CMS 2016 Paper I \u2013 Part A (Q1\u2013Q40)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&display=swap\" rel=\"stylesheet\">\n<style>\n\/* \u2500\u2500 Namespace: cms16p1a \u2500\u2500 *\/\n#cms16p1a *,#cms16p1a *::before,#cms16p1a *::after{box-sizing:border-box;margin:0;padding:0}\n\n#cms16p1a{\n --ter:#C0603A;--ter-light:#e8825f;--ter-pale:#fdf1ec;\n --teal:#2A7A6F;--teal-light:#3da394;--teal-pale:#eaf4f3;\n --ink:#1a1a1a;--ink-mid:#444;--ink-soft:#777;\n --line:#e0d8d4;--bg:#fdfaf8;--white:#ffffff;\n --correct:#1e6f46;--correct-bg:#eaf7ef;--correct-border:#43a047;\n --wrong:#b83232;--wrong-bg:#fdf0f0;--wrong-border:#e53935;\n --warn:#b85c00;--warn-bg:#fff4e5;\n --radius:10px;\n font-family:'Source Serif 4',Georgia,serif;\n font-size:16px;color:var(--ink);background:var(--bg);\n line-height:1.7;padding:0 0 48px;\n}\n\n\/* Sentinel *\/\n#cms16p1a .cq-sentinel{height:1px}\n\n\/* 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.cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms16p1a .cq-retry-btn{\n margin-top:22px;background:transparent;border:2px solid var(--teal);\n color:var(--teal);border-radius:8px;padding:10px 28px;\n font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;\n cursor:pointer;transition:background 0.2s,color 0.2s;\n}\n#cms16p1a .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n\n@media(max-width:480px){\n #cms16p1a .cq-header h1{font-size:1.15rem}\n #cms16p1a .cq-qtext{font-size:0.88rem}\n #cms16p1a .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms16p1a\">\n\n <div class=\"cq-sentinel\" id=\"cms16p1a-sentinel\"><\/div>\n\n \n <div class=\"cq-statusbar\" id=\"cms16p1a-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms16p1a-timer-item\">\u23f1 <strong id=\"cms16p1a-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms16p1a-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms16p1a-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms16p1a-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms16p1a-sn\">0<\/strong> \/ <strong id=\"cms16p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms16p1a-fill\"><\/div><\/div>\n <\/div>\n\n \n <div class=\"cq-grace\" id=\"cms16p1a-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3>\n <p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms16p1a-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms16p1a-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n\n \n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2016<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine \u00b7 Paediatrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 1 \u2013 40<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms16p1a-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-body\">\n <div id=\"cms16p1a-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms16p1a-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms16p1a-score\">\n <div class=\"cq-score-ring\" id=\"cms16p1a-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms16p1a-ring-pct\">0%<\/span>\n <span class=\"cq-ring-sub\">score<\/span>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms16p1a-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms16p1a-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms16p1a-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms16p1a-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms16p1a-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms16p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms16p1a', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60; \/\/ 40 minutes\n const GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:1,\n stem:'A 40-year-old male is admitted with acute inferior wall myocardial infarction. Half an hour later his B.P. is 80\/50 mm Hg and heart rate is 40\/minute with sinus rhythm. The most appropriate step in the management of this patient would be:',\n correct:'Intravenous administration of atropine sulfate',\n options:['Administration of normal saline 300 ml over 15 minutes','Immediate insertion of temporary pacemaker','Intravenous administration of atropine sulfate','Intravenous administration of iso-prenaline 50 \u00b5g\/minute'],\n exp:'Acute inferior wall MI commonly involves the RCA which supplies the SA and AV nodes. Sinus bradycardia (HR 40) with hypotension in this context is vagally mediated. First-line treatment is IV atropine sulfate (0.5\u20131 mg, repeat to max 3 mg), which reverses vagal inhibition. Temporary pacemaker is reserved if atropine fails. Isoprenaline is not first-line. Saline loading is used in right ventricular infarction but is not the priority here.'\n },\n {\n id:2,\n stem:'The characteristic feature of tricuspid insufficiency in the jugular venous pulse is:',\n correct:'Obliteration of the \\'x\\' descent and prominent \\'CV\\' wave',\n options:['Prominent \\'a\\' wave','Exaggerated \\'x\\' and \\'y\\' descents','Cannon waves','Obliteration of the \\'x\\' descent and prominent \\'CV\\' wave'],\n exp:'In tricuspid regurgitation, blood regurgitates into the right atrium during systole. This abolishes the normal x descent (systolic collapse) and produces a large systolic wave (the c and v waves merge into a prominent CV wave). Cannon waves are seen in complete heart block. Prominent a waves occur in pulmonary hypertension or tricuspid stenosis.'\n },\n {\n id:3,\n stem:'Match List I (Clinical Features) with List II (Diagnosis):\\nA. Osler\\'s node\\nB. Differential cyanosis\\nC. Bisferiens pulse\\nD. Graham Steell murmur\\n\\n1. Patent ductus arteriosus with reversal of shunt\\n2. Aortic stenosis with aortic regurgitation\\n3. Pulmonary hypertension\\n4. Subacute bacterial endocarditis',\n correct:'A-4, B-1, C-2, D-3',\n options:['A-4, B-1, C-2, D-3','A-4, B-1, C-3, D-2','A-1, B-4, C-2, D-3','A-1, B-4, C-3, D-2'],\n exp:'Osler\\'s nodes are painful, tender nodules in the pulp of fingers\/toes, pathognomonic of SBE (4). Differential cyanosis (lower limbs cyanosed, upper limbs pink) is characteristic of PDA with reversed shunt (Eisenmenger) (1). Bisferiens pulse (double-peaked systolic pulse) is classic for combined AS + AR (2). Graham Steell murmur is an early diastolic murmur of pulmonary regurgitation due to pulmonary hypertension (3).'\n },\n {\n id:4,\n stem:'Acute aortic regurgitation occurs in:',\n correct:'Infective endocarditis',\n options:['Infective endocarditis','Ankylosing spondylitis','Marfan\\'s syndrome','Rheumatoid arthritis'],\n exp:'Acute aortic regurgitation requires a sudden disruption of the aortic valve or root. Infective endocarditis causes acute cusp destruction\/perforation leading to acute AR \u2014 a surgical emergency. Ankylosing spondylitis, Marfan\\'s syndrome, and rheumatoid arthritis all cause chronic, slowly progressive AR through aortic root dilatation or valve fibrosis, not the acute form.'\n },\n {\n id:5,\n stem:'The following are early complications of acute myocardial infarction EXCEPT:',\n correct:'Dressler\\'s syndrome',\n options:['Papillary muscle dysfunction','Ventricular septal defect','Ventricular free wall rupture','Dressler\\'s syndrome'],\n exp:'Dressler\\'s syndrome (post-MI pericarditis) is a late complication, typically occurring 2\u201310 weeks after AMI. It is an autoimmune pericarditis with fever, pleuritic chest pain, and pericardial\/pleural effusion. Early complications (within 1\u20132 weeks) include arrhythmias, papillary muscle dysfunction (mitral regurgitation), ventricular septal rupture, and ventricular free wall rupture \u2014 all occurring in the first few days.'\n },\n {\n id:6,\n stem:'For which one of the following serum proteins do the levels NOT decrease in nephrotic syndrome?',\n correct:'Fibrinogen',\n options:['Albumin','Transferrin','Fibrinogen','Ceruloplasmin'],\n exp:'In nephrotic syndrome, the glomerular barrier selectively loses low-molecular-weight proteins. Albumin (69 kDa), transferrin (80 kDa), and ceruloplasmin (160 kDa) are all lost in urine and their serum levels fall. Fibrinogen (340 kDa) is a large-molecular-weight protein that does NOT filter through the damaged glomerulus; in fact, fibrinogen levels are elevated in nephrotic syndrome, contributing to the hypercoagulable state.'\n },\n {\n id:7,\n stem:'Following are the causes of high anion-gap acidosis EXCEPT:',\n correct:'Renal tubular acidosis',\n options:['Renal tubular acidosis','Acute renal failure','Chronic renal failure','Diabetic ketoacidosis'],\n exp:'Renal tubular acidosis (RTA) causes a NORMAL anion-gap (hyperchloraemic) metabolic acidosis. The anion gap stays normal because the acidosis results from failure to excrete H\u207a or reabsorb HCO\u2083\u207b, with compensatory Cl\u207b retention. High anion-gap acidosis (MUDPILES) includes acute and chronic renal failure (retained phosphates, sulphates), DKA, and lactic acidosis.'\n },\n {\n id:8,\n stem:'A patient of cirrhosis develops oliguria and worsening azotemia. Urinary sediment is normal. Urinary sodium concentration is 5 mEq\/L. The most likely cause could be:',\n correct:'Hepato-renal syndrome',\n options:['Interstitial nephritis','Acute tubular necrosis','Acute glomerulonephritis','Hepato-renal syndrome'],\n exp:'Hepato-renal syndrome (HRS) presents in cirrhotic patients with oliguria, rising creatinine, bland urinary sediment, and very low urinary sodium (<10 mEq\/L) \u2014 indicating intense renal vasoconstriction with intact tubular function. ATN would show muddy brown casts and urinary Na >20 mEq\/L. Glomerulonephritis shows active sediment (casts, RBCs). Interstitial nephritis shows WBC casts. The triad of cirrhosis + normal sediment + urinary Na <10 = HRS.'\n },\n {\n id:9,\n stem:'Which one of the following infections is related to subacute sclerosing panencephalitis (SSPE)?',\n correct:'Measles virus',\n options:['HIV','Measles virus','Japanese B encephalitis virus','JC virus'],\n exp:'SSPE is a late, progressive, fatal encephalitis caused by a defective mutant measles virus that persists in the CNS years after the primary infection (usually in childhood). It presents in young adults with cognitive decline, myoclonic jerks, and EEG changes (periodic complexes). JC virus causes PML (in immunocompromised). Japanese B encephalitis is an acute arboviral encephalitis. HIV causes AIDS dementia, not SSPE.'\n },\n {\n id:10,\n stem:'Consider the following:\\n1. Failure to swing the arms while walking\\n2. Nystagmus\\n3. Cogwheel rigidity\\n4. Festinant gait\\n\\nTypical features of Parkinsonism include which of the above?',\n correct:'1, 3 and 4',\n options:['2, 3 and 4','1, 2 and 4','1 and 3 only','1, 3 and 4'],\n exp:'Classic features of Parkinsonism: resting tremor, rigidity (lead-pipe and cogwheel = 3), bradykinesia, postural instability, festinant (shuffling, accelerating) gait (= 4), and loss of arm swing (= 1). Nystagmus (= 2) is NOT a feature of Parkinson\\'s disease; it suggests cerebellar or brainstem pathology (e.g., PSP may show gaze palsies but not nystagmus in the classic sense). All three \u2014 1, 3, and 4 \u2014 are correct.'\n },\n {\n id:11,\n stem:'Consider the following sites of lesion:\\n1. Left optic tract\\n2. Left optic radiation\\n3. Optic chiasma\\n4. Left lateral geniculate body\\n\\nRight homonymous hemianopia will result from lesions at which of the above?',\n correct:'1, 2 and 4',\n options:['1 and 3 only','1, 2 and 4','2, 3 and 4','1, 2 and 3'],\n exp:'Right homonymous hemianopia = loss of the right visual field in BOTH eyes. Visual fibres from both nasal retinae (carrying temporal field information) cross at the chiasma and travel in the LEFT optic tract, LEFT LGB, and LEFT optic radiation. Therefore a lesion anywhere in the left retrochiasmal pathway (left optic tract = 1, left LGB = 4, left optic radiation = 2) produces right homonymous hemianopia. Chiasmal lesion (3) produces bitemporal hemianopia.'\n },\n {\n id:12,\n stem:'Raised alkaline phosphatase is seen in the following EXCEPT:',\n correct:'Multiple myeloma',\n options:['Hyperparathyroidism','Obstructive jaundice','Osteomalacia','Multiple myeloma'],\n exp:'Alkaline phosphatase (ALP) is raised when bone osteoblast activity is increased or bile ducts are obstructed. It is elevated in hyperparathyroidism (increased bone resorption\/turnover), obstructive jaundice (biliary ALP isoenzyme), and osteomalacia (increased osteoblast activity attempting mineralisation). Multiple myeloma causes osteolytic lesions via osteoclast activation \u2014 ALP is characteristically NORMAL or only mildly elevated because osteoblastic activity is suppressed.'\n },\n {\n id:13,\n stem:'Consider the following statements about acromegaly:\\n1. Fibroma molluscum and acanthosis nigricans are common findings.\\n2. Growth hormone secretion is increased by TRH in 50 to 80% of acromegalics.\\n3. Acroosteolysis is a common radiological finding.\\n4. Diabetes mellitus may be associated in nearly 25% of acromegalics.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 4',\n options:['1, 2 and 3','1, 3 and 4','1, 2 and 4','2, 3 and 4'],\n exp:'In acromegaly: skin tags (fibroma molluscum) and acanthosis nigricans are common soft tissue findings (1 = correct). GH paradoxically rises with TRH in 50\u201380% of acromegalics \u2014 a useful diagnostic test (2 = correct). DM\/IGT occurs in ~25% due to GH insulin antagonism (4 = correct). Statement 3 is WRONG: acroosteolysis (terminal phalangeal resorption) is seen in hyperparathyroidism, psoriasis, and vinyl chloride exposure \u2014 NOT acromegaly. Acromegaly shows increased terminal phalangeal tufting and heel pad thickening.'\n },\n {\n id:14,\n stem:'Causes of hypomagnesaemia include all of the following EXCEPT:',\n correct:'Beta-blocker',\n options:['Beta-blocker','Chronic pancreatic insufficiency','Poorly controlled diabetes mellitus','Alcoholism'],\n exp:'Hypomagnesaemia causes: alcoholism (poor intake + renal wasting), poorly controlled DM (osmotic diuresis), chronic diarrhoea, malabsorption (including pancreatic insufficiency causing fat malabsorption and Mg soap formation), loop diuretics, aminoglycosides, cisplatin, and PPIs. Beta-blockers have no established mechanism for causing hypomagnesaemia and are NOT a recognised cause.'\n },\n {\n id:15,\n stem:'Which of the following conditions are associated with secondary diabetes mellitus?\\n1. Thyrotoxicosis, pheochromocytoma and acromegaly\\n2. Haemochromatosis\\n3. Pancreatic carcinoma\\n\\nSelect the correct answer:',\n correct:'1, 2 and 3',\n options:['2 and 3 only','1, 2 and 3','1 and 3 only','1 and 2 only'],\n exp:'Secondary DM arises from identifiable causes outside the islets: (1) Counter-regulatory hormones \u2014 GH (acromegaly), catecholamines (phaeochromocytoma), T3\/T4 (thyrotoxicosis) all cause insulin resistance. (2) Haemochromatosis deposits iron in the pancreas destroying beta cells (\"bronze diabetes\"). (3) Pancreatic carcinoma destroys exocrine and endocrine tissue. All three are well-recognised causes of secondary diabetes mellitus.'\n },\n {\n id:16,\n stem:'Consider the following statements:\\n1. Boils\/suppurative lesions around the nose must be promptly treated with antibiotics.\\n2. Suppurative lesions around the nose lead to cavernous sinus thrombosis.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'Both 1 and 2',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'The \"danger triangle of the face\" (nasal tip to mouth corners) is drained by valveless facial veins that communicate with the cavernous sinus via the ophthalmic veins. Septic emboli from boils in this area can cause septic cavernous sinus thrombosis \u2014 a life-threatening condition (statement 2 correct). Therefore, suppurative lesions here must be treated early with antibiotics and must NOT be squeezed (statement 1 correct). Both statements are correct.'\n },\n {\n id:17,\n stem:'Which one of the following is NOT an ECG change of hyperkalaemia?',\n correct:'Tall P-wave',\n options:['Tall T-wave','Tall P-wave','Prolonged PR interval','QRS widening'],\n exp:'ECG changes of hyperkalaemia in sequence: tall peaked T-waves \u2192 prolonged PR interval \u2192 flattening\/disappearance of P-wave \u2192 widening of QRS \u2192 sine-wave pattern \u2192 VF\/asystole. A TALL P-wave is NOT a feature \u2014 in fact, P-waves progressively diminish and disappear with rising K\u207a. Tall P-waves suggest right atrial hypertrophy or ectopic atrial rhythms, not hyperkalaemia.'\n },\n {\n id:18,\n stem:'Which one of the following tests has the highest chance of detecting HIV infection in a blood donor during the window period?',\n correct:'p24 antigen detection',\n options:['Demonstration of antibody to HIV by ELISA','CD4 count','p24 antigen detection','Western blot test'],\n exp:'The window period is the time between HIV infection and detectable antibody response (3\u201312 weeks). During this period, ELISA and Western blot (antibody tests) are NEGATIVE. p24 antigen (HIV core protein) appears in blood 2\u20133 weeks after infection, well before antibody seroconversion, making it the best single marker during the window period. Modern 4th-generation tests combine p24 Ag + Ab. CD4 count falls but is non-specific.'\n },\n {\n id:19,\n stem:'Which of the following features are characteristic of tuberculoid leprosy?\\n1. Type 2 lepra reaction\\n2. A few lesions with well-demarcated edges\\n3. Early and marked nerve damage\\n4. Tendency to heal spontaneously\\n\\nSelect the correct answer:',\n correct:'2, 3 and 4',\n options:['1, 2 and 3','2, 3 and 4','1 and 4','2 and 3 only'],\n exp:'Tuberculoid leprosy (TT): high cellular immunity, few well-demarcated hypopigmented anaesthetic plaques (statement 2), early and severe nerve involvement leading to nerve thickening\/damage (statement 3), tendency to heal spontaneously (statement 4). Type 2 lepra reaction (erythema nodosum leprosum) is a feature of LEPROMATOUS leprosy (BL\/LL), not tuberculoid \u2014 statement 1 is incorrect. Type 1 (reversal) reaction occurs in tuberculoid\/borderline types.'\n },\n {\n id:20,\n stem:'Which one of the following immunological reactions occurs in Goodpasture\\'s syndrome?',\n correct:'Type II cytotoxicity',\n options:['Type I Atopy','Type II cytotoxicity','Type III immune complex','Type IV cell mediation'],\n exp:'Goodpasture\\'s syndrome is caused by autoantibodies (anti-GBM IgG) directed against the alpha-3 chain of type IV collagen in the glomerular and alveolar basement membranes. These antibodies activate complement and recruit neutrophils causing crescentic glomerulonephritis and pulmonary haemorrhage. This is a classic Type II (cytotoxic\/antibody-mediated) hypersensitivity reaction. Linear IgG deposits are seen on immunofluorescence.'\n },\n {\n id:21,\n stem:'Consider the following statements about leptospirosis:\\n1. It is a ubiquitous enzootic disease.\\n2. Its incubation period ranges from 2 to 20 days.\\n3. The intensity of jaundice is directly related to prognosis.\\n4. Urine may show microscopic haematuria.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 4',\n options:['1, 2 and 4','1, 2 and 3','1, 3 and 4','2, 3 and 4'],\n exp:'Leptospirosis (Weil\\'s disease): (1) It is indeed an enzootic (reservoir in animals, esp. rodents) zoonosis found worldwide \u2014 correct. (2) Incubation 2\u201320 days (mean 10 days) \u2014 correct. (3) Intensity of jaundice does NOT directly predict prognosis; patients with deep jaundice may survive if renal function is maintained \u2014 statement 3 is FALSE. (4) Microscopic haematuria is common due to renal tubular involvement \u2014 correct. So 1, 2, and 4 are correct.'\n },\n {\n id:22,\n stem:'SVC syndrome can occur in the following EXCEPT:',\n correct:'Pneumomediastinum',\n options:['Pneumomediastinum','Goitre','Bronchogenic carcinoma','Lymphoma'],\n exp:'Superior vena cava syndrome results from external compression or thrombosis of the SVC, causing facial\/arm oedema, dilated neck veins, and plethora. Causes include bronchogenic carcinoma (right-sided; most common), lymphoma, goitre, aortic aneurysm, pericardial effusion, and mediastinal fibrosis. Pneumomediastinum (air in mediastinum from alveolar rupture) does NOT compress the SVC and is NOT a cause of SVC syndrome.'\n },\n {\n id:23,\n stem:'Match List I (Physical Sign) with List II (Medical Condition):\\nA. Koebner phenomenon\\nB. Erythema nodosum\\nC. Erythema multiforme\\nD. Nikolsky\\'s sign\\n\\n1. Lepra reaction\\n2. Pemphigus vulgaris\\n3. Stevens-Johnson syndrome\\n4. Psoriasis',\n correct:'A-4, B-1, C-3, D-2',\n options:['A-1, B-4, C-3, D-2','A-4, B-1, C-2, D-3','A-1, B-4, C-2, D-3','A-4, B-1, C-3, D-2'],\n exp:'Koebner phenomenon (new lesions at trauma sites) = Psoriasis (4). Erythema nodosum (painful red nodules on shins) = Type 2 lepra reaction \/ ENL (1) among these options. Erythema multiforme (target lesions) at severe end = Stevens-Johnson syndrome (3). Nikolsky\\'s sign (skin slippage with lateral pressure) = Pemphigus vulgaris (2), confirming loss of keratinocyte adhesion (acantholysis).'\n },\n {\n id:24,\n stem:'Which one of the following is the major site of absorption of Vitamin B12?',\n correct:'Terminal ileum',\n options:['Stomach','Terminal ileum','Duodenum','Mid Jejunum'],\n exp:'Vitamin B12 (cobalamin) is bound to intrinsic factor (IF) secreted by gastric parietal cells. The IF-B12 complex is specifically absorbed by cubilin receptors located exclusively in the terminal ileum. Disease of the terminal ileum (Crohn\\'s, ileal resection) or absence of IF (pernicious anaemia, gastrectomy) causes B12 deficiency. No other segment of the gut can absorb the IF-B12 complex in physiological quantities.'\n },\n {\n id:25,\n stem:'The following features regarding polymyositis are true EXCEPT:',\n correct:'Ocular muscle involvement is common',\n options:['Progressive proximal muscle involvement','25% patients may present with dysphagia','Ocular muscle involvement is common','Elevated levels of serum creatine kinase'],\n exp:'Polymyositis characteristically involves proximal limb muscles (shoulders, hips), and pharyngeal muscles causing dysphagia (~25%). Serum CK is markedly elevated. Ocular muscles are SPARED in polymyositis \u2014 this is an important distinguishing feature from myasthenia gravis (which commonly involves ocular muscles causing ptosis and diplopia). Sparing of ocular muscles is a hallmark of inflammatory myopathies.'\n },\n {\n id:26,\n stem:'Match List I (Inflammatory Joint Disease) with List II (Clinical Finding):\\nA. Reiter\\'s Syndrome\\nB. Rheumatoid arthritis\\nC. Psoriatic arthritis\\nD. Sj\u00f6gren\\'s syndrome\\n\\n1. Onycholysis\\n2. Keratoderma blenorrhagica\\n3. Xerostomia\\n4. Baker\\'s cysts',\n correct:'A-2, B-4, C-1, D-3',\n options:['A-4, B-2, C-3, D-1','A-2, B-4, C-1, D-3','A-2, B-4, C-3, D-1','A-4, B-2, C-1, D-3'],\n exp:'Reiter\\'s syndrome = keratoderma blenorrhagica (hyperkeratotic skin lesions on palms\/soles) (2). Rheumatoid arthritis = Baker\\'s cysts (popliteal cysts from knee joint effusion) (4). Psoriatic arthritis = onycholysis (nail lifting\/separation) (1). Sj\u00f6gren\\'s syndrome = xerostomia (dry mouth due to salivary gland infiltration by lymphocytes) (3).'\n },\n {\n id:27,\n stem:'The following drugs are useful in generalised anxiety disorders EXCEPT:',\n correct:'Risperidone',\n options:['Risperidone','Amitriptyline','Buspirone','Venlafaxine'],\n exp:'Generalised anxiety disorder is treated with: SSRIs\/SNRIs (venlafaxine = first-line), TCAs (amitriptyline), buspirone (5-HT1A partial agonist), and benzodiazepines (short-term). Risperidone is an atypical antipsychotic (D2\/5-HT2A antagonist) used for schizophrenia, bipolar disorder, and irritability in autism. It is not a recognised treatment for GAD and would not be appropriate first- or second-line.'\n },\n {\n id:28,\n stem:'Systemic inflammatory response syndrome (SIRS) can have the following features EXCEPT:',\n correct:'Bradycardia',\n options:['Hypothermia','Bradycardia','Tachypnoea','Leucopenia (WBC < 4000)'],\n exp:'SIRS criteria (2 or more of): temperature >38\u00b0C or <36\u00b0C (hypothermia is included), heart rate >90\/min (TACHYCARDIA \u2014 bradycardia is NOT a criterion), respiratory rate >20\/min or PaCO\u2082 <32 mmHg, WBC >12,000 or <4,000 or >10% bands. Bradycardia is specifically excluded \u2014 it would suggest vagal response or heart block, not the hyperadrenergic, inflammatory state of SIRS.'\n },\n {\n id:29,\n stem:'Which of the following is NOT a complication of malaria?',\n correct:'Hyperglycaemia',\n options:['ARDS','Acidosis','Hyperglycaemia','Coma'],\n exp:'Severe falciparum malaria complications (WHO criteria): cerebral malaria (coma), ARDS, metabolic acidosis, severe anaemia, renal failure, hypoglycaemia (NOT hyperglycaemia), hyperparasitaemia, abnormal bleeding, and jaundice. Hypoglycaemia occurs due to parasite glucose consumption and quinine\/quinidine-stimulated insulin release. Hyperglycaemia is NOT a complication of malaria.'\n },\n {\n id:30,\n stem:'Cardiac troponin may be elevated in:',\n correct:'Chronic kidney failure',\n options:['Muscular dystrophy','Chronic kidney failure','Acute liver failure','Epilepsy'],\n exp:'Cardiac troponins (cTnI, cTnT) are cardiac-specific markers. Elevated troponins are seen in: ACS, myocarditis, PE, cardiac contusion, severe sepsis, and importantly in chronic kidney disease (CKD) \u2014 likely due to reduced clearance, subclinical myocardial injury, and LVH. Troponin elevation in CKD is a significant prognostic marker. Skeletal muscle disorders like Duchenne\\'s dystrophy rarely cause troponin elevation since they mainly release skeletal isoforms. Acute liver failure does not elevate cardiac troponins.'\n },\n {\n id:31,\n stem:'Which of the following are the physiological abnormalities in chronic obstructive lung disease?\\n1. Reduced total lung capacity (TLC)\\n2. Increased functional residual capacity\\n3. Increased residual volume (RV)\\n4. Increased RV\/TLC ratio\\n\\nSelect the correct answer:',\n correct:'2, 3 and 4',\n options:['1 and 2 only','2, 3 and 4','1, 3 and 4','3 and 4 only'],\n exp:'In COPD, air trapping and loss of elastic recoil leads to: (1) TLC is INCREASED (not reduced) due to hyperinflation \u2014 statement 1 is WRONG. (2) FRC is increased (premature airway closure, air trapping) \u2014 correct. (3) RV is increased (incomplete emptying) \u2014 correct. (4) RV\/TLC ratio is increased (air trapping, barrel chest) \u2014 correct. TLC reduction would suggest restrictive disease. All of 2, 3, and 4 are correct.'\n },\n {\n id:32,\n stem:'Acute respiratory distress syndrome characteristically occurs in:\\n1. Gram-negative septicaemia\\n2. Gastric aspiration\\n3. Pancreatitis\\n4. Severe burns\\n5. Myocarditis\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2, 3 and 4',\n options:['2, 3, 4 and 5','1, 3, 4 and 5','1, 2 and 5','1, 2, 3 and 4'],\n exp:'ARDS is a non-cardiogenic pulmonary oedema triggered by direct or indirect lung injury. Direct causes: aspiration (2), pneumonia, inhalation injury. Indirect causes: gram-negative sepsis (1) \u2014 most common, pancreatitis (3), severe burns (4), massive transfusion, trauma. Myocarditis (5) causes cardiogenic pulmonary oedema (due to LV failure) \u2014 NOT ARDS. All of 1, 2, 3, and 4 are recognised ARDS causes.'\n },\n {\n id:33,\n stem:'Botulism can have the following clinical features EXCEPT:',\n correct:'Hyperpyrexia',\n options:['Hyperpyrexia','Sudden onset quadriplegia','Cranial nerve deficits','Respiratory failure'],\n exp:'Botulism (Clostridium botulinum toxin) causes flaccid descending paralysis by blocking presynaptic ACh release at the NMJ. Features: cranial nerve palsies (ptosis, diplopia, dysarthria), descending symmetrical weakness\/paralysis, respiratory failure \u2014 ALL correct features. Crucially, botulism is classically AFEBRILE \u2014 hyperpyrexia is NOT a feature. Fever would suggest wound botulism with secondary infection, but not the disease itself.'\n },\n {\n id:34,\n stem:'A 55-year-old man, non-smoker, presents with sudden onset of shortness of breath. Pulse rate is 110\/minute and B.P. 180\/110 mm Hg. Patient is restless and anxious. Chest examination shows bilateral rhonchi and crepitations. S3 gallop is heard on auscultation. There is no history of chronic bronchitis. The most likely diagnosis is:',\n correct:'Acute LVF',\n options:['Bronchial asthma','Acute LVF','Pneumothorax','Acute exacerbation of COPD'],\n exp:'The clinical picture \u2014 sudden dyspnoea, severe hypertension, bilateral crepitations (alveolar oedema) with rhonchi (cardiac asthma), S3 gallop (ventricular dysfunction), tachycardia, in a non-smoker without prior bronchitis \u2014 is classic acute left ventricular failure. S3 gallop specifically points to a failing, volume-overloaded ventricle. Asthma\/COPD exacerbations would not produce an S3 gallop and typically have a prior history. Pneumothorax causes unilateral signs.'\n },\n {\n id:35,\n stem:'Small cell carcinoma of lung is commonly associated with the following paraneoplastic syndromes:\\n1. Ectopic ACTH production\\n2. Lambert-Eaton syndrome\\n3. Syndrome of inappropriate ADH (SIADH)\\n4. Addison\\'s disease\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 3',\n options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],\n exp:'Small cell lung carcinoma (SCLC) is a neuroendocrine tumour notorious for paraneoplastic syndromes: ectopic ACTH (Cushing\\'s syndrome, 1), Lambert-Eaton myasthenic syndrome (antibodies against VGCC, 2), SIADH (hyponatraemia, 3), and also carcinoid-like features. Addison\\'s disease (adrenocortical insufficiency, 4) is NOT caused by SCLC paraneoplastic mechanisms. Adrenal metastases can replace adrenal tissue but this is not a paraneoplastic syndrome.'\n },\n {\n id:36,\n stem:'On abdominal percussion, liver dullness may be obliterated in the following EXCEPT:',\n correct:'Fatty liver',\n options:['Fatty liver','Emphysema','Perforated viscus','Fulminant hepatitis'],\n exp:'Liver dullness is obliterated when air intervenes between the abdominal wall and the liver: emphysema (hyperinflated lung pushes down, gas above liver), perforated viscus (free intraperitoneal air rises to lie anterior to liver), and fulminant hepatic failure (massive hepatocyte loss causes the liver to shrink dramatically, replacing dullness with resonance). Fatty liver (hepatomegaly) INCREASES liver dullness \u2014 the area of dullness enlarges, it is not obliterated.'\n },\n {\n id:37,\n stem:'Consider the following statements regarding Helicobacter pylori:\\n1. It is a gram-negative bacterium.\\n2. It invades the epithelium.\\n3. It produces urease.\\n4. It produces chronic gastritis.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 3 and 4',\n options:['1, 2 and 4','1 and 3 only','2 and 4 only','1, 3 and 4'],\n exp:'H. pylori: (1) Gram-negative curved\/spiral rod \u2014 correct. (2) Does NOT invade the epithelium \u2014 it colonises the gastric mucus layer overlying the epithelium without actual cellular invasion, unlike Salmonella\/Shigella. Statement 2 is FALSE. (3) Produces urease (splits urea \u2192 NH\u2083 + CO\u2082), neutralising local acid and enabling survival \u2014 correct; basis of CLO\/urea breath test. (4) Causes type B chronic antral gastritis \u2014 correct. So 1, 3, and 4 are correct.'\n },\n {\n id:38,\n stem:'Consider the following conditions:\\n1. Steroid therapy\\n2. Hypertriglyceridaemia\\n3. Hypercalcaemia\\n4. Azathioprine therapy\\n\\nAcute pancreatitis may occur in which of the above conditions?',\n correct:'1, 2, 3 and 4',\n options:['1, 2 and 3 only','2 and 4 only','1, 3 and 4 only','1, 2, 3 and 4'],\n exp:'All four are recognised causes of acute pancreatitis: (1) Corticosteroids \u2014 can cause pancreatitis (mechanism debated but well documented). (2) Hypertriglyceridaemia >1000 mg\/dL \u2014 a major cause via free fatty acid toxicity to acinar cells. (3) Hypercalcaemia (hyperparathyroidism) \u2014 calcium activates trypsinogen prematurely. (4) Azathioprine \u2014 drug-induced pancreatitis (class effect with 6-mercaptopurine). All four cause acute pancreatitis.'\n },\n {\n id:39,\n stem:'A 60-year-old patient presents with gradually increasing dysphagia to solids for 3 months with significant loss of weight. The most probable diagnosis is:',\n correct:'Carcinoma oesophagus',\n options:['Stricture oesophagus','Carcinoma oesophagus','Reflux oesophagitis','Neurogenic oesophagus'],\n exp:'Progressive dysphagia to solids (then liquids), age >50, significant weight loss \u2014 this is the classic presentation of carcinoma of the oesophagus until proved otherwise. The insidious onset and marked weight loss strongly suggest malignancy. Benign stricture (post-reflux\/corrosive) has a slower, less dramatic course. Achalasia (neurogenic) typically affects both solids and liquids from the start. Reflux oesophagitis causes heartburn\/regurgitation, not predominantly dysphagia.'\n },\n {\n id:40,\n stem:'Consider the following statements:\\n1. Gentamicin should be added to the empirical regime for acute meningitis for patients aged more than 55 years.\\n2. Ampicillin covers Listeria monocytogenes.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'2 only',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'For bacterial meningitis in patients >55 years, empirical therapy is ceftriaxone + AMPICILLIN (to cover Listeria monocytogenes, which is seen in the elderly and immunocompromised). Gentamicin is NOT routinely added \u2014 statement 1 is FALSE. Ampicillin is indeed the drug of choice for Listeria (which is intrinsically resistant to cephalosporins) \u2014 statement 2 is CORRECT. Vancomycin may be added if MRSA\/resistant pneumococcus is suspected.'\n }\n ];\n\n \/\/ Fisher-Yates shuffle\n function shuffle(arr){\n const a=[...arr];\n for(let i=a.length-1;i>0;i--){const j=Math.floor(Math.random()*(i+1));[a[i],a[j]]=[a[j],a[i]];}\n return a;\n }\n\n const LETTERS=['A','B','C','D'];\n let userAnswers={}, answered=0, shuffledOpts={};\n\n \/\/ \u2500\u2500 Timer state \u2500\u2500\n let timerRunning=false, timerRemaining=TIMER_SECS, timerInterval=null, graceInterval=null;\n let quizSubmitted=false;\n\n function fmtTime(s){\n const m=Math.floor(s\/60), sec=s%60;\n return String(m).padStart(2,'0')+':'+String(sec).padStart(2,'0');\n }\n\n function startTimer(){\n if(timerRunning||quizSubmitted)return;\n timerRunning=true;\n const btn=document.getElementById(NS+'-timer-btn');\n btn.textContent='\u23f1 '+fmtTime(timerRemaining);\n btn.classList.add('running');\n document.getElementById(NS+'-timer-item').classList.add('active');\n\n timerInterval=setInterval(function(){\n timerRemaining--;\n const disp=fmtTime(timerRemaining);\n document.getElementById(NS+'-timer-display').textContent=disp;\n btn.textContent='\u23f1 '+disp;\n\n const item=document.getElementById(NS+'-timer-item');\n if(timerRemaining<=300) item.classList.add('warning'); \/\/ red at 5 min\n\n if(timerRemaining<=0){\n clearInterval(timerInterval);\n timerInterval=null;\n triggerGrace();\n }\n },1000);\n }\n\n function stopTimer(){\n if(timerInterval){clearInterval(timerInterval);timerInterval=null;}\n timerRunning=false;\n }\n\n function triggerGrace(){\n if(quizSubmitted)return;\n let g=GRACE_SECS;\n document.getElementById(NS+'-grace-count').textContent=g;\n document.getElementById(NS+'-grace').classList.add('show');\n graceInterval=setInterval(function(){\n g--;\n document.getElementById(NS+'-grace-count').textContent=g;\n if(g<=0){\n clearInterval(graceInterval);\n dismissGrace();\n showScore();\n }\n },1000);\n }\n\n function dismissGrace(){\n document.getElementById(NS+'-grace').classList.remove('show');\n if(graceInterval){clearInterval(graceInterval);graceInterval=null;}\n }\n\n function build(){\n const container=document.getElementById(NS+'-questions');\n container.innerHTML='';\n userAnswers={};answered=0;shuffledOpts={};\n quizSubmitted=false;timerRunning=false;timerRemaining=TIMER_SECS;\n stopTimer();\n if(graceInterval){clearInterval(graceInterval);graceInterval=null;}\n dismissGrace();\n document.getElementById(NS+'-score').style.display='none';\n document.getElementById(NS+'-timer-item').classList.remove('active','warning');\n const btn=document.getElementById(NS+'-timer-btn');\n btn.textContent='\u23f1 Start Timed Mode';btn.classList.remove('running');\n document.getElementById(NS+'-timer-display').textContent=fmtTime(TIMER_SECS);\n updateStats();\n\n QUESTIONS.forEach(function(q){\n \/\/ Shuffle answer options; correct answer tracked by text content\n const opts=shuffle(q.options);shuffledOpts[q.id]=opts;\n const card=document.createElement('div');card.className='cq-card';\n card.innerHTML=\n '<div class=\"cq-qhead\">'+\n '<div class=\"cq-qnum\" id=\"'+NS+'-n'+q.id+'\">'+q.id+'<\/div>'+\n '<div class=\"cq-qtext\">'+q.stem.replace(\/\\n\/g,'<br>')+'<\/div>'+\n '<\/div>'+\n '<div class=\"cq-options\" id=\"'+NS+'-opts'+q.id+'\">'+\n opts.map(function(o,i){\n return '<div class=\"cq-opt\" id=\"'+NS+'-o'+q.id+'-'+i+'\" role=\"button\" tabindex=\"0\">'+\n '<span class=\"cq-opt-letter\">'+LETTERS[i]+'<\/span>'+\n '<span class=\"cq-opt-text\">'+o+'<\/span><\/div>';\n }).join('')+\n '<\/div>'+\n '<div class=\"cq-explanation\" id=\"'+NS+'-exp'+q.id+'\">'+\n '<div class=\"cq-exp-label\">Explanation<\/div>'+q.exp+'<\/div>';\n container.appendChild(card);\n \/\/ Attach click listeners to each option\n opts.forEach(function(_,i){\n document.getElementById(NS+'-o'+q.id+'-'+i).addEventListener('click',function(){pick(q.id,i);});\n });\n });\n }\n\n function pick(qid,oi){\n 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14px;\n font-family:'Source Serif 4',serif;font-size:0.78rem;\n cursor:pointer;letter-spacing:0.03em;\n transition:background 0.2s,border-color 0.2s;\n display:flex;align-items:center;gap:6px;\n}\n#cms16p1a .cq-timer-btn:hover{background:rgba(255,255,255,0.15)}\n#cms16p1a .cq-timer-btn.running{\n background:rgba(255,255,255,0.2);border-color:var(--white);\n}\n\n\/* Body *\/\n#cms16p1a .cq-body{max-width:760px;margin:0 auto;padding:0 16px}\n\n\/* Cards *\/\n#cms16p1a .cq-card{\n background:var(--white);border:1px solid var(--line);\n border-radius:var(--radius);margin:24px 0;overflow:hidden;transition:box-shadow 0.2s;\n}\n#cms16p1a .cq-card:hover{box-shadow:0 2px 12px rgba(192,96,58,0.1)}\n#cms16p1a .cq-qhead{\n background:var(--ter-pale);border-bottom:1px solid var(--line);\n padding:14px 18px;display:flex;gap:12px;align-items:flex-start;\n}\n#cms16p1a .cq-qnum{\n flex-shrink:0;width:26px;height:26px;border-radius:50%;\n 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18px 12px;font-size:0.82rem;color:#1a4f49;line-height:1.62;\n}\n#cms16p1a .cq-exp-label{\n font-size:0.7rem;font-weight:700;letter-spacing:0.08em;\n text-transform:uppercase;color:var(--teal);margin-bottom:4px;\n}\n\n#cms16p1a .cq-submit-wrap{text-align:center;padding:28px 16px 8px}\n#cms16p1a .cq-btn{\n background:var(--teal);color:var(--white);border:none;border-radius:8px;\n padding:13px 36px;font-family:'Playfair Display',serif;\n font-size:1rem;font-weight:700;cursor:pointer;letter-spacing:0.02em;\n transition:background 0.2s,transform 0.1s;\n}\n#cms16p1a .cq-btn:hover{background:var(--teal-light)}\n#cms16p1a .cq-btn:active{transform:scale(0.98)}\n\n\/* Score panel *\/\n#cms16p1a .cq-score{\n display:none;background:var(--white);border:2px solid var(--teal);\n border-radius:var(--radius);margin:28px 0 0;padding:28px 24px;text-align:center;\n}\n#cms16p1a .cq-score-ring{\n width:110px;height:110px;border-radius:50%;\n background:conic-gradient(var(--teal) 0%,var(--line) 0%);\n display:flex;align-items:center;justify-content:center;\n margin:0 auto 20px;position:relative;\n}\n#cms16p1a .cq-score-ring::before{\n content:'';position:absolute;width:86px;height:86px;\n border-radius:50%;background:var(--white);\n}\n#cms16p1a .cq-ring-inner{position:relative;display:flex;flex-direction:column;align-items:center;line-height:1.2}\n#cms16p1a .cq-ring-pct{font-family:'Playfair Display',serif;font-size:1.3rem;font-weight:700;color:var(--teal)}\n#cms16p1a .cq-ring-sub{font-size:0.6rem;color:var(--ink-soft);text-transform:uppercase;letter-spacing:0.05em}\n#cms16p1a .cq-score h2{font-family:'Playfair Display',serif;font-size:1.2rem;color:var(--ink);margin-bottom:8px}\n#cms16p1a .cq-net-line{font-size:1rem;color:var(--teal);font-weight:600;margin-bottom:6px}\n#cms16p1a .cq-verdict{font-size:0.85rem;color:var(--ink-soft);margin-bottom:20px}\n#cms16p1a .cq-score-bands{display:flex;justify-content:center;gap:10px;flex-wrap:wrap;font-size:0.8rem}\n#cms16p1a .cq-band{padding:4px 12px;border-radius:16px;font-weight:600}\n#cms16p1a .cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms16p1a .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms16p1a .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms16p1a .cq-retry-btn{\n margin-top:22px;background:transparent;border:2px solid var(--teal);\n color:var(--teal);border-radius:8px;padding:10px 28px;\n font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;\n cursor:pointer;transition:background 0.2s,color 0.2s;\n}\n#cms16p1a .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n\n@media(max-width:480px){\n #cms16p1a .cq-header h1{font-size:1.15rem}\n #cms16p1a .cq-qtext{font-size:0.88rem}\n #cms16p1a .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms16p1a\">\n\n <div class=\"cq-sentinel\" id=\"cms16p1a-sentinel\"><\/div>\n\n \n <div class=\"cq-statusbar\" id=\"cms16p1a-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms16p1a-timer-item\">\u23f1 <strong id=\"cms16p1a-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms16p1a-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms16p1a-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms16p1a-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms16p1a-sn\">0<\/strong> \/ <strong id=\"cms16p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms16p1a-fill\"><\/div><\/div>\n <\/div>\n\n \n <div class=\"cq-grace\" id=\"cms16p1a-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3>\n <p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms16p1a-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms16p1a-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n\n \n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2016<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine \u00b7 Paediatrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 1 \u2013 40<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms16p1a-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-body\">\n <div id=\"cms16p1a-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms16p1a-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms16p1a-score\">\n <div class=\"cq-score-ring\" id=\"cms16p1a-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms16p1a-ring-pct\">0%<\/span>\n <span class=\"cq-ring-sub\">score<\/span>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms16p1a-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms16p1a-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms16p1a-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms16p1a-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms16p1a-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms16p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms16p1a', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60; \/\/ 40 minutes\n const GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:1,\n stem:'A 40-year-old male is admitted with acute inferior wall myocardial infarction. Half an hour later his B.P. is 80\/50 mm Hg and heart rate is 40\/minute with sinus rhythm. The most appropriate step in the management of this patient would be:',\n correct:'Intravenous administration of atropine sulfate',\n options:['Administration of normal saline 300 ml over 15 minutes','Immediate insertion of temporary pacemaker','Intravenous administration of atropine sulfate','Intravenous administration of iso-prenaline 50 \u00b5g\/minute'],\n exp:'Acute inferior wall MI commonly involves the RCA which supplies the SA and AV nodes. Sinus bradycardia (HR 40) with hypotension in this context is vagally mediated. First-line treatment is IV atropine sulfate (0.5\u20131 mg, repeat to max 3 mg), which reverses vagal inhibition. Temporary pacemaker is reserved if atropine fails. Isoprenaline is not first-line. Saline loading is used in right ventricular infarction but is not the priority here.'\n },\n {\n id:2,\n stem:'The characteristic feature of tricuspid insufficiency in the jugular venous pulse is:',\n correct:'Obliteration of the \\'x\\' descent and prominent \\'CV\\' wave',\n options:['Prominent \\'a\\' wave','Exaggerated \\'x\\' and \\'y\\' descents','Cannon waves','Obliteration of the \\'x\\' descent and prominent \\'CV\\' wave'],\n exp:'In tricuspid regurgitation, blood regurgitates into the right atrium during systole. This abolishes the normal x descent (systolic collapse) and produces a large systolic wave (the c and v waves merge into a prominent CV wave). Cannon waves are seen in complete heart block. Prominent a waves occur in pulmonary hypertension or tricuspid stenosis.'\n },\n {\n id:3,\n stem:'Match List I (Clinical Features) with List II (Diagnosis):\\nA. Osler\\'s node\\nB. Differential cyanosis\\nC. Bisferiens pulse\\nD. Graham Steell murmur\\n\\n1. Patent ductus arteriosus with reversal of shunt\\n2. Aortic stenosis with aortic regurgitation\\n3. Pulmonary hypertension\\n4. Subacute bacterial endocarditis',\n correct:'A-4, B-1, C-2, D-3',\n options:['A-4, B-1, C-2, D-3','A-4, B-1, C-3, D-2','A-1, B-4, C-2, D-3','A-1, B-4, C-3, D-2'],\n exp:'Osler\\'s nodes are painful, tender nodules in the pulp of fingers\/toes, pathognomonic of SBE (4). Differential cyanosis (lower limbs cyanosed, upper limbs pink) is characteristic of PDA with reversed shunt (Eisenmenger) (1). Bisferiens pulse (double-peaked systolic pulse) is classic for combined AS + AR (2). Graham Steell murmur is an early diastolic murmur of pulmonary regurgitation due to pulmonary hypertension (3).'\n },\n {\n id:4,\n stem:'Acute aortic regurgitation occurs in:',\n correct:'Infective endocarditis',\n options:['Infective endocarditis','Ankylosing spondylitis','Marfan\\'s syndrome','Rheumatoid arthritis'],\n exp:'Acute aortic regurgitation requires a sudden disruption of the aortic valve or root. Infective endocarditis causes acute cusp destruction\/perforation leading to acute AR \u2014 a surgical emergency. Ankylosing spondylitis, Marfan\\'s syndrome, and rheumatoid arthritis all cause chronic, slowly progressive AR through aortic root dilatation or valve fibrosis, not the acute form.'\n },\n {\n id:5,\n stem:'The following are early complications of acute myocardial infarction EXCEPT:',\n correct:'Dressler\\'s syndrome',\n options:['Papillary muscle dysfunction','Ventricular septal defect','Ventricular free wall rupture','Dressler\\'s syndrome'],\n exp:'Dressler\\'s syndrome (post-MI pericarditis) is a late complication, typically occurring 2\u201310 weeks after AMI. It is an autoimmune pericarditis with fever, pleuritic chest pain, and pericardial\/pleural effusion. Early complications (within 1\u20132 weeks) include arrhythmias, papillary muscle dysfunction (mitral regurgitation), ventricular septal rupture, and ventricular free wall rupture \u2014 all occurring in the first few days.'\n },\n {\n id:6,\n stem:'For which one of the following serum proteins do the levels NOT decrease in nephrotic syndrome?',\n correct:'Fibrinogen',\n options:['Albumin','Transferrin','Fibrinogen','Ceruloplasmin'],\n exp:'In nephrotic syndrome, the glomerular barrier selectively loses low-molecular-weight proteins. Albumin (69 kDa), transferrin (80 kDa), and ceruloplasmin (160 kDa) are all lost in urine and their serum levels fall. Fibrinogen (340 kDa) is a large-molecular-weight protein that does NOT filter through the damaged glomerulus; in fact, fibrinogen levels are elevated in nephrotic syndrome, contributing to the hypercoagulable state.'\n },\n {\n id:7,\n stem:'Following are the causes of high anion-gap acidosis EXCEPT:',\n correct:'Renal tubular acidosis',\n options:['Renal tubular acidosis','Acute renal failure','Chronic renal failure','Diabetic ketoacidosis'],\n exp:'Renal tubular acidosis (RTA) causes a NORMAL anion-gap (hyperchloraemic) metabolic acidosis. The anion gap stays normal because the acidosis results from failure to excrete H\u207a or reabsorb HCO\u2083\u207b, with compensatory Cl\u207b retention. High anion-gap acidosis (MUDPILES) includes acute and chronic renal failure (retained phosphates, sulphates), DKA, and lactic acidosis.'\n },\n {\n id:8,\n stem:'A patient of cirrhosis develops oliguria and worsening azotemia. Urinary sediment is normal. Urinary sodium concentration is 5 mEq\/L. The most likely cause could be:',\n correct:'Hepato-renal syndrome',\n options:['Interstitial nephritis','Acute tubular necrosis','Acute glomerulonephritis','Hepato-renal syndrome'],\n exp:'Hepato-renal syndrome (HRS) presents in cirrhotic patients with oliguria, rising creatinine, bland urinary sediment, and very low urinary sodium (<10 mEq\/L) \u2014 indicating intense renal vasoconstriction with intact tubular function. ATN would show muddy brown casts and urinary Na >20 mEq\/L. Glomerulonephritis shows active sediment (casts, RBCs). Interstitial nephritis shows WBC casts. The triad of cirrhosis + normal sediment + urinary Na <10 = HRS.'\n },\n {\n id:9,\n stem:'Which one of the following infections is related to subacute sclerosing panencephalitis (SSPE)?',\n correct:'Measles virus',\n options:['HIV','Measles virus','Japanese B encephalitis virus','JC virus'],\n exp:'SSPE is a late, progressive, fatal encephalitis caused by a defective mutant measles virus that persists in the CNS years after the primary infection (usually in childhood). It presents in young adults with cognitive decline, myoclonic jerks, and EEG changes (periodic complexes). JC virus causes PML (in immunocompromised). Japanese B encephalitis is an acute arboviral encephalitis. HIV causes AIDS dementia, not SSPE.'\n },\n {\n id:10,\n stem:'Consider the following:\\n1. Failure to swing the arms while walking\\n2. Nystagmus\\n3. Cogwheel rigidity\\n4. Festinant gait\\n\\nTypical features of Parkinsonism include which of the above?',\n correct:'1, 3 and 4',\n options:['2, 3 and 4','1, 2 and 4','1 and 3 only','1, 3 and 4'],\n exp:'Classic features of Parkinsonism: resting tremor, rigidity (lead-pipe and cogwheel = 3), bradykinesia, postural instability, festinant (shuffling, accelerating) gait (= 4), and loss of arm swing (= 1). Nystagmus (= 2) is NOT a feature of Parkinson\\'s disease; it suggests cerebellar or brainstem pathology (e.g., PSP may show gaze palsies but not nystagmus in the classic sense). All three \u2014 1, 3, and 4 \u2014 are correct.'\n },\n {\n id:11,\n stem:'Consider the following sites of lesion:\\n1. Left optic tract\\n2. Left optic radiation\\n3. Optic chiasma\\n4. Left lateral geniculate body\\n\\nRight homonymous hemianopia will result from lesions at which of the above?',\n correct:'1, 2 and 4',\n options:['1 and 3 only','1, 2 and 4','2, 3 and 4','1, 2 and 3'],\n exp:'Right homonymous hemianopia = loss of the right visual field in BOTH eyes. Visual fibres from both nasal retinae (carrying temporal field information) cross at the chiasma and travel in the LEFT optic tract, LEFT LGB, and LEFT optic radiation. Therefore a lesion anywhere in the left retrochiasmal pathway (left optic tract = 1, left LGB = 4, left optic radiation = 2) produces right homonymous hemianopia. Chiasmal lesion (3) produces bitemporal hemianopia.'\n },\n {\n id:12,\n stem:'Raised alkaline phosphatase is seen in the following EXCEPT:',\n correct:'Multiple myeloma',\n options:['Hyperparathyroidism','Obstructive jaundice','Osteomalacia','Multiple myeloma'],\n exp:'Alkaline phosphatase (ALP) is raised when bone osteoblast activity is increased or bile ducts are obstructed. It is elevated in hyperparathyroidism (increased bone resorption\/turnover), obstructive jaundice (biliary ALP isoenzyme), and osteomalacia (increased osteoblast activity attempting mineralisation). Multiple myeloma causes osteolytic lesions via osteoclast activation \u2014 ALP is characteristically NORMAL or only mildly elevated because osteoblastic activity is suppressed.'\n },\n {\n id:13,\n stem:'Consider the following statements about acromegaly:\\n1. Fibroma molluscum and acanthosis nigricans are common findings.\\n2. Growth hormone secretion is increased by TRH in 50 to 80% of acromegalics.\\n3. Acroosteolysis is a common radiological finding.\\n4. Diabetes mellitus may be associated in nearly 25% of acromegalics.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 4',\n options:['1, 2 and 3','1, 3 and 4','1, 2 and 4','2, 3 and 4'],\n exp:'In acromegaly: skin tags (fibroma molluscum) and acanthosis nigricans are common soft tissue findings (1 = correct). GH paradoxically rises with TRH in 50\u201380% of acromegalics \u2014 a useful diagnostic test (2 = correct). DM\/IGT occurs in ~25% due to GH insulin antagonism (4 = correct). Statement 3 is WRONG: acroosteolysis (terminal phalangeal resorption) is seen in hyperparathyroidism, psoriasis, and vinyl chloride exposure \u2014 NOT acromegaly. Acromegaly shows increased terminal phalangeal tufting and heel pad thickening.'\n },\n {\n id:14,\n stem:'Causes of hypomagnesaemia include all of the following EXCEPT:',\n correct:'Beta-blocker',\n options:['Beta-blocker','Chronic pancreatic insufficiency','Poorly controlled diabetes mellitus','Alcoholism'],\n exp:'Hypomagnesaemia causes: alcoholism (poor intake + renal wasting), poorly controlled DM (osmotic diuresis), chronic diarrhoea, malabsorption (including pancreatic insufficiency causing fat malabsorption and Mg soap formation), loop diuretics, aminoglycosides, cisplatin, and PPIs. Beta-blockers have no established mechanism for causing hypomagnesaemia and are NOT a recognised cause.'\n },\n {\n id:15,\n stem:'Which of the following conditions are associated with secondary diabetes mellitus?\\n1. Thyrotoxicosis, pheochromocytoma and acromegaly\\n2. Haemochromatosis\\n3. Pancreatic carcinoma\\n\\nSelect the correct answer:',\n correct:'1, 2 and 3',\n options:['2 and 3 only','1, 2 and 3','1 and 3 only','1 and 2 only'],\n exp:'Secondary DM arises from identifiable causes outside the islets: (1) Counter-regulatory hormones \u2014 GH (acromegaly), catecholamines (phaeochromocytoma), T3\/T4 (thyrotoxicosis) all cause insulin resistance. (2) Haemochromatosis deposits iron in the pancreas destroying beta cells (\"bronze diabetes\"). (3) Pancreatic carcinoma destroys exocrine and endocrine tissue. All three are well-recognised causes of secondary diabetes mellitus.'\n },\n {\n id:16,\n stem:'Consider the following statements:\\n1. Boils\/suppurative lesions around the nose must be promptly treated with antibiotics.\\n2. Suppurative lesions around the nose lead to cavernous sinus thrombosis.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'Both 1 and 2',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'The \"danger triangle of the face\" (nasal tip to mouth corners) is drained by valveless facial veins that communicate with the cavernous sinus via the ophthalmic veins. Septic emboli from boils in this area can cause septic cavernous sinus thrombosis \u2014 a life-threatening condition (statement 2 correct). Therefore, suppurative lesions here must be treated early with antibiotics and must NOT be squeezed (statement 1 correct). Both statements are correct.'\n },\n {\n id:17,\n stem:'Which one of the following is NOT an ECG change of hyperkalaemia?',\n correct:'Tall P-wave',\n options:['Tall T-wave','Tall P-wave','Prolonged PR interval','QRS widening'],\n exp:'ECG changes of hyperkalaemia in sequence: tall peaked T-waves \u2192 prolonged PR interval \u2192 flattening\/disappearance of P-wave \u2192 widening of QRS \u2192 sine-wave pattern \u2192 VF\/asystole. A TALL P-wave is NOT a feature \u2014 in fact, P-waves progressively diminish and disappear with rising K\u207a. Tall P-waves suggest right atrial hypertrophy or ectopic atrial rhythms, not hyperkalaemia.'\n },\n {\n id:18,\n stem:'Which one of the following tests has the highest chance of detecting HIV infection in a blood donor during the window period?',\n correct:'p24 antigen detection',\n options:['Demonstration of antibody to HIV by ELISA','CD4 count','p24 antigen detection','Western blot test'],\n exp:'The window period is the time between HIV infection and detectable antibody response (3\u201312 weeks). During this period, ELISA and Western blot (antibody tests) are NEGATIVE. p24 antigen (HIV core protein) appears in blood 2\u20133 weeks after infection, well before antibody seroconversion, making it the best single marker during the window period. Modern 4th-generation tests combine p24 Ag + Ab. CD4 count falls but is non-specific.'\n },\n {\n id:19,\n stem:'Which of the following features are characteristic of tuberculoid leprosy?\\n1. Type 2 lepra reaction\\n2. A few lesions with well-demarcated edges\\n3. Early and marked nerve damage\\n4. Tendency to heal spontaneously\\n\\nSelect the correct answer:',\n correct:'2, 3 and 4',\n options:['1, 2 and 3','2, 3 and 4','1 and 4','2 and 3 only'],\n exp:'Tuberculoid leprosy (TT): high cellular immunity, few well-demarcated hypopigmented anaesthetic plaques (statement 2), early and severe nerve involvement leading to nerve thickening\/damage (statement 3), tendency to heal spontaneously (statement 4). Type 2 lepra reaction (erythema nodosum leprosum) is a feature of LEPROMATOUS leprosy (BL\/LL), not tuberculoid \u2014 statement 1 is incorrect. Type 1 (reversal) reaction occurs in tuberculoid\/borderline types.'\n },\n {\n id:20,\n stem:'Which one of the following immunological reactions occurs in Goodpasture\\'s syndrome?',\n correct:'Type II cytotoxicity',\n options:['Type I Atopy','Type II cytotoxicity','Type III immune complex','Type IV cell mediation'],\n exp:'Goodpasture\\'s syndrome is caused by autoantibodies (anti-GBM IgG) directed against the alpha-3 chain of type IV collagen in the glomerular and alveolar basement membranes. These antibodies activate complement and recruit neutrophils causing crescentic glomerulonephritis and pulmonary haemorrhage. This is a classic Type II (cytotoxic\/antibody-mediated) hypersensitivity reaction. Linear IgG deposits are seen on immunofluorescence.'\n },\n {\n id:21,\n stem:'Consider the following statements about leptospirosis:\\n1. It is a ubiquitous enzootic disease.\\n2. Its incubation period ranges from 2 to 20 days.\\n3. The intensity of jaundice is directly related to prognosis.\\n4. Urine may show microscopic haematuria.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 4',\n options:['1, 2 and 4','1, 2 and 3','1, 3 and 4','2, 3 and 4'],\n exp:'Leptospirosis (Weil\\'s disease): (1) It is indeed an enzootic (reservoir in animals, esp. rodents) zoonosis found worldwide \u2014 correct. (2) Incubation 2\u201320 days (mean 10 days) \u2014 correct. (3) Intensity of jaundice does NOT directly predict prognosis; patients with deep jaundice may survive if renal function is maintained \u2014 statement 3 is FALSE. (4) Microscopic haematuria is common due to renal tubular involvement \u2014 correct. So 1, 2, and 4 are correct.'\n },\n {\n id:22,\n stem:'SVC syndrome can occur in the following EXCEPT:',\n correct:'Pneumomediastinum',\n options:['Pneumomediastinum','Goitre','Bronchogenic carcinoma','Lymphoma'],\n exp:'Superior vena cava syndrome results from external compression or thrombosis of the SVC, causing facial\/arm oedema, dilated neck veins, and plethora. Causes include bronchogenic carcinoma (right-sided; most common), lymphoma, goitre, aortic aneurysm, pericardial effusion, and mediastinal fibrosis. Pneumomediastinum (air in mediastinum from alveolar rupture) does NOT compress the SVC and is NOT a cause of SVC syndrome.'\n },\n {\n id:23,\n stem:'Match List I (Physical Sign) with List II (Medical Condition):\\nA. Koebner phenomenon\\nB. Erythema nodosum\\nC. Erythema multiforme\\nD. Nikolsky\\'s sign\\n\\n1. Lepra reaction\\n2. Pemphigus vulgaris\\n3. Stevens-Johnson syndrome\\n4. Psoriasis',\n correct:'A-4, B-1, C-3, D-2',\n options:['A-1, B-4, C-3, D-2','A-4, B-1, C-2, D-3','A-1, B-4, C-2, D-3','A-4, B-1, C-3, D-2'],\n exp:'Koebner phenomenon (new lesions at trauma sites) = Psoriasis (4). Erythema nodosum (painful red nodules on shins) = Type 2 lepra reaction \/ ENL (1) among these options. Erythema multiforme (target lesions) at severe end = Stevens-Johnson syndrome (3). Nikolsky\\'s sign (skin slippage with lateral pressure) = Pemphigus vulgaris (2), confirming loss of keratinocyte adhesion (acantholysis).'\n },\n {\n id:24,\n stem:'Which one of the following is the major site of absorption of Vitamin B12?',\n correct:'Terminal ileum',\n options:['Stomach','Terminal ileum','Duodenum','Mid Jejunum'],\n exp:'Vitamin B12 (cobalamin) is bound to intrinsic factor (IF) secreted by gastric parietal cells. The IF-B12 complex is specifically absorbed by cubilin receptors located exclusively in the terminal ileum. Disease of the terminal ileum (Crohn\\'s, ileal resection) or absence of IF (pernicious anaemia, gastrectomy) causes B12 deficiency. No other segment of the gut can absorb the IF-B12 complex in physiological quantities.'\n },\n {\n id:25,\n stem:'The following features regarding polymyositis are true EXCEPT:',\n correct:'Ocular muscle involvement is common',\n options:['Progressive proximal muscle involvement','25% patients may present with dysphagia','Ocular muscle involvement is common','Elevated levels of serum creatine kinase'],\n exp:'Polymyositis characteristically involves proximal limb muscles (shoulders, hips), and pharyngeal muscles causing dysphagia (~25%). Serum CK is markedly elevated. Ocular muscles are SPARED in polymyositis \u2014 this is an important distinguishing feature from myasthenia gravis (which commonly involves ocular muscles causing ptosis and diplopia). Sparing of ocular muscles is a hallmark of inflammatory myopathies.'\n },\n {\n id:26,\n stem:'Match List I (Inflammatory Joint Disease) with List II (Clinical Finding):\\nA. Reiter\\'s Syndrome\\nB. Rheumatoid arthritis\\nC. Psoriatic arthritis\\nD. Sj\u00f6gren\\'s syndrome\\n\\n1. Onycholysis\\n2. Keratoderma blenorrhagica\\n3. Xerostomia\\n4. Baker\\'s cysts',\n correct:'A-2, B-4, C-1, D-3',\n options:['A-4, B-2, C-3, D-1','A-2, B-4, C-1, D-3','A-2, B-4, C-3, D-1','A-4, B-2, C-1, D-3'],\n exp:'Reiter\\'s syndrome = keratoderma blenorrhagica (hyperkeratotic skin lesions on palms\/soles) (2). Rheumatoid arthritis = Baker\\'s cysts (popliteal cysts from knee joint effusion) (4). Psoriatic arthritis = onycholysis (nail lifting\/separation) (1). Sj\u00f6gren\\'s syndrome = xerostomia (dry mouth due to salivary gland infiltration by lymphocytes) (3).'\n },\n {\n id:27,\n stem:'The following drugs are useful in generalised anxiety disorders EXCEPT:',\n correct:'Risperidone',\n options:['Risperidone','Amitriptyline','Buspirone','Venlafaxine'],\n exp:'Generalised anxiety disorder is treated with: SSRIs\/SNRIs (venlafaxine = first-line), TCAs (amitriptyline), buspirone (5-HT1A partial agonist), and benzodiazepines (short-term). Risperidone is an atypical antipsychotic (D2\/5-HT2A antagonist) used for schizophrenia, bipolar disorder, and irritability in autism. It is not a recognised treatment for GAD and would not be appropriate first- or second-line.'\n },\n {\n id:28,\n stem:'Systemic inflammatory response syndrome (SIRS) can have the following features EXCEPT:',\n correct:'Bradycardia',\n options:['Hypothermia','Bradycardia','Tachypnoea','Leucopenia (WBC < 4000)'],\n exp:'SIRS criteria (2 or more of): temperature >38\u00b0C or <36\u00b0C (hypothermia is included), heart rate >90\/min (TACHYCARDIA \u2014 bradycardia is NOT a criterion), respiratory rate >20\/min or PaCO\u2082 <32 mmHg, WBC >12,000 or <4,000 or >10% bands. Bradycardia is specifically excluded \u2014 it would suggest vagal response or heart block, not the hyperadrenergic, inflammatory state of SIRS.'\n },\n {\n id:29,\n stem:'Which of the following is NOT a complication of malaria?',\n correct:'Hyperglycaemia',\n options:['ARDS','Acidosis','Hyperglycaemia','Coma'],\n exp:'Severe falciparum malaria complications (WHO criteria): cerebral malaria (coma), ARDS, metabolic acidosis, severe anaemia, renal failure, hypoglycaemia (NOT hyperglycaemia), hyperparasitaemia, abnormal bleeding, and jaundice. Hypoglycaemia occurs due to parasite glucose consumption and quinine\/quinidine-stimulated insulin release. Hyperglycaemia is NOT a complication of malaria.'\n },\n {\n id:30,\n stem:'Cardiac troponin may be elevated in:',\n correct:'Chronic kidney failure',\n options:['Muscular dystrophy','Chronic kidney failure','Acute liver failure','Epilepsy'],\n exp:'Cardiac troponins (cTnI, cTnT) are cardiac-specific markers. Elevated troponins are seen in: ACS, myocarditis, PE, cardiac contusion, severe sepsis, and importantly in chronic kidney disease (CKD) \u2014 likely due to reduced clearance, subclinical myocardial injury, and LVH. Troponin elevation in CKD is a significant prognostic marker. Skeletal muscle disorders like Duchenne\\'s dystrophy rarely cause troponin elevation since they mainly release skeletal isoforms. Acute liver failure does not elevate cardiac troponins.'\n },\n {\n id:31,\n stem:'Which of the following are the physiological abnormalities in chronic obstructive lung disease?\\n1. Reduced total lung capacity (TLC)\\n2. Increased functional residual capacity\\n3. Increased residual volume (RV)\\n4. Increased RV\/TLC ratio\\n\\nSelect the correct answer:',\n correct:'2, 3 and 4',\n options:['1 and 2 only','2, 3 and 4','1, 3 and 4','3 and 4 only'],\n exp:'In COPD, air trapping and loss of elastic recoil leads to: (1) TLC is INCREASED (not reduced) due to hyperinflation \u2014 statement 1 is WRONG. (2) FRC is increased (premature airway closure, air trapping) \u2014 correct. (3) RV is increased (incomplete emptying) \u2014 correct. (4) RV\/TLC ratio is increased (air trapping, barrel chest) \u2014 correct. TLC reduction would suggest restrictive disease. All of 2, 3, and 4 are correct.'\n },\n {\n id:32,\n stem:'Acute respiratory distress syndrome characteristically occurs in:\\n1. Gram-negative septicaemia\\n2. Gastric aspiration\\n3. Pancreatitis\\n4. Severe burns\\n5. Myocarditis\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2, 3 and 4',\n options:['2, 3, 4 and 5','1, 3, 4 and 5','1, 2 and 5','1, 2, 3 and 4'],\n exp:'ARDS is a non-cardiogenic pulmonary oedema triggered by direct or indirect lung injury. Direct causes: aspiration (2), pneumonia, inhalation injury. Indirect causes: gram-negative sepsis (1) \u2014 most common, pancreatitis (3), severe burns (4), massive transfusion, trauma. Myocarditis (5) causes cardiogenic pulmonary oedema (due to LV failure) \u2014 NOT ARDS. All of 1, 2, 3, and 4 are recognised ARDS causes.'\n },\n {\n id:33,\n stem:'Botulism can have the following clinical features EXCEPT:',\n correct:'Hyperpyrexia',\n options:['Hyperpyrexia','Sudden onset quadriplegia','Cranial nerve deficits','Respiratory failure'],\n exp:'Botulism (Clostridium botulinum toxin) causes flaccid descending paralysis by blocking presynaptic ACh release at the NMJ. Features: cranial nerve palsies (ptosis, diplopia, dysarthria), descending symmetrical weakness\/paralysis, respiratory failure \u2014 ALL correct features. Crucially, botulism is classically AFEBRILE \u2014 hyperpyrexia is NOT a feature. Fever would suggest wound botulism with secondary infection, but not the disease itself.'\n },\n {\n id:34,\n stem:'A 55-year-old man, non-smoker, presents with sudden onset of shortness of breath. Pulse rate is 110\/minute and B.P. 180\/110 mm Hg. Patient is restless and anxious. Chest examination shows bilateral rhonchi and crepitations. S3 gallop is heard on auscultation. There is no history of chronic bronchitis. The most likely diagnosis is:',\n correct:'Acute LVF',\n options:['Bronchial asthma','Acute LVF','Pneumothorax','Acute exacerbation of COPD'],\n exp:'The clinical picture \u2014 sudden dyspnoea, severe hypertension, bilateral crepitations (alveolar oedema) with rhonchi (cardiac asthma), S3 gallop (ventricular dysfunction), tachycardia, in a non-smoker without prior bronchitis \u2014 is classic acute left ventricular failure. S3 gallop specifically points to a failing, volume-overloaded ventricle. Asthma\/COPD exacerbations would not produce an S3 gallop and typically have a prior history. Pneumothorax causes unilateral signs.'\n },\n {\n id:35,\n stem:'Small cell carcinoma of lung is commonly associated with the following paraneoplastic syndromes:\\n1. Ectopic ACTH production\\n2. Lambert-Eaton syndrome\\n3. Syndrome of inappropriate ADH (SIADH)\\n4. Addison\\'s disease\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 3',\n options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],\n exp:'Small cell lung carcinoma (SCLC) is a neuroendocrine tumour notorious for paraneoplastic syndromes: ectopic ACTH (Cushing\\'s syndrome, 1), Lambert-Eaton myasthenic syndrome (antibodies against VGCC, 2), SIADH (hyponatraemia, 3), and also carcinoid-like features. Addison\\'s disease (adrenocortical insufficiency, 4) is NOT caused by SCLC paraneoplastic mechanisms. Adrenal metastases can replace adrenal tissue but this is not a paraneoplastic syndrome.'\n },\n {\n id:36,\n stem:'On abdominal percussion, liver dullness may be obliterated in the following EXCEPT:',\n correct:'Fatty liver',\n options:['Fatty liver','Emphysema','Perforated viscus','Fulminant hepatitis'],\n exp:'Liver dullness is obliterated when air intervenes between the abdominal wall and the liver: emphysema (hyperinflated lung pushes down, gas above liver), perforated viscus (free intraperitoneal air rises to lie anterior to liver), and fulminant hepatic failure (massive hepatocyte loss causes the liver to shrink dramatically, replacing dullness with resonance). Fatty liver (hepatomegaly) INCREASES liver dullness \u2014 the area of dullness enlarges, it is not obliterated.'\n },\n {\n id:37,\n stem:'Consider the following statements regarding Helicobacter pylori:\\n1. It is a gram-negative bacterium.\\n2. It invades the epithelium.\\n3. It produces urease.\\n4. It produces chronic gastritis.\\n\\nWhich of the statements given above are correct?',\n correct:'1, 3 and 4',\n options:['1, 2 and 4','1 and 3 only','2 and 4 only','1, 3 and 4'],\n exp:'H. pylori: (1) Gram-negative curved\/spiral rod \u2014 correct. (2) Does NOT invade the epithelium \u2014 it colonises the gastric mucus layer overlying the epithelium without actual cellular invasion, unlike Salmonella\/Shigella. Statement 2 is FALSE. (3) Produces urease (splits urea \u2192 NH\u2083 + CO\u2082), neutralising local acid and enabling survival \u2014 correct; basis of CLO\/urea breath test. (4) Causes type B chronic antral gastritis \u2014 correct. So 1, 3, and 4 are correct.'\n },\n {\n id:38,\n stem:'Consider the following conditions:\\n1. Steroid therapy\\n2. Hypertriglyceridaemia\\n3. Hypercalcaemia\\n4. Azathioprine therapy\\n\\nAcute pancreatitis may occur in which of the above conditions?',\n correct:'1, 2, 3 and 4',\n options:['1, 2 and 3 only','2 and 4 only','1, 3 and 4 only','1, 2, 3 and 4'],\n exp:'All four are recognised causes of acute pancreatitis: (1) Corticosteroids \u2014 can cause pancreatitis (mechanism debated but well documented). (2) Hypertriglyceridaemia >1000 mg\/dL \u2014 a major cause via free fatty acid toxicity to acinar cells. (3) Hypercalcaemia (hyperparathyroidism) \u2014 calcium activates trypsinogen prematurely. (4) Azathioprine \u2014 drug-induced pancreatitis (class effect with 6-mercaptopurine). All four cause acute pancreatitis.'\n },\n {\n id:39,\n stem:'A 60-year-old patient presents with gradually increasing dysphagia to solids for 3 months with significant loss of weight. The most probable diagnosis is:',\n correct:'Carcinoma oesophagus',\n options:['Stricture oesophagus','Carcinoma oesophagus','Reflux oesophagitis','Neurogenic oesophagus'],\n exp:'Progressive dysphagia to solids (then liquids), age >50, significant weight loss \u2014 this is the classic presentation of carcinoma of the oesophagus until proved otherwise. The insidious onset and marked weight loss strongly suggest malignancy. Benign stricture (post-reflux\/corrosive) has a slower, less dramatic course. Achalasia (neurogenic) typically affects both solids and liquids from the start. Reflux oesophagitis causes heartburn\/regurgitation, not predominantly dysphagia.'\n },\n {\n id:40,\n stem:'Consider the following statements:\\n1. Gentamicin should be added to the empirical regime for acute meningitis for patients aged more than 55 years.\\n2. Ampicillin covers Listeria monocytogenes.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'2 only',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'For bacterial meningitis in patients >55 years, empirical therapy is ceftriaxone + AMPICILLIN (to cover Listeria monocytogenes, which is seen in the elderly and immunocompromised). Gentamicin is NOT routinely added \u2014 statement 1 is FALSE. Ampicillin is indeed the drug of choice for Listeria (which is intrinsically resistant to cephalosporins) \u2014 statement 2 is CORRECT. Vancomycin may be added if MRSA\/resistant pneumococcus is suspected.'\n }\n ];\n\n \/\/ Fisher-Yates shuffle\n function shuffle(arr){\n const a=[...arr];\n for(let i=a.length-1;i>0;i--){const j=Math.floor(Math.random()*(i+1));[a[i],a[j]]=[a[j],a[i]];}\n return a;\n }\n\n const LETTERS=['A','B','C','D'];\n let userAnswers={}, answered=0, shuffledOpts={};\n\n \/\/ \u2500\u2500 Timer state \u2500\u2500\n let timerRunning=false, timerRemaining=TIMER_SECS, timerInterval=null, graceInterval=null;\n let quizSubmitted=false;\n\n function fmtTime(s){\n const m=Math.floor(s\/60), sec=s%60;\n return String(m).padStart(2,'0')+':'+String(sec).padStart(2,'0');\n }\n\n function startTimer(){\n if(timerRunning||quizSubmitted)return;\n timerRunning=true;\n const btn=document.getElementById(NS+'-timer-btn');\n btn.textContent='\u23f1 '+fmtTime(timerRemaining);\n btn.classList.add('running');\n document.getElementById(NS+'-timer-item').classList.add('active');\n\n timerInterval=setInterval(function(){\n timerRemaining--;\n const disp=fmtTime(timerRemaining);\n document.getElementById(NS+'-timer-display').textContent=disp;\n btn.textContent='\u23f1 '+disp;\n\n const item=document.getElementById(NS+'-timer-item');\n if(timerRemaining<=300) item.classList.add('warning'); \/\/ red at 5 min\n\n if(timerRemaining<=0){\n clearInterval(timerInterval);\n timerInterval=null;\n triggerGrace();\n }\n },1000);\n }\n\n function stopTimer(){\n if(timerInterval){clearInterval(timerInterval);timerInterval=null;}\n timerRunning=false;\n }\n\n function triggerGrace(){\n if(quizSubmitted)return;\n let g=GRACE_SECS;\n document.getElementById(NS+'-grace-count').textContent=g;\n document.getElementById(NS+'-grace').classList.add('show');\n graceInterval=setInterval(function(){\n g--;\n document.getElementById(NS+'-grace-count').textContent=g;\n if(g<=0){\n clearInterval(graceInterval);\n dismissGrace();\n showScore();\n }\n },1000);\n }\n\n function dismissGrace(){\n document.getElementById(NS+'-grace').classList.remove('show');\n if(graceInterval){clearInterval(graceInterval);graceInterval=null;}\n }\n\n function build(){\n const container=document.getElementById(NS+'-questions');\n container.innerHTML='';\n userAnswers={};answered=0;shuffledOpts={};\n quizSubmitted=false;timerRunning=false;timerRemaining=TIMER_SECS;\n stopTimer();\n if(graceInterval){clearInterval(graceInterval);graceInterval=null;}\n dismissGrace();\n document.getElementById(NS+'-score').style.display='none';\n document.getElementById(NS+'-timer-item').classList.remove('active','warning');\n const btn=document.getElementById(NS+'-timer-btn');\n btn.textContent='\u23f1 Start Timed Mode';btn.classList.remove('running');\n document.getElementById(NS+'-timer-display').textContent=fmtTime(TIMER_SECS);\n updateStats();\n\n QUESTIONS.forEach(function(q){\n \/\/ Shuffle answer options; correct answer tracked by text content\n const opts=shuffle(q.options);shuffledOpts[q.id]=opts;\n const card=document.createElement('div');card.className='cq-card';\n card.innerHTML=\n '<div class=\"cq-qhead\">'+\n '<div class=\"cq-qnum\" id=\"'+NS+'-n'+q.id+'\">'+q.id+'<\/div>'+\n '<div class=\"cq-qtext\">'+q.stem.replace(\/\\n\/g,'<br>')+'<\/div>'+\n '<\/div>'+\n '<div class=\"cq-options\" id=\"'+NS+'-opts'+q.id+'\">'+\n opts.map(function(o,i){\n return '<div class=\"cq-opt\" id=\"'+NS+'-o'+q.id+'-'+i+'\" role=\"button\" tabindex=\"0\">'+\n '<span class=\"cq-opt-letter\">'+LETTERS[i]+'<\/span>'+\n '<span class=\"cq-opt-text\">'+o+'<\/span><\/div>';\n }).join('')+\n '<\/div>'+\n '<div class=\"cq-explanation\" id=\"'+NS+'-exp'+q.id+'\">'+\n '<div class=\"cq-exp-label\">Explanation<\/div>'+q.exp+'<\/div>';\n container.appendChild(card);\n \/\/ Attach click listeners to each option\n opts.forEach(function(_,i){\n document.getElementById(NS+'-o'+q.id+'-'+i).addEventListener('click',function(){pick(q.id,i);});\n });\n });\n }\n\n function pick(qid,oi){\n if(userAnswers[qid]!==undefined||quizSubmitted)return;\n const q=QUESTIONS.find(function(x){return x.id===qid;});\n const opts=shuffledOpts[qid];\n \/\/ Correct answer determined by matching text, not index\n const correct=opts[oi]===q.correct;\n userAnswers[qid]=correct?'correct':'wrong';\n answered++;\n opts.forEach(function(o,i){\n const el=document.getElementById(NS+'-o'+qid+'-'+i);\n if(o===q.correct) el.classList.add('cq-correct','cq-locked');\n else if(i===oi) el.classList.add('cq-wrong','cq-locked');\n else el.classList.add('cq-dimmed','cq-locked');\n });\n document.getElementById(NS+'-n'+qid).classList.add(correct?'ans-c':'ans-w');\n document.getElementById(NS+'-exp'+qid).style.display='block';\n updateStats();\n }\n\n function updateStats(){\n const c=Object.values(userAnswers).filter(function(v){return v==='correct';}).length;\n const w=Object.values(userAnswers).filter(function(v){return v==='wrong';}).length;\n \/\/ Score formula: c \u00d7 4 \u2212 w\n const net=(c*4)-w;\n 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