• Wide, fixed splitting of S2
• Systolic ejection murmur at the upper left sternal border; mid-diastolic rumble lower left

Investigations — what will you order?

• CXR, ECG (right axis deviation in secundum, left axis in primum)
• Echo; cardiac catheterisation occasionally

DDx — what else could it be?

• VSD
• PDA
• Pulmonary stenosis
• Partial anomalous pulmonary venous return

Management — what will you do?

• Yearly follow-up; diuretics if symptomatic
• Device closure for a large shunt (Amplatzer, Gore helix, CardioSEAL, BioSTAR)
• Complications — pulmonary hypertension, HF, paradoxical emboli, AF, Eisenmenger

C. Patent ductus arteriosus (PDA)

Scenario. Infant or adult with a continuous machinery murmur in the second left intercostal space and a wide pulse pressure; small ducts are asymptomatic, large ones cause HF and pulmonary hypertension.

History — what will you ask?

• Asymptomatic if small
• Exercise intolerance, recurrent infections
• Failure to thrive in a large duct

Signs — what will you find?

• Wide pulse pressure, bounding peripheral pulses
• Prominent apical impulse; thrill in the 2nd left intercostal space
• Classic continuous murmur at the 2nd left interspace, radiating to the left clavicle or apex

Investigations — what will you order?

• Clinical; CXR, ECG, echocardiography

DDx — what else could it be?

• VSD with aortic regurgitation
• Aortopulmonary window
• Ruptured sinus of Valsalva aneurysm
• AV fistula (other continuous murmurs)

Management — what will you do?

• Closure — device or surgical ligation
• Treat HF; complications — HF, Eisenmenger, infective endarteritis, emboli

D. Coarctation of the aorta

Scenario. Young patient with hypertension and upper-limb pulses stronger than femoral — 98% of coarctations are juxtaductal; arch hypoplasia can give differential cyanosis.

History — what will you ask?

• Often asymptomatic; headache from hypertension
• Exercise intolerance, cold legs
• Differential cyanosis if arch hypoplasia

Signs — what will you find?

• Disparity in pulse and BP between arms and legs; radio-femoral delay
• Systolic murmur at the left mid-sternal border and between the scapulae; occasional back thrill
• Hypertension

Investigations — what will you order?

• CXR — cardiomegaly, pulmonary congestion, rib notching
• ECG; echocardiography

DDx — what else could it be?

• Aortic stenosis
• VSD
• Essential hypertension
• Takayasu arteritis

Management — what will you do?

• Surgical or catheter repair
• Treat hypertension and HF; endocarditis prophylaxis

E. Bicuspid aortic valve

Scenario. Adult with an ejection systolic murmur and two aortic cusps instead of three, from fusion of two leaflets — a common congenital anomaly that may present with stenosis, regurgitation or an aortic complication.

History — what will you ask?

• Often asymptomatic
• Exertional dyspnoea, angina or syncope if stenosis develops
• Family history of bicuspid valve or aortic disease

Signs — what will you find?

• Ejection systolic murmur at the aortic area, radiating to the carotids
• Early diastolic murmur if regurgitation
• Signs of aortic stenosis or ascending aortic dilatation

Investigations — what will you order?

• Echo — two cusps, valve function, ascending aortic diameter
• CXR; ECG

DDx — what else could it be?

• Aortic stenosis of other cause
• VSD
• Mitral regurgitation
• Coarctation

Management — what will you do?

• Follow valve function and aortic root size
• Treat stenosis/regurgitation; aortic surgery for dilatation
• Endocarditis prophylaxis

F. Eisenmenger syndrome

Scenario. Long-standing left-to-right shunt (VSD, ASD, less often PDA) raises pulmonary pressure until the shunt reverses — the patient becomes cyanosed and clubbed with polycythaemia.

History — what will you ask?

• Cyanosis, exertional dyspnoea, syncope
• Haemoptysis, bleeding tendency, gout
• Recurrent infections

Signs — what will you find?

• Central cyanosis, clubbing
• Right ventricular heave, loud P2
• Signs of HF and pulmonary hypertension

Investigations — what will you order?

• CXR — enlarged pulmonary arteries, peripheral pruning
• ECG — RVH; echo — shunt reversal, pulmonary pressure
• FBC — secondary polycythaemia; iron studies

DDx — what else could it be?

• Pulmonary arterial hypertension of other cause
• Cyanotic congenital heart disease
• Chronic lung disease with cor pulmonale

Management — what will you do?

• Avoid pregnancy and dehydration; manage cyanosis, HF, arrhythmia, bleeding and hyperviscosity
• No shunt closure once reversed
• Transplant assessment in selected cases

Hypertension-2

A. Chronic hypertension

Scenario. Adult with systolic BP >130 or diastolic >80 on repeated measurement, usually asymptomatic, at risk of stroke, retinopathy, LVH/HF, coronary disease, nephropathy and peripheral vascular disease.

History — what will you ask?

• Usually asymptomatic; headache, dizziness, blurred vision
• Symptoms of end-organ damage — focal weakness, visual loss, chest pain, haematuria
• Adherence; smoking, salt, obesity, diabetes, family history

Signs — what will you find?

• Correct technique — relaxed, no smoking, no fever, arm at heart level; both arms
• Fundoscopy — papilloedema, haemorrhages
• LVH, S3, murmurs; lung crackles; peripheral pulses and bruits; focal deficit

Investigations — what will you order?

• Repeated BP; urinalysis, creatinine and electrolytes
• Fasting glucose/HbA1c, lipid profile
• ECG (LVH), echo, fundoscopy, CXR, renal ultrasound/Doppler

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Essential vs secondary — renal, renovascular, hyperaldosteronism, phaeochromocytoma, Cushing, thyroid, coarctation
• White-coat hypertension

Management — what will you do?

• Lifestyle — salt restriction, weight loss, exercise, DASH, stop smoking, reduce alcohol
• Thiazide, ACEI/ARB, calcium channel blocker, beta-blocker, spironolactone by comorbidity
• Counsel and follow up; screen for complications

B. Hypertensive crisis — urgency and emergency

Scenario. Adult with very high BP who is either without acute end-organ damage (urgency) or with it (emergency): encephalopathy or stroke, blurred vision from papilloedema, chest pain from angina/MI, or haematuria from acute kidney injury.

History — what will you ask?

• Headache, confusion, seizure, focal deficit
• Visual blurring or loss
• Chest pain, dyspnoea, palpitations
• Reduced urine output or haematuria
• Missed medication, cocaine or stimulants

Signs — what will you find?

• BP very high; fundoscopy for papilloedema and haemorrhage
• Neurological deficit, encephalopathy
• Signs of LVF, aortic dissection or AKI
• Signs of the precipitant

Investigations — what will you order?

• Targeted to the organ — ECG and troponin, creatinine and urinalysis, fundoscopy
• CT head if neurological deficit; CXR; echo
• Toxicology screen

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Stroke
• Encephalopathy of other cause
• Aortic dissection
• Phaeochromocytoma crisis
• Pre-eclampsia

Management — what will you do?

• Urgency — no acute end-organ damage: lower BP gradually, without a parenteral rush
• Emergency — controlled IV lowering with continuous monitoring, specific to the organ involved
• Treat the precipitant and complications

Infective Endocarditis-2

A. Native valve, acute endocarditis

Scenario. Very sick adult with high fever and rigors and a new regurgitant murmur — a virulent organism (S. aureus) destroying a native valve; emboli and shock can follow within days.

History — what will you ask?

• Fever and rigors, night sweats, weight loss, malaise
• New or changing murmur, exertional dyspnoea
• Embolic events — stroke, limb pain, haematuria, splenic or back pain
• IV drug use (right-sided/tricuspid), recent procedure, lines

Signs — what will you find?

• Fever; new regurgitant murmur
• Splinter haemorrhages, Janeway lesions, Osler nodes, Roth spots
• Tender splenomegaly; HF/pulmonary oedema; hypotension and shock
• Septic arthritis or spondylodiscitis

Investigations — what will you order?

• Three blood cultures from different sites at different times — 2 positive is diagnostic
• TTE and TEE (vegetation, new regurgitation, abscess, prosthetic leak)
• MRI brain/spine, splenic and renal ultrasound; urine for RBC casts, fundoscopy, rheumatoid factor
• DUCKS criteria — 2 major, or 1 major + 3 minor, or 5 minor

DDx — what else could it be?

• Libman–Sacks endocarditis of SLE
• Marantic endocarditis
• Rheumatic fever
• Atrial myxoma
• Non-bacterial thrombotic endocarditis

Management — what will you do?

• Cultures before antibiotics; empiric vancomycin + cefazolin + nafcillin
• Surgery for acute LHF, pulmonary oedema, recurrent emboli, shock, prosthetic dehiscence, perivalvular abscess, failure of antibiotics, fungal IE
• Prophylaxis before high-risk procedures

B. Native valve, subacute endocarditis

Scenario. Indolent adult with weeks of low-grade fever, fatigue and weight loss and a changing murmur — Streptococcus viridans on a previously damaged valve; the classic Osler/Roth/splinter picture.

History — what will you ask?

• Prolonged low-grade fever, night sweats, fatigue, weight loss
• Exertional dyspnoea; back pain; stroke or embolic episode
• Known rheumatic or congenital valve disease, dental procedure

Signs — what will you find?

• Fever; changing murmur
• Splinter haemorrhages, Osler nodes, Roth spots
• Tender splenomegaly; pallor; signs of HF

Investigations — what will you order?

• Three sets of blood cultures; TTE and TEE
• Brain/spine MRI, splenic and renal ultrasound; urinalysis and fundoscopy
• DUCKS criteria

DDx — what else could it be?

• Libman–Sacks endocarditis
• Marantic endocarditis
• Atrial myxoma
• Rheumatic fever

Management — what will you do?

• Empiric vancomycin + ampicillin/sulbactam; ceftriaxone if penicillin allergy
• Surgery for the same indications as acute disease
• Prophylaxis for high-risk procedures

C. Prosthetic valve, acute endocarditis

Scenario. Fever and a new murmur within weeks of valve replacement, with paravalvular leak or dehiscence — acute prosthetic valve endocarditis.

History — what will you ask?

• Fever, rigors, malaise since surgery
• Dyspnoea and orthopnoea from valve dysfunction
• Embolic phenomena

Signs — what will you find?

• Fever; new or changing prosthetic murmur
• Signs of HF; paravalvular leak murmur
• Embolic stigmata

Investigations — what will you order?

• Blood cultures ×3; TEE is confirmatory — abscess, dehiscence, vegetation
• Echo for paravalvular leakage and ventricular function
• DUCKS criteria

DDx — what else could it be?

• Marantic or Libman–Sacks endocarditis
• Prosthetic valve thrombosis
• Paravalvular leak without infection

Management — what will you do?

• Empiric vancomycin + cefepime + gentamicin + rifampin (rifampin added a week later)
• Early surgery for dehiscence, abscess, HF or persistent bacteraemia
• Prophylaxis for procedures

D. Prosthetic valve, subacute endocarditis

Scenario. Months after valve surgery, indolent fever and a parvavalvular leak — Staphylococcus epidermidis growing on the prosthesis.

History — what will you ask?

• Low-grade fever, fatigue, weight loss
• Dyspnoea, embolic events

Signs — what will you find?

• New prosthetic murmur or leak; fever
• Splenomegaly; peripheral stigmata

Investigations — what will you order?

• Blood cultures ×3; TEE
• Echo for dehiscence/abscess; DUCKS criteria

DDx — what else could it be?

• Non-infective thrombus
• Marantic endocarditis
• Prosthetic dysfunction of other cause

Management — what will you do?

• Empiric vancomycin + ampicillin/sulbactam + gentamicin + rifampin
• Surgery for dehiscence, abscess or failure to clear
• Long-term suppressive therapy in selected cases

Section 3 — Respiratory Disease (Pulmonology)

Sarcoidosis-2

A. Acute sarcoidosis — Löfgren and Heerfordt syndromes

Scenario. Young adult with an acute febrile illness: erythema nodosum, bilateral hilar lymphadenopathy and arthritis (Löfgren), or uveitis, parotid swelling, fever and facial nerve palsy (Heerfordt).

History — what will you ask?

• Fever, fatigue, night sweats, weight loss
• Painful raised skin lesions (erythema nodosum)
• Red painful eye, visual change; dry mouth or parotid swelling
• Facial weakness, arthralgia

Signs — what will you find?

• Erythema nodosum — raised tender lesions, usually shins
• Uveitis, conjunctival granulomas, lacrimal or parotid enlargement
• Facial nerve palsy
• Bilateral hilar lymphadenopathy on CXR

Investigations — what will you order?

• CXR — bilateral hilar lymphadenopathy (± stage 2 infiltration)
• Serum ACE ↑, calcium ↑, ESR ↑
• Biopsy — non-caseating granulomas (diagnostic)
• Exclude TB and fungal infection

DDx — what else could it be?

• Tuberculosis (unilateral hilar nodes)
• Lymphoma
• Fungal infection
• Hypersensitivity pneumonitis

Management — what will you do?

• Often resolves spontaneously over 2–5 years
• Corticosteroids are the mainstay; methotrexate/azathioprine if resistant
• Steroid eye drops for uveitis to protect vision

B. Chronic pulmonary sarcoidosis

Scenario. Adult with months of dry cough and progressive dyspnoea and bilateral hilar lymphadenopathy that has progressed to pulmonary infiltration and fibrosis — restrictive lung disease, sometimes with cardiac or neurological involvement.

History — what will you ask?

• Dry cough, dyspnoea, chest pain
• Fatigue, weight loss, night sweats
• Palpitations or syncope (cardiac sarcoid), facial palsy or neuropathy
• Loin pain or stones (hypercalcaemia)

Signs — what will you find?

• Fine crackles; signs of fibrosis
• Arrhythmia, cardiomyopathy
• Cranial nerve palsy; hepatosplenomegaly

Investigations — what will you order?

• CXR staging — 0 none (5–10%), 1 lymphadenopathy (50%), 2 lymphadenopathy + infiltration (25–30%), 3 infiltration (10–12%), 4 fibrosis (5%)
• HRCT — infiltrates, fibrosis
• Serum ACE, calcium, ESR; PFTs (restrictive); biopsy; exclude TB/fungi

DDx — what else could it be?

• TB
• Lymphoma
• Fungal infection
• Hypersensitivity pneumonitis
• Vasculitis

Management — what will you do?

• Corticosteroids; methotrexate/azathioprine in resistant disease
• Treat organ involvement; monitor for complications
• Poor prognosis with cardiac, neurological or fibrotic lung disease

ILD

A. Idiopathic pulmonary fibrosis (UIP pattern)

Scenario. Older adult with progressive exertional dyspnoea and a persistent dry cough, fine Velcro crackles at the bases and clubbing; HRCT shows basal, subpleural reticulation and honeycombing with traction bronchiectasis.

History — what will you ask?

• Progressive exertional dyspnoea, dry cough
• Occupational or drug exposure; connective tissue disease symptoms
• Smoking; family history of pulmonary fibrosis

Signs — what will you find?

• Fine end-inspiratory Velcro crackles, bibasal
• Clubbing, central cyanosis
• Signs of cor pulmonale and right heart failure

Investigations — what will you order?

• HRCT — basal subpleural honeycombing, reticulation, traction bronchiectasis, no alternative features
• PFTs — restrictive (↓FVC, normal/↑ ratio, ↓TLC, ↓DLCO)
• Autoimmune screen; BAL/biopsy only if diagnosis unclear

DDx — what else could it be?

• Hypersensitivity pneumonitis
• Asbestosis
• CTD-associated ILD
• Drug-induced ILD
• Sarcoidosis

Management — what will you do?

• Nintedanib 150 mg BID or pirfenidone slow progression, do not reverse scar
• Oxygen, pulmonary rehabilitation, vaccination, smoking cessation
• Steroids/azathioprine are not routine in IPF (increased mortality); transplant referral

B. Hypersensitivity pneumonitis

Scenario. Adult with recurrent dyspnoea, cough and fever hours after exposure to an organic antigen — bird fancier’s, farmer’s lung; upper-zone changes and a restrictive defect.

History — what will you ask?

• Symptoms recurring after exposure; improvement away from the exposure
• Bird, mould, hay or occupational antigen; hobbies and work
• Fever, chills, weight loss in subacute disease

Signs — what will you find?

• Crackles; clubbing in chronic disease
• Signs of restriction and right heart failure

Investigations — what will you order?

• HRCT — upper-zone GGO, centrilobular nodules, air trapping, fibrosis in chronic disease
• PFTs restrictive; DLCO low
• Serum precipitins to the antigen; BAL lymphocytosis

DDx — what else could it be?

• IPF/UIP
• Sarcoidosis
• Pneumoconiosis
• Infection

Management — what will you do?

• Remove the antigen — the single most effective step
• Corticosteroids in inflammatory disease; immunosuppression in chronic progressive disease
• Oxygen, rehabilitation, transplant referral

C. Silicosis

Scenario. Stone cutter, sandblaster or engineered-stone worker with years of silica exposure, progressive dyspnoea and upper-lobe nodules ± eggshell calcification of hilar nodes.

History — what will you ask?

• Exposure — mining, quarrying, sandblasting, construction, engineered-stone countertops; duration and PPE
• Dyspnoea, cough, reduced exercise tolerance
• Course — chronic >10–20 years, accelerated 3–10 years, acute weeks–months

Signs — what will you find?

• Fine crackles; signs of restriction and cor pulmonale
• Clubbing uncommon

Investigations — what will you order?

• CXR — small well-defined upper-lobe nodules, hilar/mediastinal nodes ± eggshell calcification
• HRCT — centrilobular/perilymphatic nodules; PMF (confluent upper-lobe masses)
• PFTs restrictive ± obstruction; assess for TB

DDx — what else could it be?

• Miliary TB
• Sarcoidosis
• Coal-worker pneumoconiosis
• Lung cancer
• Hypersensitivity pneumonitis

Management — what will you do?

• Stop exposure, stop smoking, vaccinate
• Surveillance with PFT and imaging; investigate TB (critical risk)
• Oxygen, rehabilitation, treat complications; transplant in selected cases — fibrosis is irreversible

D. Asbestosis

Scenario. Construction or shipyard worker, 20–40 years after asbestos exposure, with gradual dyspnoea, dry cough and bibasal Velcro crackles; pleural plaques mark exposure but are not the disease.

History — what will you ask?

• Exposure — construction/demolition, ships, insulation, roofing, older buildings; latency 20–40 years
• Gradual dyspnoea, dry cough
• Smoking history (multiplies lung-cancer risk)

Signs — what will you find?

• Bibasal Velcro crackles, clubbing
• Signs of pulmonary hypertension and right heart failure

Investigations — what will you order?

• HRCT — basal subpleural reticulation, septal thickening, parenchymal bands, GGO, traction bronchiectasis ± honeycombing
• Pleural plaques — exposure marker, not proof of asbestosis
• PFTs restrictive, DLCO low

DDx — what else could it be?

• IPF
• Silicosis
• CTD-associated ILD
• Drug-induced ILD

Management — what will you do?

• End exposure, smoking cessation, vaccination
• PFT follow-up, oxygen, rehabilitation; treat pulmonary hypertension
• Screen for lung cancer and mesothelioma — smoking greatly increases lung-cancer risk; fibrosis is not reversible

ARDS

Scenario. Acutely and severely ill patient within 1 week of an inciting event: sepsis (commonest), burns, severe pneumonia, trauma/fractures, acute pancreatitis, aspiration. Non-cardiogenic pulmonary oedema from increased capillary permeability with severe hypoxaemia, stiff lungs and diffuse infiltrates; mortality very high. Symptoms begin hours to days after the insult.

History — what will you ask?

• Timing and nature of the precipitant — fever/infection, burns, trauma, pancreatitis, vomiting/aspiration
• acute dyspnoea, tachypnoea
• rapid deterioration
• no history of cardiac disease or fluid overload

Signs — what will you find?

• Acutely dyspnoeic, tachypnoeic, cyanosed, anxious, febrile
• crackles on auscultation
• severe respiratory distress, accessory muscle use
• hypoxia not correctable with oxygen
• signs of the underlying cause (sepsis, burns, trauma)

Investigations — what will you order?

• CXR — bilateral diffuse pulmonary infiltrates appearing quickly and progressing rapidly (improve after 2 weeks in survivors)
• echo/BNP to exclude cardiogenic oedema
• CT chest (more detail, not mandatory — weigh transport risk in ventilated patient)
• PET
• chest ultrasound
• ABG — hypoxaemia with high A–a gradient
• Berlin criteria for diagnosis and severity grading (PaO₂/FiO₂)

DDx — what else could it be?

• Cardiogenic pulmonary oedema (CHF)
• diffuse pneumonia
• pulmonary haemorrhage
• acute exacerbation of interstitial lung disease
• aspiration pneumonia

Management — what will you do?

• Oxygen and mechanical ventilation with low tidal volume
• prone positioning in selected cases
• treat the precipitating cause. Corticosteroids and inhaled nitric oxide have no role
• no drug has shown definitive mortality benefit
• Monitor for complications
• prognosis guarded

Pneumonia-2

A. Community-acquired pneumonia

Scenario. Adult from the community with fever, cough and yellow-green or rust-coloured sputum and pleuritic chest pain — Streptococcus pneumoniae overall, Mycoplasma the commonest atypical.

History — what will you ask?

• Fever, rigors, cough and sputum colour, pleuritic pain, dyspnoea
• Confusion in the elderly
• Risk factors — COPD/asthma, diabetes, HIV, aspiration

Signs — what will you find?

• Fever; bronchial breath sounds and dullness over the affected lobe
• Crackles, tachypnoea, cyanosis
• Hypotension (systolic <90); confusion

Investigations — what will you order?

• CBC (↑WBC); CXR — homogeneous consolidation (may be normal early; 4–6 weeks to clear)
• Sputum Gram stain and culture; ABG if severe
• CURB 65 — confusion, urea, RR ≥30, systolic <90, age >65; ≥3 = severe

DDx — what else could it be?

• Lung abscess
• Bronchial carcinoma
• TB
• PE with infarction

Management — what will you do?

• No risk factors — clarithromycin or azithromycin 7 days
• Risk factors/chronic disease — levofloxacin or Augmentin; severe — hospital IV broad spectrum ~1 week
• Supportive — antipyretics, analgesia, oxygen, fluids, physiotherapy; do not repeat CXR before 4–6 weeks; Pneumovax

B. Hospital-acquired pneumonia

Scenario. Patient developing pneumonia ≥48 hours after admission, often ventilated or with lines and resistant organisms — a different flora from community disease.

History — what will you ask?

• Fever, new purulent sputum, worsening oxygen requirement
• Mechanical ventilation, recent antibiotics, surgery, immunosuppression
• Comorbid disease and prior hospital stay

Signs — what will you find?

• Fever; dullness and bronchial breathing; crackles
• Tachypnoea, desaturation, confusion

Investigations — what will you order?

• CXR — new or progressive infiltrate
• Sputum/tracheal aspirate culture and sensitivity; blood cultures
• CBC, ABG, CURB 65 for severity

DDx — what else could it be?

• Atelectasis
• Pulmonary oedema
• ARDS
• PE
• Empyema

Management — what will you do?

• Broad-spectrum IV antibiotics guided by local flora and culture
• Supportive care, oxygen/ventilation, physiotherapy
• Prevention — hand hygiene, head-up positioning, early mobilisation

COPD

A. Stable COPD

Scenario. Adult with tobacco or biomass exposure and progressive persistent exertional dyspnoea, recurrent wheeze and chronic cough; spirometry shows post-bronchodilator FEV₁/FVC <0.70, with emphysema (pink puffer) or chronic bronchitis (blue bloater) patterns.

History — what will you ask?

• Dyspnoea, wheeze, chronic cough and sputum, recurrent infections
• Smoking pack-years, household fuel, occupational fumes
• Exacerbations in the past 12 months; exercise tolerance; oedema

Signs — what will you find?

• Tripod posture, pursed-lip breathing, barrel chest
• Reduced air entry, wheeze, crackles; cyanosis
• Oedema and raised JVP in cor pulmonale; cachexia or obesity

Investigations — what will you order?

• Spirometry — FEV₁/FVC <0.70; ↑RV; bronchodilator reversibility >12% and 200 mL favours asthma
• GOLD 1–4 by FEV₁; ABE groups by exacerbations and CAT/mMRC
• ABG, α1-antitrypsin, eosinophils, ECG/echo; LTOT assessment (PaO₂ ≤55 or SpO₂ ≤88%)

DDx — what else could it be?

• Asthma
• TB
• Congestive heart failure
• Bronchiectasis
• Obliterative bronchiolitis

Management — what will you do?

• Group A bronchodilator; B LABA + LAMA; E LABA + LAMA + ICS if eosinophils ≥300/µL
• Roflumilast or azithromycin in selected patients
• Smoking cessation, vaccination, rehabilitation, NIV for hypercapnia, LTOT, LVRS/valves/transplant

B. Acute exacerbation of COPD (ECOPD)

Scenario. Known COPD with worsening dyspnoea, cough and sputum over <14 days, often after a viral infection or pollution — tachypnoeic, using accessory muscles, with falling saturation.

History — what will you ask?

• Speed of worsening, sputum volume and purulence, fever
• Trigger — infection, pollution; chest pain or palpitations (mimics)
• Recent exacerbations, inhalers, steroids, oxygen at home

Signs — what will you find?

• Tachypnoea, accessory muscle use, pursed lips, cyanosis
• Reduced air entry, wheeze, confusion/drowsiness
• Cor pulmonale signs; asterixis if CO₂ retention

Investigations — what will you order?

• ABG — hypercapnia and acidosis; CXR to exclude pneumonia/pneumothorax
• ECG and troponin (MI, arrhythmia); BNP (HF)
• Sputum culture if ventilated or failing

DDx — what else could it be?

• Pneumonia
• Pulmonary embolism
• Pneumothorax
• Heart failure
• MI
• Arrhythmia

Management — what will you do?

• Nebulised salbutamol 2.5–5 mg ± ipratropium 500 µg hourly ×2–3 then q2–4h; oxygen to SaO₂ 88–92% (24–35% Venturi)
• Prednisone 40 mg ×5 days; antibiotics if 3 cardinal symptoms (or 2 with purulence, or ventilated) — aminopenicillin–clavulanate, macrolide, tetracycline
• NIV if PaCO₂ ≥45 and pH ≤7.35; avoid IV methylxanthines

Section 3 — Gastroenterology and Hepatology

Gastrointestinal Bleeding-2

A. Upper gastrointestinal bleeding

Scenario. Adult with haematemesis, coffee-ground vomiting or melena — bleeding proximal to the ligament of Treitz; the commonest cause is peptic ulcer disease, followed by varices.

History — what will you ask?

• Nature and volume of bleeding; melena or haematemesis
• Peptic ulcer history, NSAIDs/aspirin/anticoagulants, alcohol, liver disease
• Epigastric pain, weight loss, dysphagia; previous bleeding

Signs — what will you find?

• Tachycardia, postural drop, hypotension; pallor
• Abdominal tenderness; stigmata of chronic liver disease and ascites
• Digital rectal examination — melena

Investigations — what will you order?

• CBC, cross-match, coagulation, urea/creatinine, LFTs, lactate
• EGD — diagnostic of choice (within 24 h; 12 h if shocked)
• Glasgow-Blatchford for triage; Rockall for prognosis
• CT angiography if endoscopy inconclusive

DDx — what else could it be?

• Peptic ulcer
• Oesophageal/gastric varices
• Mallory–Weiss tear
• Gastritis/portal gastropathy
• Vascular lesion
• Malignancy

Management — what will you do?

• ABCDE, two wide-bore lines, crystalloid 1 L then reassess; transfuse to Hb ≥7 g/dL (≥8–9 if CAD/shock)
• Correct coagulopathy; alert endoscopy; ICU if unstable
• IV PPI 80 mg bolus then 8 mg/h for 72 h for ulcer bleeding; if variceal — octreotide/terlipressin + IV ceftriaxone at once
• Endoscopic haemostasis — adrenaline + thermal/hemoclips; varices — EVL, sclerotherapy, cyanoacrylate, TIPS

B. Lower gastrointestinal bleeding

Scenario. Adult with haematochezia — fresh blood per rectum from a source distal to the ligament of Treitz; diverticulosis is the commonest cause, with haemorrhoids, IBD, angiodysplasia and cancer behind it.

History — what will you ask?

• Fresh blood per rectum, amount and duration; mixed with stool?
• Change in bowel habit, weight loss, tenesmus
• Previous bleeding, anticoagulants, NSAIDs; family history of colorectal cancer

Signs — what will you find?

• Pallor, tachycardia, postural drop
• Abdominal mass or tenderness; rectal examination — haemorrhoids, fissure, mass

Investigations — what will you order?

• CBC, cross-match, coagulation
• Colonoscopy — investigation of choice
• CT angiography for brisk bleeding; radionuclide scan for intermittent bleeding
• Capsule endoscopy

DDx — what else could it be?

• Haemorrhoids/anal fissure
• IBD/ulcerative colitis
• Diverticulosis
• Angiodysplasia
• Colorectal cancer
• Ischaemic colitis
• Meckel’s diverticulum

Management — what will you do?

• Resuscitate as for upper bleeding; transfuse to target Hb
• Colonoscopy with endoscopic therapy — clipping, cautery, injection
• CT angiography ± embolisation for ongoing brisk bleed; surgery for massive or refractory bleeding
• Treat the cause; screen for colorectal cancer

Jaundice-2

A. Prehepatic jaundice

Scenario. Young patient with jaundice and unconjugated hyperbilirubinaemia, no bilirubin in urine, and anaemia or splenomegaly — haemolysis, Gilbert syndrome or Crigler–Najjar; physiological in the newborn.

History — what will you ask?

• Jaundice, dark urine (haemolysis gives dark urine from urobilinogen, not bilirubin), fatigue
• Family history of anaemia or jaundice; episodes with stress, fasting or menstruation (Gilbert)
• Blood transfusion, sickle cell disease; drugs

Signs — what will you find?

• Pallor, splenomegaly (haemolysis)
• No scratch marks, no hepatomegaly
• Mild jaundice in Gilbert without stigmata of liver disease

Investigations — what will you order?

• CBC, reticulocytes, blood film, LDH, haptoglobin, bilirubin (unconjugated)
• Urine bilirubin absent, urobilinogen increased
• Coombs test, Hb electrophoresis, G6PD assay; exclude Gilbert

DDx — what else could it be?

• Haemolytic anaemia
• Gilbert syndrome
• Crigler–Najjar
• Physiological neonatal jaundice

Management — what will you do?

• Treat the underlying haemolysis; stop the offending drug
• Gilbert — reassurance, no treatment
• Neonatal — phototherapy if required; genetic counselling for Crigler–Najjar

B. Hepatic jaundice

Scenario. Adult with jaundice, malaise and mixed hyperbilirubinaemia and raised transaminases — viral, alcoholic or autoimmune hepatitis, NASH, drug toxicity or vascular injury.

History — what will you ask?

• Prodrome — fever, malaise, anorexia, myalgia, nausea
• Alcohol intake; drugs and toxins (cocaine, paracetamol); blood transfusion, tattoos, unprotected sex
• Itch, dark urine, pale stool; confusion (failure)

Signs — what will you find?

• Jaundice, tender hepatomegaly
• Signs of chronic liver disease and portal hypertension
• Encephalopathy if acute liver failure

Investigations — what will you order?

• LFTs — ALT/AST high, bilirubin mixed; albumin and INR for severity
• Viral serology (A/B/C/E), autoimmune markers (ANA, ASMA, anti-LKM1), ferritin, caeruloplasmin
• Ultrasound; liver biopsy if diagnosis unclear

DDx — what else could it be?

• Post-hepatic obstruction
• Prehepatic haemolysis
• Drug-induced liver injury
• Ischaemic hepatitis

Management — what will you do?

• Supportive care; stop alcohol and hepatotoxic drugs
• Antivirals where indicated; steroids + azathioprine for autoimmune hepatitis
• Treat complications of liver failure; transplant if fulminant

C. Post-hepatic (obstructive) jaundice

Scenario. Adult with jaundice, dark urine and pale stool, itching and right upper quadrant pain — bile duct obstruction by gallstones, cholangiocarcinoma, pancreatic head tumour, PSC or Budd-Chiari.

History — what will you ask?

• Pain (RUQ, colicky or constant), fever with rigors (cholangitis)
• Pruritus, pale stool, dark urine, weight loss
• Previous biliary surgery or stones; jaundice that fluctuates

Signs — what will you find?

• Jaundice, scratch marks
• Palpable gallbladder (Courvoisier); RUQ tenderness, Murphy’s sign
• Fever and hypotension if cholangitis

Investigations — what will you order?

• Bilirubin conjugated, alkaline phosphatase and GGT very high
• Ultrasound — dilated ducts and stones; MRCP; CT
• ERCP for diagnosis and stenting; CA 19-9

DDx — what else could it be?

• Hepatocellular jaundice
• Haemolysis
• Drug-induced cholestasis
• PSC
• Cholangiocarcinoma

Management — what will you do?

• ERCP — stone extraction or stent; surgery for tumour
• Cholangitis — IV antibiotics and urgent biliary drainage
• Pruritus — cholestyramine/antihistamines; vitamin K for coagulopathy

Section 3 — Nephrology and Fluid/Electrolytes

Electrolyte imbalance

A. Hyponatraemia

Scenario. Adult with confusion, headache or seizure and Na⁺ <135 mmol/L — hypotonic hyponatraemia classified by volume: hypovolaemic (vomiting, diarrhoea, thiazides, Addison), euvolaemic (SIADH — CNS disease, pneumonia, SSRIs, carbamazepine, small-cell lung cancer) or hypervolaemic (HF, cirrhosis, nephrotic syndrome).

History — what will you ask?

• Fluid loss or intake; diuretics; vomiting, diarrhoea
• Drugs — SSRIs, carbamazepine, thiazides; lung or CNS disease
• Headache, confusion, seizure, coma (acute <48 h); chronic often asymptomatic

Signs — what will you find?

• Volume status — dehydration, oedema or neither
• Confusion, seizures, coma
• Signs of the cause — pneumonia, Addison, HF, cirrhosis

Investigations — what will you order?

• Serum osmolality first; urine Na⁺ and osmolality
• Thyroid and adrenal function; glucose, urea (calculated osmolality)
• Exclude pseudohyponatraemia

DDx — what else could it be?

• Hyperglycaemia
• Pseudohyponatraemia
• Hypothyroidism
• Adrenal insufficiency
• SIADH

Management — what will you do?

• Severe symptomatic — 3% hypertonic saline, rise 4–6 mmol/L, limits <10/24 h and <18/48 h (avoid osmotic demyelination)
• Hypovolaemic — 0.9% saline; SIADH — restrict 800–1000 mL/day, demeclocycline or tolvaptan; hypervolaemic — restriction + loop diuretics
• Treat the cause

B. Hypernatraemia

Scenario. Adult with thirst, lethargy, irritability or seizures and Na⁺ >145 mmol/L — a water deficit (osmotic diuresis, diabetes insipidus, diarrhoea, burns, sweating) or sodium gain (hypertonic saline, bicarbonate).

History — what will you ask?

• Water intake and access; polyuria, nocturia
• Diarrhoea, burns, fever, sweating
• Lithium, demeclocycline; head injury or pituitary surgery (central DI)

Signs — what will you find?

• Cellular dehydration — dry mucosa, reduced skin turgor
• Lethargy, irritability, seizures, coma
• Signs of the cause

Investigations — what will you order?

• Serum and urine osmolality; urine Na⁺
• Water-deprivation test to separate central from nephrogenic DI
• Glucose, calcium, potassium

DDx — what else could it be?

• Osmotic diuresis (diabetes)
• Diabetes insipidus
• Extrarenal water loss
• Sodium administration

Management — what will you do?

• Oral free water if possible; otherwise IV 5% dextrose or 0.45% saline
• Correct over 48–72 h — avoid rapid correction (cerebral oedema)
• Treat the cause; desmopressin for central DI

C. Hypokalaemia

Scenario. Adult with weakness, cramps, ileus or palpitations and K⁺ <3.5 mmol/L — from intracellular shift (insulin, β₂ agonists, alkalosis, refeeding) or, most commonly, increased loss (vomiting, diarrhoea, NG suction, loop/thiazide diuretics, hyperaldosteronism).

History — what will you ask?

• Vomiting, diarrhoea, NG suction; diuretic use
• Weakness, cramps, paralysis, constipation
• Digoxin use (toxicity risk); palpitations

Signs — what will you find?

• Weakness, hyporeflexia, ileus
• Arrhythmia; ECG — flat T, prominent U, ST depression, apparent QT/QU prolongation
• Hypertension suggesting hyperaldosteronism

Investigations — what will you order?

• Confirm K⁺; acid–base status; 24-h urinary K⁺ — <20 mmol/day extrarenal, >20 renal
• Magnesium; aldosterone/renin if hypertension
• ECG

DDx — what else could it be?

• Diuretic-induced
• Gastrointestinal loss
• Hyperaldosteronism (Conn, renal artery stenosis)
• Refeeding, insulin, β₂ agonists

Management — what will you do?

• Mild/asymptomatic — oral KCl
• Severe/symptomatic — IV K⁺ with ECG monitoring, peripheral max 10 mmol/h, never bolus
• Replace Mg²⁺ if low — otherwise K⁺ stays refractory

D. Hyperkalaemia

Scenario. Adult with weakness, paraesthesia or a peri-arrest ECG and K⁺ >5.0 mmol/L — usually reduced renal excretion (CKD, hypoaldosteronism, ACEI/ARB, K⁺-sparing diuretics) or shift/release (acidosis, DKA, rhabdomyolysis, tumour lysis).

History — what will you ask?

• CKD or dialysis; ACEI/ARB, spironolactone, trimethoprim
• Weakness, palpitations, syncope
• Crush injury, chemotherapy, insulin omission

Signs — what will you find?

• Weakness, paraesthesia, areflexia
• ECG progression — peaked T, shortened QT, PR prolongation, QRS widening, sine wave → VF/asystole
• Signs of the cause

Investigations — what will you order?

• Confirm K⁺ — exclude pseudohyperkalaemia (haemolysis, thrombocytosis, difficult venepuncture)
• Creatinine, glucose, CK, ABG
• ECG immediately

DDx — what else could it be?

• Pseudohyperkalaemia
• Renal failure
• Hypoaldosteronism/Addison
• Drug-induced
• Tumour lysis/rhabdomyolysis

Management — what will you do?

• IV calcium gluconate to stabilise the myocardium (does not lower K⁺)
• Shift — insulin + glucose, nebulised salbutamol, bicarbonate if acidotic
• Remove — loop diuretics, K⁺ binders, dialysis for severe/refractory or ECG toxicity

E. Hypercalcaemia

Scenario. Adult with stones, bone pain, abdominal pain/constipation, depression or confusion, polyuria and dehydration, Ca²⁺ >2.6 mmol/L — primary hyperparathyroidism (commonest overall) or malignancy (commonest inpatient, via PTHrP, bone metastases or myeloma).

History — what will you ask?

• Renal stones, polyuria/polydipsia
• Bone pain, fractures, constipation, nausea
• Depression, confusion, drowsiness; weight loss (malignancy)
• Vitamin D, thiazides, sarcoidosis, immobility, family history of MEN

Signs — what will you find?

• “Stones, bones, groans, psychic moans”
• Dehydration, hypertension
• ECG — short QT; >3.5 mmol/L is a medical emergency

Investigations — what will you order?

• Repeat and albumin-adjust Ca²⁺; PTH is key — high/inappropriately normal = PTH-mediated, suppressed = malignancy/other
• U&E, vitamin D, myeloma screen, CXR, parathyroid imaging
• 24-h urine calcium

DDx — what else could it be?

• Primary hyperparathyroidism
• Malignancy (PTHrP, myeloma, bone metastases)
• Vitamin D excess
• Sarcoidosis
• Thiazides
• Immobilisation
• Addison disease

Management — what will you do?

• IV 0.9% saline first, then IV bisphosphonate (zoledronic acid) ± calcitonin
• Steroids if vitamin-D mediated; dialysis if refractory
• Parathyroidectomy for primary hyperparathyroidism with symptoms, Ca²⁺ >0.25 mmol/L above normal, osteoporosis, stones or age <50

F. Hypocalcaemia

Scenario. Adult with perioral numbness, cramps, tetany, seizures or laryngospasm and Ca²⁺ <2.2 mmol/L — hypoparathyroidism (post-thyroidectomy), vitamin D deficiency, CKD, acute pancreatitis or massive transfusion.

History — what will you ask?

• Perioral and acral numbness, cramps, twitching
• Seizures, stridor, carpopedal spasm
• Thyroid surgery, malabsorption, alcohol, CKD, pancreatitis, transfusion

Signs — what will you find?

• Trousseau sign — BP cuff inflated 1–4 min → palmar-flexion spasm
• Chvostek sign — tap anterior/inferior to the ear → ipsilateral facial twitch
• ECG — prolonged QT; cataract; dry skin

Investigations — what will you order?

• Albumin-adjusted Ca²⁺, PTH, vitamin D, Mg²⁺, phosphate
• ECG; renal function
• Look for the cause — post-surgical, malabsorption, CKD

DDx — what else could it be?

• Hypoparathyroidism (post-thyroidectomy)
• Vitamin D deficiency
• CKD
• Acute pancreatitis
• Massive transfusion (citrate)
• Hypomagnesaemia

Management — what will you do?

• Acute symptomatic — slow IV 10% calcium gluconate with cardiac monitoring
• Chronic — oral calcium + cholecalciferol, calcitriol in CKD, replace Mg²⁺
• Treat the cause; monitor for arrhythmia and seizures

Section 3 — Endocrinology and Metabolism

Dyslipidemia-2

A. Familial hypercholesterolaemia

Scenario. Young adult with a strong family history of premature cardiovascular disease and very high LDL (≥190 mg/dL), tendon xanthomas, xanthelasma or corneal arcus — an inherited defect of LDL clearance.

History — what will you ask?

• Family history of premature ASCVD or sudden death
• Xanthelasma, tendon xanthomas, corneal arcus at a young age
• Diet and lifestyle; statin intolerance

Signs — what will you find?

• Tendon xanthomas, xanthelasma, corneal arcus
• Absent peripheral pulses or bruits (established ASCVD)
• Blood pressure and BMI

Investigations — what will you order?

• Fasting lipid panel — LDL ≥190 mg/dL
• Exclude secondary causes — TSH, HbA1c, renal and liver function, urinalysis
• Screen first-degree relatives; genetic testing where available
• ASCVD risk assessment

DDx — what else could it be?

• Secondary hyperlipidaemia (hypothyroidism, nephrotic syndrome, cholestasis, drugs)
• Familial combined hyperlipidaemia
• Sitosterolaemia

Management — what will you do?

• High-intensity statin — atorvastatin 40–80 mg or rosuvastatin 20–40 mg
• Add ezetimibe, then a PCSK9 inhibitor if LDL remains high
• Lifestyle for all; family cascade screening

B. Hypertriglyceridaemia

Scenario. Adult with triglycerides ≥500 mg/dL, often with obesity, diabetes or alcohol use — the risk here is acute pancreatitis, not just atherosclerosis; at ≥1000 mg/dL the risk is high.

History — what will you ask?

• Abdominal pain (pancreatitis); alcohol intake
• Diabetes, obesity, high-carbohydrate diet, oestrogens, steroids
• Family history of hypertriglyceridaemia

Signs — what will you find?

• Xanthomas (eruptive) on the trunk and limbs
• Hepatosplenomegaly; signs of pancreatitis
• Signs of the secondary cause

Investigations — what will you order?

• Fasting lipid panel — TG ≥500 mg/dL
• Lipase/amylase if abdominal pain; glucose and HbA1c
• Exclude secondary causes — alcohol, diabetes, hypothyroidism, nephrotic syndrome, drugs

DDx — what else could it be?

• Type I familial chylomicronaemia
• Type IV/V familial hypertriglyceridaemia
• Secondary hypertriglyceridaemia
• Pancreatitis of other cause

Management — what will you do?

• TG ≥500 mg/dL — fibrate first-line plus omega-3 to prevent pancreatitis
• Add a statin if ASCVD risk; icosapent ethyl in high-risk patients
• Stop alcohol, very-low-fat diet, weight loss, strict glucose control; hospitalise if symptomatic

Section 3 — Rheumatology and Connective Tissue Diseases

Dermatomyositis

Scenario. Female-predominant idiopathic inflammatory myopathy (juvenile peak 5–15 years, adult 45–65) with autoimmune microangiopathy: complement-mediated capillary destruction, muscle ischaemia and perifascicular atrophy with perimysial inflammation. Presents with symmetrical proximal muscle weakness (difficulty climbing stairs, rising from a chair, lifting arms) and distinctive skin signs; strongly associated with malignancy in adults (up to 30% — ovarian, breast, lung, gastric).

History — what will you ask?

• Weakness pattern and progression, difficulty with stairs/chair/overhead work, muscle pain (less than weakness), dysphagia, fatigue, fever, weight loss, Raynaud, breathlessness, joint pain, palpitations
• smoking
• age
• cancer screening history
• family history and HLA-DR

Signs — what will you find?

• Heliotrope rash (violaceous eyelids), Gottron’s papules (erythematous scaly papules over knuckles), shawl sign and photosensitive rash on face, neck and upper chest, mechanic’s hands (rough cracked palms)
• proximal muscle tenderness and weakness
• dysphagia
• calcinosis in juvenile cases
• signs of ILD or cardiomyopathy

Investigations — what will you order?

• ↑CK, ↑AST/ALT, ↑LDH
• autoantibodies — anti-Mi-2, anti-TIF1-γ (malignancy association)
• EMG myopathic pattern
• MRI muscle oedema
• muscle biopsy — perifascicular atrophy with perimysial inflammation (vs endomysial inflammation in polymyositis)
• spirometry (restrictive pattern) and HRCT for ILD
• echo/ECG
• age-appropriate cancer screening in all adults

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Polymyositis (endomysial inflammation, no rash)
• inclusion body myositis
• immune-mediated necrotising myopathy
• SLE
• scleroderma
• drug-induced myopathy (statins)
• muscular dystrophy
• hypothyroidism

Management — what will you do?

• First-line corticosteroids (prednisolone)
• immunosuppressants — methotrexate, azathioprine
• IVIG or rituximab in resistant cases
• physiotherapy to prevent contractures
• sun protection for skin lesions
• treat associated malignancy. 5-year survival ~75–80%, worse with malignancy

Vasculitis

A. Giant cell arteritis

Scenario. Elderly woman with a new temporal headache, scalp tenderness, jaw claudication and blurring of vision — granulomatous inflammation of the external carotid branches; blindness is the feared complication.

History — what will you ask?

• Temporal headache, scalp tenderness on combing
• Jaw claudication; blurring or transient visual loss
• Fever, malaise, myalgia; polymyalgia rheumatica
• Age >50; visual loss may be permanent if untreated

Signs — what will you find?

• Tender, thickened, pulseless temporal artery
• Visual acuity and fields — anterior ischaemic optic neuropathy
• Signs of polymyalgia rheumatica

Investigations — what will you order?

• ESR and CRP very high
• Temporal artery biopsy — long segment (up to 2 cm), tunica media granuloma, elastic lamina destruction, adventitial thickening
• Fundoscopy; consider PET/CT if biopsy negative

DDx — what else could it be?

• Atherosclerotic carotid disease
• Migraine
• Trigeminal neuralgia
• Infection
• Takayasu arteritis

Management — what will you do?

• High-dose glucocorticoids immediately — before the biopsy result (delay risks ophthalmic artery occlusion and blindness)
• Taper slowly; steroid-sparing agent if relapsing
• Aspirin for visual ischaemia; monitor for aortic involvement

B. Takayasu arteritis

Scenario. Young Asian woman under 35 with arm claudication, dizziness and absent or unequal pulses — granulomatous inflammation of the aorta and its branches, most often the subclavian (pulseless disease).

History — what will you ask?

• Arm claudication, fatigue, dizziness, syncope
• Fever, myalgia, weight loss (active phase)
• Hypertension; visual disturbance

Signs — what will you find?

• Absent or unequal pulses and blood-pressure disparity between arms
• Bruits over the aorta, carotids or subclavian
• Signs of aortic regurgitation or heart failure

Investigations — what will you order?

• ESR/CRP high; anaemia
• Angiography/MRA — aortic and branch stenosis
• Echo for aortic valve and root; PET/CT for active inflammation
• Exclude GCA by age and distribution

DDx — what else could it be?

• Giant cell arteritis
• Atherosclerosis
• Fibromuscular dysplasia
• Coarctation
• Behçet with aortic involvement

Management — what will you do?

• Corticosteroids; immunosuppression if refractory
• Revascularisation for critical stenosis once inflammation is controlled
• Control hypertension; monitor for aneurysm

C. Kawasaki disease

Scenario. Infant under 4 years with prolonged fever, rash, cervical adenopathy and mucocutaneous ulceration — a medium-vessel vasculitis that attacks the coronary arteries.

History — what will you ask?

• Fever >5 days, irritability, poor feeding
• Rash; red eyes, red cracked lips, oral or genital ulcers
• Cervical swelling

Signs — what will you find?

• Fever + cervical adenopathy, rash, mucocutaneous oral and genital ulceration, erythema
• Conjunctival injection, strawberry tongue, desquamation
• Signs of coronary ischaemia or shock

Investigations — what will you order?

• Echocardiography — coronary artery beading/aneurysm
• ESR, CRP, platelets, anaemia
• ECG for ischaemia

DDx — what else could it be?

• Mononucleosis
• Hand-foot syndrome (Coxsackie)
• HIV
• Scarlet fever
• Measles

Management — what will you do?

• High-dose aspirin — beware Reye syndrome
• IV immunoglobulin; cardiology follow-up for aneurysms
• Treat complications — thrombosis, myocardial ischaemia

D. Thromboangiitis obliterans (Buerger disease)

Scenario. Male smoker over 40 with claudication of the calf or forearm, Raynaud’s phenomenon and fingertip ulceration or autoamputation — segmental thrombosing inflammation of medium vessels.

History — what will you ask?

• Claudication — calf or forearm, intermittent
• Raynaud’s phenomenon; painful fingertip ulcers
• Heavy smoking; young age for peripheral vascular disease

Signs — what will you find?

• Absent distal pulses; ischaemic digits, ulceration, autoamputation
• Signs of superficial thrombophlebitis
• No proximal bruits

Investigations — what will you order?

• Angiography — segmental occlusion with corkscrew collaterals, distal disease
• ESR normal; thrombophilia and autoimmune screen negative
• Exclude diabetes and embolic source

DDx — what else could it be?

• Atherosclerosis (older, proximal disease)
• Thromboembolism
• Scleroderma with digital ulcers
• Takayasu arteritis

Management — what will you do?

• Smoking cessation — the only measure that stops progression
• Prostaglandins, calcium channel blockers (vasoselective, e.g. nifedipine); beta-blockers are contraindicated
• Endothelin receptor antagonist in severe cases; amputation for gangrene

E. Polyarteritis nodosa

Scenario. Adult with palpable purpura, fever, weight loss, abdominal pain and mononeuritis multiplex (wrist or foot drop) — necrotising inflammation of medium arteries that spares the pulmonary artery; 30% are hepatitis B positive.

History — what will you ask?

• Fever, weight loss, myalgia, arthralgia
• Abdominal pain; testicular pain
• Numbness or weakness in a single nerve territory
• Hepatitis B risk; dialysis fistula infection

Signs — what will you find?

• Palpable purpura, subcutaneous nodules in a string-of-pearls distribution
• Peripheral neuropathy — wrist drop, foot drop
• Hypertension and renal impairment
• Abdominal tenderness

Investigations — what will you order?

• Hepatitis B serology positive in 30%
• Angiography — multiple microaneurysms (string of pearls), beading of medium arteries, pulmonary artery spared
• Urinalysis and creatinine; biopsy of skin, nerve or kidney
• ESR/CRP, ANCA usually negative

DDx — what else could it be?

• GPA/MPA (pulmonary involvement, ANCA)
• Cryoglobulinaemia
• HSP
• Endocarditis with emboli
• Cholesterol embolisation

Management — what will you do?

• Corticosteroids; add cyclophosphamide for severe disease
• Treat hepatitis B; dialysis and transplant for renal failure
• Control hypertension

F. Granulomatosis with polyangiitis (GPA)

Scenario. Adult with haemoptysis, chronic sinusitis, nasal crusting or saddle-nose deformity and a rising creatinine — small-vessel ANCA vasculitis with granulomas and pauci-immune glomerulonephritis.

History — what will you ask?

• Upper airway — sinusitis, runny nose, nasal crusting, saddle-nose deformity
• Lower airway — haemoptysis, cough, pulmonary infiltrates
• Haematuria, oedema, hypertension
• Weight loss, fever, arthralgia, neuropathy

Signs — what will you find?

• Saddle-nose deformity, nasal crusting, septal perforation
• Purpura; mononeuritis multiplex
• Signs of renal failure and pulmonary haemorrhage

Investigations — what will you order?

• c-ANCA against PR3
• Urinalysis — haematuria, RBC casts; rising creatinine
• CXR/CT — nodules, cavitation, alveolar haemorrhage
• Biopsy — necrotising granuloma, pauci-immune crescentic GN

DDx — what else could it be?

• MPA (no upper-airway disease, no granuloma)
• Churg–Strauss (asthma, eosinophilia)
• Infection — TB, fungal
• Malignancy
• Goodpasture disease

Management — what will you do?

• Corticosteroids + cyclophosphamide or rituximab
• Plasma exchange for pulmonary haemorrhage or severe renal disease
• Treat infection; monitor for relapse

G. Microscopic polyangiitis

Scenario. Adult with haemoptysis, haematuria and a rising creatinine but no upper-airway disease and no granuloma — small-vessel ANCA vasculitis, the closest mimic of GPA.

History — what will you ask?

• Haemoptysis, dyspnoea
• Haematuria, oedema, hypertension
• Fever, weight loss, arthralgia, purpura, neuropathy

Signs — what will you find?

• Purpura, peripheral neuropathy
• Signs of pulmonary haemorrhage and renal failure
• No saddle nose or sinus disease

Investigations — what will you order?

• p-ANCA against MPO
• Urinalysis — haematuria, RBC casts; creatinine
• CXR/CT — pulmonary infiltrates/haemorrhage
• Biopsy — pauci-immune necrotising crescentic GN, no granuloma

DDx — what else could it be?

• GPA (upper-airway disease, granuloma)
• Churg–Strauss (asthma, eosinophilia)
• Anti-GBM disease
• Lupus nephritis
• Infection

Management — what will you do?

• Corticosteroids + cyclophosphamide or rituximab
• Plasma exchange for severe renal or pulmonary disease
• Monitor for relapse and infection

H. Eosinophilic granulomatosis with polyangiitis (Churg–Strauss)

Scenario. Adult with late-onset asthma, eosinophilia, pericarditis and purpura — small-vessel ANCA vasculitis with eosinophilic inflammation.

History — what will you ask?

• Allergic asthma, often severe and late-onset
• Allergic rhinitis, sinusitis, nasal polyps
• Purpura, numbness, abdominal pain
• Fever, weight loss

Signs — what will you find?

• Eosinophilia, purpura, peripheral neuropathy
• Pericarditis; signs of heart failure
• Wheeze, crackles

Investigations — what will you order?

• p-ANCA against MPO; marked eosinophilia
• CXR/CT — transient infiltrates; echo — pericarditis, cardiomyopathy
• Biopsy — eosinophilic necrotising vasculitis and granulomas
• IgE raised

DDx — what else could it be?

• GPA/MPA
• Hypereosinophilic syndrome
• Severe asthma with infection
• Eosinophilic pneumonia

Management — what will you do?

• Corticosteroids; immunosuppression for severe organ disease
• Treat asthma and cardiac involvement; leukotriene antagonists may unmask vasculitis
• Monitor for relapse

I. Henoch–Schönlein purpura (IgA vasculitis)

Scenario. Child or young adult with palpable purpura over the buttocks and extensor legs, arthralgia and colicky abdominal pain, days after an upper respiratory infection; the kidney may be the only organ involved (Berger disease).

History — what will you ask?

• Recent upper respiratory infection within a week
• Purpura over buttocks, legs and thighs (extensor surfaces)
• Joint pain; abdominal pain, bloody diarrhoea, vomiting

Signs — what will you find?

• Palpable purpura on the extensor surfaces — back, buttocks, legs, thighs
• Arthralgia; abdominal tenderness
• Strawberry-jelly stool; signs of intussusception
• Haematuria and hypertension (glomerulonephritis)

Investigations — what will you order?

• Urinalysis — haematuria and protein (IgA nephropathy); renal function
• Stool for blood; abdominal ultrasound if intussusception suspected
• IgA immune complexes on biopsy; ANCA negative
• CBC, ESR

DDx — what else could it be?

• Berger disease (kidney only)
• ITP
• Meningococcaemia
• Cryoglobulinaemia
• Post-streptococcal glomerulonephritis

Management — what will you do?

• Plasmapheresis (most important)
• Corticosteroids and immunoglobulin
• Supportive care; nephrology follow-up for persistent proteinuria

J. Behçet disease

Scenario. Young adult from the Silk Road (Middle East, Mediterranean, East Asia) with recurrent painful oral and genital ulcers, red painful eye and attacks of aseptic meningitis or dural sinus thrombosis — vasculitis of arteries, veins and capillaries.

History — what will you ask?

• Recurrent oral ulcers (mandatory) and genital ulcers
• Red painful eye, blurred vision
• Headache, photophobia, neck stiffness; focal deficit
• Skin lesions — erythema nodosum; joint pain
• Family history; HLA-B51

Signs — what will you find?

• Oral and genital aphthous ulcers
• Uveitis (anterior and posterior); hypopyon
• Meningism — aseptic meningitis with lymphocytic CSF, no organisms
• Erythema nodosum; pulmonary aneurysms; sagittal sinus thrombosis with spastic paraparesis

Investigations — what will you order?

• Clinical criteria; HLA-B51
• CSF — lymphocytosis, sterile; MRI/MRV for sinus thrombosis
• Fundoscopy and slit lamp; CXR/CT for pulmonary aneurysms
• ESR/CRP; pathergy test

DDx — what else could it be?

• Herpes simplex stomatitis
• Syphilis
• Reactive arthritis
• Inflammatory bowel disease
• Antiphospholipid syndrome

Management — what will you do?

• Steroids in flares, then a steroid-sparing agent — azathioprine, methotrexate or cyclosporine
• Anticoagulation for dural sinus thrombosis
• Immunosuppression for eye, CNS and vascular disease

K. Cryoglobulinaemia

Scenario. Adult presenting in cold weather with purpura, arthralgia, Raynaud’s phenomenon and neuropathy — immunoglobulins that precipitate below 37 °C, deposit in vessels and activate complement (low C4).

History — what will you ask?

• Cold-provoked rash and Raynaud’s phenomenon
• Arthralgia, fatigue, fever
• Neuropathy — numbness, weakness
• Hepatitis C, HIV, Sjögren or haematological malignancy

Signs — what will you find?

• Palpable purpura, livedo reticularis, chronic leg ulcers
• Peripheral neuropathy; arthropathy
• Membranoproliferative glomerulonephritis — oedema, hypertension
• Hepatosplenomegaly, lymphadenopathy (type 1)

Investigations — what will you order?

• Cryoglobulins positive; complement C4 low
• Hepatitis C and HIV serology; rheumatoid factor; SPEP/UPEP
• Urinalysis, creatinine; nerve conduction
• Skin or renal biopsy — immune-complex deposition

DDx — what else could it be?

• Type 1 — monoclonal (Waldenström, myeloma)
• Type 2 — mixed, hepatitis C/HIV
• Type 3 — polyclonal (SLE, Sjögren)
• HSP
• Cryofibrinogenaemia

Management — what will you do?

• Treat the cause — antiviral for HCV, antiretroviral for HIV
• Corticosteroids, rituximab; plasmapheresis for severe disease
• Avoid cold exposure; treat renal and neurological complications

Section 3 — Neurology

Parkinsons disease

Scenario. Older adult with progressive neurodegeneration from loss of dopaminergic neurons in the substantia nigra pars compacta with Lewy bodies (α-synuclein), causing dopamine deficiency in the basal ganglia and dopamine–acetylcholine imbalance. Motor features “TRAP”: resting pill-rolling tremor, rigidity, akinesia/bradykinesia and late postural instability. Non-motor: depression/anxiety, constipation, urinary frequency and orthostatic hypotension (late), cognitive decline/Parkinson’s dementia, REM sleep behaviour disorder, early hyposmia.

History — what will you ask?

• Onset and asymmetry of tremor (rest vs action), stiffness, slowness, falls, handwriting and walking change
• sleep disturbance, anosmia, constipation, mood, memory
• drug history — antipsychotics (haloperidol, risperidone), antiemetics (metoclopramide)
• young onset with psychiatric or liver features (Wilson)
• family history (Huntington)
• response to levodopa

Signs — what will you find?

• Resting pill-rolling tremor, cogwheel/lead-pipe rigidity, bradykinesia, postural instability
• hypophonia
• symmetric signs and absent resting tremor with drug-induced parkinsonism
• vertical gaze palsy and early falls (PSP)
• early dementia with visual hallucinations and fluctuation (DLB)
• hyperreflexia (vascular)
• Kayser-Fleischer rings

Investigations — what will you order?

• Clinical diagnosis (UK Brain Bank criteria)
• MRI usually normal — used to exclude other causes
• DAT-SPECT showing reduced striatal dopamine uptake
• Red flags against idiopathic PD: poor or no levodopa response, early postural instability/falls, rapid progression, early autonomic failure or dementia, symmetrical onset

DDx — what else could it be?

• Drug-induced parkinsonism
• vascular parkinsonism
• normal pressure hydrocephalus (gait disturbance, incontinence, dementia, enlarged ventricles)
• essential tremor (action tremor, alcohol-responsive, no rigidity)
• Parkinson-plus syndromes — MSA (autonomic failure, cerebellar signs), PSP, corticobasal degeneration, dementia with Lewy bodies
• Wilson’s disease
• Huntington’s
• post-encephalitic parkinsonism

Management — what will you do?

• Levodopa + carbidopa (Sinemet; not preferred early; nausea, dyskinesias, on–off, hallucinations, initial hypertension then orthostatic hypotension)
• dopamine agonists (pramipexole, ropinirole, bromocriptine — impulse control disorders, sleep attacks)
• MAO-B inhibitors (selegiline, rasagiline)
• COMT inhibitors (entacapone, tolcapone — orange urine, hepatotoxicity)
• amantadine (livedo reticularis, oedema, hallucinations)
• anticholinergics (trihexyphenidyl, benztropine — tremor, avoid in elderly)
• Surgery: thalamotomy for tremor, pallidotomy for rigidity
• stem cell transplantation experimental

Paraplegia

A. Compressive myelopathy

Scenario. Adult with progressive spastic paraparesis, a sensory level, root pain and sphincter disturbance — cord compression by vertebral disease, extradural or intradural tumour, abscess or disc; 95% of compressive lesions are extramedullary.

History — what will you ask?

• Back pain and root pain in a dermatome
• Progressive weakness and stiffness; falls
• Sphincter disturbance; weight loss, fever, TB contact, known cancer
• Mode of onset — acute (trauma, metastasis), subacute (Pott’s, epidural abscess, tumour 2–6 weeks), chronic (>6 weeks)

Signs — what will you find?

• Sensory level and motor level; Beevor’s sign (T10)
• Inverted supinator reflex (C5); hyperreflexia below the lesion with LMN signs at the level
• Spinal tenderness, gibbus, deformity
• Bladder involvement; saddle sensory loss

Investigations — what will you order?

• MRI spine — investigation of choice (level, cause, cord signal)
• Plain X-ray, CT; ESR/CRP, calcium, B12
• CSF if infection or malignancy suspected; biopsy of the vertebral lesion

DDx — what else could it be?

• Vertebral — fracture/dislocation, disc prolapse, Pott’s, primary or metastatic tumour, kyphoscoliosis
• Meningeal — leukaemic deposits, meningioma, pachymeningitis, neurofibroma, arachnoiditis
• Intramedullary — syringomyelia, glioma, ependymoma

Management — what will you do?

• Surgical decompression and stabilisation; urgent decompression for cord compression
• Antibiotics and drainage for epidural abscess; anti-TB therapy for Pott’s disease
• Steroids for inflammatory myelitis; radiotherapy for metastasis; bladder and pressure-area care, DVT prophylaxis, rehabilitation

B. Intramedullary non-compressive myelopathy

Scenario. Adult with a dissociated sensory loss (pain/temperature lost, proprioception preserved), wasting at the level and slowly progressive spasticity — disease within the cord itself, without external compression.

History — what will you ask?

• Neck or back pain; burning dysaesthesia
• Weakness and wasting of the hands; unsteadiness
• Fever (infection); known cancer; radiation

Signs — what will you find?

• Dissociated sensory loss; suspended sensory level
• Lower motor neuron signs at the level, upper motor neuron signs below
• Trophic changes, neuropathic joints (syringomyelia)

Investigations — what will you order?

• MRI cord — intrinsic signal change, expansion, syrinx
• CSF — cells, protein, oligoclonal bands, culture
• B12, HIV, syphilis serology; autoimmune screen; biopsy if tumour

DDx — what else could it be?

• Demyelinating — MS, transverse myelitis
• Tumour — glioma, ependymoma, metastasis
• Vascular — anterior spinal artery occlusion
• Inflammatory/infective — myelitis, abscess, TB, HIV
• Syringomyelia

Management — what will you do?

• Treat the cause — steroids for inflammatory myelitis, antimicrobials for infection, oncology for tumour
• Drainage of syrinx; rehabilitation and spasticity management
• Bladder care and prevention of contractures

C. Systemic causes of paraplegia

Scenario. Adult with bilateral, symmetrical spastic paraparesis without a sensory level — a systemic disease affecting the pyramidal tracts: hereditary spastic paraplegia, Friedreich/Marie ataxia, subacute combined degeneration, pellagra or motor neuron disease.

History — what will you ask?

• Slowly progressive stiffness and gait disturbance
• Family history (hereditary spastic paraplegia, ataxias)
• Diet, alcohol, gastric surgery (B12); malnutrition (pellagra)
• Fasciculations, wasting, bulbar symptoms (MND)

Signs — what will you find?

• Symmetrical spasticity, hyperreflexia, upgoing plantars
• Absent sensory level; posterior column signs in SACD
• Ataxia, scoliosis, cardiomyopathy (Friedreich)
• Wasting and fasciculation (MND)

Investigations — what will you order?

• B12, folate, MMA; copper; HIV/syphilis
• MRI spine (to exclude compression) and brain
• Genetic testing; nerve conduction/EMG; visual evoked potentials

DDx — what else could it be?

• Compressive myelopathy
• MS
• MND
• Hereditary ataxia
• Vitamin E deficiency

Management — what will you do?

• Treat the deficiency — B12 replacement, correct diet/alcohol
• Physiotherapy and spasticity management; genetic counselling for hereditary forms
• Multidisciplinary care for MND

Section 3 — Infectious Diseases

PARASITIC INFECTIONS

A. Asymptomatic amoebiasis

Scenario. Patient from an area of poor sanitation with Entamoeba cysts in the stool but no symptoms — E. dispar never needs treatment, but E. histolytica is treated even when asymptomatic to prevent transmission and invasion.

History — what will you ask?

• No bowel symptoms; incidental stool finding
• Sanitation, water source, flies, human faeces as fertiliser
• Travel or residence in an endemic area

Signs — what will you find?

• Normal abdominal examination
• No hepatomegaly or tenderness

Investigations — what will you order?

• Stool — cysts only, no trophozoites
• Stool antigen test for E. histolytica
• Serology not recommended for this stage

DDx — what else could it be?

• E. dispar (no treatment)
• Non-pathogenic protozoa
• Carrier state of other parasites

Management — what will you do?

• DIP — diloxanide furoate, iodoquinol or paromomycin for 7–10 days
• Health education and sanitation

B. Amoebic colitis (dysentery)

Scenario. Adult with diarrhoea, gas and abdominal pain, or severe dysentery with 10–20 bloody stools a day, fever, vomiting and tenderness — E. histolytica trophozoites invading the colon.

History — what will you ask?

• Diarrhoea — frequency, blood, mucus; abdominal pain and gas
• Fever, weakness, vomiting in severe disease
• Weight loss; recent travel or poor sanitation

Signs — what will you find?

• Abdominal tenderness; increased bowel sounds
• Dehydration; fever in dysentery
• Peritonism if perforation

Investigations — what will you order?

• Stool — cysts and trophozoites, blood and WBCs
• Stool antigen test positive for E. histolytica
• Serology available but not recommended
• Exclude other causes — stool culture, PCR

DDx — what else could it be?

• Bacillary dysentery (Shigella)
• Giardiasis
• Inflammatory bowel disease
• Colorectal carcinoma
• Intestinal TB

Management — what will you do?

• Metronidazole 500 mg TID for 10 days + diloxanide furoate (kills cysts)
• Increased fluids; correct dehydration
• Complications — intestinal perforation (high mortality), chronic diarrhoea with weight loss

C. Amoebic liver abscess

Scenario. Adult with right upper quadrant pain, fever with chills and sweating and tender hepatomegaly — often without a preceding diarrhoeal illness; ultrasound shows an abscess.

History — what will you ask?

• RUQ pain, fever, chills, sweating
• Weight loss, anorexia; may have had diarrhoea earlier
• Travel or residence in an endemic area

Signs — what will you find?

• Tender hepatomegaly; RUQ tenderness
• Fever; jaundice uncommon
• Signs of sepsis

Investigations — what will you order?

• Ultrasound — abscess (non-specific)
• Serology for anti-amoeba antibodies is a very good test
• Aspiration — brownish-yellow pus, check for E. histolytica antigens
• CBC, LFTs

DDx — what else could it be?

• Pyogenic liver abscess
• Hepatocellular carcinoma
• Hydatid cyst
• Cholecystitis
• Malaria with hepatomegaly

Management — what will you do?

• Metronidazole + diloxanide furoate
• Drain if the abscess is very large or the patient is very sick
• Treat complications — rupture, secondary infection

D. Hydatid disease (echinococcosis)

Scenario. Adult with a slowly enlarging hydatid cyst in the liver (or lung, brain) years after ingesting Echinococcus eggs from a dog — a zoonosis; E. granulosus gives cystic disease and E. multilocularis a more aggressive alveolar form.

History — what will you ask?

• RUQ pain, nausea, malaise, hepatomegaly
• Cough, chest pain, dyspnoea, haemoptysis (lung cyst)
• Headache or seizures (brain cyst)
• Dog/sheep contact, farming, endemic region

Signs — what will you find?

• Hepatomegaly with a smooth palpable mass
• Signs of lung cyst; focal neurological signs
• Anaphylaxis if the cyst ruptures

Investigations — what will you order?

• CBC — eosinophilia
• Anti-echinococcus antibodies
• Ultrasound — smooth-walled cyst with eggshell calcification, daughter cysts and septa
• CT — best for extrahepatic (brain, lung) cysts

DDx — what else could it be?

• Amoebic liver abscess
• Simple hepatic cyst
• Hepatocellular carcinoma
• Haemangioma
• Lung abscess

Management — what will you do?

• Small cyst — albendazole alone (alternatives mebendazole, praziquantel)
• Large or complicated cyst — surgical resection of the whole cyst
• Never spill cyst contents — fatal anaphylaxis and daughter-cyst spread

Visceral Leishmaniasis

Scenario. Patient from an endemic area (90% of cases in India, Bangladesh, Sudan, Brazil, Ethiopia; also Asia, Africa, South America, Mediterranean) with kala-azar (black fever): Leishmania donovani or L. infantum/chagasi, an obligate intracellular protozoon transmitted by the bite of the female sandfly (Phlebotomus Old World, Lutzomyia New World) from reservoirs in dogs, rodents, foxes, jackals and humans. Incubation 2–6 months (up to 2 years). Amastigotes multiply in macrophages and invade the reticuloendothelial system (spleen, liver, bone marrow, lymph nodes) with progressive immune suppression; fatal in >95% if untreated.

History — what will you ask?

• Prolonged irregular fever with chills and night sweats, progressive weight loss and anorexia, abdominal fullness, weakness and malaise, bleeding/petechiae
• poverty, malnutrition, poor housing, HIV co-infection, population movement, rainforest/peri-urban residence, proximity to animal reservoirs

Signs — what will you find?

• Ill-looking, pale and emaciated
• fever
• hepatosplenomegaly — enlarged non-tender spleen and liver causing abdominal swelling
• generalized lymphadenopathy
• skin darkening/hyperpigmentation
• petechiae and bruising
• jaundice
• signs of secondary infection

Investigations — what will you order?

• Gold standard: amastigotes (Leishman–Donovan bodies) — splenic aspirate ~95% (bleeding risk), bone marrow ~60–85% (safer), lymph node, culture
• serology — rK39 rapid test, DAT, ELISA, IFA (persist after cure, lower in HIV)
• KAtex urine antigen
• PCR (HIV/relapse)
• Montenegro skin test negative in active disease
• supportive — pancytopenia, hypergammaglobulinaemia, raised ESR, hypoalbuminaemia

DDx — what else could it be? (standard differential; the note gives no list of its own)

• Malaria
• typhoid
• tuberculosis
• brucellosis
• lymphoma with splenomegaly
• chronic myeloid leukaemia
• cirrhosis with hypersplenism
• HIV with opportunistic infection
• other causes of pancytopenia and fever of unknown origin

Management — what will you do?

• Supportive — nutrition, anaemia, infections, antipyretics, bleeding
• WHO drugs: pentavalent antimony, amphotericin B deoxycholate, liposomal amphotericin B, paromomycin, miltefosine
• Saudi-registered: sodium stibogluconate or meglumine antimoniate 20 mg/kg/day ×30 days IM/IV — cardiotoxicity, fatal arrhythmia
• avoid in elderly, organ disease, pregnancy. Liposomal amphotericin B 3 mg/kg/day IV — nephrotoxicity, thrombocytopenia, hypokalaemia
• reserve for resistant/contraindicated cases
• Death from overwhelming bacterial infection
• Prevention: bed nets, spraying, sanitation
• no vaccine

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