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id=\"qz-sr\">40<\/strong> left<\/div>\n <div class=\"qz-timer-wrap\">\n <div class=\"qz-timer\" id=\"qz-timer\">⏱ <strong id=\"qz-td\">40:00<\/strong><\/div>\n <div class=\"qz-stat net-score\">Net <strong id=\"qz-sn\">0<\/strong> \/ 160<\/div>\n <\/div>\n <\/div>\n <div class=\"qz-prog-track\"><div class=\"qz-prog-fill\" id=\"qz-fill\"><\/div><\/div>\n<\/div>\n\n<div class=\"qz-grace\" id=\"qz-grace\">\n <div class=\"qz-grace-box\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"qz-grace-n\" id=\"qz-gn\">10<\/div>\n <button class=\"qz-grace-now\" id=\"qz-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n\n<div class=\"qz-header\">\n <h1>Combined Medical Services Examination 2023<br>General Medicine & Paediatrics · Paper I · Part A<\/h1>\n <p>Cardiology · Respiratory · Gastroenterology & Hepatology · Neurology · Haematology & Endocrinology<\/p>\n <div class=\"qz-meta\">\n <span class=\"qz-badge\">Questions 1–40<\/span>\n <span class=\"qz-badge\">Options reshuffled<\/span>\n <span class=\"qz-badge\">Score = c × 4 − w<\/span>\n <button class=\"qz-timer-btn\" id=\"qz-tbtn\">⏱ Start Timed Mode<\/button>\n <\/div>\n<\/div>\n\n<div class=\"qz-body\">\n <div id=\"qz-questions\"><\/div>\n <div class=\"qz-submit-wrap\">\n <button class=\"qz-submit\" id=\"qz-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"qz-result\" id=\"qz-result\">\n <div class=\"qz-ring\" id=\"qz-ring\">\n <div class=\"qz-ring-inner\">\n <div class=\"qz-ring-pct\" id=\"qz-rpct\">0%<\/div>\n <div class=\"qz-ring-sub\">score<\/div>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"qz-net\" id=\"qz-rnet\"><\/div>\n <div class=\"qz-verdict\" id=\"qz-rv\"><\/div>\n <div class=\"qz-bands\">\n <span class=\"qz-band bc\" id=\"qz-bc\"><\/span>\n <span class=\"qz-band bw\" id=\"qz-bw\"><\/span>\n <span class=\"qz-band bs\" id=\"qz-bs\"><\/span>\n <\/div>\n <button class=\"qz-retry\" id=\"qz-retry\">↺ Retry Quiz<\/button>\n <\/div>\n<\/div>\n\n<\/div>\n\n<script>\n(function(){\n\nvar TOTAL = 40, MAX = 160;\nvar TSECS = 2400, GSECS = 10;\nvar LTRS = [\"A\",\"B\",\"C\",\"D\"];\n\nvar QQ = [\n{id:1,\nstem:\"Thickened ventricular wall with normal diastolic function is a feature of\",\ncorrect:\"athlete's heart\",\nopts:[\"hypertrophic cardiomyopathy\",\"restrictive cardiomyopathy\",\"endomyocardial fibrosis\",\"athlete's heart\"],\nexp:\"Athlete's heart (physiological cardiac remodelling) shows concentric LV hypertrophy with preserved or supranormal diastolic function. This distinguishes it from pathological hypertrophy. Hypertrophic cardiomyopathy shows asymmetric septal hypertrophy with impaired diastolic filling. Restrictive cardiomyopathy shows markedly impaired diastolic function. Normal diastolic function with wall thickening = athlete's heart.\"\n},\n{id:2,\nstem:\"In which of the following cases does paradoxical splitting occur?<br>1. Severe aortic stenosis<br>2. Right bundle branch block<br>3. Right ventricular pacing<br>4. Hypertrophic obstructive cardiomyopathy<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Paradoxical (reversed) splitting of S2 occurs when A2 is delayed beyond P2, heard on expiration. Causes that delay aortic valve closure: LBBB (classic), severe aortic stenosis (prolonged LV ejection), HOCM (dynamic obstruction), and right ventricular pacing (creates LBBB activation pattern). Right bundle branch block causes WIDE splitting (P2 delayed) NOT paradoxical splitting. Statements 1, 3, and 4 are correct.\"\n},\n{id:3,\nstem:\"A patient with peripheral oedema has the following findings on clinical examination: A soft systolic murmur at the lower left sternal border with raised JVP showing prominent C-V wave. The murmur increases in intensity on deep inspiration. The most likely valvular abnormality is\",\ncorrect:\"tricuspid regurgitation\",\nopts:[\"ventricular septal defect\",\"mitral regurgitation\",\"tricuspid regurgitation\",\"mitral valve prolapse\"],\nexp:\"The clinical triad is pathognomonic of tricuspid regurgitation (TR): pansystolic murmur at the lower left sternal border, Carvallo sign (murmur increases on deep inspiration), and prominent C-V wave in JVP (systolic regurgitant wave merging C and V waves). Peripheral oedema from right heart failure confirms the diagnosis. Mitral regurgitation does NOT increase with inspiration. Tricuspid regurgitation is correct.\"\n},\n{id:4,\nstem:\"Kussmaul's sign is a clinical feature of\",\ncorrect:\"constrictive pericarditis\",\nopts:[\"constrictive pericarditis\",\"hypertrophic obstructive cardiomyopathy\",\"anteroseptal myocardial infarction\",\"dilated cardiomyopathy\"],\nexp:\"Kussmaul's sign is a paradoxical rise in jugular venous pressure on inspiration. In constrictive pericarditis, the rigid fibrocalcific pericardium cannot expand to accommodate increased venous return during inspiration, forcing JVP upward. Also seen in restrictive cardiomyopathy and massive pericardial effusion with tamponade. Not a feature of HOCM, STEMI, or dilated cardiomyopathy.\"\n},\n{id:5,\nstem:\"A patient has a cardiac murmur best heard at the right second intercostal space. It increases with expiration. The murmur reduces in intensity during sustained handgrip but increases on inhalation of amyl nitrite. The likely lesion is\",\ncorrect:\"hypertrophic obstructive cardiomyopathy\",\nopts:[\"ventricular septal defect\",\"aortic stenosis\",\"hypertrophic obstructive cardiomyopathy\",\"mitral regurgitation\"],\nexp:\"HOCM bedside manoeuvres: Handgrip increases LV afterload and preload, larger LV cavity reduces obstruction, murmur SOFTER. Amyl nitrite reduces preload and afterload, smaller LV cavity worsens obstruction, murmur LOUDER. These responses are the opposite of aortic stenosis. The HOCM murmur can radiate to the aortic area mimicking AS, but dynamic manoeuvre responses clinch HOCM.\"\n},\n{id:6,\nstem:\"In the modified Duke criteria for infective endocarditis, which one of the following is NOT a major criterion?\",\ncorrect:\"Roth's spots\",\nopts:[\"New partial dehiscence of prosthetic valve\",\"Positive blood culture\",\"Roth's spots\",\"New valvular regurgitation\"],\nexp:\"Modified Duke MAJOR criteria: (1) Positive blood cultures with typical organisms; (2) Endocardial involvement on echo (oscillating mass, abscess, new prosthetic valve dehiscence, or new valvular regurgitation). Roth's spots are flame-shaped retinal haemorrhages with pale centres; they are an immunological phenomenon and a MINOR criterion. New prosthetic valve dehiscence and new valvular regurgitation are major criteria. Roth's spots is NOT a major criterion.\"\n},\n{id:7,\nstem:\"Which one of the following diseases affects predominantly large arteries?\",\ncorrect:\"Giant cell arteritis\",\nopts:[\"Granulomatosis with polyangiitis\",\"Polyarteritis nodosa\",\"Giant cell arteritis\",\"Eosinophilic granulomatosis with polyangiitis\"],\nexp:\"Vasculitides by vessel size: Large vessel: Giant cell arteritis (aorta, major branches, temporal artery) and Takayasu arteritis. Medium vessel: Polyarteritis nodosa, Kawasaki disease. Small vessel: Granulomatosis with polyangiitis (GPA\/Wegener's), Microscopic polyangiitis, Eosinophilic granulomatosis with polyangiitis (EGPA\/Churg-Strauss), IgA vasculitis. Giant cell arteritis is the large artery vasculitis among the options.\"\n},\n{id:8,\nstem:\"Osborn waves in ECG show prolonged repolarization with a distinctive convex elevation of the J point. These waves are associated with\",\ncorrect:\"systemic hypothermia\",\nopts:[\"systemic hypothermia\",\"acute pericarditis\",\"acute myocarditis\",\"Brugada syndrome\"],\nexp:\"Osborn waves (J waves) are pathognomonic of systemic hypothermia (core temperature typically below 30 degrees C). They appear as a positive deflection at the J point, most prominent in V4-V6 and inferior leads. Amplitude increases as temperature falls. Other features: bradycardia, prolonged PR\/QRS\/QT, ventricular fibrillation below 28 degrees C. Brugada syndrome shows an RBBB-like pattern with ST elevation in V1-V3, not Osborn waves.\"\n},\n{id:9,\nstem:\"A decline in total lung capacity to less than 80% of patient's predictive value is an indication of\",\ncorrect:\"restrictive lung disease\",\nopts:[\"restrictive lung disease\",\"obstructive lung disease\",\"pulmonary artery hypertension\",\"pulmonary embolism\"],\nexp:\"Total lung capacity (TLC) below 80% of predicted defines restrictive lung disease. Restriction means the lungs cannot expand to normal total volume, caused by interstitial fibrosis (IPF), chest wall disease (kyphoscoliosis, obesity), neuromuscular weakness, or pleural disease. In obstructive lung disease (COPD, asthma), TLC is normal or increased due to air trapping. Pulmonary artery hypertension and embolism affect vasculature and do not primarily reduce TLC.\"\n},\n{id:10,\nstem:\"A 28-year male is suspected of having hypertrophic obstructive cardiomyopathy (HOCM). Which of the following statements are likely to be true on his examination?<br>1. Maneuvers that decrease LV preload will cause the murmur to intensify.<br>2. Maneuvers that decrease LV afterload will cause decrease in intensity of murmur.<br>3. Murmur of HOCM becomes softer with passive leg raising.<br>4. Murmur of HOCM becomes louder with squatting.<br>Select the correct answer using the code given below.\",\ncorrect:\"1 and 3\",\nopts:[\"1 and 3\",\"2 and 3\",\"2 and 4\",\"1 and 4\"],\nexp:\"HOCM murmur worsens when the LV cavity is smaller (less preload) and improves when larger. Statement 1 TRUE: decreased preload (Valsalva, standing) gives smaller LV, worse obstruction, louder murmur. Statement 2 FALSE: decreased afterload gives smaller LV, LOUDER murmur (not softer). Statement 3 TRUE: passive leg raising increases preload, larger LV, murmur softer. Statement 4 FALSE: squatting increases preload and afterload, larger LV, murmur SOFTER. Statements 1 and 3 are correct.\"\n},\n{id:11,\nstem:\"A 56-year male, chronic heavy smoker, presented with breathlessness. Pulse: 96\/min, BP: 112\/70 mm Hg and a pansystolic murmur showing Carvallo's sign with murmur getting louder on deep inspiration. Which one of the following statements is true regarding examination of JVP in him?\",\ncorrect:\"V wave and C wave merge.\",\nopts:[\"V wave is attenuated.\",\"C wave is attenuated and V wave is accentuated.\",\"V wave and C wave merge.\",\"V wave and C wave merge and Y descent is blunted.\"],\nexp:\"In tricuspid regurgitation (confirmed by Carvallo's sign in this COPD\/cor pulmonale patient), the regurgitant systolic jet into the right atrium merges the C wave (tricuspid valve closure) and V wave (venous filling) into a single large CV fusion wave. This is the characteristic JVP finding in TR. The Y descent is typically sharp. Blunted Y descent is seen in cardiac tamponade or tricuspid stenosis.\"\n},\n{id:12,\nstem:\"Which one of the following is a manifestation of vascular phenomenon in modified Duke criteria?\",\ncorrect:\"Janeway's lesions\",\nopts:[\"Osler's node\",\"Roth's spots\",\"Janeway's lesions\",\"Glomerulonephritis\"],\nexp:\"Modified Duke MINOR criteria include immunological phenomena (Osler's nodes, Roth's spots, rheumatoid factor, glomerulonephritis) and vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway's lesions). Janeway's lesions are painless erythematous macules on palms and soles resulting from septic emboli (vascular phenomenon). Osler's nodes (painful tender nodules on fingertips) are immunological phenomena.\"\n},\n{id:13,\nstem:\"The volume of air remaining in the lungs after a normal expiration is called\",\ncorrect:\"functional residual capacity\",\nopts:[\"expiratory residual volume\",\"functional residual capacity\",\"residual volume\",\"vital capacity\"],\nexp:\"Functional Residual Capacity (FRC) is the volume of air remaining in the lungs at the end of a normal passive (tidal) expiration. FRC equals ERV plus RV. It represents the resting equilibrium position where outward chest wall recoil balances inward lung recoil. Residual volume (RV) is the air remaining after maximal forced expiration. Vital capacity is the maximum volume exhaled after maximal inhalation. FRC is the correct answer.\"\n},\n{id:14,\nstem:\"The investigation of choice for early follow-up in patients treated for anti-H. pylori drugs is\",\ncorrect:\"urea breath test\",\nopts:[\"urea breath test\",\"rapid urease test\",\"stool H. pylori antigen test\",\"serology for H. pylori\"],\nexp:\"The urea breath test (UBT) is the investigation of choice for confirming H. pylori eradication after treatment. The patient ingests labelled urea; if H. pylori is present, its urease splits the urea and labelled CO2 is detected in exhaled breath. Performed at least 4 weeks after completing antibiotics and 2 weeks after stopping PPIs. Sensitivity and specificity approximately 95%. Serology remains positive for months to years after eradication and cannot confirm cure. UBT is the gold standard for follow-up.\"\n},\n{id:15,\nstem:\"The most common non-pancreatic site for tumour distribution in Zollinger-Ellison syndrome is\",\ncorrect:\"duodenum\",\nopts:[\"duodenum\",\"ovaries\",\"stomach\",\"liver\"],\nexp:\"In Zollinger-Ellison syndrome (ZES), the gastrinoma arises in the pancreas in approximately 25-40% of cases. Among extra-pancreatic locations, the duodenum is the most common site (50-70% of sporadic gastrinomas). The gastrinoma triangle (Passaro triangle) is defined by the biliary confluence, the junction of 2nd and 3rd duodenum, and the pancreatic neck. Most sporadic gastrinomas lie within this triangle. MEN-1 associated gastrinomas are frequently duodenal, often multiple and small.\"\n},\n{id:16,\nstem:\"Which of the following are the risk factors for the acquisition of hepatitis C infection?<br>1. Faeco-oral transmission<br>2. Intravenous drug abuse<br>3. Vertical transmission<br>4. Sharing toothbrush and razors<br>Select the correct answer using the code given below.\",\ncorrect:\"2, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"HCV is transmitted via blood-to-blood contact. IV drug abuse (sharing needles) is the leading route of HCV transmission. Vertical transmission from HCV-positive mother to neonate occurs in approximately 5% of pregnancies. Sharing toothbrushes and razors involves percutaneous\/permucosal blood exposure and is a recognised risk factor. Faeco-oral transmission is NOT a route for HCV (unlike HAV and HEV). Statement 1 is false. Statements 2, 3, and 4 are correct.\"\n},\n{id:17,\nstem:\"The most common cause of shock in severe acute pancreatitis (SAP) is\",\ncorrect:\"hypovolemic shock resulting from third space loss\",\nopts:[\"hypovolemic shock resulting from third space loss\",\"septic shock resulting from infected pancreatic necrosis\",\"cardiogenic shock resulting from SIRS\",\"abdominal compartment syndrome\"],\nexp:\"In the early phase of severe acute pancreatitis, massive third-space fluid sequestration occurs as plasma leaks into the retroperitoneum, peritoneal cavity, and bowel wall due to inflammatory capillary leak syndrome. This results in hypovolemic shock, the most common cause of shock in SAP. Septic shock from infected necrosis is a later complication, usually after week 2. Aggressive IV fluid resuscitation (lactated Ringer's preferred) in the first 24-48 hours is the cornerstone of SAP management.\"\n},\n{id:18,\nstem:\"The most common causative agent for spontaneous bacterial peritonitis is\",\ncorrect:\"Escherichia coli\",\nopts:[\"Escherichia coli\",\"Enterococcus sp.\",\"Staphylococcus aureus\",\"Streptococcus viridans\"],\nexp:\"Spontaneous bacterial peritonitis (SBP) occurs in cirrhotic patients when gut bacteria translocate into ascitic fluid. Escherichia coli is the most common causative organism (40-50%), followed by Klebsiella pneumoniae and Streptococcus pneumoniae. SBP is typically monomicrobial. Diagnosis: ascitic fluid neutrophil count at least 250\/mm3. Treatment: cefotaxime IV plus IV albumin (to prevent hepatorenal syndrome). Prophylaxis: norfloxacin or ciprofloxacin in high-risk cirrhotics.\"\n},\n{id:19,\nstem:\"The serologic marker detectable during the window period of hepatitis B infection is\",\ncorrect:\"anti-HBc IgM\",\nopts:[\"anti-HBsAb\",\"anti-HBc IgG\",\"anti-HBc IgM\",\"HBeAg\"],\nexp:\"The serological window period in acute HBV infection is when HBsAg has become undetectable but anti-HBs has not yet appeared. During this window, the ONLY detectable marker is anti-HBc IgM (IgM antibody to hepatitis B core antigen). Anti-HBc IgM is the diagnostic marker of acute HBV infection. It appears in the prodromal phase, peaks during acute illness, and declines over 3-6 months. Anti-HBc IgG persists lifelong indicating past or chronic infection. In the window period, anti-HBc IgM is the only positive marker.\"\n},\n{id:20,\nstem:\"A 14-year boy came with chronic diarrhoea and malnutrition. The physician suspected celiac disease. Which of the following are correct in his diagnostic workup?<br>1. Presence of IgA antiendomysial antibody<br>2. Absence of reduced height of villi on intestinal biopsy<br>3. Increased lymphocytes in lamina propria in small intestine biopsy<br>4. Absence of tTG antibody in serum<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 3\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Celiac disease diagnostic features: IgA anti-endomysial antibody (EMA) is highly specific (at least 95%) for celiac disease and its presence strongly supports the diagnosis. On intestinal biopsy, villous atrophy (reduced height of villi) IS present, confirming celiac disease. Increased intraepithelial and lamina propria lymphocytes with crypt hyperplasia are characteristic Marsh lesions. Anti-tTG antibodies are ELEVATED (not absent) in celiac disease, so statement 4 is false. Statements 1, 2, and 3 are correct diagnostic features.\"\n},\n{id:21,\nstem:\"Which of the following statements are correct for the treatment of chronic hepatitis B with pegylated interferon (PEG-IFN)?<br>1. PEG-IFN is poorly tolerated drug as compared to nucleoside analogues.<br>2. Resistance to treatment with PEG-IFN is more common than nucleoside analogues.<br>3. PEG-IFN is not useful in patients of cirrhosis.<br>4. PEG-IFN is administered every week for 48 weeks.<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 3 and 4\",\nopts:[\"1, 3 and 4\",\"1, 2 and 3\",\"2 and 4\",\"1 and 3 only\"],\nexp:\"Statement 1 TRUE: PEG-IFN has significant adverse effects (flu-like symptoms, cytopenias, depression) making it poorly tolerated compared to nucleoside analogues. Statement 2 FALSE: Resistance to PEG-IFN does NOT occur as it acts via immune mechanisms with no resistance mutations. Statement 3 TRUE: PEG-IFN is contraindicated in decompensated cirrhosis (Child-Pugh B\/C) due to risk of hepatic decompensation. Statement 4 TRUE: Standard PEG-IFN for HBV is 180 mcg SC weekly for 48 weeks. Statements 1, 3, and 4 are correct.\"\n},\n{id:22,\nstem:\"Which of the following are recommended for management of tumour lysis syndrome?<br>1. Urinary alkalinisation<br>2. Intravenous fluids<br>3. Rasburicase<br>4. Febuxostat<br>Select the correct answer using the code given below.\",\ncorrect:\"2, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Current guidelines for tumour lysis syndrome: IV fluids (aggressive hydration 2-3 L\/m2\/day) is the cornerstone. Rasburicase (recombinant urate oxidase) converts uric acid to allantoin (more soluble) and is the treatment of choice for established hyperuricaemia. Febuxostat (xanthine oxidase inhibitor) is used for TLS prophylaxis. Urinary alkalinisation is now discouraged: it promotes calcium phosphate precipitation in tubules (worsening nephropathy) and is contraindicated with rasburicase. Current guidelines do NOT recommend urinary alkalinisation. Statements 2, 3, and 4 are correct.\"\n},\n{id:23,\nstem:\"Focal seizures may be associated with which of the following?<br>1. Jacksonian march<br>2. Todd's paralysis<br>3. Epilepsia partialis continua<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 3\",\nopts:[\"1 and 2 only\",\"2 and 3 only\",\"1 and 3 only\",\"1, 2 and 3\"],\nexp:\"All three are features of focal (partial) seizures. Jacksonian march: focal motor seizure beginning in one body part and spreading sequentially along the motor homunculus. Todd's paralysis (post-ictal paresis): transient focal weakness (minutes to hours) following a focal motor seizure due to neuronal exhaustion. Epilepsia partialis continua (Kojewnikow syndrome): continuous focal motor seizure (clonic jerking) lasting hours to days without loss of consciousness, a form of focal status epilepticus. All three are correct.\"\n},\n{id:24,\nstem:\"Typical absence seizures are characterized by\",\ncorrect:\"abrupt 3 Hz spike-and-slow wave discharges on EEG\",\nopts:[\"abrupt 3 Hz spike-and-slow wave discharges on EEG\",\"postictal confusion in children\",\"multifocal structural abnormalities of brain\",\"less responsiveness to anticonvulsants as compared to atypical absence seizures\"],\nexp:\"Typical absence seizures have a pathognomonic EEG: bilateral, synchronous, symmetric 3 Hz spike-and-slow wave complexes, arising abruptly on a normal background. Clinically: brief (5-30 seconds) staring spells with no aura and NO postictal confusion (child resumes activity immediately). No structural brain abnormality is present. Typical absence seizures respond well to ethosuximide, valproate, or lamotrigine. Atypical absence (Lennox-Gastaut) is less responsive to treatment. Option (a) is the only correct statement.\"\n},\n{id:25,\nstem:\"Which of the following are contraindications to thrombolysis in acute ischemic stroke?<br>1. Recent head injury<br>2. Recent MI<br>3. Hypertension > 150\/100 mm Hg<br>4. GI bleeding in last 3 weeks<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Absolute contraindications to IV tPA for acute ischemic stroke include: serious head trauma in previous 3 months, recent MI (within 3 months), active internal bleeding including GI bleeding within 21 days, history of intracranial haemorrhage, and BP greater than 185\/110 mmHg that cannot be controlled. The threshold BP contraindication is greater than 185\/110 mmHg, NOT 150\/100 mmHg. A BP of 150\/100 is entirely acceptable for thrombolysis. Statement 3 is NOT a contraindication. Statements 1, 2, and 4 are correct.\"\n},\n{id:26,\nstem:\"Which one of the following distinguishes axonal degeneration from segmental demyelination on electrophysiological studies?\",\ncorrect:\"Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\",\nopts:[\"Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\",\"Conduction velocity is slow in axonal degeneration and normal in segmental demyelination.\",\"Conduction block is present in axonal degeneration and absent in segmental demyelination.\",\"Temporal dispersion is prominent in axonal degeneration and absent in segmental demyelination.\"],\nexp:\"Key distinction: In axonal neuropathy, myelin is intact so conduction velocity and distal latency are relatively preserved; the main finding is reduced CMAP\/SNAP amplitude. In demyelinating neuropathy (GBS, CIDP), myelin damage causes slowed conduction: prolonged distal latency, slowed NCV below 75% of lower normal limit, conduction block, and temporal dispersion. Conduction block and temporal dispersion are features of demyelination, not axonal degeneration. Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\"\n},\n{id:27,\nstem:\"Which one of the following drugs helps to maintain abstinence by reducing craving for alcohol?\",\ncorrect:\"Acamprosate\",\nopts:[\"Apomorphine\",\"Acamprosate\",\"Atropine\",\"Azathioprine\"],\nexp:\"Acamprosate (calcium acetylhomotaurinate) is a structural analogue of GABA that modulates glutamate (NMDA receptor antagonism) and GABA neurotransmission. It reduces the craving and protracted withdrawal discomfort associated with alcohol abstinence. It does not cause aversion reactions. Naltrexone (opioid antagonist) also reduces craving by blocking alcohol-induced dopamine release. Disulfiram causes aversion via acetaldehyde accumulation, not craving reduction. Apomorphine is a dopamine agonist used in Parkinson disease. Acamprosate is correct for reducing alcohol craving.\"\n},\n{id:28,\nstem:\"The BCR-ABL 1 oncoprotein exhibits constitutive activity of which one of the following enzymes?\",\ncorrect:\"Tyrosine kinase\",\nopts:[\"Alanine kinase\",\"Tyrosine kinase\",\"Leucine kinase\",\"Cysteine kinase\"],\nexp:\"The Philadelphia chromosome t(9;22)(q34;q11) results from fusion of the BCR gene to the ABL1 proto-oncogene. The BCR-ABL1 fusion protein is a constitutively active TYROSINE KINASE that phosphorylates downstream substrates continuously without normal regulatory control. This drives uncontrolled proliferation and resistance to apoptosis in CML haematopoietic stem cells. This is the therapeutic target of imatinib (Gleevec) and subsequent TKIs. Tyrosine kinase is the correct answer.\"\n},\n{id:29,\nstem:\"Imatinib, Dasatinib, Nilotinib and Ponatinib are examples of which class of drugs?\",\ncorrect:\"Tyrosine kinase inhibitors\",\nopts:[\"Interferons\",\"Monovalent antibodies\",\"Bivalent antibodies\",\"Tyrosine kinase inhibitors\"],\nexp:\"All four drugs are BCR-ABL tyrosine kinase inhibitors (TKIs) used in CML and Philadelphia chromosome-positive ALL. Imatinib (Gleevec) was the first-generation TKI that validated targeted therapy. Dasatinib and nilotinib are second-generation TKIs active against imatinib-resistant mutants. Ponatinib is a third-generation TKI designed to overcome the T315I gatekeeper mutation. They are small-molecule inhibitors, not antibodies. The class is tyrosine kinase inhibitors.\"\n},\n{id:30,\nstem:\"Helicobacter pylori infection is associated with the development of which one of the following lymphoid malignancies?\",\ncorrect:\"Mucosa-associated lymphoid tissue lymphoma\",\nopts:[\"Burkitt lymphoma\",\"Hodgkin lymphoma\",\"Mucosa-associated lymphoid tissue lymphoma\",\"Adult T-cell leukemia\/lymphoma\"],\nexp:\"H. pylori infection drives development of gastric MALT (mucosa-associated lymphoid tissue) lymphoma. Chronic H. pylori inflammation leads to antigen-driven clonal B-cell expansion. In early-stage MALT lymphoma, H. pylori eradication alone achieves complete remission in approximately 75% of cases. Advanced cases acquire chromosomal translocations t(11;18) making them H. pylori-independent. Burkitt lymphoma is associated with EBV. Adult T-cell leukaemia\/lymphoma is associated with HTLV-1.\"\n},\n{id:31,\nstem:\"The Duffy antigen system serves as receptor for which one of the following protozoal parasites?\",\ncorrect:\"Plasmodium vivax\",\nopts:[\"Giardia lamblia\",\"Plasmodium vivax\",\"Entamoeba histolytica\",\"Balantidium coli\"],\nexp:\"The Duffy antigen (ACKR1\/DARC) on red blood cells is the obligate receptor used by Plasmodium vivax merozoites to invade erythrocytes via the Duffy-binding protein. Individuals who are Duffy-negative (common in West Africa) are naturally resistant to P. vivax infection, explaining the near-absence of P. vivax in sub-Saharan Africa. This receptor is not used by P. falciparum (which uses glycophorin A\/B and Band 3). No other protozoa listed use the Duffy antigen.\"\n},\n{id:32,\nstem:\"With regard to transfusion therapy, cryoprecipitate is a rich source of which of the following?<br>1. Fibrinogen<br>2. Clotting factor VIII<br>3. Clotting factor IX<br>4. von Willebrand factor<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Cryoprecipitate is prepared by thawing fresh frozen plasma at 1-6 degrees C and collecting the cold-insoluble precipitate. It is rich in: fibrinogen (primary indication for hypofibrinogenaemia in DIC), Factor VIII (haemophilia A), von Willebrand factor (von Willebrand disease), Factor XIII, and fibronectin. Factor IX is NOT in cryoprecipitate; it is present in FFP and Factor IX concentrate. Cryoprecipitate is NOT the source for haemophilia B (Factor IX deficiency). Statements 1, 2, and 4 are correct.\"\n},\n{id:33,\nstem:\"Which of the following viruses can be transmitted via transfusion of infected blood?<br>1. Hepatitis B virus<br>2. Hepatitis C virus<br>3. Human immunodeficiency virus<br>4. Parvovirus B19<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2, 3 and 4\",\nopts:[\"1 and 3 only\",\"2 and 4 only\",\"1, 2 and 3 only\",\"1, 2, 3 and 4\"],\nexp:\"All four viruses are recognised transfusion-transmitted pathogens. HBV, HCV, and HIV are the three major transfusion-transmitted infections for which mandatory blood screening is performed globally. Parvovirus B19 is also transmissible by transfusion; it is a small non-enveloped DNA virus resistant to pathogen inactivation methods used for lipid-enveloped viruses. It is clinically significant in immunocompromised patients (pure red cell aplasia) and in those with chronic haemolytic anaemias (aplastic crisis). All four statements are correct.\"\n},\n{id:34,\nstem:\"Which one of the following correctly describes the mode of inheritance of haemophilia B?\",\ncorrect:\"X-linked recessive\",\nopts:[\"Autosomal dominant\",\"Autosomal recessive\",\"X-linked dominant\",\"X-linked recessive\"],\nexp:\"Haemophilia B (Christmas disease) is caused by deficiency of clotting Factor IX due to mutations in the F9 gene on the X chromosome (Xq27.1). It follows X-linked recessive inheritance: affected males (XY) have one defective X chromosome and manifest the disease; females (XX) are usually carriers and unaffected. Sons of carrier females have a 50% chance of being affected; daughters have a 50% chance of being carriers. This pattern is identical to haemophilia A (Factor VIII deficiency). X-linked recessive is correct.\"\n},\n{id:35,\nstem:\"Which one of the following conditions characteristically may present with a triad of haemolysis, pancytopenia and venous thrombosis?\",\ncorrect:\"Paroxysmal nocturnal haemoglobinuria\",\nopts:[\"Glucose-6-phosphate dehydrogenase deficiency\",\"Hereditary spherocytosis\",\"Haemolytic uremic syndrome\",\"Paroxysmal nocturnal haemoglobinuria\"],\nexp:\"Paroxysmal nocturnal haemoglobinuria (PNH) is a clonal stem cell disorder caused by a somatic PIG-A gene mutation, resulting in deficiency of GPI-anchored complement-regulatory proteins CD55 and CD59. Classic triad: (1) Intravascular haemolysis (complement-mediated, CD59 deficiency); (2) Pancytopenia (underlying bone marrow failure); (3) Venous thrombosis in unusual sites (hepatic veins causing Budd-Chiari syndrome, portal, mesenteric, cerebral veins) which is the leading cause of death in PNH. Eculizumab (anti-C5 antibody) is the specific treatment.\"\n},\n{id:36,\nstem:\"Which one of the following is associated with low MCV of red blood cells?\",\ncorrect:\"Thalassaemia\",\nopts:[\"Thalassaemia\",\"Vitamin B12 deficiency anaemia\",\"Folate deficiency anaemia\",\"Sickle cell anaemia\"],\nexp:\"MCV classification: Microcytic (low MCV below 80 fL): iron deficiency anaemia, thalassaemia (alpha and beta), anaemia of chronic disease, sideroblastic anaemia, lead poisoning. Macrocytic (high MCV above 100 fL): Vitamin B12 deficiency, folate deficiency, hypothyroidism, liver disease, alcohol. Sickle cell anaemia: MCV is typically NORMAL as sickle cells are normocytic; HbS produces normocytic red cells. Thalassaemia is characterised by microcytic hypochromic anaemia with low MCV. Thalassaemia is the correct answer.\"\n},\n{id:37,\nstem:\"GnRH deficiency with hyposmia is typically seen in\",\ncorrect:\"Kallmann syndrome\",\nopts:[\"Kallmann syndrome\",\"Bardet-Biedl syndrome\",\"Prader-Willi syndrome\",\"Wallenberg syndrome\"],\nexp:\"Kallmann syndrome is characterised by hypogonadotropic hypogonadism (GnRH deficiency) and anosmia or hyposmia (absent\/reduced sense of smell). The olfactory defect arises because GnRH-secreting neurons fail to migrate from the olfactory placode to the hypothalamus during foetal development. Associated features include anosmia\/hyposmia (pathognomonic), absence of puberty, and cryptorchidism. Bardet-Biedl and Prader-Willi syndromes cause obesity and hypogonadism but not specific anosmia. Wallenberg syndrome is a brainstem stroke. Kallmann syndrome is correct.\"\n},\n{id:38,\nstem:\"Iodine has complex effects on thyroid function. Very high concentrations of iodine inhibit thyroid hormone synthesis and release. This effect is known as\",\ncorrect:\"Wolff-Chaikoff effect\",\nopts:[\"Wolff-Chaikoff effect\",\"Jod-Basedow effect\",\"reverse Wolff-Chaikoff effect\",\"reverse Jod-Basedow effect\"],\nexp:\"The Wolff-Chaikoff effect: high inorganic iodide concentrations acutely suppress thyroid hormone synthesis by inhibiting iodide organification. This is a protective autoregulatory mechanism. Normal thyroid glands escape this effect after 10-14 days by downregulating the sodium-iodide symporter. Failure to escape leads to hypothyroidism (e.g. amiodarone-induced). The Jod-Basedow effect is the opposite: excess iodine in an iodine-deficient or autonomous thyroid gland triggers hyperthyroidism. Wolff-Chaikoff = iodine-induced suppression of hormone synthesis.\"\n},\n{id:39,\nstem:\"Consider the following pharmacological agents:<br>1. Propranolol<br>2. Sodium ipodate<br>3. Propylthiouracil<br>4. Liothyronine<br>Which of the above can be used for the treatment of thyrotoxic crisis?\",\ncorrect:\"1, 2 and 3\",\nopts:[\"3 only\",\"1 and 2 only\",\"1, 2 and 3\",\"2, 3 and 4\"],\nexp:\"Thyrotoxic crisis management requires multiple simultaneous interventions. Propylthiouracil (PTU) blocks new thyroid hormone synthesis AND inhibits peripheral T4 to T3 conversion, preferred in thyroid storm. Propranolol controls tachycardia and inhibits T4 to T3 conversion at high doses. Sodium ipodate blocks T4 to T3 conversion and inhibits thyroid hormone release. Liothyronine (T3) is an active thyroid hormone; administering it in thyrotoxic crisis would dramatically WORSEN the condition. Liothyronine is used in myxoedema coma, not thyroid storm. Statements 1, 2, and 3 are correct.\"\n},\n{id:40,\nstem:\"Consider the following pharmacological agents:<br>1. Liothyronine<br>2. Levothyroxine<br>3. Carbimazole<br>4. Sodium ipodate<br>Which of the above may be included in the treatment of myxoedema coma?\",\ncorrect:\"1 and 2\",\nopts:[\"1 only\",\"1 and 2\",\"2 and 3\",\"3 and 4\"],\nexp:\"Myxoedema coma is a life-threatening emergency of severe hypothyroidism requiring urgent thyroid hormone replacement. Liothyronine (T3): the active hormone, given IV for immediate effect; crosses the blood-brain barrier more readily; preferred for acute treatment. Levothyroxine (T4): given IV or via NG tube for sustained replacement. Carbimazole BLOCKS thyroid hormone synthesis and would worsen hypothyroidism; absolutely contraindicated. Sodium ipodate blocks T4 to T3 conversion; also contraindicated in myxoedema coma. Additional management: IV hydrocortisone, IV fluids, passive warming. 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Submitting in 10 Submit Now Combined Medical Services Examination 2023General Medicine & Paediatrics · Paper I · Part A Cardiology · Respiratory · Gastroenterology & Hepatology · Neurology · Haematology & Endocrinology Questions 1–40… <\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36727","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2023 P1 Part-A - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/04\/30\/cms-2023-p1-part-a\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2023 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2023 | General Medicine & Paediatrics | Paper I | Part A ✓️ 0 ❌ 0 ⏳ 40 left ⏱ 40:00 Net 0 \/ 160 Time's Up! 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Display\",serif;font-size:1.15rem;color:var(--bad);margin-bottom:8px}\n.qz-grace-box p{font-size:0.85rem;color:var(--ink-mid);margin-bottom:14px}\n.qz-grace-n{font-family:\"Playfair Display\",serif;font-size:2.8rem;font-weight:700;color:var(--bad);line-height:1;margin-bottom:16px}\n.qz-grace-now{background:var(--bad);color:#fff;border:none;border-radius:8px;padding:10px 24px;font-family:\"Playfair Display\",serif;font-size:0.9rem;font-weight:700;cursor:pointer}\n.qz-grace-now:hover{background:#c62828}\n\n@media(max-width:480px){\n .qz-header h1{font-size:1.05rem}\n .qz-stem{font-size:0.87rem}\n .qz-opt-txt{font-size:0.84rem}\n .qz-prog-stats{font-size:0.68rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms23p1a\">\n\n<div class=\"qz-prog-bar\" id=\"qz-prog-bar\">\n <div class=\"qz-prog-stats\">\n <div class=\"qz-stat\">✓️ <strong id=\"qz-sc\">0<\/strong><\/div>\n <div class=\"qz-stat\">❌ <strong id=\"qz-sw\">0<\/strong><\/div>\n <div class=\"qz-stat\">⏳ <strong id=\"qz-sr\">40<\/strong> left<\/div>\n <div class=\"qz-timer-wrap\">\n <div class=\"qz-timer\" id=\"qz-timer\">⏱ <strong id=\"qz-td\">40:00<\/strong><\/div>\n <div class=\"qz-stat net-score\">Net <strong id=\"qz-sn\">0<\/strong> \/ 160<\/div>\n <\/div>\n <\/div>\n <div class=\"qz-prog-track\"><div class=\"qz-prog-fill\" id=\"qz-fill\"><\/div><\/div>\n<\/div>\n\n<div class=\"qz-grace\" id=\"qz-grace\">\n <div class=\"qz-grace-box\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"qz-grace-n\" id=\"qz-gn\">10<\/div>\n <button class=\"qz-grace-now\" id=\"qz-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n\n<div class=\"qz-header\">\n <h1>Combined Medical Services Examination 2023<br>General Medicine & Paediatrics · Paper I · Part A<\/h1>\n <p>Cardiology · Respiratory · Gastroenterology & Hepatology · Neurology · Haematology & Endocrinology<\/p>\n <div class=\"qz-meta\">\n <span class=\"qz-badge\">Questions 1–40<\/span>\n <span class=\"qz-badge\">Options reshuffled<\/span>\n <span class=\"qz-badge\">Score = c × 4 − w<\/span>\n <button class=\"qz-timer-btn\" id=\"qz-tbtn\">⏱ Start Timed Mode<\/button>\n <\/div>\n<\/div>\n\n<div class=\"qz-body\">\n <div id=\"qz-questions\"><\/div>\n <div class=\"qz-submit-wrap\">\n <button class=\"qz-submit\" id=\"qz-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"qz-result\" id=\"qz-result\">\n <div class=\"qz-ring\" id=\"qz-ring\">\n <div class=\"qz-ring-inner\">\n <div class=\"qz-ring-pct\" id=\"qz-rpct\">0%<\/div>\n <div class=\"qz-ring-sub\">score<\/div>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"qz-net\" id=\"qz-rnet\"><\/div>\n <div class=\"qz-verdict\" id=\"qz-rv\"><\/div>\n <div class=\"qz-bands\">\n <span class=\"qz-band bc\" id=\"qz-bc\"><\/span>\n <span class=\"qz-band bw\" id=\"qz-bw\"><\/span>\n <span class=\"qz-band bs\" id=\"qz-bs\"><\/span>\n <\/div>\n <button class=\"qz-retry\" id=\"qz-retry\">↺ Retry Quiz<\/button>\n <\/div>\n<\/div>\n\n<\/div>\n\n<script>\n(function(){\n\nvar TOTAL = 40, MAX = 160;\nvar TSECS = 2400, GSECS = 10;\nvar LTRS = [\"A\",\"B\",\"C\",\"D\"];\n\nvar QQ = [\n{id:1,\nstem:\"Thickened ventricular wall with normal diastolic function is a feature of\",\ncorrect:\"athlete's heart\",\nopts:[\"hypertrophic cardiomyopathy\",\"restrictive cardiomyopathy\",\"endomyocardial fibrosis\",\"athlete's heart\"],\nexp:\"Athlete's heart (physiological cardiac remodelling) shows concentric LV hypertrophy with preserved or supranormal diastolic function. This distinguishes it from pathological hypertrophy. Hypertrophic cardiomyopathy shows asymmetric septal hypertrophy with impaired diastolic filling. Restrictive cardiomyopathy shows markedly impaired diastolic function. Normal diastolic function with wall thickening = athlete's heart.\"\n},\n{id:2,\nstem:\"In which of the following cases does paradoxical splitting occur?<br>1. Severe aortic stenosis<br>2. Right bundle branch block<br>3. Right ventricular pacing<br>4. Hypertrophic obstructive cardiomyopathy<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Paradoxical (reversed) splitting of S2 occurs when A2 is delayed beyond P2, heard on expiration. Causes that delay aortic valve closure: LBBB (classic), severe aortic stenosis (prolonged LV ejection), HOCM (dynamic obstruction), and right ventricular pacing (creates LBBB activation pattern). Right bundle branch block causes WIDE splitting (P2 delayed) NOT paradoxical splitting. Statements 1, 3, and 4 are correct.\"\n},\n{id:3,\nstem:\"A patient with peripheral oedema has the following findings on clinical examination: A soft systolic murmur at the lower left sternal border with raised JVP showing prominent C-V wave. The murmur increases in intensity on deep inspiration. The most likely valvular abnormality is\",\ncorrect:\"tricuspid regurgitation\",\nopts:[\"ventricular septal defect\",\"mitral regurgitation\",\"tricuspid regurgitation\",\"mitral valve prolapse\"],\nexp:\"The clinical triad is pathognomonic of tricuspid regurgitation (TR): pansystolic murmur at the lower left sternal border, Carvallo sign (murmur increases on deep inspiration), and prominent C-V wave in JVP (systolic regurgitant wave merging C and V waves). Peripheral oedema from right heart failure confirms the diagnosis. Mitral regurgitation does NOT increase with inspiration. Tricuspid regurgitation is correct.\"\n},\n{id:4,\nstem:\"Kussmaul's sign is a clinical feature of\",\ncorrect:\"constrictive pericarditis\",\nopts:[\"constrictive pericarditis\",\"hypertrophic obstructive cardiomyopathy\",\"anteroseptal myocardial infarction\",\"dilated cardiomyopathy\"],\nexp:\"Kussmaul's sign is a paradoxical rise in jugular venous pressure on inspiration. In constrictive pericarditis, the rigid fibrocalcific pericardium cannot expand to accommodate increased venous return during inspiration, forcing JVP upward. Also seen in restrictive cardiomyopathy and massive pericardial effusion with tamponade. Not a feature of HOCM, STEMI, or dilated cardiomyopathy.\"\n},\n{id:5,\nstem:\"A patient has a cardiac murmur best heard at the right second intercostal space. It increases with expiration. The murmur reduces in intensity during sustained handgrip but increases on inhalation of amyl nitrite. The likely lesion is\",\ncorrect:\"hypertrophic obstructive cardiomyopathy\",\nopts:[\"ventricular septal defect\",\"aortic stenosis\",\"hypertrophic obstructive cardiomyopathy\",\"mitral regurgitation\"],\nexp:\"HOCM bedside manoeuvres: Handgrip increases LV afterload and preload, larger LV cavity reduces obstruction, murmur SOFTER. Amyl nitrite reduces preload and afterload, smaller LV cavity worsens obstruction, murmur LOUDER. These responses are the opposite of aortic stenosis. The HOCM murmur can radiate to the aortic area mimicking AS, but dynamic manoeuvre responses clinch HOCM.\"\n},\n{id:6,\nstem:\"In the modified Duke criteria for infective endocarditis, which one of the following is NOT a major criterion?\",\ncorrect:\"Roth's spots\",\nopts:[\"New partial dehiscence of prosthetic valve\",\"Positive blood culture\",\"Roth's spots\",\"New valvular regurgitation\"],\nexp:\"Modified Duke MAJOR criteria: (1) Positive blood cultures with typical organisms; (2) Endocardial involvement on echo (oscillating mass, abscess, new prosthetic valve dehiscence, or new valvular regurgitation). Roth's spots are flame-shaped retinal haemorrhages with pale centres; they are an immunological phenomenon and a MINOR criterion. New prosthetic valve dehiscence and new valvular regurgitation are major criteria. Roth's spots is NOT a major criterion.\"\n},\n{id:7,\nstem:\"Which one of the following diseases affects predominantly large arteries?\",\ncorrect:\"Giant cell arteritis\",\nopts:[\"Granulomatosis with polyangiitis\",\"Polyarteritis nodosa\",\"Giant cell arteritis\",\"Eosinophilic granulomatosis with polyangiitis\"],\nexp:\"Vasculitides by vessel size: Large vessel: Giant cell arteritis (aorta, major branches, temporal artery) and Takayasu arteritis. Medium vessel: Polyarteritis nodosa, Kawasaki disease. Small vessel: Granulomatosis with polyangiitis (GPA\/Wegener's), Microscopic polyangiitis, Eosinophilic granulomatosis with polyangiitis (EGPA\/Churg-Strauss), IgA vasculitis. Giant cell arteritis is the large artery vasculitis among the options.\"\n},\n{id:8,\nstem:\"Osborn waves in ECG show prolonged repolarization with a distinctive convex elevation of the J point. These waves are associated with\",\ncorrect:\"systemic hypothermia\",\nopts:[\"systemic hypothermia\",\"acute pericarditis\",\"acute myocarditis\",\"Brugada syndrome\"],\nexp:\"Osborn waves (J waves) are pathognomonic of systemic hypothermia (core temperature typically below 30 degrees C). They appear as a positive deflection at the J point, most prominent in V4-V6 and inferior leads. Amplitude increases as temperature falls. Other features: bradycardia, prolonged PR\/QRS\/QT, ventricular fibrillation below 28 degrees C. Brugada syndrome shows an RBBB-like pattern with ST elevation in V1-V3, not Osborn waves.\"\n},\n{id:9,\nstem:\"A decline in total lung capacity to less than 80% of patient's predictive value is an indication of\",\ncorrect:\"restrictive lung disease\",\nopts:[\"restrictive lung disease\",\"obstructive lung disease\",\"pulmonary artery hypertension\",\"pulmonary embolism\"],\nexp:\"Total lung capacity (TLC) below 80% of predicted defines restrictive lung disease. Restriction means the lungs cannot expand to normal total volume, caused by interstitial fibrosis (IPF), chest wall disease (kyphoscoliosis, obesity), neuromuscular weakness, or pleural disease. In obstructive lung disease (COPD, asthma), TLC is normal or increased due to air trapping. Pulmonary artery hypertension and embolism affect vasculature and do not primarily reduce TLC.\"\n},\n{id:10,\nstem:\"A 28-year male is suspected of having hypertrophic obstructive cardiomyopathy (HOCM). Which of the following statements are likely to be true on his examination?<br>1. Maneuvers that decrease LV preload will cause the murmur to intensify.<br>2. Maneuvers that decrease LV afterload will cause decrease in intensity of murmur.<br>3. Murmur of HOCM becomes softer with passive leg raising.<br>4. Murmur of HOCM becomes louder with squatting.<br>Select the correct answer using the code given below.\",\ncorrect:\"1 and 3\",\nopts:[\"1 and 3\",\"2 and 3\",\"2 and 4\",\"1 and 4\"],\nexp:\"HOCM murmur worsens when the LV cavity is smaller (less preload) and improves when larger. Statement 1 TRUE: decreased preload (Valsalva, standing) gives smaller LV, worse obstruction, louder murmur. Statement 2 FALSE: decreased afterload gives smaller LV, LOUDER murmur (not softer). Statement 3 TRUE: passive leg raising increases preload, larger LV, murmur softer. Statement 4 FALSE: squatting increases preload and afterload, larger LV, murmur SOFTER. Statements 1 and 3 are correct.\"\n},\n{id:11,\nstem:\"A 56-year male, chronic heavy smoker, presented with breathlessness. Pulse: 96\/min, BP: 112\/70 mm Hg and a pansystolic murmur showing Carvallo's sign with murmur getting louder on deep inspiration. Which one of the following statements is true regarding examination of JVP in him?\",\ncorrect:\"V wave and C wave merge.\",\nopts:[\"V wave is attenuated.\",\"C wave is attenuated and V wave is accentuated.\",\"V wave and C wave merge.\",\"V wave and C wave merge and Y descent is blunted.\"],\nexp:\"In tricuspid regurgitation (confirmed by Carvallo's sign in this COPD\/cor pulmonale patient), the regurgitant systolic jet into the right atrium merges the C wave (tricuspid valve closure) and V wave (venous filling) into a single large CV fusion wave. This is the characteristic JVP finding in TR. The Y descent is typically sharp. Blunted Y descent is seen in cardiac tamponade or tricuspid stenosis.\"\n},\n{id:12,\nstem:\"Which one of the following is a manifestation of vascular phenomenon in modified Duke criteria?\",\ncorrect:\"Janeway's lesions\",\nopts:[\"Osler's node\",\"Roth's spots\",\"Janeway's lesions\",\"Glomerulonephritis\"],\nexp:\"Modified Duke MINOR criteria include immunological phenomena (Osler's nodes, Roth's spots, rheumatoid factor, glomerulonephritis) and vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway's lesions). Janeway's lesions are painless erythematous macules on palms and soles resulting from septic emboli (vascular phenomenon). Osler's nodes (painful tender nodules on fingertips) are immunological phenomena.\"\n},\n{id:13,\nstem:\"The volume of air remaining in the lungs after a normal expiration is called\",\ncorrect:\"functional residual capacity\",\nopts:[\"expiratory residual volume\",\"functional residual capacity\",\"residual volume\",\"vital capacity\"],\nexp:\"Functional Residual Capacity (FRC) is the volume of air remaining in the lungs at the end of a normal passive (tidal) expiration. FRC equals ERV plus RV. It represents the resting equilibrium position where outward chest wall recoil balances inward lung recoil. Residual volume (RV) is the air remaining after maximal forced expiration. Vital capacity is the maximum volume exhaled after maximal inhalation. FRC is the correct answer.\"\n},\n{id:14,\nstem:\"The investigation of choice for early follow-up in patients treated for anti-H. pylori drugs is\",\ncorrect:\"urea breath test\",\nopts:[\"urea breath test\",\"rapid urease test\",\"stool H. pylori antigen test\",\"serology for H. pylori\"],\nexp:\"The urea breath test (UBT) is the investigation of choice for confirming H. pylori eradication after treatment. The patient ingests labelled urea; if H. pylori is present, its urease splits the urea and labelled CO2 is detected in exhaled breath. Performed at least 4 weeks after completing antibiotics and 2 weeks after stopping PPIs. Sensitivity and specificity approximately 95%. Serology remains positive for months to years after eradication and cannot confirm cure. UBT is the gold standard for follow-up.\"\n},\n{id:15,\nstem:\"The most common non-pancreatic site for tumour distribution in Zollinger-Ellison syndrome is\",\ncorrect:\"duodenum\",\nopts:[\"duodenum\",\"ovaries\",\"stomach\",\"liver\"],\nexp:\"In Zollinger-Ellison syndrome (ZES), the gastrinoma arises in the pancreas in approximately 25-40% of cases. Among extra-pancreatic locations, the duodenum is the most common site (50-70% of sporadic gastrinomas). The gastrinoma triangle (Passaro triangle) is defined by the biliary confluence, the junction of 2nd and 3rd duodenum, and the pancreatic neck. Most sporadic gastrinomas lie within this triangle. MEN-1 associated gastrinomas are frequently duodenal, often multiple and small.\"\n},\n{id:16,\nstem:\"Which of the following are the risk factors for the acquisition of hepatitis C infection?<br>1. Faeco-oral transmission<br>2. Intravenous drug abuse<br>3. Vertical transmission<br>4. Sharing toothbrush and razors<br>Select the correct answer using the code given below.\",\ncorrect:\"2, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"HCV is transmitted via blood-to-blood contact. IV drug abuse (sharing needles) is the leading route of HCV transmission. Vertical transmission from HCV-positive mother to neonate occurs in approximately 5% of pregnancies. Sharing toothbrushes and razors involves percutaneous\/permucosal blood exposure and is a recognised risk factor. Faeco-oral transmission is NOT a route for HCV (unlike HAV and HEV). Statement 1 is false. Statements 2, 3, and 4 are correct.\"\n},\n{id:17,\nstem:\"The most common cause of shock in severe acute pancreatitis (SAP) is\",\ncorrect:\"hypovolemic shock resulting from third space loss\",\nopts:[\"hypovolemic shock resulting from third space loss\",\"septic shock resulting from infected pancreatic necrosis\",\"cardiogenic shock resulting from SIRS\",\"abdominal compartment syndrome\"],\nexp:\"In the early phase of severe acute pancreatitis, massive third-space fluid sequestration occurs as plasma leaks into the retroperitoneum, peritoneal cavity, and bowel wall due to inflammatory capillary leak syndrome. This results in hypovolemic shock, the most common cause of shock in SAP. Septic shock from infected necrosis is a later complication, usually after week 2. Aggressive IV fluid resuscitation (lactated Ringer's preferred) in the first 24-48 hours is the cornerstone of SAP management.\"\n},\n{id:18,\nstem:\"The most common causative agent for spontaneous bacterial peritonitis is\",\ncorrect:\"Escherichia coli\",\nopts:[\"Escherichia coli\",\"Enterococcus sp.\",\"Staphylococcus aureus\",\"Streptococcus viridans\"],\nexp:\"Spontaneous bacterial peritonitis (SBP) occurs in cirrhotic patients when gut bacteria translocate into ascitic fluid. Escherichia coli is the most common causative organism (40-50%), followed by Klebsiella pneumoniae and Streptococcus pneumoniae. SBP is typically monomicrobial. Diagnosis: ascitic fluid neutrophil count at least 250\/mm3. Treatment: cefotaxime IV plus IV albumin (to prevent hepatorenal syndrome). Prophylaxis: norfloxacin or ciprofloxacin in high-risk cirrhotics.\"\n},\n{id:19,\nstem:\"The serologic marker detectable during the window period of hepatitis B infection is\",\ncorrect:\"anti-HBc IgM\",\nopts:[\"anti-HBsAb\",\"anti-HBc IgG\",\"anti-HBc IgM\",\"HBeAg\"],\nexp:\"The serological window period in acute HBV infection is when HBsAg has become undetectable but anti-HBs has not yet appeared. During this window, the ONLY detectable marker is anti-HBc IgM (IgM antibody to hepatitis B core antigen). Anti-HBc IgM is the diagnostic marker of acute HBV infection. It appears in the prodromal phase, peaks during acute illness, and declines over 3-6 months. Anti-HBc IgG persists lifelong indicating past or chronic infection. In the window period, anti-HBc IgM is the only positive marker.\"\n},\n{id:20,\nstem:\"A 14-year boy came with chronic diarrhoea and malnutrition. The physician suspected celiac disease. Which of the following are correct in his diagnostic workup?<br>1. Presence of IgA antiendomysial antibody<br>2. Absence of reduced height of villi on intestinal biopsy<br>3. Increased lymphocytes in lamina propria in small intestine biopsy<br>4. Absence of tTG antibody in serum<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 3\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Celiac disease diagnostic features: IgA anti-endomysial antibody (EMA) is highly specific (at least 95%) for celiac disease and its presence strongly supports the diagnosis. On intestinal biopsy, villous atrophy (reduced height of villi) IS present, confirming celiac disease. Increased intraepithelial and lamina propria lymphocytes with crypt hyperplasia are characteristic Marsh lesions. Anti-tTG antibodies are ELEVATED (not absent) in celiac disease, so statement 4 is false. Statements 1, 2, and 3 are correct diagnostic features.\"\n},\n{id:21,\nstem:\"Which of the following statements are correct for the treatment of chronic hepatitis B with pegylated interferon (PEG-IFN)?<br>1. PEG-IFN is poorly tolerated drug as compared to nucleoside analogues.<br>2. Resistance to treatment with PEG-IFN is more common than nucleoside analogues.<br>3. PEG-IFN is not useful in patients of cirrhosis.<br>4. PEG-IFN is administered every week for 48 weeks.<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 3 and 4\",\nopts:[\"1, 3 and 4\",\"1, 2 and 3\",\"2 and 4\",\"1 and 3 only\"],\nexp:\"Statement 1 TRUE: PEG-IFN has significant adverse effects (flu-like symptoms, cytopenias, depression) making it poorly tolerated compared to nucleoside analogues. Statement 2 FALSE: Resistance to PEG-IFN does NOT occur as it acts via immune mechanisms with no resistance mutations. Statement 3 TRUE: PEG-IFN is contraindicated in decompensated cirrhosis (Child-Pugh B\/C) due to risk of hepatic decompensation. Statement 4 TRUE: Standard PEG-IFN for HBV is 180 mcg SC weekly for 48 weeks. Statements 1, 3, and 4 are correct.\"\n},\n{id:22,\nstem:\"Which of the following are recommended for management of tumour lysis syndrome?<br>1. Urinary alkalinisation<br>2. Intravenous fluids<br>3. Rasburicase<br>4. Febuxostat<br>Select the correct answer using the code given below.\",\ncorrect:\"2, 3 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Current guidelines for tumour lysis syndrome: IV fluids (aggressive hydration 2-3 L\/m2\/day) is the cornerstone. Rasburicase (recombinant urate oxidase) converts uric acid to allantoin (more soluble) and is the treatment of choice for established hyperuricaemia. Febuxostat (xanthine oxidase inhibitor) is used for TLS prophylaxis. Urinary alkalinisation is now discouraged: it promotes calcium phosphate precipitation in tubules (worsening nephropathy) and is contraindicated with rasburicase. Current guidelines do NOT recommend urinary alkalinisation. Statements 2, 3, and 4 are correct.\"\n},\n{id:23,\nstem:\"Focal seizures may be associated with which of the following?<br>1. Jacksonian march<br>2. Todd's paralysis<br>3. Epilepsia partialis continua<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 3\",\nopts:[\"1 and 2 only\",\"2 and 3 only\",\"1 and 3 only\",\"1, 2 and 3\"],\nexp:\"All three are features of focal (partial) seizures. Jacksonian march: focal motor seizure beginning in one body part and spreading sequentially along the motor homunculus. Todd's paralysis (post-ictal paresis): transient focal weakness (minutes to hours) following a focal motor seizure due to neuronal exhaustion. Epilepsia partialis continua (Kojewnikow syndrome): continuous focal motor seizure (clonic jerking) lasting hours to days without loss of consciousness, a form of focal status epilepticus. All three are correct.\"\n},\n{id:24,\nstem:\"Typical absence seizures are characterized by\",\ncorrect:\"abrupt 3 Hz spike-and-slow wave discharges on EEG\",\nopts:[\"abrupt 3 Hz spike-and-slow wave discharges on EEG\",\"postictal confusion in children\",\"multifocal structural abnormalities of brain\",\"less responsiveness to anticonvulsants as compared to atypical absence seizures\"],\nexp:\"Typical absence seizures have a pathognomonic EEG: bilateral, synchronous, symmetric 3 Hz spike-and-slow wave complexes, arising abruptly on a normal background. Clinically: brief (5-30 seconds) staring spells with no aura and NO postictal confusion (child resumes activity immediately). No structural brain abnormality is present. Typical absence seizures respond well to ethosuximide, valproate, or lamotrigine. Atypical absence (Lennox-Gastaut) is less responsive to treatment. Option (a) is the only correct statement.\"\n},\n{id:25,\nstem:\"Which of the following are contraindications to thrombolysis in acute ischemic stroke?<br>1. Recent head injury<br>2. Recent MI<br>3. Hypertension > 150\/100 mm Hg<br>4. GI bleeding in last 3 weeks<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Absolute contraindications to IV tPA for acute ischemic stroke include: serious head trauma in previous 3 months, recent MI (within 3 months), active internal bleeding including GI bleeding within 21 days, history of intracranial haemorrhage, and BP greater than 185\/110 mmHg that cannot be controlled. The threshold BP contraindication is greater than 185\/110 mmHg, NOT 150\/100 mmHg. A BP of 150\/100 is entirely acceptable for thrombolysis. Statement 3 is NOT a contraindication. Statements 1, 2, and 4 are correct.\"\n},\n{id:26,\nstem:\"Which one of the following distinguishes axonal degeneration from segmental demyelination on electrophysiological studies?\",\ncorrect:\"Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\",\nopts:[\"Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\",\"Conduction velocity is slow in axonal degeneration and normal in segmental demyelination.\",\"Conduction block is present in axonal degeneration and absent in segmental demyelination.\",\"Temporal dispersion is prominent in axonal degeneration and absent in segmental demyelination.\"],\nexp:\"Key distinction: In axonal neuropathy, myelin is intact so conduction velocity and distal latency are relatively preserved; the main finding is reduced CMAP\/SNAP amplitude. In demyelinating neuropathy (GBS, CIDP), myelin damage causes slowed conduction: prolonged distal latency, slowed NCV below 75% of lower normal limit, conduction block, and temporal dispersion. Conduction block and temporal dispersion are features of demyelination, not axonal degeneration. Distal latency is normal in axonal degeneration and prolonged in segmental demyelination.\"\n},\n{id:27,\nstem:\"Which one of the following drugs helps to maintain abstinence by reducing craving for alcohol?\",\ncorrect:\"Acamprosate\",\nopts:[\"Apomorphine\",\"Acamprosate\",\"Atropine\",\"Azathioprine\"],\nexp:\"Acamprosate (calcium acetylhomotaurinate) is a structural analogue of GABA that modulates glutamate (NMDA receptor antagonism) and GABA neurotransmission. It reduces the craving and protracted withdrawal discomfort associated with alcohol abstinence. It does not cause aversion reactions. Naltrexone (opioid antagonist) also reduces craving by blocking alcohol-induced dopamine release. Disulfiram causes aversion via acetaldehyde accumulation, not craving reduction. Apomorphine is a dopamine agonist used in Parkinson disease. Acamprosate is correct for reducing alcohol craving.\"\n},\n{id:28,\nstem:\"The BCR-ABL 1 oncoprotein exhibits constitutive activity of which one of the following enzymes?\",\ncorrect:\"Tyrosine kinase\",\nopts:[\"Alanine kinase\",\"Tyrosine kinase\",\"Leucine kinase\",\"Cysteine kinase\"],\nexp:\"The Philadelphia chromosome t(9;22)(q34;q11) results from fusion of the BCR gene to the ABL1 proto-oncogene. The BCR-ABL1 fusion protein is a constitutively active TYROSINE KINASE that phosphorylates downstream substrates continuously without normal regulatory control. This drives uncontrolled proliferation and resistance to apoptosis in CML haematopoietic stem cells. This is the therapeutic target of imatinib (Gleevec) and subsequent TKIs. Tyrosine kinase is the correct answer.\"\n},\n{id:29,\nstem:\"Imatinib, Dasatinib, Nilotinib and Ponatinib are examples of which class of drugs?\",\ncorrect:\"Tyrosine kinase inhibitors\",\nopts:[\"Interferons\",\"Monovalent antibodies\",\"Bivalent antibodies\",\"Tyrosine kinase inhibitors\"],\nexp:\"All four drugs are BCR-ABL tyrosine kinase inhibitors (TKIs) used in CML and Philadelphia chromosome-positive ALL. Imatinib (Gleevec) was the first-generation TKI that validated targeted therapy. Dasatinib and nilotinib are second-generation TKIs active against imatinib-resistant mutants. Ponatinib is a third-generation TKI designed to overcome the T315I gatekeeper mutation. They are small-molecule inhibitors, not antibodies. The class is tyrosine kinase inhibitors.\"\n},\n{id:30,\nstem:\"Helicobacter pylori infection is associated with the development of which one of the following lymphoid malignancies?\",\ncorrect:\"Mucosa-associated lymphoid tissue lymphoma\",\nopts:[\"Burkitt lymphoma\",\"Hodgkin lymphoma\",\"Mucosa-associated lymphoid tissue lymphoma\",\"Adult T-cell leukemia\/lymphoma\"],\nexp:\"H. pylori infection drives development of gastric MALT (mucosa-associated lymphoid tissue) lymphoma. Chronic H. pylori inflammation leads to antigen-driven clonal B-cell expansion. In early-stage MALT lymphoma, H. pylori eradication alone achieves complete remission in approximately 75% of cases. Advanced cases acquire chromosomal translocations t(11;18) making them H. pylori-independent. Burkitt lymphoma is associated with EBV. Adult T-cell leukaemia\/lymphoma is associated with HTLV-1.\"\n},\n{id:31,\nstem:\"The Duffy antigen system serves as receptor for which one of the following protozoal parasites?\",\ncorrect:\"Plasmodium vivax\",\nopts:[\"Giardia lamblia\",\"Plasmodium vivax\",\"Entamoeba histolytica\",\"Balantidium coli\"],\nexp:\"The Duffy antigen (ACKR1\/DARC) on red blood cells is the obligate receptor used by Plasmodium vivax merozoites to invade erythrocytes via the Duffy-binding protein. Individuals who are Duffy-negative (common in West Africa) are naturally resistant to P. vivax infection, explaining the near-absence of P. vivax in sub-Saharan Africa. This receptor is not used by P. falciparum (which uses glycophorin A\/B and Band 3). No other protozoa listed use the Duffy antigen.\"\n},\n{id:32,\nstem:\"With regard to transfusion therapy, cryoprecipitate is a rich source of which of the following?<br>1. Fibrinogen<br>2. Clotting factor VIII<br>3. Clotting factor IX<br>4. von Willebrand factor<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2 and 4\",\nopts:[\"1, 2 and 3\",\"1, 2 and 4\",\"1, 3 and 4\",\"2, 3 and 4\"],\nexp:\"Cryoprecipitate is prepared by thawing fresh frozen plasma at 1-6 degrees C and collecting the cold-insoluble precipitate. It is rich in: fibrinogen (primary indication for hypofibrinogenaemia in DIC), Factor VIII (haemophilia A), von Willebrand factor (von Willebrand disease), Factor XIII, and fibronectin. Factor IX is NOT in cryoprecipitate; it is present in FFP and Factor IX concentrate. Cryoprecipitate is NOT the source for haemophilia B (Factor IX deficiency). Statements 1, 2, and 4 are correct.\"\n},\n{id:33,\nstem:\"Which of the following viruses can be transmitted via transfusion of infected blood?<br>1. Hepatitis B virus<br>2. Hepatitis C virus<br>3. Human immunodeficiency virus<br>4. Parvovirus B19<br>Select the correct answer using the code given below.\",\ncorrect:\"1, 2, 3 and 4\",\nopts:[\"1 and 3 only\",\"2 and 4 only\",\"1, 2 and 3 only\",\"1, 2, 3 and 4\"],\nexp:\"All four viruses are recognised transfusion-transmitted pathogens. HBV, HCV, and HIV are the three major transfusion-transmitted infections for which mandatory blood screening is performed globally. Parvovirus B19 is also transmissible by transfusion; it is a small non-enveloped DNA virus resistant to pathogen inactivation methods used for lipid-enveloped viruses. It is clinically significant in immunocompromised patients (pure red cell aplasia) and in those with chronic haemolytic anaemias (aplastic crisis). All four statements are correct.\"\n},\n{id:34,\nstem:\"Which one of the following correctly describes the mode of inheritance of haemophilia B?\",\ncorrect:\"X-linked recessive\",\nopts:[\"Autosomal dominant\",\"Autosomal recessive\",\"X-linked dominant\",\"X-linked recessive\"],\nexp:\"Haemophilia B (Christmas disease) is caused by deficiency of clotting Factor IX due to mutations in the F9 gene on the X chromosome (Xq27.1). It follows X-linked recessive inheritance: affected males (XY) have one defective X chromosome and manifest the disease; females (XX) are usually carriers and unaffected. Sons of carrier females have a 50% chance of being affected; daughters have a 50% chance of being carriers. This pattern is identical to haemophilia A (Factor VIII deficiency). X-linked recessive is correct.\"\n},\n{id:35,\nstem:\"Which one of the following conditions characteristically may present with a triad of haemolysis, pancytopenia and venous thrombosis?\",\ncorrect:\"Paroxysmal nocturnal haemoglobinuria\",\nopts:[\"Glucose-6-phosphate dehydrogenase deficiency\",\"Hereditary spherocytosis\",\"Haemolytic uremic syndrome\",\"Paroxysmal nocturnal haemoglobinuria\"],\nexp:\"Paroxysmal nocturnal haemoglobinuria (PNH) is a clonal stem cell disorder caused by a somatic PIG-A gene mutation, resulting in deficiency of GPI-anchored complement-regulatory proteins CD55 and CD59. Classic triad: (1) Intravascular haemolysis (complement-mediated, CD59 deficiency); (2) Pancytopenia (underlying bone marrow failure); (3) Venous thrombosis in unusual sites (hepatic veins causing Budd-Chiari syndrome, portal, mesenteric, cerebral veins) which is the leading cause of death in PNH. Eculizumab (anti-C5 antibody) is the specific treatment.\"\n},\n{id:36,\nstem:\"Which one of the following is associated with low MCV of red blood cells?\",\ncorrect:\"Thalassaemia\",\nopts:[\"Thalassaemia\",\"Vitamin B12 deficiency anaemia\",\"Folate deficiency anaemia\",\"Sickle cell anaemia\"],\nexp:\"MCV classification: Microcytic (low MCV below 80 fL): iron deficiency anaemia, thalassaemia (alpha and beta), anaemia of chronic disease, sideroblastic anaemia, lead poisoning. Macrocytic (high MCV above 100 fL): Vitamin B12 deficiency, folate deficiency, hypothyroidism, liver disease, alcohol. Sickle cell anaemia: MCV is typically NORMAL as sickle cells are normocytic; HbS produces normocytic red cells. Thalassaemia is characterised by microcytic hypochromic anaemia with low MCV. Thalassaemia is the correct answer.\"\n},\n{id:37,\nstem:\"GnRH deficiency with hyposmia is typically seen in\",\ncorrect:\"Kallmann syndrome\",\nopts:[\"Kallmann syndrome\",\"Bardet-Biedl syndrome\",\"Prader-Willi syndrome\",\"Wallenberg syndrome\"],\nexp:\"Kallmann syndrome is characterised by hypogonadotropic hypogonadism (GnRH deficiency) and anosmia or hyposmia (absent\/reduced sense of smell). The olfactory defect arises because GnRH-secreting neurons fail to migrate from the olfactory placode to the hypothalamus during foetal development. Associated features include anosmia\/hyposmia (pathognomonic), absence of puberty, and cryptorchidism. Bardet-Biedl and Prader-Willi syndromes cause obesity and hypogonadism but not specific anosmia. Wallenberg syndrome is a brainstem stroke. Kallmann syndrome is correct.\"\n},\n{id:38,\nstem:\"Iodine has complex effects on thyroid function. Very high concentrations of iodine inhibit thyroid hormone synthesis and release. This effect is known as\",\ncorrect:\"Wolff-Chaikoff effect\",\nopts:[\"Wolff-Chaikoff effect\",\"Jod-Basedow effect\",\"reverse Wolff-Chaikoff effect\",\"reverse Jod-Basedow effect\"],\nexp:\"The Wolff-Chaikoff effect: high inorganic iodide concentrations acutely suppress thyroid hormone synthesis by inhibiting iodide organification. This is a protective autoregulatory mechanism. Normal thyroid glands escape this effect after 10-14 days by downregulating the sodium-iodide symporter. Failure to escape leads to hypothyroidism (e.g. amiodarone-induced). The Jod-Basedow effect is the opposite: excess iodine in an iodine-deficient or autonomous thyroid gland triggers hyperthyroidism. Wolff-Chaikoff = iodine-induced suppression of hormone synthesis.\"\n},\n{id:39,\nstem:\"Consider the following pharmacological agents:<br>1. Propranolol<br>2. Sodium ipodate<br>3. Propylthiouracil<br>4. Liothyronine<br>Which of the above can be used for the treatment of thyrotoxic crisis?\",\ncorrect:\"1, 2 and 3\",\nopts:[\"3 only\",\"1 and 2 only\",\"1, 2 and 3\",\"2, 3 and 4\"],\nexp:\"Thyrotoxic crisis management requires multiple simultaneous interventions. Propylthiouracil (PTU) blocks new thyroid hormone synthesis AND inhibits peripheral T4 to T3 conversion, preferred in thyroid storm. Propranolol controls tachycardia and inhibits T4 to T3 conversion at high doses. Sodium ipodate blocks T4 to T3 conversion and inhibits thyroid hormone release. Liothyronine (T3) is an active thyroid hormone; administering it in thyrotoxic crisis would dramatically WORSEN the condition. Liothyronine is used in myxoedema coma, not thyroid storm. Statements 1, 2, and 3 are correct.\"\n},\n{id:40,\nstem:\"Consider the following pharmacological agents:<br>1. Liothyronine<br>2. Levothyroxine<br>3. Carbimazole<br>4. Sodium ipodate<br>Which of the above may be included in the treatment of myxoedema coma?\",\ncorrect:\"1 and 2\",\nopts:[\"1 only\",\"1 and 2\",\"2 and 3\",\"3 and 4\"],\nexp:\"Myxoedema coma is a life-threatening emergency of severe hypothyroidism requiring urgent thyroid hormone replacement. Liothyronine (T3): the active hormone, given IV for immediate effect; crosses the blood-brain barrier more readily; preferred for acute treatment. Levothyroxine (T4): given IV or via NG tube for sustained replacement. Carbimazole BLOCKS thyroid hormone synthesis and would worsen hypothyroidism; absolutely contraindicated. Sodium ipodate blocks T4 to T3 conversion; also contraindicated in myxoedema coma. Additional management: IV hydrocortisone, IV fluids, passive warming. 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Submitting in 10 Submit Now Combined Medical Services Examination 2023General Medicine & Paediatrics · Paper I · Part A Cardiology · Respiratory · Gastroenterology & Hepatology · Neurology · Haematology & Endocrinology Questions 1–40… <\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36727","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2023 P1 Part-A - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/04\/30\/cms-2023-p1-part-a\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2023 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2023 | General Medicine & Paediatrics | Paper I | Part A ✓️ 0 ❌ 0 ⏳ 40 left ⏱ 40:00 Net 0 \/ 160 Time's Up! 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