100 High-Yield MBBS General Medicine Q&A

GASTROINTESTINAL BLEED (Q1-5)

• Forrest Ia: Active spurting arterial bleed - highest risk (~90%)
• Forrest Ib: Oozing bleed
• Forrest IIa: Visible non-bleeding vessel (~50% rebleed risk)
• Forrest IIb: Adherent clot
• Forrest IIc: Flat pigmented spot
• Forrest III: Clean base - lowest risk (~5%) Forrest Ia, Ib, IIa require endoscopic therapy.

JAUNDICE (Q6-10)

• Pre-hepatic (hemolytic): Malaria, hereditary spherocytosis. Unconjugated hyperbilirubinemia, urine normal (no bilirubin), increased urobilinogen.
• Hepatic (hepatocellular): Viral hepatitis, alcoholic hepatitis. Both conjugated and unconjugated raised, bilirubinuria present.
• Post-hepatic (obstructive/cholestatic): Choledocholithiasis, carcinoma head of pancreas. Conjugated hyperbilirubinemia, dark urine, pale stools, pruritus.

• Gilbert's: Mild unconjugated hyperbilirubinemia, autosomal dominant/recessive (UGT1A1 promoter mutation), benign, triggered by fasting/stress, no treatment needed.
• Crigler-Najjar Type I: Severe, complete absence of UGT1A1, kernicterus/death without liver transplant.
• Crigler-Najjar Type II (Arias): Partial UGT1A1 deficiency, responds to phenobarbital, better prognosis.

CONGENITAL HEART DISEASE (Q11-15)

• Acyanotic (left-to-right shunt initially): ASD, VSD, PDA, AVSD - become cyanotic after Eisenmenger's.
• Cyanotic (right-to-left shunt): Tetralogy of Fallot (most common cyanotic CHD in children >1 year), Transposition of Great Arteries (most common in neonates), Tricuspid atresia, Total anomalous pulmonary venous connection (TAPVC), Truncus arteriosus. Mnemonic: "5 Ts."

1. Pulmonary stenosis (infundibular > valvular)
2. Right ventricular hypertrophy
3. Overiding aorta
4. VSD (large, perimembranous) Pulmonary stenosis is the key determinant of severity. CXR shows "boot-shaped heart" (coeur en sabot).

STROKE (Q16-20)

• Stroke: Sudden focal neurological deficit lasting >24 hours due to vascular cause (ischemic 85%, hemorrhagic 15%).
• TIA (Transient Ischemic Attack): Focal neurological deficit resolving within 24 hours (usually <1 hour), with no infarction on imaging. High risk of subsequent stroke - use ABCD2 score to risk-stratify.

• IV tPA (alteplase): Within 4.5 hours of symptom onset (3 hours in some guidelines). Contraindicated if: hemorrhage on CT, BP >185/110 (treat first), recent surgery, INR >1.7, platelets <100,000, blood glucose <50 or >400.
• Mechanical thrombectomy: Within 6 hours (up to 24 hours with favorable imaging - DAWN/DEFUSE-3 trials) for large vessel occlusion (ICA, M1, basilar).

• Age ≥60 = 1
• BP ≥140/90 = 1
• Clinical features: unilateral weakness = 2, speech disturbance without weakness = 1
• Duration: ≥60 min = 2, 10-59 min = 1
• Diabetes = 1 Score ≥4 = high risk, admit for urgent investigation.

• Antiplatelet: Aspirin 75-150mg ± clopidogrel (dual for 21 days if minor stroke/TIA, then single agent)
• Statin: High-dose (atorvastatin 40-80mg) even if normal cholesterol
• Antihypertensives: Start after acute phase (ACE inhibitor + thiazide)
• AF-related stroke: Anticoagulation (DOACs preferred over warfarin)
• Carotid endarterectomy: If symptomatic carotid stenosis 70-99%

BRAINSTEM STROKE (Q21-24)

• Ipsilateral: Facial pain/numbness (V), Horner's syndrome, palatal/pharyngeal weakness (IX,X - dysphagia, hoarseness), cerebellar signs (ataxia)
• Contralateral: Spinothalamic loss (pain/temperature in limbs/trunk)
• No hemiplegia (pyramidal tracts spared - lateral location)
• Hiccups, nausea, vertigo

• Midbrain (Weber's syndrome - PCA): Ipsilateral CN III palsy (ptosis, mydriasis, "down and out" eye) + contralateral hemiplegia (crossed hemiplegia)
• Pons (Millard-Gubler): Ipsilateral CN VI (lateral gaze palsy) and CN VII palsy + contralateral hemiplegia
• Pons (Foville's): Ipsilateral gaze palsy toward lesion + contralateral hemiplegia; eyes deviate AWAY from side of lesion (contrast to cortical stroke where eyes deviate TOWARD lesion)
• Bilateral pontine stroke: Locked-in syndrome (intact consciousness, quadriplegia, only vertical eye movements preserved)

• Ipsilateral gaze palsy ("one") - cannot look toward lesion
• Ipsilateral internuclear ophthalmoplegia ("half") - cannot adduct ipsilateral eye on contralateral gaze Only movement preserved: contralateral abduction (exotropia = "wall-eyed" appearance). Causes: MS, brainstem stroke, tumor.

ALTERED SENSORIUM (Q25-28)

• Alcohol (intoxication/withdrawal)
• Epilepsy (post-ictal)
• Insulin (hypoglycemia - must always check BGL immediately)
• Opiates/overdose
• Uremia
• Trauma
• Infection (meningitis, encephalitis, sepsis)
• Poisons/metabolic (hyponatremia, hypercalcemia, liver failure, CO)
• Stroke/structural Always check: BSL (hypoglycemia), BMP (electrolytes), ABG, CT head, blood cultures.

• Grade I: Trivial lack of awareness, euphoria/anxiety, impaired attention, asterixis absent
• Grade II: Lethargy, disorientation, obvious personality change, asterixis present
• Grade III: Somnolence, confusion, gross disorientation, bizarre behavior
• Grade IV: Coma Treatment: Lactulose (reduces ammonia production), rifaximin (non-absorbable antibiotic), treat precipitants (GI bleed, infection, electrolyte disturbance, constipation).

• Metabolic coma: Pupils reactive (light reflex preserved until late)
• Midbrain lesion: Fixed mid-position pupils (~5mm)
• CN III compression (transtentorial herniation): Unilateral fixed, dilated pupil (mydriasis) - neurosurgical emergency
• Pontine lesion: Bilateral pinpoint pupils (due to loss of sympathetics, intact parasympathetics)
• Opiates: Bilateral pinpoint pupils (reversed by naloxone)
• Atropine/anticholinergics: Bilateral fixed, dilated pupils

PARKINSON'S DISEASE (Q29-32)

1. Tremor - resting, "pill-rolling," 4-6 Hz, worse at rest, better with movement
2. Rigidity - "lead pipe" rigidity, or "cogwheel" if combined with tremor
3. Akinesia/Bradykinesia - slowness of movement, shuffling gait, micrographia, hypomimia (masked facies), hypophonia
4. Postural instability - late feature, festinant gait, falls Diagnosis is clinical. Loss of dopaminergic neurons in substantia nigra pars compacta with Lewy bodies (alpha-synuclein).

• Levodopa + Carbidopa (Sinemet): Most effective, gold standard. Carbidopa is peripheral DOPA decarboxylase inhibitor (reduces peripheral conversion of levodopa, reduces side effects, increases CNS availability). Complications: wearing off, on-off phenomenon, dyskinesias (long-term use).
• Dopamine agonists (pramipexole, ropinirole, rotigotine): Used early, especially in young patients to delay levodopa. Risk: impulse control disorders, somnolence.
• MAO-B inhibitors (selegiline, rasagiline): Mild benefit, possible neuroprotection.
• COMT inhibitors (entacapone): Used with levodopa to prolong effect (reduce "off" time).

• No tremor (or action > resting)
• Symmetrical onset
• Early falls (PSP - Progressive Supranuclear Palsy)
• Early autonomic failure (MSA - Multiple System Atrophy)
• Early dementia or hallucinations (DLB - Dementia with Lewy Bodies)
• Vertical gaze palsy (PSP)
• Poor response to levodopa
• Cerebellar signs (MSA-C)

• Anticholinergics (trihexyphenidyl/benzhexol, benztropine): Block muscarinic receptors in striatum; effective for tremor dominant PD in young patients; avoid in elderly (cognitive side effects).
• Beta-blockers (propranolol): For essential tremor - also reduces action tremor in PD.
• Levodopa: Reduces all features including tremor.
• Deep brain stimulation (STN/GPi): Highly effective for tremor when medications fail.

EPILEPSY (Q33-37)

• Focal onset: Aware (formerly simple partial) / Impaired awareness (formerly complex partial) / focal to bilateral tonic-clonic
• Generalized onset: Motor (tonic-clonic, tonic, clonic, myoclonic, atonic, epileptic spasms) / Non-motor (absence: typical/atypical)
• Unknown onset EEG and MRI are key investigations for classification.

• Focal seizures: Carbamazepine (first-line), lamotrigine, levetiracetam, oxcarbazepine
• Generalized tonic-clonic: Valproate (most effective, avoid in women of childbearing age), levetiracetam, lamotrigine
• Absence seizures: Ethosuximide (first-line for pure absence), valproate, lamotrigine
• Myoclonic: Valproate, levetiracetam, clonazepam (avoid carbamazepine - worsens myoclonus)
• Infantile spasms (West syndrome): ACTH or vigabatrin
• Lennox-Gastaut: Valproate, rufinamide, clobazam

• 0-5 min: ABCs, oxygen, glucose, IV access
• 5-20 min (Phase 1): Lorazepam 4mg IV (or diazepam 10mg IV/rectal, midazolam 10mg IM/buccal)
• 20-40 min (Phase 2): IV levetiracetam 60mg/kg OR valproate 40mg/kg OR phenytoin 20mg/kg (fosphenytoin preferred)
• >40 min (Phase 3 - Refractory SE): ICU - propofol, midazolam infusion, thiopental, phenobarbital, ketamine
• Always check for precipitants: low AED levels, CNS infection, metabolic, structural

• Valproate: Highest risk - neural tube defects (spina bifida 1-2%), cardiac, facial, cognitive impairment. Avoid in women of childbearing age unless no alternative.
• Phenytoin: Fetal hydantoin syndrome (facial dysmorphism, digit hypoplasia, growth restriction)
• Carbamazepine: Neural tube defects (0.5%)
• Lamotrigine and levetiracetam: Considered relatively safer in pregnancy
• All women on AEDs: folic acid 5mg/day preconception

ACUTE MENINGITIS (Q38-42)

• Kernig's sign: Inability to extend knee when hip flexed at 90°
• Brudzinski's sign: Involuntary hip/knee flexion on neck flexion
• Immediate LP (if no papilledema, no focal signs, GCS >12, no coagulopathy)
• CT first if: papilledema, focal signs, immunocompromised, seizures, GCS <12
• Do not delay antibiotics for CT - give ceftriaxone before CT if concerned

• Adults (18-60): Ceftriaxone 2g IV BD (covers S. pneumoniae, N. meningitidis)
• >60 years / immunocompromised: Add ampicillin 2g IV 4-hourly (covers Listeria monocytogenes, which cephalosporins miss)
• Neonates: Ampicillin + cefotaxime (or aminoglycoside)
• Add dexamethasone 0.15mg/kg IV QDS for 4 days - reduces mortality, hearing loss (most benefit in S. pneumoniae meningitis; evidence weaker for N. meningitidis)
• Give dexamethasone before or with first antibiotic dose

CHRONIC LIVER DISEASE (Q43-46)

• Hands: Leukonychia, clubbing, palmar erythema, Dupuytren's contracture, asterixis
• Skin/general: Spider nevi (>5 significant), jaundice, parotid enlargement (alcohol), gynecomastia, testicular atrophy, loss of secondary sexual hair, bruising
• Abdomen: Hepatomegaly (early) or small liver (late/cirrhosis), splenomegaly, caput medusae, ascites
• Eyes: Kayser-Fleischer rings (Wilson's disease), xanthelasma (PBC)

• Bilirubin, Albumin, PT/INR, Ascites (none/mild/severe), Encephalopathy (none/grade I-II/grade III-IV) Child A: Good surgical risk (1-year mortality ~5%) Child C: Poor risk (~85% mortality)

• Ascites (and SBP)
• Bleeding (varices, coagulopathy)
• Cerebral - hepatic encephalopathy
• Death (HCC - hepatocellular carcinoma; screen 6-monthly USS + AFP)
• Endocrine - hypogonadism, diabetes (hepatogenous)

• Hepatorenal syndrome, Hepatopulmonary syndrome, Portopulmonary hypertension

PORTAL HYPERTENSION (Q47-50)

• Pre-hepatic: Portal vein thrombosis, splenic vein thrombosis
• Intrahepatic (sinusoidal): Cirrhosis (most common overall), alcoholic hepatitis
• Intrahepatic (pre-sinusoidal): Schistosomiasis (most common worldwide), PBC (early), sarcoidosis, nodular regenerative hyperplasia
• Post-hepatic: Budd-Chiari syndrome, cardiac failure (congestive), constrictive pericarditis

• Primary prophylaxis: Non-selective beta-blockers (propranolol, carvedilol) OR band ligation. Reduce portal pressure, prevent first bleed.
• Acute variceal bleed: Terlipressin (vasoconstrictor, reduces portal pressure) + IV ceftriaxone (antibiotic prophylaxis) + urgent endoscopic band ligation within 12 hours. Sengstaken-Blakemore tube as bridge to TIPS if uncontrolled bleeding. TIPSS (transjugular intrahepatic portosystemic shunt) if refractory.
• Secondary prophylaxis: Combination of beta-blockers + band ligation (reduces rebleed from 60% to 20%).

ACUTE PANCREATITIS (Q51-54)

• Gallstones (most common overall, 45%)
• Ethanol/Alcohol (2nd most common, 35%)
• Trauma
• Steroids
• Mumps (viral: CMV, HIV, coxsackie)
• Autoimmune (Type 1 - IgG4, Type 2)
• Scorpion venom (tropical)
• Hyperlipidemia (triglycerides >1000 mg/dL), Hypercalcemia
• ERCP (post-procedure)
• Drugs: azathioprine, valproate, thiazides, tetracycline, furosemide

• Revised Atlanta Classification: Mild (no organ failure, no local complications), Moderately severe (transient organ failure <48h or local complications), Severe (persistent organ failure >48h)
• Ranson's Criteria: At admission (5 parameters) + at 48 hours (6 parameters). Score ≥3 = severe.
• BISAP Score: BUN >25, Impaired mental status, SIRS, Age >60, Pleural effusion (score >2 = severe)
• CT Severity Index (Balthazar): CT grade (A-E) + necrosis score
• CRP >150 mg/L at 48 hours = severe pancreatitis

• Pain control: IV opioids (morphine/pethidine - meperidine traditionally used but morphine acceptable)
• Analgesia + Nursing: IV fluids - aggressive early resuscitation (Ringer's lactate preferred over NS, 250-500ml/hr initially)
• Critical care if severe; HDU/ICU
• Rest bowel (nil by mouth initially); early enteral feeding (nasojejunal tube) preferred over parenteral in severe cases
• ERCP within 24-48 hours if gallstone pancreatitis + cholangitis/persistent obstruction
• Antibiotics: Only if infected necrosis suspected (NOT prophylactic)
• Surgery/intervention: Necrosectomy for infected pancreatic necrosis (delay 3-4 weeks for walling off - "step-up approach": percutaneous drainage first, then surgery)

• Local: Acute peripancreatic fluid collection → pseudocyst (>4 weeks, encapsulated, no necrosis); Acute necrotic collection → Walled-off necrosis (>4 weeks); pancreatic abscess; pseudoaneurysm (splenic artery - rupture risk); splenic vein thrombosis; fistula; "left-sided portal hypertension"
• Systemic: ARDS, AKI (acute kidney injury), DIC, hypocalcemia (saponification - tetany), hyperglycemia, sepsis, multi-organ failure
• Chronic sequelae: Chronic pancreatitis, exocrine insufficiency, endocrine insufficiency (diabetes)

ACID PEPTIC DISEASE (Q55-58)

• Triple therapy (7-14 days): PPI (BD) + Clarithromycin 500mg BD + Amoxicillin 1g BD (or Metronidazole 400mg BD if penicillin allergy)
• Quadruple therapy (if clarithromycin resistance >15% locally): PPI + Bismuth + Tetracycline + Metronidazole for 10-14 days (bismuth-based)
• Or Concomitant 4-drug (non-bismuth): PPI + Clarithromycin + Amoxicillin + Metronidazole
• Confirm eradication 4-6 weeks after treatment with urea breath test (or stool antigen test) - NOT serology (remains positive even after eradication)
• Eradication rates: ~80-90% with first-line regimens

• PPIs (omeprazole, pantoprazole, lansoprazole, rabeprazole, esomeprazole): Irreversibly inhibit H⁺/K⁺-ATPase (proton pump) in parietal cell canaliculi. Are prodrugs - activated in acidic environment of canaliculus. Most effective acid suppressants. Take 30 min before meals for maximum effect.
• H2 blockers (ranitidine, famotidine, cimetidine): Competitively block H2 receptors on parietal cells, reducing histamine-stimulated acid secretion. Less effective than PPIs. Cimetidine: multiple drug interactions (CYP450 inhibitor), anti-androgenic (gynecomastia).

• Emergency: Perforation (pneumoperitoneum on erect CXR - "free air under diaphragm"), bleeding not controllable endoscopically, obstruction (pyloric stenosis - unresponsive to medical therapy)
• Elective: Very rare now with H. pylori eradication and PPIs
• Most common emergency: Perforated DU - emergency laparotomy, omental patch repair (Graham's patch), peritoneal lavage + H. pylori eradication + PPI

IRRITABLE BOWEL SYNDROME (Q59-61)

1. Related to defecation
2. Associated with change in frequency of stool
3. Associated with change in form (appearance) of stool Criteria fulfilled for last 3 months with symptom onset ≥6 months prior to diagnosis. Subtypes: IBS-C (constipation predominant), IBS-D (diarrhea predominant), IBS-M (mixed), IBS-U (unclassified).

• Anemia (iron deficiency)
• Late onset (>50 years)
• Anoreexia/weight loss
• Rectal bleeding
• Mass (abdominal or rectal)
• Stronger family history of CRC or IBD Also: Nocturnal symptoms, fever, raised inflammatory markers. These warrant colonoscopy and other investigations before IBS diagnosis.

• Explanation, reassurance, doctor-patient relationship
• Diet: Low FODMAP diet (Fermentable Oligosaccharides Disaccharides Monosaccharides And Polyols) - reduces symptoms in 50-70%
• IBS-C: Fiber supplement (psyllium/ispaghula), osmotic laxatives (PEG), linaclotide, lubiprostone
• IBS-D: Loperamide, bile acid sequestrants (if BAM), rifaximin (non-absorbable antibiotic), eluxadoline
• Pain: Antispasmodics (mebeverine, hyoscine, peppermint oil), low-dose tricyclics (amitriptyline - also help diarrhea), SSRIs (for pain + anxiety, better for constipation)
• Psychological: CBT, hypnotherapy (evidence-based for IBS)

BUDD-CHIARI SYNDROME (Q62-64)

• Myeloproliferative neoplasms (JAK2 mutation - most common, especially Polycythemia Vera)
• Antiphospholipid syndrome
• Factor V Leiden, Protein C/S/antithrombin III deficiency
• PNH (paroxysmal nocturnal hemoglobinuria)
• Pregnancy/OCP (estrogen-related)
• Hepatocellular carcinoma (local invasion)
• Behcet's disease
• Membranous obstruction of IVC (in Asia/Africa)

• Acute: RUQ pain, hepatomegaly, jaundice, rapid ascites
• Chronic: Massive hepatomegaly (caudate lobe hypertrophy - caudate has direct drainage to IVC), ascites, splenomegaly, varices
• Fulminant: Liver failure, encephalopathy Classic triad: Hepatomegaly + Ascites + Abdominal pain Diagnosis: Doppler USS (absent/reversed flow in hepatic veins - first-line), CT/MRI (spider-web pattern), liver biopsy (zone 3 congestion/necrosis - centrilobular).

1. Anticoagulation (LMWH then warfarin/DOAC) - all patients unless contraindicated
2. Treat underlying cause (hydroxyurea for MPN, immunosuppression for Behcet's)
3. Diuretics for ascites, therapeutic paracentesis
4. Angioplasty/thrombolysis for short-segment stenosis/recent thrombosis
5. TIPS - for failure of above; effective for decompression
6. Liver transplant - for fulminant or end-stage; lifelong anticoagulation post-transplant

ALCOHOLIC LIVER DISEASE (Q65-67)

1. Alcoholic steatosis (fatty liver): Reversible on abstinence; asymptomatic usually; hepatomegaly; raised GGT
2. Alcoholic hepatitis: Fever, jaundice, tender hepatomegaly, raised AST:ALT ratio >2:1 (both rarely >300 IU/L), raised GGT, leukocytosis; can progress to liver failure
3. Alcoholic cirrhosis: Irreversible; all complications of cirrhosis

• Prednisolone 40mg/day for 28 days (Lille model score at day 7 - if >0.45, no response, consider stopping steroids)
• If steroids contraindicated: Pentoxifylline (now less favored - not shown superior in recent trials)
• Abstinence from alcohol (most important long-term factor)
• Nutritional support (protein-calorie malnutrition common)
• Liver transplant: Considered in "super-urgent" cases not responding (controversial, requires MDT)

• Wernicke's encephalopathy (thiamine B1 deficiency): CONFUSION + OPHTHALMOPLEGIA (nystagmus, lateral gaze palsy, CN VI) + ATAXIA (classic triad, often incomplete). Treat with IV thiamine (Pabrinex) immediately - before glucose. MRI: mamillary body hyperintensity.
• Korsakoff's syndrome: Anterograde amnesia, confabulation - chronic irreversible state post-Wernicke's
• Alcoholic cerebellar degeneration: Truncal ataxia, wide-based gait
• Peripheral neuropathy: Mainly sensory, stocking-glove distribution
• Alcohol withdrawal: Seizures (6-48h after last drink), delirium tremens (24-96h), Rx with benzodiazepines (chlordiazepoxide or diazepam in UK/India)

MASH - Metabolic Dysfunction-Associated Steatohepatitis (Q68-70)

• Steatosis: 0-3
• Lobular inflammation: 0-3
• Hepatocyte ballooning: 0-2 NAS 0-2: Not MASH; NAS 3-4: borderline; NAS ≥5: Definite MASH Also staged separately: Fibrosis (F0-F4). F3-F4 has worst prognosis.

• Lifestyle modification (cornerstone): Weight loss of 7-10% body weight reduces steatohepatitis and fibrosis. Exercise independently beneficial.
• Control metabolic risk factors: T2DM (pioglitazone - shown to improve histology; GLP-1 agonists - semaglutide; SGLT2 inhibitors), hypertension, dyslipidemia (statins safe in MASH)
• FDA-approved (2024): Resmetirom (thyroid hormone receptor-beta agonist) - first approved medication specifically for MASH with fibrosis
• Vitamin E: Shown to improve histology in non-diabetic MASH (but safety concerns limit use)
• Bariatric surgery for morbid obesity improves MASH
• Liver transplant for decompensated MASH cirrhosis or HCC

CHRONIC DIARRHOEA (Q71-73)

• Osmotic: Stops with fasting; osmotic gap >125 mOsm/kg (stool osmotic gap = 290 - 2×(Na+K)). Causes: lactose intolerance, sorbitol, Mg antacids, osmotic laxative abuse
• Secretory: Persists with fasting; large volume (>1L/day); normal osmotic gap (<50). Causes: VIPoma, carcinoid, microscopic colitis, bile acid malabsorption, cholera
• Malabsorptive/fatty: Steatorrhea, weight loss. Causes: celiac disease, chronic pancreatitis, small bowel bacterial overgrowth, Crohn's ileitis
• Inflammatory: Blood/mucus, fever. Causes: IBD, microscopic colitis, infective colitis
• Functional: IBS-D, normal investigations

INFLAMMATORY BOWEL DISEASE (Q74-77)

• Parallel disease activity (improve with IBD control): Peripheral arthropathy (type 1 - pauciarticular, large joints), oral aphthous ulcers, erythema nodosum, episcleritis
• Independent of disease activity: Axial arthropathy (ankylosing spondylitis - HLA-B27), pyoderma gangrenosum, uveitis/iritis, primary sclerosing cholangitis (PSC - especially UC, p-ANCA positive)
• PSC: Bile duct strictures + beading on ERCP/MRCP, increased risk cholangiocarcinoma and CRC; treat with UDCA (ursodeoxycholic acid)

• UC mild-moderate: 5-ASA (mesalazine) oral + rectal, or systemic/topical steroids
• UC severe/steroid-refractory: IV hydrocortisone; rescue therapy: IV ciclosporin or infliximab; if fails: colectomy
• Crohn's induction: Steroids, elemental/polymeric diet; biologics early in fistulising/complex disease
• Maintenance (both): 5-ASA (UC), azathioprine/6-MP (both), methotrexate (Crohn's), biologics: anti-TNF (infliximab, adalimumab), anti-integrin (vedolizumab), anti-IL-12/23 (ustekinumab), anti-IL-23 (risankizumab - newer)
• Assess remission: Calprotectin, endoscopy (mucosa healing is treatment target)

CORONARY ARTERY DISEASE (Q78-82)

• Anterior (LAD): ST elevation V1-V4 (proximal LAD = V1-V6 + I, aVL)
• Inferior (RCA or LCx): ST elevation II, III, aVF; reciprocal depression I, aVL
• Lateral (LCx or diagonal): ST elevation I, aVL, V5-V6
• Posterior (RCA/LCx): ST depression V1-V3 (mirror image) + tall R waves V1-V2; confirm with posterior leads V7-V9 (ST elevation)
• Right ventricular (proximal RCA): Inferior STEMI + ST elevation V4R. Important: RV infarct - avoid nitrates and diuretics (preload-dependent); treat with IV fluids

• Age ≥65
• ≥3 CAD risk factors
• Prior coronary stenosis ≥50%
• ST deviation on ECG
• ≥2 anginal events in 24 hours
• Aspirin use in past 7 days
• Elevated cardiac biomarkers Score 0-2: Low risk (4.7% adverse events); 3-4: Intermediate (13.2%); 5-7: High (40.9%) Higher scores warrant early invasive strategy.

• Clopidogrel: Prodrug (requires CYP2C19 activation), check for poor metabolizers
• Ticagrelor: Preferred over clopidogrel (PLATO trial), direct P2Y12 inhibitor, more potent, reversible
• Prasugrel: Most potent; contraindicated in >75 years, <60kg, prior TIA/stroke Duration after PCI:
• Elective PCI (stable angina): 6 months DAPT then aspirin alone
• ACS + PCI: 12 months DAPT (irrespective of stent type)
• High bleeding risk: DAPT can be shortened to 3-6 months
• High thrombotic risk: Extended DAPT >12 months

• Previous intracranial hemorrhage (any time)
• Ischemic stroke <3 months (unless within 4.5h window - complex decision)
• Known intracranial malignancy, AVM, or aneurysm
• Active bleeding or bleeding diathesis (excluding menses)
• Significant closed-head/face trauma <3 months
• Aortic dissection
• Severe uncontrolled hypertension >180/110 unresponsive to treatment (relative) PCI is preferred over thrombolysis when available within 120 minutes of first medical contact.

• Beta-blocker (bisoprolol, carvedilol, metoprolol) - reduce mortality/remodeling, continue indefinitely
• ACE inhibitor (ramipril, lisinopril) - reduce remodeling, heart failure prevention, all post-MI patients, especially if EF reduced; ARB if ACEi intolerant
• Statin - high dose (atorvastatin 40-80mg) - LDL target <1.4 mmol/L (<55 mg/dL); add ezetimibe, PCSK9i if needed
• Mineral receptor antagonist (eplerenone/spironolactone) - if EF ≤35% and HF/DM
• Antiplatelet - DAPT for 12 months, then aspirin indefinitely

APPROACH TO SHOCK (Q83-87)

1. Distributive (vasodilatory - warm shock): Septic (most common), anaphylactic, neurogenic, adrenal crisis - decreased SVR, high CO (in sepsis initially)
2. Hypovolemic: Blood loss (hemorrhagic), fluid loss (vomiting, diarrhea, burns) - decreased preload, decreased CO
3. Cardiogenic: MI, cardiomyopathy, arrhythmia, myocarditis - pump failure, decreased CO, high SVR
4. Obstructive: Tension pneumothorax, cardiac tamponade, massive PE, aortic stenosis - mechanical obstruction to flow

1. Measure lactate (if >2 mmol/L, remeasure if initial >4 mmol/L)
2. Blood cultures x2 (before antibiotics, but do not delay)
3. Broad-spectrum antibiotics - within 1 hour (every hour delay increases mortality)
4. 30ml/kg IV crystalloids if hypotensive or lactate ≥4 mmol/L
5. Vasopressors if hypotensive during/after fluids to target MAP ≥65 mmHg (Norepinephrine first-line)

• Norepinephrine (noradrenaline): First-line in septic shock - α1 > β1, increases SVR and MAP
• Vasopressin: Add-on in refractory septic shock (0.03 units/min) - V1 receptor, vasopressor; may spare norepinephrine
• Dopamine: Low dose (2-5 mcg/kg/min): D1 (renal/splanchnic); Mid (5-10): β1 (inotrope); High (>10): α1 (vasopressor). Now rarely used for renal protection (not evidence-based); 2nd line vasopressor in septic shock.
• Dobutamine: β1 > β2 agonist; inotrope without vasoconstriction; used in cardiogenic shock (with norepinephrine if hypotensive)
• Epinephrine (adrenaline): α1+β1+β2; used in anaphylaxis (IM) and refractory shock/cardiac arrest
• Phenylephrine: Pure α1 vasopressor; useful in septic shock with tachyarrhythmia

1. Epinephrine (adrenaline) 0.5mg IM into anterolateral thigh (1:1000 solution) - most important
2. IV fluids (500ml-1L rapid)
3. Antihistamine (chlorphenamine 10mg IV)
4. Hydrocortisone 200mg IV (delays recurrence, biphasic reaction)
5. Nebulized salbutamol if bronchospasm
6. Observe 4-12 hours (biphasic reaction in 5-20%)

INTEGRATED/CROSS-TOPIC QUESTIONS (Q88-100)

• Unconjugated (physiological/pathological): Physiological jaundice (2nd-4th day, benign), ABO/Rh hemolysis, G6PD deficiency, spherocytosis, Crigler-Najjar, hypothyroidism, breast milk jaundice
• Conjugated (always pathological): Biliary atresia (Kasai procedure urgently if <60 days), neonatal hepatitis, choledochal cyst, Alagille syndrome, metabolic (galactosemia, alpha-1-antitrypsin deficiency) Direct bilirubin >20% of total = conjugated hyperbilirubinemia; always investigate.

• K+ 5.5-6.5: Tall peaked T waves (narrow base)
• K+ 6.5-7: Prolonged PR, widened QRS
• K+ >7: Sine wave pattern, loss of P waves
• K+ >8: Ventricular fibrillation/asystole Treatment (severe K+ >6.5 or ECG changes):

1. IV calcium gluconate 10% 10ml - membrane stabilization (immediate, 1-3 min)
2. Insulin 10U + 50ml 50% dextrose IV - shifts K into cells (30-60 min)
3. Salbutamol nebulized 10-20mg - also shifts K+ in (additive with insulin)
4. Remove K+: Furosemide, kayexalate/patiromer (GI binding), dialysis (definitive if AKI/renal failure)
5. Sodium bicarbonate - if concurrent severe acidosis

1. Blood cultures x2 (immediately)
2. Dexamethasone 0.15mg/kg IV
3. IV Ceftriaxone 2g immediately (do not wait)
4. CT head
5. LP when safe LP findings will still be meaningful even after antibiotics (for a few hours - cell counts, protein, glucose remain diagnostic). Never delay antibiotics for investigations.

• Postprandial distress syndrome (PDS) - meal-related fullness/satiation
• Epigastric pain syndrome (EPS) - pain/burning not necessarily meal-related Treatment: H. pylori eradication if positive, low-dose TCAs, prokinetics (itopride, domperidone), PPIs (limited benefit), psychological therapies.

• Alcoholic hepatitis: History of significant alcohol use (>40g/day women, >60g/day men, for years), recent drinking + symptoms; AST:ALT ratio >2:1; both rarely >300 IU/L; raised GGT; often raised MCV; elevated IgA on serum immunoglobulins
• MASH: No significant alcohol; metabolic syndrome (obesity, DM, dyslipidemia); ALT > AST typically; raised ALT with AST:ALT <1 Can co-exist. Liver biopsy can help differentiate but histology overlaps.

• Wernicke's: Medical emergency. IV thiamine (Pabrinex 2 pairs of ampoules - 500mg thiamine) 3x daily for 3 days before any glucose administration. Glucose without thiamine precipitates/worsens Wernicke's by exhausting already depleted thiamine. 80% recover with prompt treatment; 20% develop Korsakoff's.
• Korsakoff's: Irreversible anterograde amnesia + confabulation. Only 25% show significant recovery with prolonged abstinence and thiamine. Institutionalization often required.

• Elevated ALP (predominantly): Cholestasis (biliary obstruction - gallstones, PSC, PBC, biliary stricture), bone disease (Paget's disease, bone metastases, rickets), pregnancy (placental ALP), hepatic infiltration (sarcoid, lymphoma, metastases). Confirm hepatic source with GGT (GGT elevated in hepatic causes, not bone).
• Elevated AST/ALT (transaminases - predominantly hepatocellular injury): Viral hepatitis (ALT > AST), alcoholic hepatitis (AST:ALT >2:1), MASH, ischemic hepatitis ("shock liver" - very high transaminases >1000), autoimmune hepatitis, Wilson's disease.
• Both elevated together: Mixed picture: drug-induced liver injury, decompensated cirrhosis.

• Most common cause: Large LV infarction (EF reduced) - LAD territory
• Mechanical complications: VSD (harsh systolic murmur + new left step-up on Swan-Ganz), acute mitral regurgitation (ruptured papillary muscle - apical systolic murmur, acute pulmonary edema), free wall rupture (Beck's triad - hypotension, JVP elevation, muffled heart sounds = tamponade) Management:

1. Primary PCI (early revascularization - SHOCK trial: improves 1-year survival)
2. Vasopressors: Norepinephrine > dopamine (SOAP-II trial: less arrhythmias with norepinephrine)
3. Inotropes: Dobutamine (if low CO but not severely hypotensive)
4. Intra-aortic balloon pump: Counterpulsation (reduces afterload, improves coronary perfusion) - consider as bridge
5. Mechanical circulatory support: Impella, VA-ECMO in refractory cases
6. Treat mechanical complications (urgent surgery for VSD/acute MR)

Summary Table: Key High-Yield Mnemonics