{"id":36767,"date":"2026-05-06T22:12:36","date_gmt":"2026-05-06T16:42:36","guid":{"rendered":"https:\/\/atsixty.com\/?p=36767"},"modified":"2026-05-06T22:13:57","modified_gmt":"2026-05-06T16:43:57","slug":"cms-2017-p1-part-a","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/06\/cms-2017-p1-part-a\/","title":{"rendered":"CMS 2017 P1 Part-A"},"content":{"rendered":"\n\n\n\n\n\n\n\nCMS 2017 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: cms17p1a \u2500\u2500 *\/\n#cms17p1a *,#cms17p1a *::before,#cms17p1a *::after{box-sizing:border-box;margin:0;padding:0}\n#cms17p1a{\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 --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#cms17p1a .cq-sentinel{height:1px}\n#cms17p1a .cq-statusbar{\n position:fixed;top:0;left:0;right:0;z-index:99999;\n background:var(--white);border-bottom:2px solid var(--line);\n border-left:4px solid var(--ter);box-shadow:0 2px 12px rgba(0,0,0,0.11);\n opacity:0;pointer-events:none;transform:translateY(-110%);\n transition:opacity 0.22s ease,transform 0.22s ease;\n}\n#cms17p1a .cq-statusbar.visible{opacity:1;pointer-events:auto;transform:translateY(0)}\n#cms17p1a .cq-sb-stats{display:flex;align-items:center;padding:0.38rem 0.7rem;font-size:0.73rem;color:var(--ink-soft);}\n#cms17p1a .cq-sb-item{display:flex;align-items:center;gap:0.18rem;padding:0.1rem 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.cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms17p1a .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms17p1a .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms17p1a .cq-retry-btn{margin-top:22px;background:transparent;border:2px solid var(--teal);color:var(--teal);border-radius:8px;padding:10px 28px;font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;cursor:pointer;transition:background 0.2s,color 0.2s;}\n#cms17p1a .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n@media(max-width:480px){\n #cms17p1a .cq-header h1{font-size:1.15rem}\n #cms17p1a .cq-qtext{font-size:0.88rem}\n #cms17p1a .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms17p1a\">\n <div class=\"cq-sentinel\" id=\"cms17p1a-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms17p1a-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms17p1a-timer-item\">\u23f1 <strong id=\"cms17p1a-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms17p1a-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms17p1a-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms17p1a-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms17p1a-sn\">0<\/strong> \/ <strong id=\"cms17p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms17p1a-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms17p1a-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=\"cms17p1a-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms17p1a-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2017<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine<\/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=\"cms17p1a-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms17p1a-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms17p1a-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms17p1a-score\">\n <div class=\"cq-score-ring\" id=\"cms17p1a-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms17p1a-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=\"cms17p1a-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms17p1a-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms17p1a-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms17p1a-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms17p1a-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms17p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms17p1a', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60, GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:1,\n stem:'Which of the following is NOT correct?',\n correct:'Hepatitis A does not lead to massive hepatic necrosis',\n options:['Hepatitis A does not lead to massive hepatic necrosis','Hepatitis B vaccination is part of universal childhood vaccination','Hepatitis C is commonest cause of transfusion-transmitted hepatitis','Hepatitis E carries very high mortality in pregnant women'],\n exp:'Hepatitis A CAN lead to massive hepatic necrosis (fulminant hepatic failure) in rare cases (~0.1\u20130.3%) \u2014 so statement (a) is INCORRECT (the NOT correct option). HAV is usually self-limiting but massive necrosis\/ALF does occur. HBV is in the universal childhood schedule (correct). HCV is the predominant transfusion-transmitted hepatitis since HBV screening (correct). HEV carries 15\u201325% mortality in pregnant women, especially in 3rd trimester (correct). Statement (a) is the false one.'\n },\n {\n id:2,\n stem:'Which of the following antihypertensive drugs is contraindicated in pregnancy?',\n correct:'Ramipril',\n options:['Hydralazine','Amlodipine','Labetalol','Ramipril'],\n exp:'ACE inhibitors (ramipril, enalapril, lisinopril) are ABSOLUTELY CONTRAINDICATED in pregnancy \u2014 they cause fetal ACE inhibitor fetopathy: oligohydramnios (from reduced fetal urine output), renal tubular dysplasia, hypocalvaria, and neonatal renal failure. They are teratogenic in the 2nd and 3rd trimesters. Safe antihypertensives in pregnancy: methyldopa (1st choice), labetalol, hydralazine (IV for acute), nifedipine\/amlodipine (calcium channel blockers). Ramipril is the contraindicated option.'\n },\n {\n id:3,\n stem:'Which of the following least predisposes to infective endocarditis?',\n correct:'Atrial septal defect',\n options:['Ventricular septal defect','Atrial septal defect','Patent ductus arteriosus','Tetralogy of Fallot'],\n exp:'The risk of infective endocarditis depends on the turbulence and pressure gradient created by the defect. High-risk lesions: VSD (high-velocity jet damages endocardium), PDA (turbulent flow), Tetralogy of Fallot (complex cyanotic lesion). Atrial septal defect (ASD \u2014 secundum type) creates LOW-velocity, low-pressure shunting \u2014 the RIGHT atrial endocardium is not subjected to the same high-speed jets. ASD is the congenital defect with the LOWEST risk of IE. It is specifically listed as a low-risk lesion in IE prophylaxis guidelines.'\n },\n {\n id:4,\n stem:'A 60-year-old male with Marfan\\'s syndrome comes to the emergency department with severe generalised tearing pain in the chest anteriorly and interscapular region, sweating and weakness. BP is 200\/140 mm Hg. Chest X-ray shows widening of the superior mediastinum. ECG shows sinus tachycardia. What is the most likely diagnosis?',\n correct:'Dissection of aorta',\n options:['Acute pulmonary embolism','Dissection of aorta','Acute myocardial infarction','Acute pericarditis'],\n exp:'The clinical triad \u2014 Marfan\\'s syndrome (aortic root dilatation predisposes), tearing\/ripping chest-to-back pain, widened mediastinum on CXR, and severe hypertension \u2014 is diagnostic of acute aortic dissection (Type A). Marfan\\'s is the most common connective tissue disease predisposing to dissection. The pain radiates from anterior chest to interscapular region as the dissection propagates. Mediastinal widening reflects haematoma around the aorta. MI causes ST changes; PE causes right heart strain; pericarditis causes saddle-shaped ST elevation without widened mediastinum.'\n },\n {\n id:5,\n stem:'A patient who is allergic to penicillin can be prescribed which of the following drugs for prophylaxis of acute rheumatic fever?',\n correct:'Erythromycin',\n options:['Ciprofloxacin','Erythromycin','Cotrimoxazole','Tetracycline'],\n exp:'Secondary prophylaxis of acute rheumatic fever (to prevent recurrence): first choice is benzathine penicillin G (monthly IM injection) or oral phenoxymethylpenicillin. For penicillin-allergic patients, ERYTHROMYCIN (macrolide) is the recommended alternative \u2014 250 mg twice daily. Sulfonamides (including cotrimoxazole) prevent streptococcal spread but do NOT eradicate carriage and are not recommended as sole prophylaxis. Ciprofloxacin and tetracycline are not used for RF prophylaxis. Erythromycin is the established penicillin-alternative.'\n },\n {\n id:6,\n stem:'QT interval is prolonged in:',\n correct:'Hypocalcaemia',\n options:['Hypocalcaemia','Hyperkalaemia','Hypermagnesaemia','Digoxin therapy'],\n exp:'QT prolongation occurs when ventricular repolarisation is delayed. Hypocalcaemia prolongs the plateau phase of the action potential (calcium is needed to terminate it) \u2192 prolonged QT \u2014 a classic and important association. Hyperkalaemia causes tall peaked T waves, widened QRS, and shortened QT. Hypermagnesaemia shortens QT and slows conduction. Digoxin causes ST scooping (\"dig effect\"), shortened QT, and T-wave changes \u2014 it shortens, not prolongs, the QT. Hypocalcaemia is the correct answer for QT prolongation.'\n },\n {\n id:7,\n stem:'Differential cyanosis is seen in:',\n correct:'Patent ductus arteriosus with pulmonary arterial hypertension',\n options:['Atrial septal defect with pulmonary arterial hypertension','Ventricular septal defect with pulmonary arterial hypertension','Patent ductus arteriosus with pulmonary arterial hypertension','Fallot tetralogy'],\n exp:'Differential cyanosis (lower limbs\/toes cyanosed, upper limbs\/fingers pink) occurs only in PDA with Eisenmenger physiology (pulmonary arterial hypertension causing reversal of shunt). In PDA, the ductus connects the descending aorta (post-left subclavian) to the pulmonary artery \u2014 when shunt reverses, desaturated blood enters the aorta BELOW the origin of the subclavian arteries, reaching the legs but not the arms. ASD\/VSD Eisenmenger produces generalised cyanosis (not differential). ToF produces generalised cyanosis. PDA reversal = classic differential cyanosis.'\n },\n {\n id:8,\n stem:'Wilson\\'s disease is characterised by all EXCEPT:',\n correct:'Increased serum ceruloplasmin',\n options:['Increased urinary copper','Increased hepatic copper','Deposition of copper in Descemet\\'s membrane','Increased serum ceruloplasmin'],\n exp:'Wilson\\'s disease (hepatolenticular degeneration, ATP7B mutation): features include increased urinary copper (>100 \u00b5g\/24h), increased hepatic copper (>250 \u00b5g\/g dry weight), and copper deposition in Descemet\\'s membrane of the cornea (Kayser-Fleischer rings). Serum ceruloplasmin is characteristically DECREASED (<20 mg\/dL) in 85\u201390% of cases \u2014 because ATP7B is needed for ceruloplasmin-copper incorporation in the liver. Increased serum ceruloplasmin is therefore NOT a feature of Wilson\\'s disease \u2014 it is the exception.'\n },\n {\n id:9,\n stem:'Following drugs are used for H. pylori eradication EXCEPT:',\n correct:'Cephalexin',\n options:['Amoxycillin','Bismuth subsalicylate','Tetracycline','Cephalexin'],\n exp:'H. pylori eradication regimens include: amoxycillin (first-line, disrupts cell wall), clarithromycin, metronidazole, tetracycline (used in bismuth quadruple therapy), and bismuth subsalicylate (toxic to H. pylori, part of quadruple therapy). Cephalexin (a 1st generation oral cephalosporin) has NO established activity against H. pylori and is NOT included in any eradication regimen. It is the exception.'\n },\n {\n id:10,\n stem:'A 45-year-old female comes to you with dysphagia. She is found to have anaemia and koilonychia. Most likely diagnosis is:',\n correct:'Plummer Vinson syndrome',\n options:['Plummer Vinson syndrome','Boerhaave syndrome','Carcinoma oesophagus','Reflux oesophagitis'],\n exp:'Plummer-Vinson (Patterson-Kelly-Brown) syndrome: classic triad of (1) iron-deficiency anaemia, (2) dysphagia (from upper oesophageal\/postcricoid web), and (3) koilonychia (spoon-shaped nails \u2014 iron deficiency). Occurs in middle-aged women. Important because it is a premalignant condition (postcricoid carcinoma risk). Koilonychia specifically points to iron deficiency. Boerhaave = oesophageal perforation from vomiting. Reflux oesophagitis causes heartburn. Carcinoma oesophagus would not explain koilonychia. The triad points exclusively to Plummer-Vinson syndrome.'\n },\n {\n id:11,\n stem:'Chest tube insertion should be considered in a patient with parapneumonic effusion \u2014 EXCEPT when:',\n correct:'Pleural effusion is less than 10 mm thickness on decubitus',\n options:['Loculated pleural effusion','Positive Gram stain\/culture of pleural fluid','Pleural effusion is less than 10 mm thickness on decubitus','Pleural fluid pH less than 7.20'],\n exp:'Indications for chest tube drainage in parapneumonic effusion (complicated effusion\/empyema): loculated effusion, positive Gram stain or culture (infected fluid), pleural fluid pH <7.20 (or glucose <60 mg\/dL or LDH >1000 IU\/L), frank pus (empyema), and large effusion (>half hemithorax). A pleural effusion <10 mm on decubitus X-ray is a FREE, small effusion that is too thin to drain safely \u2014 it does NOT require chest tube insertion. This is actually a contraindication\/non-indication for drainage. The other three are all indications.'\n },\n {\n id:12,\n stem:'A patient underwent hip replacement surgery. On the fourth post-operative day, he had dyspnoea, pleuritic pain and haemoptysis. Most likely diagnosis is:',\n correct:'Pulmonary embolism',\n options:['Pulmonary embolism','Pneumonia','Pulmonary oedema','Pericarditis'],\n exp:'The classic triad of pulmonary embolism \u2014 dyspnoea, pleuritic chest pain, and haemoptysis \u2014 appearing on day 4 post-major orthopaedic surgery (hip replacement) is textbook pulmonary thromboembolism. Hip and knee replacement surgery carries the highest risk of DVT\/PE of any elective surgery due to venous stasis, endothelial injury, and hypercoagulability (Virchow\\'s triad). Haemoptysis results from pulmonary infarction. Pneumonia would typically present with fever and cough. Pericarditis causes positional, non-pleuritic pain. Pulmonary oedema is bilateral and not associated with haemoptysis.'\n },\n {\n id:13,\n stem:'A 55-year-old male with COPD rushed to emergency with increasing shortness of breath, fever, and productive cough. ABG shows pH 7.3, PaCO\u2082 68 mmHg, HCO\u2083 28 mmol\/L, and PaO\u2082 60 mmHg. How would you interpret this?',\n correct:'Respiratory acidosis, partially compensated',\n options:['Respiratory acidosis, uncompensated','Respiratory alkalosis, uncompensated','Respiratory acidosis, partially compensated','Respiratory alkalosis, partially compensated'],\n exp:'Step-by-step ABG analysis: pH 7.3 = acidosis. PaCO\u2082 68 mmHg (elevated) = respiratory acidosis (primary). HCO\u2083 28 mmol\/L (elevated, normal 22\u201326) = metabolic compensation \u2014 the kidneys have retained bicarbonate to buffer the acidosis. However, pH is still low (not normalised at 7.4), confirming PARTIAL compensation. This is chronic COPD with acute exacerbation \u2014 classic partially compensated respiratory acidosis. Uncompensated would show normal HCO\u2083 with low pH. Respiratory alkalosis would require low PaCO\u2082.'\n },\n {\n id:14,\n stem:'A 40-year-old woman presents with haematuria, ecchymoses and menorrhagia of six months duration. What is the most likely diagnosis?',\n correct:'Idiopathic thrombocytopaenic purpura',\n options:['Haemophilia A','Haemophilia B','Idiopathic thrombocytopaenic purpura','Henoch-Sch\u00f6nlein purpura'],\n exp:'ITP (immune thrombocytopaenic purpura) is the most common cause of isolated thrombocytopaenia in otherwise healthy adults, predominantly young women. Features: mucocutaneous bleeding \u2014 petechiae, ecchymoses (bruising), haematuria, and menorrhagia \u2014 all reflecting platelet-type (primary haemostasis) bleeding. Haemophilia A and B occur in males (X-linked), cause deep haematomas\/haemarthroses (coagulation-type bleeding), not mucocutaneous bleeding. HSP (now IgA vasculitis) occurs in children with palpable purpura on lower limbs + arthritis + abdominal pain + glomerulonephritis. ITP fits perfectly.'\n },\n {\n id:15,\n stem:'Which of the following heavy metal poisonings strictly affects the motor nerve?',\n correct:'Lead',\n options:['Cadmium','Mercury','Lead','Thallium'],\n exp:'Lead poisoning (plumbism) causes a characteristic MOTOR neuropathy \u2014 specifically affecting upper limb extensors (wrist drop, lead palsy) with sparing of sensory nerves. The classic \"Saturday night palsy\" in painters using lead paint. Lead accumulates in anterior horn cells and motor neurons. Mercury causes sensorimotor neuropathy plus cerebellar and visual effects. Cadmium causes renal tubular damage (Fanconi syndrome, Itai-Itai disease) and lung toxicity. Thallium causes painful sensorimotor neuropathy + alopecia. Lead is the heavy metal with a purely\/predominantly MOTOR nerve effect.'\n },\n {\n id:16,\n stem:'A patient develops skin necrosis 3 days after being started on warfarin for deep vein thrombosis. What is the most likely cause?',\n correct:'Protein C deficiency',\n options:['Antiphospholipid antibody syndrome','Protein C deficiency','Disseminated intravascular coagulation','Thrombotic thrombocytopaenic purpura'],\n exp:'Warfarin-induced skin necrosis (days 3\u20135 of warfarin therapy) is the hallmark of Protein C (or Protein S) deficiency. Warfarin inhibits synthesis of ALL vitamin K-dependent factors including the anticoagulants Protein C and S. Since Protein C has the shortest half-life (~8 hours), it falls first \u2014 creating a transient hypercoagulable state before factors II, IX, X drop. This paradoxically causes microvascular thrombosis and skin necrosis (especially breasts, thighs, buttocks). Treatment: stop warfarin, give fresh frozen plasma\/Protein C concentrate, start heparin.'\n },\n {\n id:17,\n stem:'A 15-year-old boy is brought to emergency with two days\\' history of headache, vomiting and altered sensorium. His BP is 70 mmHg systolic and he has ecchymoses on his skin. Most likely organism causing his condition is:',\n correct:'Neisseria meningitidis',\n options:['Haemophilus influenzae','Listeria monocytogenes','Neisseria meningitidis','Streptococcus pneumoniae'],\n exp:'Meningococcal meningitis (Neisseria meningitidis) classically presents in adolescents with: meningitis (headache, vomiting, altered sensorium) + septicaemia (hypotension, shock) + PETECHIAE\/ECCHYMOSES (non-blanching purpuric rash from meningococcaemia and DIC). The purpuric\/petechial rash in a shocked young patient with meningitis is pathognomonic of N. meningitidis. H. influenzae meningitis is rare post-immunisation. Listeria is seen in neonates\/elderly. S. pneumoniae meningitis occurs in all ages but the purpuric rash + shock pattern is specific to meningococcal disease.'\n },\n {\n id:18,\n stem:'A child presents with an episode of haematuria soon after a respiratory tract infection. What is the most likely diagnosis?',\n correct:'IgA nephropathy',\n options:['IgA nephropathy','Wegener granulomatosis','Post-streptococcal glomerulonephritis','Churg-Strauss syndrome'],\n exp:'IgA nephropathy (Berger\\'s disease): haematuria appearing within 24\u201372 hours of an URTI (synpharyngitic haematuria) \u2014 the simultaneous onset is the key. This is because the same mucosal immune response that fights the respiratory infection stimulates IgA production, which deposits in the mesangium. Compare with PSGN: haematuria appears 1\u20133 weeks AFTER streptococcal pharyngitis (latent period). The ABSENCE of latent period (haematuria with or immediately after URTI) is the hallmark distinguishing IgA nephropathy from PSGN.'\n },\n {\n id:19,\n stem:'In microalbuminuria, 24-hour urinary albumin is:',\n correct:'30\u2013300 mg',\n options:['8\u201310 mg','30\u2013300 mg','300\u20133000 mg','>3000 mg'],\n exp:'Urinary albumin classification per 24-hour collection: Normal = <30 mg\/24h (or <30 mg\/g creatinine). Microalbuminuria = 30\u2013300 mg\/24h \u2014 the earliest marker of diabetic nephropathy and cardiovascular risk. Macroalbuminuria (clinical proteinuria) = >300 mg\/24h. Nephrotic-range proteinuria = >3500 mg\/24h (or >3.5 g\/24h). Microalbuminuria (30\u2013300 mg\/day) represents early glomerular injury before it can be detected by standard dipstick urinalysis (which detects protein only above ~300 mg\/L). It is a critical intervention point in diabetic and hypertensive nephropathy.'\n },\n {\n id:20,\n stem:'Following are complications of acute renal failure EXCEPT:',\n correct:'Metabolic alkalosis',\n options:['Intravascular volume overload','Hyponatraemia','Hyperkalaemia','Metabolic alkalosis'],\n exp:'Complications of acute kidney injury (AKI): (1) Volume overload \u2014 failure to excrete water\/sodium. (2) Hyponatraemia \u2014 water retention with dilutional hyponatraemia. (3) Hyperkalaemia \u2014 failure to excrete potassium (life-threatening). Also: metabolic ACIDOSIS (accumulation of H\u207a, phosphate, sulphate \u2014 failure to excrete acid load), uraemia, hyperphosphataemia, hypocalcaemia. Metabolic ALKALOSIS is the EXCEPTION \u2014 it does NOT occur in AKI. Alkalosis would require excessive acid loss (vomiting, NG suction, diuretics). AKI invariably causes metabolic acidosis, not alkalosis.'\n },\n {\n id:21,\n stem:'Deficiency of which vitamin causes subacute combined degeneration of spinal cord?',\n correct:'Vitamin B12',\n options:['Vitamin B1','Vitamin B6','Vitamin B2','Vitamin B12'],\n exp:'Subacute combined degeneration (SCD) of the spinal cord is caused by Vitamin B12 (cobalamin) deficiency. It affects: (1) Posterior columns (loss of vibration and proprioception), (2) Lateral\/corticospinal tracts (upper motor neuron signs \u2014 spasticity, extensor plantar), and (3) peripheral nerves. B12 is required for myelin synthesis via methylmalonyl-CoA \u2192 succinyl-CoA pathway. Deficiency causes accumulation of methylmalonic acid, which is directly toxic to myelin. Vitamin B1 deficiency causes Wernicke\\'s encephalopathy and Korsakoff\\'s syndrome. B6 deficiency causes peripheral neuropathy. B2 is riboflavin.'\n },\n {\n id:22,\n stem:'Obstructive lung function tests are seen in which of the following conditions?',\n correct:'Asthma',\n options:['Obesity','Kyphoscoliosis','Pleural effusion','Asthma'],\n exp:'Obstructive pattern (FEV\u2081\/FVC <0.70, reduced FEV\u2081, normal\/increased TLC): asthma, COPD, bronchiectasis, cystic fibrosis. Restrictive pattern (reduced FVC, reduced TLC, normal\/increased FEV\u2081\/FVC): obesity (elevated diaphragm, reduced chest excursion), kyphoscoliosis (thoracic cage deformity reducing lung expansion), and pleural effusion (external compression reducing lung volume). All three \u2014 obesity, kyphoscoliosis, and pleural effusion \u2014 cause RESTRICTIVE patterns. Only ASTHMA produces an obstructive pattern.'\n },\n {\n id:23,\n stem:'In which of the following conditions is there an INCREASE in lung diffusion capacity?',\n correct:'Alveolar haemorrhage',\n options:['Emphysema','Idiopathic pulmonary fibrosis','Alveolar haemorrhage','Pulmonary oedema'],\n exp:'Diffusing capacity (DLCO\/TLCO) is INCREASED in alveolar haemorrhage. Free haemoglobin in the alveoli avidly binds carbon monoxide (the test gas), artificially elevating the DLCO measurement. This is the classical cause of increased DLCO and is clinically useful \u2014 an unexplained high DLCO in a patient with haemoptysis\/anaemia suggests pulmonary haemorrhage. Other causes of increased DLCO: polycythaemia, high altitude, left-to-right shunts, exercise. DLCO is DECREASED in emphysema (destroyed alveoli), IPF (fibrosis), and pulmonary oedema (interstitial fluid barrier).'\n },\n {\n id:24,\n stem:'Which one of the following statements is correct?',\n correct:'Omalizumab is a blocking antibody that neutralises circulating IgE',\n options:['Omalizumab is an antileukotriene','Omalizumab is a blocking antibody that neutralises circulating IgE','Omalizumab is a newer long-acting anticholinergic agent','Omalizumab is a once-daily long-acting beta-2 agonist'],\n exp:'Omalizumab (Xolair) is a recombinant humanised monoclonal anti-IgE antibody. It binds free circulating IgE, preventing IgE from binding to mast cell\/basophil Fc\u03b5RI receptors, thereby blocking the allergic cascade. It is approved for moderate-to-severe allergic asthma and chronic urticaria. Anticoagulant therapy, not omalizumab. Antileukotrienes = montelukast\/zafirlukast. Long-acting anticholinergics = tiotropium. Long-acting beta-2 agonists = salmeterol\/formoterol. Omalizumab is specifically an anti-IgE biologic.'\n },\n {\n id:25,\n stem:'Widespread concave ST segment elevation and PR depression in most leads except aVR favours the diagnosis of:',\n correct:'Pericarditis',\n options:['Acute myocardial infarction','Pericarditis','Digoxin toxicity','Hypertrophic obstructive cardiomyopathy'],\n exp:'The ECG of acute pericarditis has characteristic features: (1) Diffuse\/widespread CONCAVE-UP (\"saddle-shaped\") ST elevation in most leads (I, II, aVF, V2\u2013V6) \u2014 unlike the convex ST elevation of STEMI. (2) ST depression and PR elevation in aVR (reciprocal). (3) PR segment DEPRESSION in most leads (subepicardial atrial inflammation). (4) No reciprocal ST depression (except aVR). AMI shows convex ST elevation with reciprocal changes and Q waves. Digoxin causes scooping ST depression. HOCM causes LVH changes. Diffuse concave ST + PR depression = pericarditis.'\n },\n {\n id:26,\n stem:'A known case of lepromatous leprosy was initiated on treatment. She developed painful erythematous papules with fever and lymphadenopathy. What is the likely reactional state?',\n correct:'Type 2 lepra reaction',\n options:['Type 1 lepra reaction','Type 2 lepra reaction','Lucio\\'s phenomenon','Lupus pernio'],\n exp:'Type 2 lepra reaction (Erythema Nodosum Leprosum, ENL): occurs in lepromatous (LL) and borderline lepromatous (BL) leprosy, typically during or after MDT. Features: crops of painful, tender erythematous papules\/nodules (ENL), fever, lymphadenopathy, orchitis, iridocyclitis \u2014 a systemic immune complex-mediated (Type III hypersensitivity) reaction. Type 1 (reversal) reaction occurs in borderline types (BT, BB, BL) and manifests as oedema and erythema of existing lesions. Lucio\\'s phenomenon = severe vasculitis in diffuse non-nodular lepromatous leprosy. Lupus pernio = sarcoidosis, not leprosy.'\n },\n {\n id:27,\n stem:'Which of the following is NOT true regarding congestive cardiac failure in the elderly?',\n correct:'Loop diuretics are usually well tolerated',\n options:['Incidence rises with age','Common causes include coronary artery disease and hypertension','Diastolic dysfunction is often present','Loop diuretics are usually well tolerated'],\n exp:'CCF in the elderly: (1) Incidence and prevalence rise sharply with age \u2014 true. (2) Most common causes are CAD and hypertension (causing ischaemic cardiomyopathy and hypertensive heart disease) \u2014 true. (3) Diastolic dysfunction (heart failure with preserved ejection fraction, HFpEF) is particularly common in the elderly because of age-related myocardial stiffening \u2014 true. (4) Loop diuretics are NOT well tolerated in the elderly \u2014 they cause dehydration, electrolyte disturbances (hypokalaemia, hyponatraemia), renal impairment, orthostatic hypotension, and falls. Elderly patients require careful, low-dose initiation. Statement (d) is NOT true.'\n },\n {\n id:28,\n stem:'Multidrug-resistant tuberculosis (MDR-TB) is defined as:',\n correct:'At least resistance to Isoniazid and Rifampicin',\n options:['At least resistance to three or more antitubercular drugs','At least resistance to Isoniazid, Streptomycin and Ethambutol','At least resistance to Isoniazid and Rifampicin','At least resistance to Streptomycin and Rifampicin'],\n exp:'MDR-TB is precisely defined as resistance to at least the two most potent first-line anti-TB drugs: ISONIAZID (INH) AND RIFAMPICIN, regardless of resistance to other drugs. This is the WHO\/RNTCP definition. XDR-TB (extensively drug-resistant) = MDR-TB + resistance to any fluoroquinolone + at least one second-line injectable (amikacin, kanamycin, or capreomycin). Resistance to three drugs, or combinations without both INH and RIF, does NOT qualify as MDR-TB by definition.'\n },\n {\n id:29,\n stem:'Aortic stenosis is associated with:',\n correct:'Pulsus parvus et tardus',\n options:['Pulsus paradoxus','Pulsus parvus et tardus','Pulsus alternans bisferiens','Pulsus bigeminus'],\n exp:'Aortic stenosis characteristically produces pulsus parvus et tardus \u2014 a SMALL (parvus) and SLOW-RISING (tardus) pulse. The LV outflow obstruction reduces and delays systolic ejection, resulting in a weak, slowly rising carotid pulse (anacrotic pulse) with a sustained upstroke and plateau (pulsus anacrotic). Pulsus paradoxus = cardiac tamponade, COPD. Bisferiens pulse = combined AS + AR, or HOCM. Pulsus alternans = severe LV failure (alternating strong\/weak beats). Pulsus bigeminus = premature beats creating alternating rhythm. Pulsus parvus et tardus is the classic pulse of severe AS.'\n },\n {\n id:30,\n stem:'Which of the following is associated with hypercoagulable state?\\n1. Protein C deficiency\\n2. Antiphospholipid syndrome\\n3. Homocysteinaemia\\n\\nSelect the correct answer:',\n correct:'1, 2 and 3',\n options:['1 only','2 and 3 only','1 and 3 only','1, 2 and 3'],\n exp:'All three are causes of hypercoagulability (thrombophilia): (1) Protein C deficiency \u2014 loss of the natural anticoagulant that inactivates factors Va and VIIIa; leads to venous thromboembolism and warfarin-induced skin necrosis. (2) Antiphospholipid syndrome \u2014 antibodies against phospholipid-binding proteins cause arterial and venous thrombosis and recurrent pregnancy loss. (3) Homocysteinaemia \u2014 elevated homocysteine damages endothelium, activates coagulation, and inhibits anticoagulant pathways; associated with arterial and venous thrombosis. All three cause hypercoagulable states.'\n },\n {\n id:31,\n stem:'A 20-year-old male walked into OPD with high-grade fever, cough and chest pain for one day. CXR showed consolidation of left upper zone. Respiratory rate 22\/min, pulse 96\/min, BP systolic 120 mmHg, blood urea 18 mg\/dL. What is his CURB-65 score?',\n correct:'1',\n options:['0','1','2','3'],\n exp:'CURB-65 score for CAP severity (1 point each): C = Confusion (new onset disorientation) \u2014 absent (0). U = Urea >7 mmol\/L (>19 mg\/dL) \u2014 urea 18 mg\/dL = <19 mg\/dL = 0 points. R = Respiratory rate \u226530\/min \u2014 RR is 22\/min = 0 points. B = BP systolic <90 or diastolic \u226460 \u2014 BP 120\/? = 0 points. 65 = Age \u226565 years \u2014 patient is 20 years old = 0 points. But wait: Fever + cough + chest pain + consolidation in a 20-year-old = pneumonia. CURB-65 = 0... However the question mentions \"high-grade fever\" which is not scored. Actually re-evaluating: C=0, U=0 (18<19), R=0 (22<30), B=0 (SBP 120), Age=0 (20yr). Score = 0. But the given answer is 1 \u2014 suggesting urea 18 mg\/dL is counted (some versions use >7 mmol\/L = >18.9 mg\/dL; 18 mg\/dL rounds to borderline). Per standard scoring, score = 0; however UPSC answer key gives 1. Score = 1 (per official key, urea threshold borderline).'\n },\n {\n id:32,\n stem:'Which of the following conditions is an autosomal dominant disorder?',\n correct:'Marfan syndrome',\n options:['G-6PD deficiency','Sickle cell disease','Fanconi anaemia','Marfan syndrome'],\n exp:'Inheritance patterns: G-6PD deficiency = X-linked recessive. Sickle cell disease = autosomal recessive. Fanconi anaemia = autosomal recessive (most subtypes). Marfan syndrome = AUTOSOMAL DOMINANT \u2014 caused by mutations in the FBN1 gene (fibrillin-1) on chromosome 15, with virtually complete penetrance but variable expressivity. Other autosomal dominant conditions: HOCM, familial hypercholesterolaemia, achondroplasia, neurofibromatosis, Huntington\\'s disease. Marfan syndrome is the autosomal dominant condition in this list.'\n },\n {\n id:33,\n stem:'Consider the following statements regarding treatment of bronchial asthma:\\n1. Tablets of \u03b22 agonist are better than aerosol therapy\\n2. Inhaled corticosteroids are contraindicated in acute severe asthma\\n3. Oral steroids may be necessary for severe acute asthma\\n4. Anticholinergic bronchodilators are muscarinic antagonists\\n5. Salmeterol and formoterol are highly selective and potent long-acting \u03b22 agonists\\n\\nWhich of the statements given above are true?',\n correct:'3, 4 and 5 only',\n options:['1, 4 and 5 only','3, 4 and 5 only','1, 2 and 5 only','1, 2 and 3 only'],\n exp:'(1) FALSE \u2014 inhaled aerosol therapy delivers drug directly to airways with minimal systemic effects; oral tablets cause more systemic side effects and slower onset. (2) FALSE \u2014 inhaled corticosteroids are NOT contraindicated in acute severe asthma; in fact, high-dose ICS are used acutely, though systemic steroids are more effective in the acute setting. (3) TRUE \u2014 systemic oral\/IV corticosteroids are essential for severe acute asthma. (4) TRUE \u2014 anticholinergics (ipratropium, tiotropium) are muscarinic (M3) receptor antagonists causing bronchodilation. (5) TRUE \u2014 salmeterol and formoterol are selective long-acting \u03b22 agonists. Statements 3, 4, and 5 are correct.'\n },\n {\n id:34,\n stem:'Acute massive pulmonary embolism is manifested by the following EXCEPT:',\n correct:'Pulmonary opacities in chest X-ray',\n options:['Reduced PaO\u2082 and reduced PaCO\u2082','Pulmonary opacities in chest X-ray','S1Q3T3 with RBBB in ECG','Reduced cardiac output and acute right heart failure'],\n exp:'Acute massive PE: (1) Reduced PaO\u2082 (V\/Q mismatch, hypoxia) and reduced PaCO\u2082 (hyperventilation) \u2014 CORRECT. (3) S1Q3T3 (deep S in I, Q wave in III, inverted T in III) with RBBB \u2014 acute right heart strain pattern \u2014 CORRECT. (4) Massive PE causes acute RV failure, reduced cardiac output, and obstructive shock \u2014 CORRECT. Pulmonary opacities on CXR are RARE in acute PE \u2014 the classic CXR in PE is normal or shows oligaemia (Westermark sign), pleural effusion, or Hampton\\'s hump (wedge-shaped pleural-based opacity from infarction, seen in ~20%). Massive PE typically has a normal or near-normal CXR \u2014 opacities are not a typical finding.'\n },\n {\n id:35,\n stem:'The side effects of isoniazid (INH) include the following EXCEPT:',\n correct:'Hyperuricaemia',\n options:['Hepatitis','Rash','Peripheral neuropathy','Hyperuricaemia'],\n exp:'Isoniazid (INH) side effects: hepatitis (dose-related, age-dependent), peripheral neuropathy (pyridoxine-responsive \u2014 INH inhibits pyridoxine metabolism), rash, drug-induced lupus, sideroblastic anaemia, and CNS effects (seizures in overdose). Hyperuricaemia is a well-known side effect of PYRAZINAMIDE (PZA) \u2014 it inhibits uric acid secretion, causing gout. Ethambutol causes optic neuritis. Rifampicin causes orange urine\/secretions, hepatitis, and drug interactions. Hyperuricaemia is NOT caused by INH \u2014 it is caused by pyrazinamide.'\n },\n {\n id:36,\n stem:'A patient of COPD develops a large pneumothorax during a violent bout of coughing. The most appropriate management would be:\\n1. Simple aspiration\\n2. Tube thoracostomy\\n3. Pleurodesis\\n\\nWhich of the above is\/are correct?',\n correct:'2 and 3',\n options:['1 and 2','2 and 3','1 and 3','2 only'],\n exp:'Management of secondary spontaneous pneumothorax (SSP) in COPD: (1) Simple aspiration alone is NOT appropriate for large SSP in COPD \u2014 it has high failure rates in secondary pneumothorax with underlying lung disease. (2) Tube thoracostomy (intercostal drain) is the treatment of choice for large SSP \u2014 required for adequate drainage given poor lung compliance. (3) Pleurodesis (chemical \u2014 via the chest tube) or surgical is recommended to prevent recurrence, as recurrence rates are high in COPD. The combination of tube thoracostomy + pleurodesis (2 and 3) is the appropriate answer for large SSP in COPD.'\n },\n {\n id:37,\n stem:'Carbon dioxide tension (PaCO\u2082) in arterial blood at sea level is:',\n correct:'35\u201345 mm of Hg',\n options:['Less than 25 mm of Hg','25\u201335 mm of Hg','35\u201345 mm of Hg','45\u201355 mm of Hg'],\n exp:'Normal arterial blood gas values at sea level: pH = 7.35\u20137.45. PaO\u2082 = 80\u2013100 mmHg. PaCO\u2082 = 35\u201345 mmHg (mean ~40 mmHg). HCO\u2083 = 22\u201326 mEq\/L. SaO\u2082 \u226595%. PaCO\u2082 below 35 mmHg = hypocapnia (respiratory alkalosis\/hyperventilation). PaCO\u2082 above 45 mmHg = hypercapnia (respiratory acidosis\/hypoventilation). The range 35\u201345 mmHg is the internationally accepted normal PaCO\u2082 range.'\n },\n {\n id:38,\n stem:'The volume of fresh air entering the alveoli each minute is called as:',\n correct:'Alveolar ventilation',\n options:['Dead space','Diffusing capacity','Alveolar ventilation','Ventilation perfusion'],\n exp:'Alveolar ventilation (V\u0307A) = the volume of fresh air reaching the alveoli per minute that participates in gas exchange. V\u0307A = (Tidal Volume \u2212 Dead Space Volume) \u00d7 Respiratory Rate. Dead space = anatomical (conducting airways) + physiological. Diffusing capacity (DLCO) = the rate of gas transfer across the alveolar-capillary membrane. Ventilation-perfusion (V\/Q ratio) compares airflow to blood flow in a lung region. Alveolar ventilation is specifically the volume of fresh gas reaching alveoli per minute for gas exchange.'\n },\n {\n id:39,\n stem:'Exacerbations of bronchial asthma that occur with little or no warning are called:',\n correct:'Brittle asthma',\n options:['Brittle asthma','Acute severe asthma','Poorly controlled asthma','Nocturnal asthma'],\n exp:'Brittle asthma is a rare, severe variant characterised by: Type 1 = chaotic, unpredictable peak flow variability despite maximal therapy (difficult to control). Type 2 = sudden severe attacks occurring with LITTLE OR NO WARNING in a patient who otherwise has good background asthma control. Type 2 brittle asthma is particularly dangerous because patients (and clinicians) are unprepared. These sudden attacks can cause death within minutes. Acute severe asthma is a specific clinical diagnosis with measurable criteria (PEFR <33%, SpO\u2082 <92%). Nocturnal asthma occurs predictably during sleep.'\n },\n {\n id:40,\n stem:'Which of the following constituents of antacid can cause constipation?',\n correct:'Aluminium hydroxide',\n options:['Magnesium hydroxide','Aluminium hydroxide','Calcium carbonate','Sodium bicarbonate'],\n exp:'Antacid side effects: Aluminium hydroxide \u2014 CONSTIPATION (Al\u00b3\u207a ions reduce intestinal motility and form insoluble aluminium faecalith). Magnesium hydroxide \u2014 diarrhoea\/laxative effect (osmotic, Mg\u00b2\u207a draws water into gut). Calcium carbonate \u2014 constipation (similar mechanism to Al) and milk-alkali syndrome with overuse. Sodium bicarbonate \u2014 belching (CO\u2082 generation), alkalosis with overuse. The question asks specifically which constituent causes CONSTIPATION \u2014 aluminium hydroxide is the classic answer (though calcium carbonate also causes constipation, aluminium hydroxide is the most commonly cited and tested). The single best answer is aluminium hydroxide.'\n }\n ];\n\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 const LETTERS=['A','B','C','D'];\n let userAnswers={},answered=0,shuffledOpts={};\n let timerRunning=false,timerRemaining=TIMER_SECS,timerInterval=null,graceInterval=null;\n let quizSubmitted=false;\n\n function fmtTime(s){const m=Math.floor(s\/60),sec=s%60;return String(m).padStart(2,'0')+':'+String(sec).padStart(2,'0');}\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);btn.classList.add('running');\n document.getElementById(NS+'-timer-item').classList.add('active');\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 if(timerRemaining<=300)document.getElementById(NS+'-timer-item').classList.add('warning');\n if(timerRemaining<=0){clearInterval(timerInterval);timerInterval=null;triggerGrace();}\n },1000);\n }\n function stopTimer(){if(timerInterval){clearInterval(timerInterval);timerInterval=null;}timerRunning=false;}\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(){g--;document.getElementById(NS+'-grace-count').textContent=g;if(g<=0){clearInterval(graceInterval);dismissGrace();showScore();}},1000);\n }\n function dismissGrace(){document.getElementById(NS+'-grace').classList.remove('show');if(graceInterval){clearInterval(graceInterval);graceInterval=null;}}\n\n function build(){\n const 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