CMS 2016 Paper I \u2013 Part B (Q41\u2013Q80)<\/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: cms16p1b \u2500\u2500 *\/\n#cms16p1b *,#cms16p1b *::before,#cms16p1b *::after{box-sizing:border-box;margin:0;padding:0}\n\n#cms16p1b{\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\n#cms16p1b .cq-sentinel{height:1px}\n\n#cms16p1b .cq-statusbar{\n 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.cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n\n@media(max-width:480px){\n #cms16p1b .cq-header h1{font-size:1.15rem}\n #cms16p1b .cq-qtext{font-size:0.88rem}\n #cms16p1b .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms16p1b\">\n\n <div class=\"cq-sentinel\" id=\"cms16p1b-sentinel\"><\/div>\n\n <div class=\"cq-statusbar\" id=\"cms16p1b-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms16p1b-timer-item\">\u23f1 <strong id=\"cms16p1b-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms16p1b-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms16p1b-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms16p1b-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms16p1b-sn\">0<\/strong> \/ <strong id=\"cms16p1b-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms16p1b-fill\"><\/div><\/div>\n <\/div>\n\n <div class=\"cq-grace\" id=\"cms16p1b-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=\"cms16p1b-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms16p1b-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2016<br>Paper I \u00b7 Part B<\/h1>\n <p>General Medicine \u00b7 Surgery \u00b7 Paediatrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 41 \u2013 80<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms16p1b-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-body\">\n <div id=\"cms16p1b-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms16p1b-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms16p1b-score\">\n <div class=\"cq-score-ring\" id=\"cms16p1b-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms16p1b-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=\"cms16p1b-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms16p1b-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms16p1b-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms16p1b-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms16p1b-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms16p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms16p1b', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60;\n const GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:41,\n stem:'Which one of the following gases is used for sterilization of pharmaceutical products?',\n correct:'Ethylene oxide',\n options:['Ethylene oxide','Ammonia','Halothane','Nitrous oxide'],\n exp:'Ethylene oxide (EO) is a highly penetrating alkylating gas used for sterilization of heat- and moisture-sensitive medical devices and pharmaceutical products (e.g., catheters, implants). It is effective at low temperatures (~50\u00b0C). It is, however, toxic and carcinogenic and requires long aeration cycles to remove residues. Ammonia is a disinfectant, not a sterilant. Halothane and nitrous oxide are anaesthetic gases.'\n },\n {\n id:42,\n stem:'The following statements about peptic ulcer are true EXCEPT:',\n correct:'Duodenal ulcer invariably changes into malignant',\n options:['Eradication of H. pylori is a part of medical management','Duodenal ulcer invariably changes into malignant','Complications are indication for surgery','Zollinger-Ellison syndrome is associated with intractable peptic ulceration'],\n exp:'Duodenal ulcers virtually NEVER undergo malignant transformation \u2014 this is a key distinguishing feature from gastric ulcers (which have a small but real malignant potential). H. pylori eradication is the cornerstone of medical management. Complications (perforation, haemorrhage, obstruction) are surgical indications. Zollinger-Ellison syndrome (gastrinoma) causes hypersecretion and intractable, multiple, atypical peptic ulcers.'\n },\n {\n id:43,\n stem:'In a patient with a lacerated foot injury who is not actively immunised against tetanus, which one of the following is indicated for tetanus prophylaxis?',\n correct:'Tetanus immunoglobulin',\n options:['Penicillin','Tetanus toxoid','Tetanus immunoglobulin','Triple vaccine'],\n exp:'A non-immunised patient with a tetanus-prone wound (lacerated, contaminated) requires immediate passive immunisation with human tetanus immunoglobulin (HTIG, 250\u2013500 IU IM) to provide immediate protection. Tetanus toxoid (active immunisation) should also be given but at a different site, starting a primary immunisation course. Penicillin is an adjunct, not prophylaxis. Triple vaccine (DPT) is for children in the primary immunisation schedule.'\n },\n {\n id:44,\n stem:'Which one of the following neoplasms can lead to \\'water intoxication\\'?',\n correct:'Oat cell carcinoma of bronchus',\n options:['Oat cell carcinoma of bronchus','Hepatocarcinoma','Testicular tumours','Rhabdomyosarcoma'],\n exp:'Water intoxication results from SIADH (syndrome of inappropriate ADH secretion), causing dilutional hyponatraemia. Oat cell (small cell) carcinoma of the bronchus is the classic cause of paraneoplastic SIADH \u2014 the tumour cells ectopically secrete ADH (vasopressin), leading to excessive water retention. This is one of the most common paraneoplastic manifestations of SCLC. The other options do not typically secrete ADH.'\n },\n {\n id:45,\n stem:'The Swan-Ganz catheter is used to measure:',\n correct:'Pulmonary wedge pressure',\n options:['Peripheral arterial blood pressure','Portal venous pressure','Pulmonary wedge pressure','Intracranial pressure monitoring'],\n exp:'The Swan-Ganz (balloon-tipped pulmonary artery) catheter is floated from a central vein through the right heart into the pulmonary artery. When the balloon is inflated it wedges distally, occluding forward flow, and the distal lumen measures pulmonary capillary wedge pressure (PCWP) \u2014 an indirect measure of left atrial pressure and left ventricular end-diastolic pressure. It also measures pulmonary artery pressure, CVP, and cardiac output (thermodilution).'\n },\n {\n id:46,\n stem:'Delirium is usually seen in:',\n correct:'Atropine toxicity',\n options:['Acetaminophen toxicity','Atropine toxicity','Kerosene poisoning','Digitalis toxicity'],\n exp:'Atropine (anticholinergic) toxicity causes the classic antimuscarinic syndrome: \"blind as a bat, dry as a bone, red as a beet, hot as a hare, mad as a hatter\" \u2014 the \"mad as a hatter\" component refers to agitated delirium and hallucinations from central anticholinergic effects. Paracetamol toxicity primarily causes hepatotoxicity. Kerosene causes chemical pneumonitis. Digitalis toxicity causes cardiac arrhythmias, visual disturbances, and nausea \u2014 not typically delirium.'\n },\n {\n id:47,\n stem:'The following statements regarding Hodgkin\\'s disease are true EXCEPT:',\n correct:'Stage III disease is confined to one side of the diaphragm',\n options:['It usually presents as painless lymphadenopathy','The Pel-Ebstein fever is a characteristic feature','Stage III disease is confined to one side of the diaphragm','Reed-Sternberg cells are a diagnostic feature'],\n exp:'Ann Arbor staging: Stage I = single lymph node region; Stage II = two or more regions on the SAME side of the diaphragm; Stage III = lymph node regions on BOTH sides of the diaphragm (spleen counts as lymphoid tissue); Stage IV = diffuse extranodal involvement. Stage III is therefore on BOTH sides \u2014 the statement \"confined to one side\" describes Stage I\/II, not Stage III. Reed-Sternberg cells (owl-eye nuclei) are diagnostic; Pel-Ebstein (cyclical) fever is characteristic.'\n },\n {\n id:48,\n stem:'Following are causes of bleeding EXCEPT:',\n correct:'Heparin-induced thrombocytopenia',\n options:['Heparin-induced thrombocytopenia','Dengue fever','ITP','Aspirin'],\n exp:'Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication of heparin where antibodies against PF4-heparin complexes activate platelets. The predominant complication is THROMBOSIS (venous and arterial), not bleeding \u2014 despite the low platelet count. This is why it is sometimes called \"the clotting disorder.\" Dengue, ITP, and aspirin (platelet dysfunction) all cause bleeding tendencies. HIT is paradoxically prothrombotic.'\n },\n {\n id:49,\n stem:'The combination of cyanosis with clubbing can be seen in the following conditions EXCEPT:',\n correct:'Chronic bronchitis',\n options:['Eisenmenger syndrome','Lung abscess','Chronic bronchitis','Pulmonary AV fistula'],\n exp:'Cyanosis with clubbing: Eisenmenger syndrome (right-to-left shunt with pulmonary hypertension), lung abscess (suppurative lung disease causing local hypoxia + chronic infection), and pulmonary AV fistula (right-to-left shunting through the fistula) all cause both. Chronic bronchitis (COPD) causes cyanosis (\"blue bloater\") but typically does NOT cause clubbing \u2014 clubbing in respiratory disease is mainly associated with lung cancer, suppurative lung disease, and fibrosing alveolitis. Clubbing in COPD alone is absent or very rare.'\n },\n {\n id:50,\n stem:'Diagnosis and grading of multi-organ failure is based on all the following criteria EXCEPT:',\n correct:'Serum albumin',\n options:['Serum bilirubin','Serum albumin','Serum creatinine','PaO\u2082\/FiO\u2082 ratio'],\n exp:'Multi-organ dysfunction\/failure scoring systems (SOFA, Marshall MOF score) use organ-specific markers: PaO\u2082\/FiO\u2082 ratio (respiratory), serum creatinine\/urine output (renal), serum bilirubin (hepatic), platelet count (coagulation), GCS (neurological), and vasopressor requirement (cardiovascular). Serum albumin reflects nutritional status and chronic synthetic function but is NOT used as an MOF grading criterion \u2014 it is too slow to change and non-specific for acute organ failure.'\n },\n {\n id:51,\n stem:'A 16-year-old boy presents with exertional dyspnoea, haemoptysis and occasionally paroxysmal nocturnal dyspnoea. There was history of joint pains five years back. The most probable diagnosis is:',\n correct:'Mitral stenosis',\n options:['Aortic regurgitation','Mitral stenosis','Tricuspid stenosis','Aortic stenosis'],\n exp:'The triad of exertional dyspnoea, haemoptysis, and PND in a young patient with a history of rheumatic joint pains (rheumatic fever) 5 years earlier is the classic presentation of rheumatic mitral stenosis. Mitral stenosis leads to left atrial hypertension \u2192 pulmonary venous hypertension \u2192 pulmonary oedema (PND) and pulmonary hypertension (haemoptysis). Rheumatic fever predominantly damages the mitral valve (70% of cases).'\n },\n {\n id:52,\n stem:'The adrenocortical insufficiency may result in:\\n1. Hyponatraemia\\n2. Hypokalaemia\\n3. Acidosis\\n4. Hyperglycaemia\\n\\nWhich of the statements given above is\/are correct?',\n correct:'1 and 3',\n options:['1 only','1 and 3','2 and 4 only','2, 3 and 4'],\n exp:'Adrenocortical insufficiency (Addison\\'s disease): loss of aldosterone \u2192 sodium wasting (hyponatraemia, 1 = correct) and potassium retention (HYPERKALAEMIA, not hypokalaemia \u2014 statement 2 is WRONG). Loss of cortisol \u2192 impaired gluconeogenesis \u2192 hypoglycaemia (not hyperglycaemia \u2014 statement 4 is WRONG). Hyperkalaemia and decreased renal acid excretion cause metabolic acidosis (3 = correct). So hyponatraemia (1) and acidosis (3) are correct.'\n },\n {\n id:53,\n stem:'Life-threatening pneumococcal infection is a complication seen in:\\n1. Idiopathic thrombocytopenic purpura\\n2. Sickle cell disease\\n3. Thalassaemia minor\\n4. Nephrotic syndrome\\n\\nWhich of the statements given above is\/are correct?',\n correct:'2 and 4 only',\n options:['1 only','1 and 3','2 and 4 only','2, 3 and 4'],\n exp:'Overwhelming pneumococcal infection (OPSI) occurs in functional\/anatomical asplenia and hyposplenic states. Sickle cell disease (2): splenic autoinfarction by 5 years causes functional asplenia \u2014 pneumococcal sepsis is a major cause of death. Nephrotic syndrome (4): loss of opsonins (immunoglobulins, properdin) in urine plus corticosteroid therapy creates susceptibility to encapsulated bacteria including pneumococcus. ITP affects platelets, not pneumococcal immunity. Thalassaemia minor has normal splenic function.'\n },\n {\n id:54,\n stem:'The following are true regarding Zollinger-Ellison syndrome EXCEPT:',\n correct:'It occurs in association with MEN-2 syndrome',\n options:['Common age group is 30 to 50 years','Gastrin level is usually high','Diarrhoea can be an associated feature','It occurs in association with MEN-2 syndrome'],\n exp:'Zollinger-Ellison syndrome (gastrinoma) occurs in 20\u201325% of cases as part of MEN-1 (multiple endocrine neoplasia type 1 = 3Ps: pituitary, parathyroid, pancreas). It is NOT associated with MEN-2 (which comprises medullary thyroid cancer, phaeochromocytoma, and hyperparathyroidism). Presentation: age 30\u201350, markedly elevated fasting gastrin, intractable peptic ulcers, secretory diarrhoea (acid inactivates pancreatic enzymes). Statement d is FALSE.'\n },\n {\n id:55,\n stem:'The following may be seen in a patient with chronic liver disease EXCEPT:',\n correct:'Decreased factor VIII',\n options:['Prolonged PT','Prolonged PTT','Thrombocytopenia','Decreased factor VIII'],\n exp:'Chronic liver disease impairs synthesis of clotting factors II, V, VII, IX, X (all made in liver) \u2192 prolonged PT and PTT. Thrombocytopenia occurs due to hypersplenism and reduced thrombopoietin. Factor VIII is unique \u2014 it is produced by vascular endothelial cells (not exclusively hepatocytes) and is also an acute phase reactant; it is therefore ELEVATED or normal in CLD. Decreased factor VIII is NOT expected in CLD; it is seen in haemophilia A or von Willebrand disease.'\n },\n {\n id:56,\n stem:'Pseudomembranous colitis is caused by which of the following organisms?',\n correct:'Clostridium difficile',\n options:['Shigella','Clostridium difficile','E. coli','Clostridium perfringens'],\n exp:'Pseudomembranous colitis (PMC) is caused by Clostridium difficile, a gram-positive spore-forming anaerobe. Following antibiotic use (classically clindamycin, broad-spectrum penicillins, cephalosporins), normal colonic flora are disrupted, allowing C. difficile to overgrow and produce toxins A (enterotoxin) and B (cytotoxin), causing colitis with the formation of yellowish-white pseudomembranous plaques on the mucosa. Diagnosed by stool toxin assay or PCR.'\n },\n {\n id:57,\n stem:'A patient presents with breathlessness and occasional dry cough. Bilateral basal crepitations are found on examination. Pulmonary function tests reveal a decrease in total lung capacity and vital capacity, with normal FEV\u2081\/FVC ratio. He is most likely suffering from:',\n correct:'Idiopathic pulmonary fibrosis',\n options:['Chronic bronchitis','Idiopathic pulmonary fibrosis','Cystic fibrosis','Allergic bronchopulmonary aspergillosis'],\n exp:'The classic restrictive pattern \u2014 reduced TLC and VC with NORMAL FEV\u2081\/FVC ratio (both volumes reduced proportionally) \u2014 combined with bilateral basal fine crepitations (\"velcro\" crepitations) and dry cough in an adult points to interstitial lung disease, specifically idiopathic pulmonary fibrosis (IPF). COPD\/chronic bronchitis causes obstructive pattern (reduced FEV\u2081\/FVC). Cystic fibrosis and ABPA cause obstructive\/mixed patterns, typically in younger patients.'\n },\n {\n id:58,\n stem:'A 45-year-old hypertensive male presented with 3-hour history of sudden onset severe headache associated with nausea and vomiting. On clinical examination, the patient had right-sided ptosis and neck stiffness. Rest of the neurological examination was normal. The most likely diagnosis is:',\n correct:'Aneurysmal subarachnoid bleed',\n options:['Hypertensive brain damage','Migraine','Aneurysmal subarachnoid bleed','Acute pyogenic meningitis'],\n exp:'The combination of sudden-onset \"thunderclap\" headache (worst headache of life), meningismus (neck stiffness), and right-sided ptosis (indicating third nerve palsy from posterior communicating artery aneurysm compressing CN III) is pathognomonic of aneurysmal subarachnoid haemorrhage. The posterior communicating artery aneurysm causes a \"surgical\" third nerve palsy with pupil involvement. This is a neurosurgical emergency. CT head non-contrast \u2192 LP if CT negative.'\n },\n {\n id:59,\n stem:'Which one of the following is NOT a treatment of hepatic encephalopathy?',\n correct:'TIPS',\n options:['Lactulose','Rifaximin','TIPS','Electrolyte supplementation'],\n exp:'Treatments for hepatic encephalopathy: lactulose (acidifies colon, traps NH\u2084\u207a, promotes bowel clearance), rifaximin (non-absorbable antibiotic reduces ammoniagenic gut bacteria), electrolyte correction (especially potassium \u2014 hypokalaemia worsens HE), and dietary protein adjustment. TIPS (transjugular intrahepatic portosystemic shunt) is used to reduce portal hypertension and treat variceal bleeding\/refractory ascites, but it actually WORSENS hepatic encephalopathy by diverting portal blood (rich in ammonia) away from the liver.'\n },\n {\n id:60,\n stem:'Features of intravascular haemolysis are the following EXCEPT:',\n correct:'Increased serum haptoglobin',\n options:['Increased LDH','Haemoglobinuria','Increased serum indirect bilirubin','Increased serum haptoglobin'],\n exp:'In intravascular haemolysis, RBCs lyse within vessels releasing haemoglobin directly into plasma. Features: raised LDH (released from RBCs), haemoglobinaemia \u2192 haemoglobinuria (dark urine), raised indirect bilirubin (from haem catabolism), haemosiderinuria, and DECREASED haptoglobin (free Hb binds and saturates haptoglobin, which is then cleared by the liver). Increased serum haptoglobin is the OPPOSITE of what occurs \u2014 it is a feature of acute phase reactions, not haemolysis.'\n },\n {\n id:61,\n stem:'Consider the following statements:\\n1. Hypertrophic cardiomyopathy can lead to sudden cardiac death.\\n2. Dressler\\'s syndrome is an early complication of acute myocardial infarction.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'1 only',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'HCM (hypertrophic cardiomyopathy) is the most common cause of sudden cardiac death in young athletes, due to dynamic LVOT obstruction and life-threatening ventricular arrhythmias \u2014 statement 1 is CORRECT. Dressler\\'s syndrome is a LATE complication of AMI (2\u201310 weeks post-MI), not early. Early complications (first days) include arrhythmias, mechanical complications (VSD, free wall rupture, papillary muscle dysfunction), and cardiogenic shock \u2014 statement 2 is WRONG. Only statement 1 is correct.'\n },\n {\n id:62,\n stem:'The common sites of hypertensive bleed are the following EXCEPT:',\n correct:'Frontal cortex',\n options:['Basal ganglion','Pons','Cerebellum','Frontal cortex'],\n exp:'Hypertensive intracerebral haemorrhage occurs in penetrating arteries damaged by chronic hypertension (Charcot-Bouchard microaneurysms). Classic sites in order of frequency: putamen\/basal ganglia (most common, ~50%), thalamus, pons, cerebellum, and subcortical white matter. The FRONTAL CORTEX is not a typical site for hypertensive bleeds \u2014 lobar haemorrhages in the cortex are more commonly associated with cerebral amyloid angiopathy (in elderly), AVM, or coagulopathy.'\n },\n {\n id:63,\n stem:'Hypoglycaemia as an adverse side effect is most commonly seen during treatment with:',\n correct:'Sulfonylureas',\n options:['Dipeptidyl peptidase-IV inhibitors','Metformin','\u03b1-glucosidase inhibitors','Sulfonylureas'],\n exp:'Sulfonylureas (e.g., glibenclamide, glipizide) stimulate insulin secretion from pancreatic beta cells in a glucose-independent manner, meaning they cause insulin release even when blood glucose is low. This is why hypoglycaemia is their most important adverse effect, especially in the elderly and with missed meals. Metformin, DPP-4 inhibitors, and \u03b1-glucosidase inhibitors do not cause hypoglycaemia when used as monotherapy because their mechanisms are glucose-dependent or act outside the pancreas.'\n },\n {\n id:64,\n stem:'Which of the following statements is\/are correct regarding Gilbert\\'s syndrome?\\n1. Inheritance of the disease is autosomal dominant.\\n2. Jaundice becomes very severe with time.\\n3. Fasting leads to increased bilirubin levels.\\n\\nSelect the correct answer:',\n correct:'1 and 3 only',\n options:['1 and 3 only','1 only','2 and 3 only','1, 2 and 3'],\n exp:'Gilbert\\'s syndrome: autosomal dominant (or recessive, depending on the mutation; classically described as dominant \u2014 statement 1 correct) reduction in UGT1A1 enzyme activity causing unconjugated hyperbilirubinaemia. Jaundice is mild and fluctuating \u2014 it does NOT become severe with time (statement 2 is WRONG). Fasting, stress, intercurrent illness, and exercise all precipitate jaundice by increasing bilirubin load and reducing hepatic uptake (statement 3 correct). Benign condition with normal liver function and life expectancy.'\n },\n {\n id:65,\n stem:'The following are causes of secondary hypertension EXCEPT:',\n correct:'Carcinoid syndrome',\n options:['Conn\\'s syndrome','Carcinoid syndrome','Cushing\\'s syndrome','Phaeochromocytoma'],\n exp:'Classic causes of secondary hypertension include: Conn\\'s syndrome (primary hyperaldosteronism \u2014 sodium\/water retention), Cushing\\'s syndrome (cortisol excess \u2014 mineralocorticoid effects), phaeochromocytoma (catecholamine excess \u2014 episodic or sustained hypertension). Carcinoid syndrome characteristically causes flushing, diarrhoea, and bronchoconstriction from serotonin and other mediators; it does NOT cause sustained hypertension and is not a recognised cause of secondary hypertension.'\n },\n {\n id:66,\n stem:'Tetralogy of Fallot is characterised by the following EXCEPT:',\n correct:'Pulmonary hypertension',\n options:['Ventricular septal defect','Overriding aorta','Pulmonary hypertension','Right ventricular hypertrophy'],\n exp:'Tetralogy of Fallot comprises four defects: (1) VSD, (2) overriding aorta, (3) pulmonary STENOSIS (infundibular \u00b1 valvular \u2014 obstruction, not hypertension), (4) right ventricular hypertrophy (secondary to outflow obstruction). Pulmonary hypertension is NOT a feature \u2014 in fact, the pulmonary stenosis reduces pulmonary blood flow and protects the pulmonary vasculature. Pulmonary hypertension with VSD (without stenosis) leads to Eisenmenger syndrome \u2014 a different entity entirely.'\n },\n {\n id:67,\n stem:'Regarding high altitude pulmonary oedema, the following statements are true EXCEPT:',\n correct:'It does not occur in a physically fit person',\n options:['It can be caused by physical exertion at high altitude','It does not occur in a physically fit person','It occurs due to leak in the alveolar capillary membrane','Portable hyperbaric chamber may be used for treatment instead of descent to a lower altitude'],\n exp:'High altitude pulmonary oedema (HAPE) occurs due to non-uniform hypoxic pulmonary vasoconstriction causing high pulmonary microvascular pressure and increased permeability of the alveolar-capillary membrane. It CAN AND DOES occur in physically fit, acclimatised mountaineers and athletes \u2014 physical fitness is NOT protective. Exertion at altitude worsens it. Treatment: immediate descent, supplemental O\u2082, portable hyperbaric chamber (Gamow bag), and nifedipine. The statement \"does not occur in physically fit person\" is FALSE.'\n },\n {\n id:68,\n stem:'Complications of myocardial infarction are all EXCEPT:',\n correct:'Dissection of aorta',\n options:['Systemic embolisation','Rupture of interventricular septum','Dissection of aorta','Ventricular fibrillation'],\n exp:'Recognised complications of MI: arrhythmias (VF, VT), mechanical complications (ventricular free wall rupture, VSD\/interventricular septal rupture, papillary muscle rupture causing acute MR), cardiogenic shock, pericarditis, Dressler\\'s syndrome, LV aneurysm, and systemic embolisation (mural thrombus). Aortic dissection is a separate condition caused by medial degeneration\/hypertension \u2014 it is NOT a complication of MI. It may mimic MI (Type A dissection can obstruct coronary ostia) but is not caused by it.'\n },\n {\n id:69,\n stem:'Philadelphia chromosome can be detected by which of the following techniques?\\n1. FISH\\n2. PCR\\n3. Cytogenetics\\n\\nSelect the correct answer:',\n correct:'1, 2 and 3',\n options:['1 only','1 and 3 only','2 and 3 only','1, 2 and 3'],\n exp:'The Philadelphia chromosome [t(9;22)(q34;q11)] creates the BCR-ABL fusion gene. All three techniques detect it: (1) FISH (fluorescence in situ hybridisation) \u2014 detects BCR-ABL fusion at chromosomal level, sensitive, used on interphase cells. (2) PCR (RT-PCR) \u2014 detects BCR-ABL mRNA\/DNA, most sensitive for minimal residual disease monitoring. (3) Conventional cytogenetics (karyotyping) \u2014 the original method, detects the translocation in dividing cells. All three are valid and complementary.'\n },\n {\n id:70,\n stem:'The following statements regarding coeliac disease are correct EXCEPT:',\n correct:'Absence of gastrointestinal symptoms rules out coeliac disease',\n options:['Absence of gastrointestinal symptoms rules out coeliac disease','Malabsorption syndrome may be a presenting feature','Duodenal biopsy shows increased intraepithelial lymphocytes','Steroid therapy may induce remission'],\n exp:'Coeliac disease (gluten-sensitive enteropathy) has a wide clinical spectrum. \"Silent\" or \"atypical\" coeliac disease is common \u2014 patients may present only with anaemia, osteoporosis, infertility, neurological symptoms, or dermatitis herpetiformis WITHOUT GI symptoms. Absence of GI symptoms does NOT rule it out \u2014 statement (a) is FALSE. Classic malabsorption, villous atrophy with increased IELs on duodenal biopsy, and response to steroids in refractory cases are all well-documented.'\n },\n {\n id:71,\n stem:'A 6-year-old child presents with oliguria, haematuria, puffiness of face, convulsions, B.P. of 200\/100 mm Hg and blood urea 80 mg%. What is the most likely diagnosis?',\n correct:'Acute glomerulonephritis with hypertensive encephalopathy',\n options:['Haemolytic uraemic syndrome','Nephrotic syndrome','Acute glomerulonephritis with hypertensive encephalopathy','Obstructive uropathy'],\n exp:'The combination of oliguria, haematuria (nephritic urine), facial oedema, severe hypertension, and convulsions in a school-age child following throat\/skin infection is classic post-streptococcal acute glomerulonephritis (PSGN) complicated by hypertensive encephalopathy. Nephrotic syndrome has heavy proteinuria, oedema but normotension. HUS features microangiopathic haemolytic anaemia + thrombocytopenia. The markedly elevated BP with convulsions confirms hypertensive encephalopathy as the complication here.'\n },\n {\n id:72,\n stem:'A 3-year-old child is brought for sudden inability to walk following fever of two days duration. Sensorium is normal. Both lower limbs are hypotonic, right more than left. Plantar reflex is equivocal. Deep tendon reflexes are not elicitable in the lower limbs. The most probable diagnosis is:',\n correct:'Acute poliomyelitis',\n options:['Acute poliomyelitis','Acute rheumatic fever','Acute transverse myelitis','Acute infective polyneuritis'],\n exp:'Acute poliomyelitis: fever followed by acute flaccid paralysis (AFP) \u2014 lower motor neuron pattern with hypotonia, areflexia, and asymmetric weakness (right > left). Sensorium is normal (pure motor involvement of anterior horn cells). The asymmetric, lower limb predominant, post-febrile AFP with preserved sensation and absent DTRs is the hallmark of acute paralytic polio. Guillain-Barr\u00e9 (infective polyneuritis) is symmetric ascending paralysis typically without fever at onset. Transverse myelitis gives a sensory level.'\n },\n {\n id:73,\n stem:'X-ray of the skull in an infant shows periventricular calcification in:',\n correct:'Cytomegalovirus infection',\n options:['Tuberculous meningitis','Cytomegalovirus infection','Japanese B encephalitis','Congenital syphilis'],\n exp:'Periventricular (subependymal) calcification on skull X-ray or CT is the hallmark of congenital cytomegalovirus (CMV) infection \u2014 the virus preferentially infects periventricular germinal matrix cells. Toxoplasmosis causes scattered intracerebral calcifications (not specifically periventricular). Congenital rubella causes periventricular leukomalacia but not discrete calcifications. TB meningitis causes basal ganglia calcification. Congenital syphilis shows bone changes, not periventricular calcification.'\n },\n {\n id:74,\n stem:'A 4-year-old boy with sickle cell disease presents with pain and swelling of bones, marked in small bones of hand and feet, severe abdominal pain, and necrosis of femoral head and upper tibia on investigation. Symptoms resolved after one week. The possible explanation is:',\n correct:'Vaso-occlusive crisis',\n options:['Aplastic crisis','Sequestration crisis','Vaso-occlusive crisis','Haemolytic crisis'],\n exp:'Vaso-occlusive (painful) crisis in sickle cell disease is caused by sickling of RBCs in small vessels causing ischaemia and infarction. Features: dactylitis (painful swelling of small bones of hands and feet \u2014 hand-foot syndrome), bone pain (avascular necrosis of femoral head), abdominal pain (mesenteric ischaemia), and resolution within days to a week. Aplastic crisis = sudden drop in Hb (parvovirus B19). Sequestration crisis = sudden splenic trapping of RBCs. Haemolytic crisis = accelerated haemolysis.'\n },\n {\n id:75,\n stem:'Match List I (Genetic disorder) with List II (Genotype):\\nA. Down Syndrome\\nB. Turner Syndrome\\nC. Noonan Syndrome\\nD. Cri-du-chat Syndrome\\n\\n1. 47, XY, +21\\n2. 46, XY\\n3. 46, XX, 5p\u2212\\n4. 45, XO\\n5. 47, XXY',\n correct:'A-1, B-4, C-2, D-3',\n options:['A-1, B-4, C-2, D-3','A-1, B-4, C-5, D-3','A-3, B-1, C-2, D-4','A-3, B-1, C-5, D-4'],\n exp:'Down syndrome = trisomy 21, karyotype 47, XY, +21 (A=1). Turner syndrome = 45, XO \u2014 monosomy X (B=4). Noonan syndrome is a RASopathy (autosomal dominant, PTPN11 mutation) \u2014 phenotypically resembles Turner but has a NORMAL karyotype: 46, XY in males (C=2). Cri-du-chat syndrome = deletion of short arm of chromosome 5 (5p\u2212), karyotype 46, XX, 5p\u2212 (D=3). Klinefelter = 47, XXY (option 5, not used here).'\n },\n {\n id:76,\n stem:'With reference to Paediatrics, the following are true of breath-holding spells EXCEPT:',\n correct:'They occur during inspiration',\n options:['They occur during inspiration','They are involuntary','Cyanosis may not occur','Bradycardia may occur'],\n exp:'Breath-holding spells occur in infants\/toddlers triggered by fright, frustration, or pain. The child cries, then holds the breath in EXPIRATION (not inspiration) until cyanosis or pallor occurs, sometimes followed by brief loss of consciousness. They are involuntary reflex events (not intentional breath-holding). Cyanosis may not occur in pallid spells (vagal). Bradycardia (vagal syncope) can occur, especially in pallid spells. \"During inspiration\" is INCORRECT \u2014 breath is held at end-expiration.'\n },\n {\n id:77,\n stem:'Match List I (Drugs for epilepsy) with List II (Dose-dependent side effects):\\nA. Sodium valproate\\nB. Carbamazepine\\nC. Phenytoin\\nD. Phenobarbitone\\n\\n1. Raised liver enzymes\\n2. Hirsutism\\n3. Hyperactivity\\n4. Drowsiness',\n correct:'A-1, B-4, C-2, D-3',\n options:['A-1, B-4, C-2, D-3','A-1, B-4, C-3, D-2','A-4, B-1, C-2, D-3','A-4, B-1, C-3, D-2'],\n exp:'Sodium valproate = raised liver enzymes \/ hepatotoxicity (A=1). Carbamazepine = dose-related drowsiness, ataxia, diplopia (B=4). Phenytoin = hirsutism, gingival hypertrophy, coarsening of features (C=2). Phenobarbitone = paradoxical hyperactivity in children (D=3) \u2014 a well-recognised dose-related behavioural effect in paediatric patients, along with sedation in adults. The paediatric hyperactivity effect is a classic exam point.'\n },\n {\n id:78,\n stem:'The confirmatory diagnostic test for thalassaemia carrier status is:',\n correct:'Haemoglobin A2 more than 3.5%',\n options:['Low haemoglobin level','Haemoglobin A2 more than 3.5%','Foetal haemoglobin more than 10%','Positive osmotic fragility test'],\n exp:'Beta-thalassaemia trait (carrier) is confirmed by HPLC or haemoglobin electrophoresis showing HbA2 >3.5% (usually 4\u20136%). HbA2 is elevated because in the absence of normal beta chains, delta chains compensate producing HbA2 (\u03b1\u2082\u03b4\u2082). Low Hb is suggestive but non-specific (many causes). Elevated HbF (>2%) can occur but is not the confirmatory test. Osmotic fragility is decreased in thalassaemia (not increased), and is used for spherocytosis diagnosis.'\n },\n {\n id:79,\n stem:'A 3-year-old male child has a poor stream of urine and strains at micturition. After voiding, the bladder is still palpable. The patient should be advised:',\n correct:'Excretory urogram',\n options:['Abdomen X-ray','Urine examination','Circumcision','Excretory urogram'],\n exp:'A 3-year-old boy with poor urinary stream, straining, and incomplete bladder emptying (palpable bladder post-void) has features of bladder outflow obstruction. The most likely cause is posterior urethral valves (PUV), a congenital obstructive uropathy. The investigation of choice is excretory urogram (IVU) or micturating cystourethrogram (MCU) to define the anatomy of the urinary tract, identify hydronephrosis, and confirm the diagnosis. Circumcision is for phimosis causing poor stream in older children but does not explain a palpable bladder.'\n },\n {\n id:80,\n stem:'A two-year-old child has weight less than 3 SD (less than \u22123 Z score) as per WHO growth chart and mid upper arm circumference less than 11 cm. What is the correct diagnosis for this child?',\n correct:'Severe acute malnutrition',\n options:['Acute malnutrition','Chronic malnutrition','Severe acute malnutrition','Moderate acute malnutrition'],\n exp:'WHO\/UNICEF criteria for Severe Acute Malnutrition (SAM): weight-for-height < \u22123 Z score (or <70% of median), AND\/OR MUAC <11.5 cm in children 6\u201359 months, AND\/OR presence of bilateral pitting oedema. This child meets BOTH criteria (weight < \u22123 SD AND MUAC <11 cm). Moderate acute malnutrition = MUAC 11.5\u201312.5 cm or weight-for-height \u22123 to \u22122 Z score. Stunting (chronic malnutrition) = low height-for-age. SAM carries high mortality and requires therapeutic feeding programme.'\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\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){\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 timerInterval=setInterval(function(){\n timerRemaining--;\n const disp=fmtTime(timerRemaining);\n document.getElementById(NS+'-timer-display').textContent=disp;\n btn.textContent='\u23f1 '+disp;\n const item=document.getElementById(NS+'-timer-item');\n if(timerRemaining<=300) item.classList.add('warning');\n if(timerRemaining<=0){clearInterval(timerInterval);timerInterval=null;triggerGrace();}\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){clearInterval(graceInterval);dismissGrace();showScore();}\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 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 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 const correct=opts[oi]===q.correct;\n userAnswers[qid]=correct?'correct':'wrong';\n answered++;\n 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.cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms16p1b .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms16p1b .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#cms16p1b .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n\n@media(max-width:480px){\n #cms16p1b .cq-header h1{font-size:1.15rem}\n #cms16p1b .cq-qtext{font-size:0.88rem}\n #cms16p1b .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms16p1b\">\n\n <div class=\"cq-sentinel\" id=\"cms16p1b-sentinel\"><\/div>\n\n <div class=\"cq-statusbar\" id=\"cms16p1b-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms16p1b-timer-item\">\u23f1 <strong id=\"cms16p1b-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms16p1b-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms16p1b-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms16p1b-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms16p1b-sn\">0<\/strong> \/ <strong id=\"cms16p1b-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms16p1b-fill\"><\/div><\/div>\n <\/div>\n\n <div class=\"cq-grace\" id=\"cms16p1b-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=\"cms16p1b-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms16p1b-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2016<br>Paper I \u00b7 Part B<\/h1>\n <p>General Medicine \u00b7 Surgery \u00b7 Paediatrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 41 \u2013 80<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms16p1b-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n\n <div class=\"cq-body\">\n <div id=\"cms16p1b-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms16p1b-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms16p1b-score\">\n <div class=\"cq-score-ring\" id=\"cms16p1b-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms16p1b-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=\"cms16p1b-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms16p1b-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms16p1b-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms16p1b-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms16p1b-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms16p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms16p1b', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60;\n const GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:41,\n stem:'Which one of the following gases is used for sterilization of pharmaceutical products?',\n correct:'Ethylene oxide',\n options:['Ethylene oxide','Ammonia','Halothane','Nitrous oxide'],\n exp:'Ethylene oxide (EO) is a highly penetrating alkylating gas used for sterilization of heat- and moisture-sensitive medical devices and pharmaceutical products (e.g., catheters, implants). It is effective at low temperatures (~50\u00b0C). It is, however, toxic and carcinogenic and requires long aeration cycles to remove residues. Ammonia is a disinfectant, not a sterilant. Halothane and nitrous oxide are anaesthetic gases.'\n },\n {\n id:42,\n stem:'The following statements about peptic ulcer are true EXCEPT:',\n correct:'Duodenal ulcer invariably changes into malignant',\n options:['Eradication of H. pylori is a part of medical management','Duodenal ulcer invariably changes into malignant','Complications are indication for surgery','Zollinger-Ellison syndrome is associated with intractable peptic ulceration'],\n exp:'Duodenal ulcers virtually NEVER undergo malignant transformation \u2014 this is a key distinguishing feature from gastric ulcers (which have a small but real malignant potential). H. pylori eradication is the cornerstone of medical management. Complications (perforation, haemorrhage, obstruction) are surgical indications. Zollinger-Ellison syndrome (gastrinoma) causes hypersecretion and intractable, multiple, atypical peptic ulcers.'\n },\n {\n id:43,\n stem:'In a patient with a lacerated foot injury who is not actively immunised against tetanus, which one of the following is indicated for tetanus prophylaxis?',\n correct:'Tetanus immunoglobulin',\n options:['Penicillin','Tetanus toxoid','Tetanus immunoglobulin','Triple vaccine'],\n exp:'A non-immunised patient with a tetanus-prone wound (lacerated, contaminated) requires immediate passive immunisation with human tetanus immunoglobulin (HTIG, 250\u2013500 IU IM) to provide immediate protection. Tetanus toxoid (active immunisation) should also be given but at a different site, starting a primary immunisation course. Penicillin is an adjunct, not prophylaxis. Triple vaccine (DPT) is for children in the primary immunisation schedule.'\n },\n {\n id:44,\n stem:'Which one of the following neoplasms can lead to \\'water intoxication\\'?',\n correct:'Oat cell carcinoma of bronchus',\n options:['Oat cell carcinoma of bronchus','Hepatocarcinoma','Testicular tumours','Rhabdomyosarcoma'],\n exp:'Water intoxication results from SIADH (syndrome of inappropriate ADH secretion), causing dilutional hyponatraemia. Oat cell (small cell) carcinoma of the bronchus is the classic cause of paraneoplastic SIADH \u2014 the tumour cells ectopically secrete ADH (vasopressin), leading to excessive water retention. This is one of the most common paraneoplastic manifestations of SCLC. The other options do not typically secrete ADH.'\n },\n {\n id:45,\n stem:'The Swan-Ganz catheter is used to measure:',\n correct:'Pulmonary wedge pressure',\n options:['Peripheral arterial blood pressure','Portal venous pressure','Pulmonary wedge pressure','Intracranial pressure monitoring'],\n exp:'The Swan-Ganz (balloon-tipped pulmonary artery) catheter is floated from a central vein through the right heart into the pulmonary artery. When the balloon is inflated it wedges distally, occluding forward flow, and the distal lumen measures pulmonary capillary wedge pressure (PCWP) \u2014 an indirect measure of left atrial pressure and left ventricular end-diastolic pressure. It also measures pulmonary artery pressure, CVP, and cardiac output (thermodilution).'\n },\n {\n id:46,\n stem:'Delirium is usually seen in:',\n correct:'Atropine toxicity',\n options:['Acetaminophen toxicity','Atropine toxicity','Kerosene poisoning','Digitalis toxicity'],\n exp:'Atropine (anticholinergic) toxicity causes the classic antimuscarinic syndrome: \"blind as a bat, dry as a bone, red as a beet, hot as a hare, mad as a hatter\" \u2014 the \"mad as a hatter\" component refers to agitated delirium and hallucinations from central anticholinergic effects. Paracetamol toxicity primarily causes hepatotoxicity. Kerosene causes chemical pneumonitis. Digitalis toxicity causes cardiac arrhythmias, visual disturbances, and nausea \u2014 not typically delirium.'\n },\n {\n id:47,\n stem:'The following statements regarding Hodgkin\\'s disease are true EXCEPT:',\n correct:'Stage III disease is confined to one side of the diaphragm',\n options:['It usually presents as painless lymphadenopathy','The Pel-Ebstein fever is a characteristic feature','Stage III disease is confined to one side of the diaphragm','Reed-Sternberg cells are a diagnostic feature'],\n exp:'Ann Arbor staging: Stage I = single lymph node region; Stage II = two or more regions on the SAME side of the diaphragm; Stage III = lymph node regions on BOTH sides of the diaphragm (spleen counts as lymphoid tissue); Stage IV = diffuse extranodal involvement. Stage III is therefore on BOTH sides \u2014 the statement \"confined to one side\" describes Stage I\/II, not Stage III. Reed-Sternberg cells (owl-eye nuclei) are diagnostic; Pel-Ebstein (cyclical) fever is characteristic.'\n },\n {\n id:48,\n stem:'Following are causes of bleeding EXCEPT:',\n correct:'Heparin-induced thrombocytopenia',\n options:['Heparin-induced thrombocytopenia','Dengue fever','ITP','Aspirin'],\n exp:'Heparin-induced thrombocytopenia (HIT) is an immune-mediated complication of heparin where antibodies against PF4-heparin complexes activate platelets. The predominant complication is THROMBOSIS (venous and arterial), not bleeding \u2014 despite the low platelet count. This is why it is sometimes called \"the clotting disorder.\" Dengue, ITP, and aspirin (platelet dysfunction) all cause bleeding tendencies. HIT is paradoxically prothrombotic.'\n },\n {\n id:49,\n stem:'The combination of cyanosis with clubbing can be seen in the following conditions EXCEPT:',\n correct:'Chronic bronchitis',\n options:['Eisenmenger syndrome','Lung abscess','Chronic bronchitis','Pulmonary AV fistula'],\n exp:'Cyanosis with clubbing: Eisenmenger syndrome (right-to-left shunt with pulmonary hypertension), lung abscess (suppurative lung disease causing local hypoxia + chronic infection), and pulmonary AV fistula (right-to-left shunting through the fistula) all cause both. Chronic bronchitis (COPD) causes cyanosis (\"blue bloater\") but typically does NOT cause clubbing \u2014 clubbing in respiratory disease is mainly associated with lung cancer, suppurative lung disease, and fibrosing alveolitis. Clubbing in COPD alone is absent or very rare.'\n },\n {\n id:50,\n stem:'Diagnosis and grading of multi-organ failure is based on all the following criteria EXCEPT:',\n correct:'Serum albumin',\n options:['Serum bilirubin','Serum albumin','Serum creatinine','PaO\u2082\/FiO\u2082 ratio'],\n exp:'Multi-organ dysfunction\/failure scoring systems (SOFA, Marshall MOF score) use organ-specific markers: PaO\u2082\/FiO\u2082 ratio (respiratory), serum creatinine\/urine output (renal), serum bilirubin (hepatic), platelet count (coagulation), GCS (neurological), and vasopressor requirement (cardiovascular). Serum albumin reflects nutritional status and chronic synthetic function but is NOT used as an MOF grading criterion \u2014 it is too slow to change and non-specific for acute organ failure.'\n },\n {\n id:51,\n stem:'A 16-year-old boy presents with exertional dyspnoea, haemoptysis and occasionally paroxysmal nocturnal dyspnoea. There was history of joint pains five years back. The most probable diagnosis is:',\n correct:'Mitral stenosis',\n options:['Aortic regurgitation','Mitral stenosis','Tricuspid stenosis','Aortic stenosis'],\n exp:'The triad of exertional dyspnoea, haemoptysis, and PND in a young patient with a history of rheumatic joint pains (rheumatic fever) 5 years earlier is the classic presentation of rheumatic mitral stenosis. Mitral stenosis leads to left atrial hypertension \u2192 pulmonary venous hypertension \u2192 pulmonary oedema (PND) and pulmonary hypertension (haemoptysis). Rheumatic fever predominantly damages the mitral valve (70% of cases).'\n },\n {\n id:52,\n stem:'The adrenocortical insufficiency may result in:\\n1. Hyponatraemia\\n2. Hypokalaemia\\n3. Acidosis\\n4. Hyperglycaemia\\n\\nWhich of the statements given above is\/are correct?',\n correct:'1 and 3',\n options:['1 only','1 and 3','2 and 4 only','2, 3 and 4'],\n exp:'Adrenocortical insufficiency (Addison\\'s disease): loss of aldosterone \u2192 sodium wasting (hyponatraemia, 1 = correct) and potassium retention (HYPERKALAEMIA, not hypokalaemia \u2014 statement 2 is WRONG). Loss of cortisol \u2192 impaired gluconeogenesis \u2192 hypoglycaemia (not hyperglycaemia \u2014 statement 4 is WRONG). Hyperkalaemia and decreased renal acid excretion cause metabolic acidosis (3 = correct). So hyponatraemia (1) and acidosis (3) are correct.'\n },\n {\n id:53,\n stem:'Life-threatening pneumococcal infection is a complication seen in:\\n1. Idiopathic thrombocytopenic purpura\\n2. Sickle cell disease\\n3. Thalassaemia minor\\n4. Nephrotic syndrome\\n\\nWhich of the statements given above is\/are correct?',\n correct:'2 and 4 only',\n options:['1 only','1 and 3','2 and 4 only','2, 3 and 4'],\n exp:'Overwhelming pneumococcal infection (OPSI) occurs in functional\/anatomical asplenia and hyposplenic states. Sickle cell disease (2): splenic autoinfarction by 5 years causes functional asplenia \u2014 pneumococcal sepsis is a major cause of death. Nephrotic syndrome (4): loss of opsonins (immunoglobulins, properdin) in urine plus corticosteroid therapy creates susceptibility to encapsulated bacteria including pneumococcus. ITP affects platelets, not pneumococcal immunity. Thalassaemia minor has normal splenic function.'\n },\n {\n id:54,\n stem:'The following are true regarding Zollinger-Ellison syndrome EXCEPT:',\n correct:'It occurs in association with MEN-2 syndrome',\n options:['Common age group is 30 to 50 years','Gastrin level is usually high','Diarrhoea can be an associated feature','It occurs in association with MEN-2 syndrome'],\n exp:'Zollinger-Ellison syndrome (gastrinoma) occurs in 20\u201325% of cases as part of MEN-1 (multiple endocrine neoplasia type 1 = 3Ps: pituitary, parathyroid, pancreas). It is NOT associated with MEN-2 (which comprises medullary thyroid cancer, phaeochromocytoma, and hyperparathyroidism). Presentation: age 30\u201350, markedly elevated fasting gastrin, intractable peptic ulcers, secretory diarrhoea (acid inactivates pancreatic enzymes). Statement d is FALSE.'\n },\n {\n id:55,\n stem:'The following may be seen in a patient with chronic liver disease EXCEPT:',\n correct:'Decreased factor VIII',\n options:['Prolonged PT','Prolonged PTT','Thrombocytopenia','Decreased factor VIII'],\n exp:'Chronic liver disease impairs synthesis of clotting factors II, V, VII, IX, X (all made in liver) \u2192 prolonged PT and PTT. Thrombocytopenia occurs due to hypersplenism and reduced thrombopoietin. Factor VIII is unique \u2014 it is produced by vascular endothelial cells (not exclusively hepatocytes) and is also an acute phase reactant; it is therefore ELEVATED or normal in CLD. Decreased factor VIII is NOT expected in CLD; it is seen in haemophilia A or von Willebrand disease.'\n },\n {\n id:56,\n stem:'Pseudomembranous colitis is caused by which of the following organisms?',\n correct:'Clostridium difficile',\n options:['Shigella','Clostridium difficile','E. coli','Clostridium perfringens'],\n exp:'Pseudomembranous colitis (PMC) is caused by Clostridium difficile, a gram-positive spore-forming anaerobe. Following antibiotic use (classically clindamycin, broad-spectrum penicillins, cephalosporins), normal colonic flora are disrupted, allowing C. difficile to overgrow and produce toxins A (enterotoxin) and B (cytotoxin), causing colitis with the formation of yellowish-white pseudomembranous plaques on the mucosa. Diagnosed by stool toxin assay or PCR.'\n },\n {\n id:57,\n stem:'A patient presents with breathlessness and occasional dry cough. Bilateral basal crepitations are found on examination. Pulmonary function tests reveal a decrease in total lung capacity and vital capacity, with normal FEV\u2081\/FVC ratio. He is most likely suffering from:',\n correct:'Idiopathic pulmonary fibrosis',\n options:['Chronic bronchitis','Idiopathic pulmonary fibrosis','Cystic fibrosis','Allergic bronchopulmonary aspergillosis'],\n exp:'The classic restrictive pattern \u2014 reduced TLC and VC with NORMAL FEV\u2081\/FVC ratio (both volumes reduced proportionally) \u2014 combined with bilateral basal fine crepitations (\"velcro\" crepitations) and dry cough in an adult points to interstitial lung disease, specifically idiopathic pulmonary fibrosis (IPF). COPD\/chronic bronchitis causes obstructive pattern (reduced FEV\u2081\/FVC). Cystic fibrosis and ABPA cause obstructive\/mixed patterns, typically in younger patients.'\n },\n {\n id:58,\n stem:'A 45-year-old hypertensive male presented with 3-hour history of sudden onset severe headache associated with nausea and vomiting. On clinical examination, the patient had right-sided ptosis and neck stiffness. Rest of the neurological examination was normal. The most likely diagnosis is:',\n correct:'Aneurysmal subarachnoid bleed',\n options:['Hypertensive brain damage','Migraine','Aneurysmal subarachnoid bleed','Acute pyogenic meningitis'],\n exp:'The combination of sudden-onset \"thunderclap\" headache (worst headache of life), meningismus (neck stiffness), and right-sided ptosis (indicating third nerve palsy from posterior communicating artery aneurysm compressing CN III) is pathognomonic of aneurysmal subarachnoid haemorrhage. The posterior communicating artery aneurysm causes a \"surgical\" third nerve palsy with pupil involvement. This is a neurosurgical emergency. CT head non-contrast \u2192 LP if CT negative.'\n },\n {\n id:59,\n stem:'Which one of the following is NOT a treatment of hepatic encephalopathy?',\n correct:'TIPS',\n options:['Lactulose','Rifaximin','TIPS','Electrolyte supplementation'],\n exp:'Treatments for hepatic encephalopathy: lactulose (acidifies colon, traps NH\u2084\u207a, promotes bowel clearance), rifaximin (non-absorbable antibiotic reduces ammoniagenic gut bacteria), electrolyte correction (especially potassium \u2014 hypokalaemia worsens HE), and dietary protein adjustment. TIPS (transjugular intrahepatic portosystemic shunt) is used to reduce portal hypertension and treat variceal bleeding\/refractory ascites, but it actually WORSENS hepatic encephalopathy by diverting portal blood (rich in ammonia) away from the liver.'\n },\n {\n id:60,\n stem:'Features of intravascular haemolysis are the following EXCEPT:',\n correct:'Increased serum haptoglobin',\n options:['Increased LDH','Haemoglobinuria','Increased serum indirect bilirubin','Increased serum haptoglobin'],\n exp:'In intravascular haemolysis, RBCs lyse within vessels releasing haemoglobin directly into plasma. Features: raised LDH (released from RBCs), haemoglobinaemia \u2192 haemoglobinuria (dark urine), raised indirect bilirubin (from haem catabolism), haemosiderinuria, and DECREASED haptoglobin (free Hb binds and saturates haptoglobin, which is then cleared by the liver). Increased serum haptoglobin is the OPPOSITE of what occurs \u2014 it is a feature of acute phase reactions, not haemolysis.'\n },\n {\n id:61,\n stem:'Consider the following statements:\\n1. Hypertrophic cardiomyopathy can lead to sudden cardiac death.\\n2. Dressler\\'s syndrome is an early complication of acute myocardial infarction.\\n\\nWhich of the statements given above is\/are correct?',\n correct:'1 only',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'HCM (hypertrophic cardiomyopathy) is the most common cause of sudden cardiac death in young athletes, due to dynamic LVOT obstruction and life-threatening ventricular arrhythmias \u2014 statement 1 is CORRECT. Dressler\\'s syndrome is a LATE complication of AMI (2\u201310 weeks post-MI), not early. Early complications (first days) include arrhythmias, mechanical complications (VSD, free wall rupture, papillary muscle dysfunction), and cardiogenic shock \u2014 statement 2 is WRONG. Only statement 1 is correct.'\n },\n {\n id:62,\n stem:'The common sites of hypertensive bleed are the following EXCEPT:',\n correct:'Frontal cortex',\n options:['Basal ganglion','Pons','Cerebellum','Frontal cortex'],\n exp:'Hypertensive intracerebral haemorrhage occurs in penetrating arteries damaged by chronic hypertension (Charcot-Bouchard microaneurysms). Classic sites in order of frequency: putamen\/basal ganglia (most common, ~50%), thalamus, pons, cerebellum, and subcortical white matter. The FRONTAL CORTEX is not a typical site for hypertensive bleeds \u2014 lobar haemorrhages in the cortex are more commonly associated with cerebral amyloid angiopathy (in elderly), AVM, or coagulopathy.'\n },\n {\n id:63,\n stem:'Hypoglycaemia as an adverse side effect is most commonly seen during treatment with:',\n correct:'Sulfonylureas',\n options:['Dipeptidyl peptidase-IV inhibitors','Metformin','\u03b1-glucosidase inhibitors','Sulfonylureas'],\n exp:'Sulfonylureas (e.g., glibenclamide, glipizide) stimulate insulin secretion from pancreatic beta cells in a glucose-independent manner, meaning they cause insulin release even when blood glucose is low. This is why hypoglycaemia is their most important adverse effect, especially in the elderly and with missed meals. Metformin, DPP-4 inhibitors, and \u03b1-glucosidase inhibitors do not cause hypoglycaemia when used as monotherapy because their mechanisms are glucose-dependent or act outside the pancreas.'\n },\n {\n id:64,\n stem:'Which of the following statements is\/are correct regarding Gilbert\\'s syndrome?\\n1. Inheritance of the disease is autosomal dominant.\\n2. Jaundice becomes very severe with time.\\n3. Fasting leads to increased bilirubin levels.\\n\\nSelect the correct answer:',\n correct:'1 and 3 only',\n options:['1 and 3 only','1 only','2 and 3 only','1, 2 and 3'],\n exp:'Gilbert\\'s syndrome: autosomal dominant (or recessive, depending on the mutation; classically described as dominant \u2014 statement 1 correct) reduction in UGT1A1 enzyme activity causing unconjugated hyperbilirubinaemia. Jaundice is mild and fluctuating \u2014 it does NOT become severe with time (statement 2 is WRONG). Fasting, stress, intercurrent illness, and exercise all precipitate jaundice by increasing bilirubin load and reducing hepatic uptake (statement 3 correct). Benign condition with normal liver function and life expectancy.'\n },\n {\n id:65,\n stem:'The following are causes of secondary hypertension EXCEPT:',\n correct:'Carcinoid syndrome',\n options:['Conn\\'s syndrome','Carcinoid syndrome','Cushing\\'s syndrome','Phaeochromocytoma'],\n exp:'Classic causes of secondary hypertension include: Conn\\'s syndrome (primary hyperaldosteronism \u2014 sodium\/water retention), Cushing\\'s syndrome (cortisol excess \u2014 mineralocorticoid effects), phaeochromocytoma (catecholamine excess \u2014 episodic or sustained hypertension). Carcinoid syndrome characteristically causes flushing, diarrhoea, and bronchoconstriction from serotonin and other mediators; it does NOT cause sustained hypertension and is not a recognised cause of secondary hypertension.'\n },\n {\n id:66,\n stem:'Tetralogy of Fallot is characterised by the following EXCEPT:',\n correct:'Pulmonary hypertension',\n options:['Ventricular septal defect','Overriding aorta','Pulmonary hypertension','Right ventricular hypertrophy'],\n exp:'Tetralogy of Fallot comprises four defects: (1) VSD, (2) overriding aorta, (3) pulmonary STENOSIS (infundibular \u00b1 valvular \u2014 obstruction, not hypertension), (4) right ventricular hypertrophy (secondary to outflow obstruction). Pulmonary hypertension is NOT a feature \u2014 in fact, the pulmonary stenosis reduces pulmonary blood flow and protects the pulmonary vasculature. Pulmonary hypertension with VSD (without stenosis) leads to Eisenmenger syndrome \u2014 a different entity entirely.'\n },\n {\n id:67,\n stem:'Regarding high altitude pulmonary oedema, the following statements are true EXCEPT:',\n correct:'It does not occur in a physically fit person',\n options:['It can be caused by physical exertion at high altitude','It does not occur in a physically fit person','It occurs due to leak in the alveolar capillary membrane','Portable hyperbaric chamber may be used for treatment instead of descent to a lower altitude'],\n exp:'High altitude pulmonary oedema (HAPE) occurs due to non-uniform hypoxic pulmonary vasoconstriction causing high pulmonary microvascular pressure and increased permeability of the alveolar-capillary membrane. It CAN AND DOES occur in physically fit, acclimatised mountaineers and athletes \u2014 physical fitness is NOT protective. Exertion at altitude worsens it. Treatment: immediate descent, supplemental O\u2082, portable hyperbaric chamber (Gamow bag), and nifedipine. The statement \"does not occur in physically fit person\" is FALSE.'\n },\n {\n id:68,\n stem:'Complications of myocardial infarction are all EXCEPT:',\n correct:'Dissection of aorta',\n options:['Systemic embolisation','Rupture of interventricular septum','Dissection of aorta','Ventricular fibrillation'],\n exp:'Recognised complications of MI: arrhythmias (VF, VT), mechanical complications (ventricular free wall rupture, VSD\/interventricular septal rupture, papillary muscle rupture causing acute MR), cardiogenic shock, pericarditis, Dressler\\'s syndrome, LV aneurysm, and systemic embolisation (mural thrombus). Aortic dissection is a separate condition caused by medial degeneration\/hypertension \u2014 it is NOT a complication of MI. It may mimic MI (Type A dissection can obstruct coronary ostia) but is not caused by it.'\n },\n {\n id:69,\n stem:'Philadelphia chromosome can be detected by which of the following techniques?\\n1. FISH\\n2. PCR\\n3. Cytogenetics\\n\\nSelect the correct answer:',\n correct:'1, 2 and 3',\n options:['1 only','1 and 3 only','2 and 3 only','1, 2 and 3'],\n exp:'The Philadelphia chromosome [t(9;22)(q34;q11)] creates the BCR-ABL fusion gene. All three techniques detect it: (1) FISH (fluorescence in situ hybridisation) \u2014 detects BCR-ABL fusion at chromosomal level, sensitive, used on interphase cells. (2) PCR (RT-PCR) \u2014 detects BCR-ABL mRNA\/DNA, most sensitive for minimal residual disease monitoring. (3) Conventional cytogenetics (karyotyping) \u2014 the original method, detects the translocation in dividing cells. All three are valid and complementary.'\n },\n {\n id:70,\n stem:'The following statements regarding coeliac disease are correct EXCEPT:',\n correct:'Absence of gastrointestinal symptoms rules out coeliac disease',\n options:['Absence of gastrointestinal symptoms rules out coeliac disease','Malabsorption syndrome may be a presenting feature','Duodenal biopsy shows increased intraepithelial lymphocytes','Steroid therapy may induce remission'],\n exp:'Coeliac disease (gluten-sensitive enteropathy) has a wide clinical spectrum. \"Silent\" or \"atypical\" coeliac disease is common \u2014 patients may present only with anaemia, osteoporosis, infertility, neurological symptoms, or dermatitis herpetiformis WITHOUT GI symptoms. Absence of GI symptoms does NOT rule it out \u2014 statement (a) is FALSE. Classic malabsorption, villous atrophy with increased IELs on duodenal biopsy, and response to steroids in refractory cases are all well-documented.'\n },\n {\n id:71,\n stem:'A 6-year-old child presents with oliguria, haematuria, puffiness of face, convulsions, B.P. of 200\/100 mm Hg and blood urea 80 mg%. What is the most likely diagnosis?',\n correct:'Acute glomerulonephritis with hypertensive encephalopathy',\n options:['Haemolytic uraemic syndrome','Nephrotic syndrome','Acute glomerulonephritis with hypertensive encephalopathy','Obstructive uropathy'],\n exp:'The combination of oliguria, haematuria (nephritic urine), facial oedema, severe hypertension, and convulsions in a school-age child following throat\/skin infection is classic post-streptococcal acute glomerulonephritis (PSGN) complicated by hypertensive encephalopathy. Nephrotic syndrome has heavy proteinuria, oedema but normotension. HUS features microangiopathic haemolytic anaemia + thrombocytopenia. The markedly elevated BP with convulsions confirms hypertensive encephalopathy as the complication here.'\n },\n {\n id:72,\n stem:'A 3-year-old child is brought for sudden inability to walk following fever of two days duration. Sensorium is normal. Both lower limbs are hypotonic, right more than left. Plantar reflex is equivocal. Deep tendon reflexes are not elicitable in the lower limbs. The most probable diagnosis is:',\n correct:'Acute poliomyelitis',\n options:['Acute poliomyelitis','Acute rheumatic fever','Acute transverse myelitis','Acute infective polyneuritis'],\n exp:'Acute poliomyelitis: fever followed by acute flaccid paralysis (AFP) \u2014 lower motor neuron pattern with hypotonia, areflexia, and asymmetric weakness (right > left). Sensorium is normal (pure motor involvement of anterior horn cells). The asymmetric, lower limb predominant, post-febrile AFP with preserved sensation and absent DTRs is the hallmark of acute paralytic polio. Guillain-Barr\u00e9 (infective polyneuritis) is symmetric ascending paralysis typically without fever at onset. Transverse myelitis gives a sensory level.'\n },\n {\n id:73,\n stem:'X-ray of the skull in an infant shows periventricular calcification in:',\n correct:'Cytomegalovirus infection',\n options:['Tuberculous meningitis','Cytomegalovirus infection','Japanese B encephalitis','Congenital syphilis'],\n exp:'Periventricular (subependymal) calcification on skull X-ray or CT is the hallmark of congenital cytomegalovirus (CMV) infection \u2014 the virus preferentially infects periventricular germinal matrix cells. Toxoplasmosis causes scattered intracerebral calcifications (not specifically periventricular). Congenital rubella causes periventricular leukomalacia but not discrete calcifications. TB meningitis causes basal ganglia calcification. Congenital syphilis shows bone changes, not periventricular calcification.'\n },\n {\n id:74,\n stem:'A 4-year-old boy with sickle cell disease presents with pain and swelling of bones, marked in small bones of hand and feet, severe abdominal pain, and necrosis of femoral head and upper tibia on investigation. Symptoms resolved after one week. The possible explanation is:',\n correct:'Vaso-occlusive crisis',\n options:['Aplastic crisis','Sequestration crisis','Vaso-occlusive crisis','Haemolytic crisis'],\n exp:'Vaso-occlusive (painful) crisis in sickle cell disease is caused by sickling of RBCs in small vessels causing ischaemia and infarction. Features: dactylitis (painful swelling of small bones of hands and feet \u2014 hand-foot syndrome), bone pain (avascular necrosis of femoral head), abdominal pain (mesenteric ischaemia), and resolution within days to a week. Aplastic crisis = sudden drop in Hb (parvovirus B19). Sequestration crisis = sudden splenic trapping of RBCs. Haemolytic crisis = accelerated haemolysis.'\n },\n {\n id:75,\n stem:'Match List I (Genetic disorder) with List II (Genotype):\\nA. Down Syndrome\\nB. Turner Syndrome\\nC. Noonan Syndrome\\nD. Cri-du-chat Syndrome\\n\\n1. 47, XY, +21\\n2. 46, XY\\n3. 46, XX, 5p\u2212\\n4. 45, XO\\n5. 47, XXY',\n correct:'A-1, B-4, C-2, D-3',\n options:['A-1, B-4, C-2, D-3','A-1, B-4, C-5, D-3','A-3, B-1, C-2, D-4','A-3, B-1, C-5, D-4'],\n exp:'Down syndrome = trisomy 21, karyotype 47, XY, +21 (A=1). Turner syndrome = 45, XO \u2014 monosomy X (B=4). Noonan syndrome is a RASopathy (autosomal dominant, PTPN11 mutation) \u2014 phenotypically resembles Turner but has a NORMAL karyotype: 46, XY in males (C=2). Cri-du-chat syndrome = deletion of short arm of chromosome 5 (5p\u2212), karyotype 46, XX, 5p\u2212 (D=3). Klinefelter = 47, XXY (option 5, not used here).'\n },\n {\n id:76,\n stem:'With reference to Paediatrics, the following are true of breath-holding spells EXCEPT:',\n correct:'They occur during inspiration',\n options:['They occur during inspiration','They are involuntary','Cyanosis may not occur','Bradycardia may occur'],\n exp:'Breath-holding spells occur in infants\/toddlers triggered by fright, frustration, or pain. The child cries, then holds the breath in EXPIRATION (not inspiration) until cyanosis or pallor occurs, sometimes followed by brief loss of consciousness. They are involuntary reflex events (not intentional breath-holding). Cyanosis may not occur in pallid spells (vagal). Bradycardia (vagal syncope) can occur, especially in pallid spells. \"During inspiration\" is INCORRECT \u2014 breath is held at end-expiration.'\n },\n {\n id:77,\n stem:'Match List I (Drugs for epilepsy) with List II (Dose-dependent side effects):\\nA. Sodium valproate\\nB. Carbamazepine\\nC. Phenytoin\\nD. Phenobarbitone\\n\\n1. Raised liver enzymes\\n2. Hirsutism\\n3. Hyperactivity\\n4. Drowsiness',\n correct:'A-1, B-4, C-2, D-3',\n options:['A-1, B-4, C-2, D-3','A-1, B-4, C-3, D-2','A-4, B-1, C-2, D-3','A-4, B-1, C-3, D-2'],\n exp:'Sodium valproate = raised liver enzymes \/ hepatotoxicity (A=1). Carbamazepine = dose-related drowsiness, ataxia, diplopia (B=4). Phenytoin = hirsutism, gingival hypertrophy, coarsening of features (C=2). Phenobarbitone = paradoxical hyperactivity in children (D=3) \u2014 a well-recognised dose-related behavioural effect in paediatric patients, along with sedation in adults. The paediatric hyperactivity effect is a classic exam point.'\n },\n {\n id:78,\n stem:'The confirmatory diagnostic test for thalassaemia carrier status is:',\n correct:'Haemoglobin A2 more than 3.5%',\n options:['Low haemoglobin level','Haemoglobin A2 more than 3.5%','Foetal haemoglobin more than 10%','Positive osmotic fragility test'],\n exp:'Beta-thalassaemia trait (carrier) is confirmed by HPLC or haemoglobin electrophoresis showing HbA2 >3.5% (usually 4\u20136%). HbA2 is elevated because in the absence of normal beta chains, delta chains compensate producing HbA2 (\u03b1\u2082\u03b4\u2082). Low Hb is suggestive but non-specific (many causes). Elevated HbF (>2%) can occur but is not the confirmatory test. Osmotic fragility is decreased in thalassaemia (not increased), and is used for spherocytosis diagnosis.'\n },\n {\n id:79,\n stem:'A 3-year-old male child has a poor stream of urine and strains at micturition. After voiding, the bladder is still palpable. The patient should be advised:',\n correct:'Excretory urogram',\n options:['Abdomen X-ray','Urine examination','Circumcision','Excretory urogram'],\n exp:'A 3-year-old boy with poor urinary stream, straining, and incomplete bladder emptying (palpable bladder post-void) has features of bladder outflow obstruction. The most likely cause is posterior urethral valves (PUV), a congenital obstructive uropathy. The investigation of choice is excretory urogram (IVU) or micturating cystourethrogram (MCU) to define the anatomy of the urinary tract, identify hydronephrosis, and confirm the diagnosis. Circumcision is for phimosis causing poor stream in older children but does not explain a palpable bladder.'\n },\n {\n id:80,\n stem:'A two-year-old child has weight less than 3 SD (less than \u22123 Z score) as per WHO growth chart and mid upper arm circumference less than 11 cm. What is the correct diagnosis for this child?',\n correct:'Severe acute malnutrition',\n options:['Acute malnutrition','Chronic malnutrition','Severe acute malnutrition','Moderate acute malnutrition'],\n exp:'WHO\/UNICEF criteria for Severe Acute Malnutrition (SAM): weight-for-height < \u22123 Z score (or <70% of median), AND\/OR MUAC <11.5 cm in children 6\u201359 months, AND\/OR presence of bilateral pitting oedema. This child meets BOTH criteria (weight < \u22123 SD AND MUAC <11 cm). Moderate acute malnutrition = MUAC 11.5\u201312.5 cm or weight-for-height \u22123 to \u22122 Z score. Stunting (chronic malnutrition) = low height-for-age. SAM carries high mortality and requires therapeutic feeding programme.'\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\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){\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 timerInterval=setInterval(function(){\n timerRemaining--;\n const disp=fmtTime(timerRemaining);\n 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Submitting in 10 Submit Now Combined Medical Services Examination 2016Paper I \u00b7 Part B General Medicine \u00b7 Surgery \u00b7 Paediatrics Questions 41 \u2013 80 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0% score Your Result \u21ba Retry Quiz<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36754","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2016 P1 Part-B - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/05\/06\/cms-2016-p1-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2016 P1 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2016 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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