Internal med y5 eop Mcq: - asthma step up step down treatment - Copd gold criteria - Multiple myeloma - First line epilepsy treatment - Hypertensive emergency - Investigation for occult stool blood - Prolonged fever - Chronic glomerulonephritis - IDA, polycythemia vera, aml/cml, g6pd MEQ 1. Pt came with edema, abd distension, early satiety and leg swelling, denies heart failure and ckd symptoms - what other history do u need to ask - What are signs u need to look for - Interpret given findings (masld) - Why is there reduced platelets (2reasons) and abnormal INR (1 reason) in cirrhosis - Pathophysio of masld and the resultinf symptoms - Complications and what oral med to give for it SEQ 1. Pt came with orthopnea, cardiomegalyand pansystolic murmur, no edema, no jvp, but bilateral crackles. What is diagnosis (LV failure) - 3 etiologies of the diagnosis - Investigations and findings - What meds do u need to give - Pathophysio of murmur OSCE 1. CXR: interpret xray, give 4 differentials, give 3 investigations and expected findings, complications (dx: pneumonia) 2. Ct brain; interpret, bamford classification, investigations and what meds does patient need, what are two brain complications 3. Picture of exophthalmos, 2 abnormal findings, signs to look for in patient, one investigation to confirm diagnosis, what is diagnosis (graves disease), 2 meds that patient shoukd be on 4. ⁠interactive osce :consent hemodialysis Give me the answers

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Finding Sources

Here is the full comprehensive answer set for your Internal Medicine Year 5 EOP exam:

INTERNAL MEDICINE Y5 EOP - COMPLETE ANSWER GUIDE

MCQ TOPICS

1. ASTHMA - Step Up / Step Down Treatment (GINA Guidelines)

Step	Controller Therapy
Step 1	As-needed low-dose ICS-formoterol (preferred) OR SABA as reliever
Step 2	Low-dose ICS daily + SABA as reliever
Step 3	Low-dose ICS-LABA OR medium-dose ICS
Step 4	Medium-dose ICS-LABA
Step 5	High-dose ICS-LABA ± LAMA; consider add-on biologic (e.g. omalizumab, dupilumab)

Step UP: If uncontrolled symptoms at current step for 2-3 months (check adherence and inhaler technique first). Step DOWN: If well-controlled for at least 3 months, consider stepping down to find minimum effective therapy.

Relievers at all steps: Low-dose ICS-formoterol (SMART therapy) preferred over SABA alone. Add-ons before Step 5: Leukotriene receptor antagonists (montelukast), theophylline, LAMA (tiotropium).

2. COPD - GOLD Criteria

Diagnosis: Post-bronchodilator FEV1/FVC < 0.70

GOLD Spirometric Grades (based on FEV1 % predicted):

GOLD Grade	Severity	FEV1
GOLD 1	Mild	≥ 80%
GOLD 2	Moderate	50-79%
GOLD 3	Severe	30-49%
GOLD 4	Very Severe	< 30%

GOLD ABE Symptom/Risk Assessment (2023 update - replaced ABCD groups):

Group A: Low symptom (mMRC 0-1 or CAT <10), 0-1 exacerbations/yr (no hospitalization) → Short-acting bronchodilator (SABA or SAMA)
Group B: High symptom (mMRC ≥2 or CAT ≥10), 0-1 exacerbations/yr → Long-acting bronchodilator (LABA or LAMA), preferred: LABA+LAMA
Group E: ≥2 exacerbations OR ≥1 leading to hospitalization → LABA+LAMA; add ICS if eosinophils ≥300 cells/μL

Oxygen therapy: Long-term O₂ if PaO₂ ≤ 55 mmHg or SpO₂ ≤ 88%

3. Multiple Myeloma

CRAB Criteria (end-organ damage - diagnostic of symptomatic MM):

C - Calcium >11 mg/dL (hypercalcemia)
R - Renal impairment (creatinine >2 mg/dL or CrCl <40 mL/min)
A - Anemia (Hb <10 g/dL or >2g below normal)
B - Bone lesions (lytic lesions, osteoporosis with fractures)

SLiM criteria (added 2014 - treat even without CRAB):

60% clonal BM plasma cells
Serum FLC ratio ≥100
1 focal lesion on MRI

Investigations: SPEP (M-spike), serum FLC, 24h urine protein electrophoresis, bone marrow biopsy (≥10% clonal plasma cells), skeletal survey/low-dose whole body CT.

Treatment:

Transplant-eligible: Bortezomib + Lenalidomide + Dexamethasone (VRd), then ASCT + maintenance lenalidomide
Transplant-ineligible: VRd or daratumumab-based regimen
Bisphosphonates (zoledronic acid) for bone disease

4. First-Line Epilepsy Treatment

Focal (Partial) Seizures:

First-line: Levetiracetam, Lamotrigine, Oxcarbazepine, Carbamazepine

Generalized Tonic-Clonic:

First-line: Sodium Valproate (most effective, but teratogenic), Levetiracetam, Lamotrigine

Absence Seizures:

First-line: Ethosuximide (drug of choice), Valproate, Lamotrigine

Myoclonic Seizures:

First-line: Sodium Valproate, Levetiracetam, Clonazepam

Juvenile Myoclonic Epilepsy: Valproate (first-line), avoid carbamazepine/phenytoin (can worsen).

Pregnancy: Levetiracetam and Lamotrigine are safest (valproate teratogenic - neural tube defects).

Status Epilepticus:

Lorazepam / Diazepam (benzodiazepine first-line)
Phenytoin / Fosphenytoin or Levetiracetam (second-line)
Phenobarbital or general anesthesia (refractory)

5. Hypertensive Emergency

Definition: Severe hypertension (usually >180/120 mmHg) WITH end-organ damage.

End-organ damage: Hypertensive encephalopathy, stroke, acute MI, acute LV failure/pulmonary oedema, aortic dissection, eclampsia, AKI, MAHA.

Management:

Admit to ICU
IV antihypertensives - reduce MAP by no more than 25% in the first hour, then gradually to 160/100 over 2-6 hours (avoid rapid drops - cerebral hypoperfusion)
Drug choices:
- Labetalol IV (versatile, most situations)
- Nitroprusside IV (most potent, titratable)
- Nicardipine IV (stroke, encephalopathy)
- Hydralazine IV (eclampsia/pregnancy)
- Esmolol IV (aortic dissection - reduce HR and BP)
- GTN/Nitroglycerine IV (ACS, pulmonary oedema)
Avoid: Sublingual nifedipine (rapid uncontrolled drop → stroke/MI)

Hypertensive Urgency: Severe BP WITHOUT organ damage → oral agents, gradual reduction over 24-48h.

6. Investigation for Occult Stool Blood

Faecal Occult Blood Testing (FOBT) - used in colorectal cancer screening:

Types:

Faecal Immunochemical Test (FIT) - preferred/gold standard for CRC screening
- Detects human globin (lower GI specific)
- No dietary restrictions needed
- Automated, quantitative
Guaiac-based FOBT (gFOBT) - older method
- Detects haem peroxidase activity
- Dietary restrictions needed (avoid red meat, vitamin C, NSAIDs)
- Less specific

Other investigations for iron deficiency anaemia with occult blood:

Upper GI endoscopy (OGD) - first if >50 years or dyspepsia
Colonoscopy - first if lower GI symptoms (PR bleeding, change in bowel habit)
CT colonography (if colonoscopy not feasible)
Capsule endoscopy (if both OGD and colonoscopy negative - small bowel source)

7. Prolonged Fever (Fever of Unknown Origin - FUO)

Definition (Classic FUO): Temperature >38.3°C on ≥3 occasions, duration >3 weeks, no diagnosis despite 3 days of investigation (or 3 outpatient visits).

Causes (3 main categories):

Category	Examples
Infections (35%)	TB (most common worldwide), endocarditis, abscesses, typhoid, brucellosis, HIV, CMV, EBV
Neoplasms (20%)	Lymphoma (Hodgkin's/NHL - classic), leukaemia, renal cell carcinoma, hepatocellular carcinoma
Non-infectious inflammatory (20%)	SLE, adult-onset Still's, RA, vasculitis, IBD, sarcoidosis
Miscellaneous/Unknown (25%)	Drug fever, factitious, pulmonary embolism

Investigations (stepwise):

FBC, ESR, CRP, LFT, RFT, LDH, uric acid, blood cultures x3
ANA, ANCA, RF, complement
CXR, CECT thorax/abdomen/pelvis
Bone marrow biopsy
PET-CT (very useful for FUO - localizes occult malignancy/infection/inflammation)

8. Chronic Glomerulonephritis

Definition: Progressive destruction of glomeruli leading to CKD.

Causes:

IgA nephropathy (most common worldwide)
Focal segmental glomerulosclerosis (FSGS)
Membranous nephropathy
Lupus nephritis (Class III/IV)
MPGN
Post-infectious GN (if unresolved)

Features:

Proteinuria (may be nephrotic range)
Haematuria (microscopic)
Hypertension
Gradually rising creatinine
Small scarred kidneys on USS (late stage)

Investigations:

Urinalysis (RBC casts = pathognomonic of GN)
24h urine protein or spot PCR
ANA, ANCA, anti-GBM, complement (C3, C4), SPEP
Renal biopsy - definitive diagnosis

Management:

ACEi/ARB (reduce proteinuria, slow progression)
BP control (<130/80)
Immunosuppression (based on cause - steroids, cyclophosphamide, MMF)
Dialysis/transplant if ESRD

9. Haematology Topics

Iron Deficiency Anaemia (IDA)

Microcytic hypochromic anaemia (MCV <80 fL)

Parameter	IDA
Serum iron	Low
TIBC	High
Serum ferritin	Low (<12 ng/mL - most specific)
Transferrin saturation	Low (<15%)
Blood film	Pencil cells, target cells, microcytes
Reticulocytes	Low (hypoproliferative)

Treatment: Oral ferrous sulphate 200mg TDS; treat underlying cause (GI bleed, poor diet, malabsorption).

Polycythaemia Vera (PV)

JAK2 V617F mutation in >95% of cases.

WHO Diagnostic Criteria: 3 major OR 2 major + 1 minor

Major: Hb >16.5 (M) / >16 (F), BM biopsy showing hypercellularity with panmyelosis, JAK2 mutation
Minor: Subnormal EPO level

Features: Plethora, pruritus after hot bath (aquagenic), splenomegaly, hyperviscosity, thrombosis.

Treatment: Phlebotomy (mainstay), low-dose aspirin, hydroxyurea (high risk), ruxolitinib (refractory).

AML vs CML

Feature	AML	CML
Age	Any (peaks elderly)	Middle-aged (40-60)
WBC	Variable	Very high (>100 × 10⁹/L)
Blast count	≥20% in BM	<10% (chronic phase)
Philadelphia chromosome	Absent (usually)	Present (BCR-ABL1, t(9;22))
Auer rods	Present (diagnostic)	Absent
Clinical	Acute onset, pancytopenia	Insidious, splenomegaly
Treatment	Cytarabine + Daunorubicin (7+3); HSCT	Imatinib (TKI) first-line
Basophilia/eosinophilia	Absent	Present (CML hallmark)

AML subtypes (know M3 - APL): t(15;17), treat with ATRA + arsenic trioxide.

G6PD Deficiency

X-linked recessive - affects RBC antioxidant defense.

Triggers: Oxidative stress - infections, drugs (dapsone, primaquine, nitrofurantoin, rasburicase), fava beans, mothballs.

Presentation: Acute intravascular haemolytic anaemia.

Blood film: Bite cells, blister cells, Heinz bodies (on supravital stain).

Investigations: G6PD enzyme assay (false normal during acute haemolysis - repeat after 3 months).

Management: Remove trigger, transfuse if severe, supportive.

MEQ - MASLD / CIRRHOSIS

Clinical Scenario: Patient with edema, abdominal distension, early satiety, leg swelling; denies heart failure and CKD.

(a) What Additional History to Take

Alcohol history: quantity, duration, last drink (CAGE score) - important even for MASLD as alcohol is a confounder
Metabolic risk factors: diabetes, obesity, dyslipidemia, hypertension
Diet history: caloric intake, dietary patterns
Medications: hepatotoxic drugs (methotrexate, amiodarone, corticosteroids, TPN)
Family history: liver disease, metabolic syndrome, haemochromatosis
Symptoms of chronic liver disease: jaundice, dark urine, pale stools, pruritus, fatigue, bruising easily, confusion (encephalopathy)
GI symptoms: haematemesis, melaena, diarrhea
Social history: IV drug use (viral hepatitis risk), occupational/chemical exposures
Review of symptoms: weight loss, anorexia, loss of libido (hypogonadism in cirrhosis)

(b) Signs to Look For on Examination

Peripheral signs of chronic liver disease:

Palmar erythema
Dupuytren's contracture
Leukonychia (white nails), Terry's nails
Clubbing
Spider naevi (>5 - significant)
Parotid enlargement (alcohol)
Gynaecomastia, testicular atrophy (hyperestrogenism)
Loss of axillary/pubic hair
Peripheral oedema (hypoalbuminaemia)
Flapping tremor/asterixis (hepatic encephalopathy)
Caput medusae (portosystemic collaterals)
Jaundice, icterus

Abdominal signs:

Ascites (shifting dullness, fluid thrill)
Hepatomegaly or small firm liver (end-stage)
Splenomegaly
Abdominal wall collaterals
Tenderness (SBP - diffuse, peritoneal signs)

Vitals: Low BP (vasodilation), low O₂ (hepatopulmonary syndrome).

(c) Interpretation of Findings - MASLD

MASLD (Metabolic dysfunction-Associated Steatotic Liver Disease) = new nomenclature for NAFLD/NASH (2023).

Diagnosis requires:

Hepatic steatosis on imaging (USS: increased echogenicity, bright liver) or histology
≥1 metabolic risk factor (obesity BMI >25, T2DM, hypertension, dyslipidemia, metabolic syndrome) AND no other cause

Given findings likely include:

Raised ALT/AST (AST:ALT <2 in MASLD; >2 suggests alcohol)
Elevated GGT
USS showing echogenic liver, splenomegaly, ascites
Low albumin, raised bilirubin, prolonged INR (decompensated cirrhosis)
Thrombocytopenia

Interpretation: Patient has progressed from MASLD → MASH (Metabolic dysfunction-Associated Steatohepatitis) → cirrhosis → portal hypertension with decompensation (ascites, varices risk).

(d) Why Reduced Platelets (2 reasons) and Abnormal INR (1 reason) in Cirrhosis

Reduced Platelets - 2 reasons:

Hypersplenism / Splenic sequestration: Portal hypertension → splenomegaly → platelets pooled and destroyed in enlarged spleen.
Reduced thrombopoietin (TPO) production: TPO is synthesized in the liver → cirrhotic liver produces less TPO → reduced platelet production from megakaryocytes in bone marrow.

(Bonus: immune-mediated destruction, reduced BM production due to nutritional deficiencies)

Abnormal (Prolonged) INR - 1 reason:

Reduced hepatic synthesis of clotting factors: The liver synthesizes all clotting factors except Factor VIII (FVIII is synthesized in endothelium). In cirrhosis, reduced synthesis of Factors I (fibrinogen), II, V, VII, IX, X, XI, and Protein C and S → prolonged PT/INR. Factor VII has the shortest half-life, so INR rises earliest.

(e) Pathophysiology of MASLD and Resulting Symptoms

Pathophysiology (Two-Hit / Multi-Hit Model):

First Hit - Hepatic steatosis: Insulin resistance → increased free fatty acid (FFA) delivery to liver → impaired beta-oxidation → triglyceride accumulation in hepatocytes (steatosis). Obesity and metabolic syndrome are key drivers.
Second Hit - Oxidative stress and inflammation: Excess FFAs undergo lipotoxicity → oxidative stress → mitochondrial dysfunction → reactive oxygen species (ROS) → lipid peroxidation → activation of stellate cells → pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) via NF-κB pathway → hepatocyte apoptosis/necrosis → inflammation (steatohepatitis = MASH).
Fibrosis progression: Activated hepatic stellate cells → myofibroblast transformation → collagen deposition → fibrosis → cirrhosis.
Portal hypertension: Distortion of hepatic architecture + increased intrahepatic vascular resistance → portal hypertension → splanchnic vasodilation (NO-mediated) → ascites, varices, splenomegaly.

Resulting Symptoms:

Ascites and leg oedema: Portal hypertension + hypoalbuminaemia → ↓oncotic pressure → fluid third-spacing
Early satiety: Ascites compresses stomach
Abdominal distension: Ascites
Fatigue: Impaired metabolism, anaemia
Jaundice: Impaired bilirubin conjugation/excretion
Bruising: Coagulopathy
Confusion: Hepatic encephalopathy (↑ammonia)

(f) Complications and Oral Medication for Each

Complication	Oral Medication
Ascites	Spironolactone (first-line; aldosterone antagonist) ± Furosemide (ratio 100:40 mg); dietary Na restriction <2g/day
Hepatic Encephalopathy	Lactulose (acidifies colon, traps NH₄⁺, reduces ammonia absorption); Rifaximin (non-absorbable antibiotic - for secondary prevention)
Oesophageal Varices (primary prophylaxis)	Non-selective beta-blocker: Propranolol or Carvedilol (reduces portal pressure)
Spontaneous Bacterial Peritonitis (SBP) prophylaxis	Norfloxacin (long-term) or Trimethoprim-sulfamethoxazole; ciprofloxacin in some centres
HCC surveillance	No drug - USS + AFP every 6 months
Coagulopathy	Vitamin K (oral) if vitamin K deficiency contributing
Osteoporosis (cirrhosis)	Calcium + Vitamin D supplementation

SEQ - LEFT VENTRICULAR FAILURE

Diagnosis: Left Ventricular (Systolic) Failure - consistent with dilated cardiomyopathy/HFrEF given cardiomegaly, pansystolic murmur (MR), bilateral basal crackles (pulmonary oedema), orthopnoea; NO peripheral oedema/JVP elevation (right heart not yet involved).

(a) Three Etiologies of LV Failure

Ischaemic Heart Disease / Coronary Artery Disease - most common cause (~60-70%); myocardial infarction → scar tissue → impaired systolic function
Dilated Cardiomyopathy (DCM) - idiopathic, or secondary to: alcohol (toxic), peripartum, viral myocarditis (Coxsackievirus B), genetic, chemotherapy (doxorubicin)
Hypertensive Heart Disease - chronic pressure overload → LV hypertrophy → diastolic then systolic dysfunction
(Bonus) Valvular disease (aortic stenosis, mitral regurgitation), thyroid disease (thyrotoxicosis), Chagas disease

(b) Investigations and Expected Findings

Investigation	Expected Finding in LV Failure
ECG	LVH, LBBB (suggests cardiomyopathy), old Q waves (IHD), AF
CXR	Cardiomegaly (CTR >0.5), upper lobe blood diversion, Kerley B lines, interstitial/alveolar oedema, pleural effusion (bilateral)
Echocardiogram (key investigation)	Dilated LV, reduced EF (<40% in HFrEF), global/regional wall motion abnormality, mitral regurgitation (functional MR due to annular dilation), elevated LVEDP
BNP / NT-proBNP	Elevated (>35 pg/mL BNP or >125 pg/mL NT-proBNP excludes HF if normal; very high in HF)
FBC	Anaemia (contributing factor), WBC (if infective cause)
U&E / Renal function	Baseline before ACEi, hyponatraemia (poor prognosis)
LFT	Elevated in right heart failure, but here left-sided dominant
Troponin	Elevated if acute ischaemic cause
Coronary angiogram / CT coronary angiography	Coronary artery disease if ischaemic cause
Cardiac MRI	Gold standard for cardiomyopathy - late gadolinium enhancement (LGE) pattern: midwall = DCM, subendocardial = IHD
TFTs	Thyrotoxicosis causing high-output failure

(c) Medications

Cornerstone therapy for HFrEF (EF <40%) - "fantastic four":

ACEi (or ARBNi/ARNi - Sacubitril/Valsartan): Ramipril/Enalapril - reduces afterload, reverses remodelling, reduces mortality. Sacubitril/valsartan (Entresto) superior to ACEi if tolerated.
Beta-blocker: Carvedilol, Bisoprolol, Metoprolol succinate - reduce HR, anti-remodelling, mortality benefit. Start low, titrate up when euvolaemic.
Mineralocorticoid receptor antagonist (MRA): Spironolactone or Eplerenone - reduce aldosterone-driven fibrosis, mortality benefit.
SGLT2 inhibitor: Dapagliflozin or Empagliflozin - reduce hospitalisation and mortality regardless of diabetes status (now standard of care in HFrEF).

Additional medications:

Diuretics (Furosemide): Symptom relief - reduce preload, treat pulmonary oedema. Does NOT reduce mortality.
Digoxin: Rate control in AF, reduces hospitalisation (not mortality).
Ivabradine: If sinus rhythm + HR >70 despite max beta-blocker, reduces hospitalisation.
Hydralazine + Isosorbide dinitrate: Alternative if ACEi/ARB not tolerated (especially in African-American patients).
Anticoagulation: If AF present (warfarin or NOAC).

Device therapy (non-oral but mention):

ICD (EF <35% despite OMT >3 months)
CRT-D (EF <35% + LBBB + QRS >150ms)

(d) Pathophysiology of the Murmur (Pansystolic Murmur = Mitral Regurgitation)

In LV failure / DCM:

LV dilation → annular dilation of mitral valve ring → the mitral valve leaflets fail to coapt properly (tethered/displaced papillary muscles in dilated ventricle)
During systole, blood is ejected forward into the aorta AND regurgitates backward through the incompetent mitral valve into the left atrium
This regurgitant jet creates a pansystolic (holosystolic) murmur at the apex - because the pressure gradient between LV and LA exists throughout systole (from S1 to S2)
The murmur radiates to the axilla (direction of regurgitant jet)
In severe MR: LA becomes dilated → AF risk, pulmonary venous hypertension → pulmonary oedema → bilateral basal crackles
This is functional (secondary) MR - the valve leaflets themselves are structurally normal; dilation of the annulus and LV is the cause

OSCE ANSWERS

OSCE 1 - CXR Interpretation (Dx: Pneumonia)

CXR Interpretation:

Consolidation: homogeneous/heterogeneous opacity with air bronchograms (air-filled bronchi visible within opacified lung parenchyma)
Location: right lower lobe most common (community-acquired); may be any lobe
Loss of right heart border (right middle lobe), loss of left heart border (lingula), loss of hemidiaphragm (lower lobes)
No volume loss (unlike atelectasis)
May show pleural effusion (parapneumonic)

4 Differentials for Consolidation on CXR:

Pneumonia (bacterial, viral, atypical)
Lung malignancy / Bronchogenic carcinoma (especially if consolidative-type adenocarcinoma)
Pulmonary oedema (bilateral, perihilar "bat wing" distribution - check CTR)
Pulmonary infarction (following PE - Hampton's Hump: wedge-shaped opacity at pleural base)
(Bonus) Cryptogenic organising pneumonia (COP), atelectasis

3 Investigations and Expected Findings:

Investigation	Expected Finding
Sputum culture & sensitivity	Identification of causative organism (Streptococcus pneumoniae most common CAP; Legionella, Mycoplasma for atypical)
FBC	Elevated WBC with neutrophilia (bacterial); lymphocytosis (viral/atypical)
CRP and procalcitonin	Elevated CRP (>100 mg/L in bacterial pneumonia); elevated procalcitonin (bacterial aetiology)
Urinary antigens	Pneumococcal UAT positive for S. pneumoniae; Legionella UAT for Legionella
Blood cultures (if severe)	Bacteraemia in ~20-25% of hospitalised CAP
SpO₂ / ABG	Hypoxia (type 1 respiratory failure: ↓PaO₂, ↓/normal PaCO₂)

Severity Assessment: CURB-65 score (Confusion, Urea >7, RR ≥30, BP <90/60, Age ≥65) - guides hospital vs outpatient vs ICU.

Complications:

Parapneumonic effusion / Empyema (exudative pleural effusion → pus)
Lung abscess (cavitation)
Septicaemia / Bacteraemia
Respiratory failure (Type 1)
Organising pneumonia (fibrosis)

OSCE 2 - CT Brain - Ischaemic Stroke + Bamford Classification

CT Brain Interpretation (Ischaemic Stroke):

Acute (<24h): CT may be normal OR show subtle signs: loss of grey-white differentiation, hyperdense MCA sign (thrombus in artery), effacement of sulci/gyri in affected territory, insular ribbon sign
24-72h: Wedge-shaped hypoattenuating (dark) area in vascular territory, loss of basal ganglia outline
Late: Well-defined low-density area (infarct) with mass effect (oedema, midline shift) then gyral enhancement
Exclude: No hyperdense area (haemorrhage would be bright/white)

Bamford (Oxford) Classification (based on clinical features, not imaging):

Classification	Full Name	Clinical Features
TACI	Total Anterior Circulation Infarct	All 3: Motor/sensory deficit (2/3 body) + Homonymous hemianopia + Higher cortical dysfunction (dysphasia/neglect); MCA territory
PACI	Partial Anterior Circulation Infarct	2 of the 3 TACI features, OR isolated higher cortical dysfunction
LACI	Lacunar Infarct	Pure motor, pure sensory, sensorimotor, or ataxic hemiparesis; NO higher cortical deficit, NO hemianopia; small vessel disease
POCI	Posterior Circulation Infarct	Cerebellar/brainstem signs: ataxia, diplopia, dysarthria, dysphagia, crossed cranial nerve + long tract signs, Wallenberg syndrome

Investigations:

Investigation	Rationale / Finding
MRI DWI (gold standard)	Restricted diffusion (bright DWI, dark ADC) within minutes of ischaemia - more sensitive than CT
CT or MR Angiography	Identifies large vessel occlusion (LVO) - target for thrombectomy
ECG	AF (cardioembolic source) - new AF in ~25%
Echocardiogram (TTE/TOE)	Cardiac thrombus, PFO, valvular vegetation
Carotid Doppler	Carotid stenosis (PACI/TACI)
Lipid profile, HbA1c, FBC, coagulation	Vascular risk factors
Holter monitor	Paroxysmal AF

Medications for Ischaemic Stroke:

Acute (within 4.5h onset): IV alteplase (tPA) thrombolysis if no contraindications; Mechanical thrombectomy (if LVO, up to 24h)
Antiplatelet: Aspirin 300mg stat → 75mg daily (from 24h post-thrombolysis) ± Clopidogrel (dual antiplatelet x21 days in minor stroke/TIA - POINT/CHANCE trial)
Anticoagulation (if AF): Warfarin or NOAC (apixaban, rivaroxaban) - start 2-14 days after stroke depending on size
Statins: Atorvastatin 40-80mg (plaque stabilisation, regardless of cholesterol)
Antihypertensives: Do NOT lower BP acutely in ischaemic stroke (unless >220/120 or thrombolysis candidate) → resume after 24-48h
Supportive: DVT prophylaxis, aspiration precautions, early physiotherapy/speech therapy, glucose control

Two Brain Complications:

Cerebral oedema with transtentorial herniation (massive MCA infarct "malignant MCA syndrome") - peak 48-72h; may require decompressive hemicraniectomy
Haemorrhagic transformation (ischaemic stroke converting to haemorrhage) - especially after thrombolysis, or large territory infarcts

OSCE 3 - Exophthalmos / Graves Disease

Diagnosis: Graves Disease (autoimmune hyperthyroidism)

2 Abnormal Findings in the Picture:

Exophthalmos (proptosis) - forward protrusion of the eyeball due to retro-orbital fat/muscle infiltration
Lid lag / Lid retraction (sclera visible above iris) OR stare

Signs to Look For in the Patient:

Eye: Exophthalmos, periorbital oedema, chemosis (conjunctival oedema), ophthalmoplegia (CN III, IV, VI involvement), corneal ulceration, visual field defect (compressive optic neuropathy)
Thyroid: Diffuse smooth goitre (non-tender), bruit over thyroid
Skin: Pretibial myxoedema (localised non-pitting oedema over shin - pathognomonic for Graves), thyroid acropachy (clubbing with soft tissue swelling)
Cardiovascular: Tachycardia, AF, wide pulse pressure, hyperdynamic circulation
Neuromuscular: Fine tremor, proximal myopathy, hyperreflexia
Metabolic: Weight loss despite good appetite, heat intolerance, sweating

One Investigation to Confirm Diagnosis:

TSH receptor antibodies (TRAb) / Thyroid Stimulating Immunoglobulin (TSI): Specific and sensitive for Graves disease. Elevated TRAb confirms autoimmune hyperthyroidism.
(Supported by): Low TSH + elevated free T3/T4; thyroid USS showing diffuse hypoechoic gland with increased vascularity (inferno pattern)

2 Medications the Patient Should Be On:

Antithyroid drug (thionamide): Carbimazole (first-line in most countries) OR Propylthiouracil (PTU - used in pregnancy first trimester, thyroid storm). Mechanism: blocks thyroid peroxidase → inhibits iodine organification → reduces T3/T4 synthesis. Monitoring: FBC (risk of agranulocytosis - stop if sore throat/fever).
Beta-blocker (Propranolol): Controls adrenergic symptoms (tachycardia, tremor, anxiety) while awaiting the antithyroid drug to take effect (4-8 weeks). Also inhibits peripheral T4 → T3 conversion.

(Long-term options: Radioactive Iodine (I-131) ablation - definitive, avoid in active ophthalmopathy; Thyroidectomy)

OSCE 4 - Interactive OSCE: Consent for Haemodialysis

Structure: Introduction → Procedure → Risks → Benefits → Alternatives → Questions → Confirm consent

SAMPLE CONSENT SCRIPT FOR HAEMODIALYSIS:

Introduction: "Hello, my name is Dr. [Name], and I am one of the doctors on the renal team. I'd like to talk to you about haemodialysis, which we are recommending for you. Do you have a moment to go through this together? Is it okay if a family member or nurse is present?"

Confirm Understanding: "Before I explain, do you have any idea what haemodialysis is?"

What is Haemodialysis: "Your kidneys are no longer working well enough to clean your blood on their own. Haemodialysis is a treatment where a machine takes over the kidney's job. It filters waste products, excess fluid, and harmful substances from your blood. Without this treatment, these substances would build up and become life-threatening."

The Procedure: "We will create an access point to your blood - usually through a fistula (a surgically joined artery and vein, usually in your arm), or temporarily through a central line (a tube inserted into a large vein in your neck or chest). Three times a week, you will be connected to the dialysis machine for about 3-4 hours each session. The machine will draw blood out, filter it, and return it to your body."

Benefits: "This treatment will: remove toxins (uraemia) from your blood, control fluid balance (reduce swelling), correct electrolyte imbalances (potassium, bicarbonate), and help you feel better and avoid life-threatening complications like seizures, pulmonary oedema, and hyperkalaemia."

Risks and Complications:

Common: Hypotension during dialysis, muscle cramps, nausea, fatigue after sessions
Access-related: Infection at the catheter/fistula site, thrombosis of fistula
Long-term: Amyloidosis (dialysis-related), anaemia, bone disease (renal osteodystrophy), cardiovascular disease
Serious but rare: Air embolism, haemorrhage, arrhythmia during session, sepsis

Alternatives:

Peritoneal dialysis (PD): Done at home daily via a catheter in the abdomen - good alternative for appropriate patients
Kidney transplant: Best long-term option if suitable; you would be assessed for the waiting list
Conservative/supportive care (if patient declines dialysis): Focus on quality of life, symptom management - should be discussed honestly

Confidentiality and Rights: "You have the right to refuse this treatment or to stop at any time. However, without dialysis, your condition will deteriorate and can become fatal within days to weeks. Please let us know your wishes and concerns - we want to make this decision together with you."

Questions: "Do you have any questions? Do you understand what we have discussed? Are you happy to proceed?"

Confirm Consent: Obtain signed written consent form. Ensure patient has capacity (understands, retains, weighs, communicates decision).

QUICK SUMMARY TABLE - Key Facts to Remember

Topic	Key Fact
Asthma Step 1	As-needed ICS-formoterol (not SABA alone)
COPD GOLD 4	FEV1 <30%
COPD Group E	≥2 exacerbations/yr → LABA+LAMA
MM CRAB	Ca, Renal, Anaemia, Bone
Epilepsy - absence	Ethosuximide first
Epilepsy - GTC	Valproate (avoid in women of childbearing age)
HTN emergency	Reduce MAP by 25% in 1st hour max
Occult blood best test	FIT (faecal immunochemical test)
FUO common cause	TB / Lymphoma / SLE
Chronic GN marker	RBC casts in urine
IDA most specific	Low serum ferritin
PV mutation	JAK2 V617F
CML	BCR-ABL (Philadelphia) t(9;22), treat with imatinib
AML diagnostic	Auer rods; ≥20% blasts
G6PD trigger	Primaquine, dapsone, fava beans
Cirrhosis low platelets	Hypersplenism + low TPO
INR prolonged	Loss of clotting factor synthesis (Factor VII first)
Ascites oral drug	Spironolactone
Encephalopathy oral	Lactulose + Rifaximin
HFrEF 4 pillars	ACEi/ARNi + beta-blocker + MRA + SGLT2i
MR murmur	Pansystolic, apex → axilla, annular dilation in LV failure
Bamford LACI	Pure motor/sensory, small vessel, no higher cortical
Bamford TACI	All 3: motor+sensory, hemianopia, higher cortical
Stroke drug	Aspirin 300mg → thrombolysis if eligible
Graves confirm	TRAb (TSH receptor antibodies)
Graves 2 drugs	Carbimazole + Propranolol
Haemodialysis access	AV fistula (long-term) or central line (temporary)

Good luck on your EOP! 🎯

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