CMS 2022 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#cms22p1b *,#cms22p1b *::before,#cms22p1b *::after{box-sizing:border-box;margin:0;padding:0}\n#cms22p1b{--ter:#1A5EA8;--ter-light:#2E82D5;--ter-pale:#EBF3FD;--teal:#1A3A5C;--teal-light:#24527F;--teal-pale:#E8F0F9;--ink:#1a1a1a;--ink-mid:#444;--ink-soft:#777;--line:#dde4ed;--bg:#f8fafd;--white:#ffffff;--correct:#1e6f46;--correct-bg:#eaf7ef;--correct-border:#43a047;--wrong:#b83232;--wrong-bg:#fdf0f0;--wrong-border:#e53935;--radius:10px;font-family:'Source Serif 4',Georgia,serif;font-size:16px;color:var(--ink);background:var(--bg);line-height:1.7;padding:0 0 48px}\n#cms22p1b .cq-sentinel{height:1px}\n#cms22p1b .cq-statusbar{position:fixed;top:0;left:0;right:0;z-index:99999;background:var(--white);border-bottom:2px solid var(--line);border-left:4px 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.cq-score-ring{width:110px;height:110px;border-radius:50%;background:conic-gradient(var(--ter) 0%,var(--line) 0%);display:flex;align-items:center;justify-content:center;margin:0 auto 20px;position:relative}\n#cms22p1b .cq-score-ring::before{content:'';position:absolute;width:86px;height:86px;border-radius:50%;background:var(--white)}\n#cms22p1b .cq-ring-inner{position:relative;display:flex;flex-direction:column;align-items:center;line-height:1.2}\n#cms22p1b .cq-ring-pct{font-family:'Playfair Display',serif;font-size:1.3rem;font-weight:700;color:var(--ter)}\n#cms22p1b .cq-ring-sub{font-size:0.6rem;color:var(--ink-soft);text-transform:uppercase;letter-spacing:0.05em}\n#cms22p1b .cq-score h2{font-family:'Playfair Display',serif;font-size:1.2rem;color:var(--ink);margin-bottom:8px}\n#cms22p1b .cq-net-line{font-size:1rem;color:var(--ter);font-weight:600;margin-bottom:6px}\n#cms22p1b .cq-verdict{font-size:0.85rem;color:var(--ink-soft);margin-bottom:20px}\n#cms22p1b 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class=\"cq-statusbar\" id=\"cms22p1b-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms22p1b-timer-item\">\u23f1 <strong id=\"cms22p1b-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms22p1b-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms22p1b-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms22p1b-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms22p1b-sn\">0<\/strong> \/ <strong id=\"cms22p1b-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms22p1b-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms22p1b-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms22p1b-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms22p1b-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2022<br>General Medicine & Paediatrics \u00b7 Paper I \u00b7 Part B<\/h1>\n <p>Endocrinology \u00b7 Rheumatology \u00b7 Nephrology \u00b7 Emergency Medicine \u00b7 Haematology \u00b7 Infectious Disease<\/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=\"cms22p1b-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms22p1b-questions\"><\/div>\n <div class=\"cq-submit-wrap\"><button class=\"cq-btn\" id=\"cms22p1b-submit\">Submit Answers<\/button><\/div>\n <div class=\"cq-score\" id=\"cms22p1b-score\">\n <div class=\"cq-score-ring\" id=\"cms22p1b-ring\"><div class=\"cq-ring-inner\"><span class=\"cq-ring-pct\" id=\"cms22p1b-ring-pct\">0%<\/span><span class=\"cq-ring-sub\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms22p1b-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms22p1b-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms22p1b-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms22p1b-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms22p1b-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms22p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms22p1b',TOTAL=40,MAX=160,TIMER_SECS=2400,GRACE_SECS=10;\n const QUESTIONS=[\n {id:41,stem:'Which of the following are useful for the treatment of Hirsutism?\\n1. Amiloride\\n2. Oestrogen\\n3. Finasteride\\n4. Spironolactone',correct:'2, 3 and 4',options:['1, 2 and 3','1, 2 and 4','3 and 4 only','2, 3 and 4'],exp:'Oestrogen (via OCP) raises SHBG, reducing free testosterone. Finasteride (5\u03b1-reductase type II inhibitor) blocks conversion of testosterone to DHT at the hair follicle. Spironolactone has significant anti-androgen activity \u2014 the most widely used pharmacological treatment for hirsutism. Amiloride is a potassium-sparing diuretic with no meaningful anti-androgen effect. Statements 2, 3, and 4 are correct.'},\n {id:42,stem:'Which of the following is a long acting insulin?',correct:'Glargine',options:['Aspart','Glargine','Lispro','Regular'],exp:'Insulin glargine (Lantus) is a long-acting basal insulin analogue with ~20\u201324 hours duration and a peakless (flat) pharmacokinetic profile \u2014 ideal for once-daily basal coverage with low hypoglycaemia risk. Aspart and lispro are rapid-acting analogues (onset 10\u201315 min, duration 3\u20135 h). Regular (soluble) insulin is short-acting (onset 30\u201360 min, duration 6\u20138 h). Other long-acting analogues: detemir and degludec (~42 h).'},\n {id:43,stem:'A 15 year girl presents to the hospital with severe abdominal pain, vomiting and cold extremities. She has tachycardia and hypotension. Lab investigations show blood glucose 400 mg\/dL, blood pH 6\u00b79, urine ketones +++ and serum creatinine of 1\u00b74 mg\/dL. She is promptly administered IV fluids and insulin. After 4 hours, she complains of inability to lift her limbs. What is the next step to be considered in her management?',correct:'Potassium repletion',options:['Intravenous normal saline','Intravenous sodium bicarbonate','Urine sample for ketones','Potassium repletion'],exp:'This is DKA. After 4 hours of insulin and IV fluid therapy, new limb weakness is caused by hypokalaemia. Insulin drives potassium into cells (K\u207a-Na\u207a-ATPase activation) and correction of acidosis shifts K\u207a intracellularly, rapidly lowering serum potassium. Total body K\u207a is severely depleted in DKA. Hypokalaemic paralysis is a well-recognised complication during DKA treatment. Potassium repletion (IV KCl) is urgently required. Sodium bicarbonate is not routinely indicated even at pH 6.9.'},\n {id:44,stem:'Composition of oral rehydration solution (WHO) is',correct:'Na\u201390 m mol\/L, K\u201320 m mol\/L, Cl\u201380 m mol\/L, Energy\u201354 kca\/L',options:['Na\u201390 m mol\/L, K\u201320 m mol\/L, Cl\u201380 m mol\/L, Energy\u201354 kca\/L','Na\u201380 m mol\/L, K\u201320 m mol\/L, Cl\u201370 m mol\/L, Energy\u201354 kca\/L','Na\u201390 m mol\/L, K\u201340 m mol\/L, Cl\u201380 m mol\/L, Energy\u201327 kca\/L','Na\u201380 m mol\/L, K\u201320 m mol\/L, Cl\u201370 m mol\/L, Energy\u201354 kca\/L'],exp:'WHO standard ORS: sodium 90 mmol\/L, potassium 20 mmol\/L, chloride 80 mmol\/L, glucose 111 mmol\/L (20 g\/L), energy approximately 54 kcal\/L, total osmolarity ~311 mOsm\/L. This is the standard formulation taught for cholera and severe dehydration and remains the standard answer in this examination context.'},\n {id:45,stem:'Which of the following are correct regarding tuberculous meningitis?\\n1. Acid-Fast Bacilli are infrequently seen on direct smear of CSF\\n2. CSF culture for MTB is the gold standard for diagnosis\\n3. Xpert MTB\/RIF assay is a preferred initial diagnostic option',correct:'1, 2 and 3',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'All three are correct. (1) AFB are seen on direct ZN smear of CSF in only 10\u201340% of TBM cases \u2014 sensitivity is low; multiple large-volume samples improve yield. (2) Mycobacterial culture (MGIT liquid culture) remains the gold standard with >80% sensitivity, though requiring 4\u20138 weeks. (3) WHO recommends Xpert MTB\/RIF as the preferred initial rapid test for TBM \u2014 same-day results with ~80% sensitivity and rifampicin resistance detection. All three are correct.'},\n {id:46,stem:'Which one of the following is a subcutaneous preparation useful for treatment of osteoporosis?',correct:'Denosumab',options:['Denosumab','Alendronate','Zoledronic acid','Raloxifene'],exp:'Denosumab (Prolia) is a fully human monoclonal antibody against RANK-L. By blocking RANK-L it prevents osteoclast differentiation and bone resorption. It is administered as a subcutaneous injection of 60 mg every 6 months. Alendronate is an oral bisphosphonate. Zoledronic acid is an intravenous bisphosphonate (annual infusion). Raloxifene is an oral SERM.'},\n {id:47,stem:'Which of the following are correct with regard to osteoporosis?\\n1. It does not cause symptoms until a fracture occurs\\n2. Vertebral fracture can present with loss of height, in absence of pain\\n3. Smoking is protective\\n4. It sometimes presents incidentally as radiological osteopenia',correct:'1, 2 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:\"Osteoporosis is a silent disease until fracture occurs \u2014 statement 1 is correct. Vertebral compression fractures frequently occur without acute pain and manifest as progressive loss of height and kyphosis ('dowager's hump') \u2014 statement 2 is correct. Smoking is a well-established RISK FACTOR for osteoporosis \u2014 statement 3 (smoking is protective) is false. Osteoporosis is often an incidental finding on plain radiographs as osteopenia \u2014 statement 4 is correct. Statements 1, 2, and 4 are correct.\"},\n {id:48,stem:'Which of the following are correct with regard to Ankylosing spondylitis?\\n1. Bamboo spine may be seen\\n2. Early morning back pain is rare\\n3. Uveitis is most common extra-articular feature\\n4. It is more common in males',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Bamboo spine (complete vertebral fusion with syndesmophytes) is the pathognomonic radiological finding in advanced AS \u2014 statement 1 is correct. Early morning back stiffness and pain that IMPROVES with exercise (not rest) is the hallmark of inflammatory back pain in AS; it is characteristic and NOT rare \u2014 statement 2 (rare) is false. Acute anterior uveitis (iritis) is the most common extra-articular manifestation occurring in 25\u201330% of patients \u2014 statement 3 is correct. AS is 2\u20133 times more common in males \u2014 statement 4 is correct. Statements 1, 3, and 4 are correct.'},\n {id:49,stem:'Carpal Tunnel Syndrome is associated with which of the following features?\\n1. Pain and tingling in hands at night\\n2. Weakness of thumb abduction\\n3. Loss of sensation over lateral half of the palm\\n4. Atrophy of hypothenar eminence',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Carpal tunnel syndrome results from compression of the median nerve at the wrist. Features: (1) Nocturnal pain and paraesthesiae in median nerve distribution \u2014 classic presenting symptom; (2) Weakness of thumb abduction (abductor pollicis brevis) \u2014 correct; (3) Loss of sensation over the lateral palm (palmar cutaneous branch) \u2014 correct. Hypothenar atrophy (statement 4) indicates ulnar nerve pathology \u2014 thenar atrophy is the CTS finding. Statements 1, 2, and 3 are correct.'},\n {id:50,stem:'Which of the following can be used to monitor disease activity in rheumatoid arthritis?\\n1. Pain (visual analogue scale)\\n2. X-Ray of hands and wrists\\n3. DAS 28 score\\n4. ESR',correct:'2, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'DAS28 is the gold standard composite measure of RA disease activity incorporating tender joint count, swollen joint count, ESR (or CRP), and patient global assessment. ESR is a validated acute-phase reactant used independently and within DAS28. X-ray of hands and wrists tracks erosive structural damage over time. Pain VAS alone is a subjective patient-reported outcome and not a validated standalone measure of objective RA disease activity. Statements 2, 3, and 4 are correct.'},\n {id:51,stem:'Which one of the following HIV-associated infections is least likely with CD4 count > 100 cells\/mm\u00b3?',correct:'Cerebral toxoplasmosis',options:['Cerebral toxoplasmosis','Tuberculosis','Herpes zoster','Pneumocystis jirovecii pneumonia'],exp:'Cerebral toxoplasmosis almost exclusively occurs when CD4 falls below 100 cells\/mm\u00b3, typically <50 \u2014 it is the OI least likely at CD4 >100. PCP typically occurs at CD4 <200 but can occur up to 200. Herpes zoster can reactivate at CD4 up to 500. TB can occur at any CD4 level. Cerebral toxoplasmosis is least likely with CD4 >100 cells\/mm\u00b3.'},\n {id:52,stem:'Tests for graphesthesia and stereognosis are used clinically to assess',correct:'Cortical sensation',options:['Cortical sensation','Posterior column','Cerebellar function','Lateral spinothalamic tract'],exp:'Graphesthesia (identifying numbers or letters traced on skin) and stereognosis (identifying objects by touch alone) are tests of cortical sensory integration \u2014 they require intact primary sensory input AND parietal cortex processing. These are examples of discriminative (cortical) sensation, processed in the contralateral somatosensory cortex (postcentral gyrus). They are impaired in parietal lobe lesions even when basic primary sensations are intact.'},\n {id:53,stem:'A blast victim is brought to the emergency. Victim is unconscious. BP is 80\/50 mm Hg. Pulse is 110 per minute and thready and SpO\u2082 is 70%. Victim has rapid shallow breathing and signs of external blood loss are present. JVP is raised and heart sounds are absent on auscultation. Which one of the following is the next single most immediate step in the management, after securing airway, breathing and circulation?',correct:'Urgent pericardiocentesis',options:['Chest X-ray PA and lateral view','Urgent needle thoracostomy','Urgent pericardiocentesis','Blood for cross match followed by blood transfusion'],exp:\"The clinical triad of hypotension + raised JVP + absent heart sounds = Beck's triad of cardiac tamponade. In a blast injury, haemopericardium causes tamponade. After ABC is secured, the next immediate life-saving step is urgent pericardiocentesis. A chest X-ray would delay definitive treatment. Needle thoracostomy treats tension pneumothorax (absent breath sounds, tracheal deviation). Blood transfusion addresses hypovolaemia but will not relieve tamponade.\"},\n {id:54,stem:'A 21 year young female was brought to Emergency Department with history of unknown substance ingestion. She was having vomiting, profuse diarrhoea, bronchorrhoea and excessive sweating. On examination miosis and muscular fasciculations were present. What is the most likely diagnosis?',correct:'Organophosphorus poisoning',options:['Corrosive substance poisoning','Aluminium phosphide poisoning','Zinc phosphide poisoning','Organophosphorus poisoning'],exp:'This is the classic SLUDGE\/DUMBELS toxidrome of cholinergic excess: Salivation, Lacrimation, Urination, Defaecation, GI distress, Emesis, Bronchospasm\/Bronchorrhoea, Bradycardia, Sweating + miosis and muscular fasciculations (nicotinic effect). All features point to organophosphorus poisoning \u2014 irreversible acetylcholinesterase inhibition causing ACh accumulation. Management: atropine (muscarinic reversal) + pralidoxime + benzodiazepines for seizures.'},\n {id:55,stem:'A young female of 22 year old presented to the medical emergency with complaints of nausea, vomiting, abdominal pain, diarrhoea, and convulsions along with methaemoglobinaemia. What is the likely diagnosis?',correct:'Copper sulphate poisoning',options:['Aluminium phosphide poisoning','Zinc phosphide poisoning','Copper sulphate poisoning','Lead poisoning'],exp:'Copper sulphate poisoning classically causes: GI symptoms (nausea, vomiting, diarrhoea, abdominal pain), neurological features (convulsions), and characteristically methaemoglobinaemia \u2014 copper oxidises haemoglobin Fe\u00b2\u207a to Fe\u00b3\u207a. The blue-green vomitus is another clue. Treatment: gastric lavage, IV fluids, D-penicillamine (chelation), and methylene blue for methaemoglobinaemia. Aluminium and zinc phosphide cause phosphine gas toxicity. Lead poisoning causes chronic encephalopathy.'},\n {id:56,stem:'Which of the following are the components of the SOFA (Sequential Organ Failure Assessment)?\\n1. Serum bilirubin\\n2. Platelet count\\n3. Leucocyte count\\n4. Serum Creatinine',correct:'1, 2 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'The SOFA score assesses six organ systems: Respiratory (PaO\u2082\/FiO\u2082), Coagulation (platelet count), Liver (serum bilirubin), Cardiovascular (MAP or vasopressor), CNS (GCS), Renal (serum creatinine or urine output). Leucocyte count is NOT a SOFA component (it is part of SIRS criteria). Serum bilirubin (1), platelet count (2), and serum creatinine (4) are all SOFA components. Statements 1, 2, and 4 are correct.'},\n {id:57,stem:\"Purtscher's retinopathy may be associated with\",correct:'Acute pancreatitis',options:['Acute fulminant hepatic failure','Acute pancreatitis','Acute peritonitis','Acute cholecystitis'],exp:\"Purtscher's retinopathy is a traumatic occlusive microangiopathy of the retinal vasculature characterised by cotton-wool spots, haemorrhages, and sudden visual loss. It classically occurs with severe crush injuries but is also a recognised complication of acute pancreatitis (Purtscher-like retinopathy) \u2014 thought to be caused by complement activation, granulocyte aggregation, and fat emboli to retinal arterioles from pancreatic lipase-mediated fat necrosis. Acute pancreatitis is the classic non-traumatic association tested in examinations.\"},\n {id:58,stem:'Which of the following may constitute the characteristic triad of Zollinger-Ellison syndrome?\\n1. Severe peptic ulceration\\n2. Gastric acid hyposecretion\\n3. Gastrinoma\\n4. Pancreatic Neuro-endocrine tumour',correct:'1, 3 and 4',options:['1 and 3 only','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'ZES is caused by a gastrin-secreting tumour (gastrinoma), typically arising in the pancreas or duodenum. The triad: (1) Severe, recurrent, often multiple peptic ulcers in unusual locations; (3) A gastrin-secreting gastrinoma; (4) The tumour is a pancreatic or duodenal neuroendocrine tumour. Statement 2 is the opposite of the truth \u2014 ZES is characterised by gastric acid HYPERsecretion (not hyposecretion). Statements 1, 3, and 4 are correct.'},\n {id:59,stem:'In a healthy young adult, what proportion of sleep time is comprised Rapid Eye Movement (REM) sleep?',correct:'20-25%',options:['5-10%','20-25%','45-50%','70-75%'],exp:'In a healthy young adult, total sleep time is divided into approximately 75\u201380% NREM sleep and 20\u201325% REM sleep. REM sleep occurs in 4\u20135 cycles per night with each cycle lasting ~90 minutes and REM periods becoming longer towards morning. REM sleep is characterised by rapid eye movements, muscle atonia, vivid dreaming, and desynchronised EEG. REM decreases with age. The 20\u201325% figure is the standard examination answer for healthy young adults.'},\n {id:60,stem:'Which of the following drugs can cause Idiopathic Intracranial Hypertension?\\n1. Tetracycline\\n2. Retinoid\\n3. Vitamin A\\n4. Sulfonamides',correct:'1, 2 and 3',options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'IIH (formerly pseudotumour cerebri) presents with headache, papilloedema, and raised CSF pressure without a space-occupying lesion. Drug causes: tetracyclines (and doxycycline, minocycline) \u2014 most commonly implicated antibiotics; retinoids (isotretinoin) \u2014 significant side effect requiring ophthalmological monitoring; vitamin A (excess\/toxicity) \u2014 shares the retinoid mechanism. Sulfonamides are a much weaker association. Statements 1, 2, and 3 represent the three firmly established drug causes.'},\n {id:61,stem:\"As per the Gell and Coombs classification, Farmer's lung is which type of hypersensitivity disease?\",correct:'Type-III',options:['Type-I','Type-II','Type-III','Type-IV'],exp:\"Farmer's lung is a hypersensitivity pneumonitis (extrinsic allergic alveolitis) caused by inhalation of thermophilic actinomycetes (Saccharopolyspora rectivirgula) from mouldy hay. It is a Type III (immune complex-mediated) hypersensitivity reaction \u2014 IgG antibody-antigen immune complexes activate complement causing alveolar inflammation. Type I = IgE-mediated immediate hypersensitivity (asthma, urticaria). Type II = cytotoxic antibody-mediated (haemolytic anaemia). Type IV = delayed T-cell-mediated (tuberculin test, contact dermatitis).\"},\n {id:62,stem:'Hormonal regulation of salt and water balance in a nephron occurs at',correct:'Collecting Ducts',options:['Proximal Convoluted Tubule (PCT)','Loop of Henle','Distal Convoluted Tubule (DCT)','Collecting Ducts'],exp:'The primary site of hormonal regulation is the collecting duct. Aldosterone acts on principal cells of the cortical collecting duct, upregulating ENaC (epithelial Na\u207a channels) and ROMK (K\u207a channels), increasing Na\u207a reabsorption and K\u207a secretion. ADH\/vasopressin acts on V2 receptors of principal cells in the medullary collecting duct, inserting aquaporin-2 (AQP2) water channels to maximise water reabsorption. The collecting duct is the principal site where both aldosterone and ADH exert their integrated regulatory effects.'},\n {id:63,stem:'Which one of the following parameters suggests pre-renal azotemia?',correct:'Hyaline casts in urine sediment',options:['Renal tubular epithelial cell casts','Granular casts in urine sediment','Hyaline casts in urine sediment','Fractional excretion of sodium > 1%'],exp:'Pre-renal azotemia arises from renal hypoperfusion with intact tubular function. Urine is concentrated (high specific gravity) with sodium retention (FENa <1%). Urine sediment in pre-renal failure is bland \u2014 hyaline casts (formed from Tamm-Horsfall protein, seen in normal individuals and concentrated urine) are consistent with pre-renal aetiology. Renal tubular epithelial cell casts and muddy-brown granular casts are characteristic of acute tubular necrosis. FENa >1% suggests intrinsic renal disease.'},\n {id:64,stem:'Most common cause of Chronic Kidney Disease (CKD) is',correct:'Diabetic nephropathy',options:['Hypertension associated CKD','Autosomal Dominant Polycystic Kidney Disease (ADPKD)','Diabetic nephropathy','Glomerulonephritis'],exp:'Diabetic nephropathy (diabetic kidney disease) is the single most common cause of CKD and ESRD worldwide, accounting for approximately 40\u201345% of new cases requiring renal replacement therapy. Hypertensive nephrosclerosis is the second most common cause (~25\u201330%). Glomerulonephritis accounts for ~10\u201315%. ADPKD is the most common hereditary kidney disease but accounts for only ~5\u20138% of ESRD. For UPSC CMS, diabetic nephropathy is the correct answer.'},\n {id:65,stem:'Which of the following statements regarding contrast induced nephrotoxicity are correct?\\n1. Diabetes Mellitus is a risk factor.\\n2. N-acetylcysteine can fully reverse the renal injury.\\n3. Hydration is necessary.\\n4. Omit Metformin if nephrotoxicity occurs.',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','2, 3 and 4','1, 3 and 4'],exp:'Statement 1 is correct \u2014 DM (especially with pre-existing diabetic nephropathy) is a major CIN risk factor. Statement 2 is false \u2014 NAC may help prevent CIN but cannot fully reverse established renal injury; its benefit has been questioned in large trials. Statement 3 is correct \u2014 adequate IV hydration (isotonic saline) before and after contrast is the most effective preventive measure. Statement 4 is correct \u2014 metformin must be withheld at the time of contrast and for 48 hours after, because CIN-induced renal impairment can lead to metformin accumulation and fatal lactic acidosis. Statements 1, 3, and 4 are correct.'},\n {id:66,stem:'Which component of auto-regulation of glomerular filtration acts on the efferent arteriole?',correct:'Angiotensin II mediated vasoconstriction',options:['Autonomous myogenic reflex','Tubuloglomerular feedback','Angiotensin II mediated vasoconstriction','None of the above'],exp:'GFR autoregulation: (1) The myogenic reflex acts on the AFFERENT arteriole \u2014 stretch-activated calcium channels cause afferent vasoconstriction limiting GFR rise. (2) Tubuloglomerular feedback: macula densa senses NaCl concentration; at high NaCl, adenosine causes AFFERENT arteriolar constriction. Angiotensin II predominantly constricts the EFFERENT arteriole (higher AT1 receptor density), maintaining glomerular filtration pressure when systemic pressure falls. ACE inhibitors\/ARBs blunt this efferent vasoconstriction \u2014 hence their care in bilateral RAS.'},\n {id:67,stem:'Which of the following are consequences of nephrotic syndrome?\\n1. Increased lipoprotein synthesis\\n2. Low serum globulin levels\\n3. Increased serum aldosterone levels\\n4. Increased serum Antithrombin III levels',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2 and 3 only'],exp:'In nephrotic syndrome: (1) The liver compensates for low oncotic pressure by synthesising more lipoproteins (VLDL, LDL) causing hyperlipidaemia \u2014 correct. (2) Small immunoglobulins (IgG) are lost in urine, lowering serum globulins and predisposing to infections \u2014 correct. (3) Hypoalbuminaemia reduces plasma oncotic pressure causing effective volume depletion which activates RAAS, elevating aldosterone \u2014 correct. (4) Antithrombin III is LOST in urine (small protein ~58 kDa) \u2014 statement 4 (increased AT III) is false. Statements 1, 2, and 3 are correct.'},\n {id:68,stem:'Sickle cell syndromes are caused by a mutation in the \u03b2-globin gene. Which one of the following correctly describes the change?',correct:'Sixth amino acid-glutamic acid is replaced by valine.',options:['Sixth amino acid-glutamic acid is replaced by valine.','Twenty-sixth amino acid-glutamic acid is replaced by lysine.','Sixth amino acid-glutamic acid is replaced by lysine','Ninety eighth amino acid-valine is replaced by methionine.'],exp:'Sickle cell disease results from a point mutation in codon 6 of the \u03b2-globin gene (HBB): GAG \u2192 GTG, causing substitution of glutamic acid (hydrophilic, negatively charged) by valine (hydrophobic, uncharged) at the 6th amino acid position. This creates HbS. Under deoxygenated conditions, valine at position 6 docks into a complementary hydrophobic pocket on an adjacent HbS molecule, initiating polymerisation and sickling. The 26th amino acid substitution (Glu \u2192 Lys) characterises HbE.'},\n {id:69,stem:'In which of the following a high reticulocyte production index is seen?\\n1. Sickle cell disease\\n2. Vitamin B-12 deficiency\\n3. Glucose-6-phosphate dehydrogenase deficiency\\n4. Blood loss',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'High RPI (>2\u20133) indicates a hyperproliferative marrow responding to peripheral RBC destruction or loss. Sickle cell disease causes chronic haemolytic anaemia \u2014 the marrow is in compensated hyperplasia producing reticulocytes at a high rate (1 correct). G6PD deficiency causes acute haemolytic episodes during which RPI is markedly elevated (3 correct). Blood loss triggers erythropoietin release and compensatory reticulocytosis (4 correct). Vitamin B12 deficiency causes megaloblastic anaemia \u2014 a hypoproliferative state with a LOW reticulocyte index (2 incorrect). Statements 1, 3, and 4 are correct.'},\n {id:70,stem:'Which one of the following combinations of drugs can be used for treatment of relapsed myeloma?',correct:'Lenalidomide, Bortezomib, Dexamethasone',options:['Infliximab, Methotrexate, Dexamethasone','Lenalidomide, Bortezomib, Dexamethasone','Rituximab, Vincristine, Cytarabine','Methotrexate, Doxorubicin, Prednisone'],exp:'The VRd regimen \u2014 Bortezomib (proteasome inhibitor) + Lenalidomide (IMiD) + Dexamethasone \u2014 is a standard, guideline-recommended regimen for relapsed myeloma. Infliximab is an anti-TNF biologic for RA and IBD. Rituximab + Vincristine + Cytarabine are used in lymphomas (myeloma cells lack CD20). Methotrexate + Doxorubicin + Prednisone is for lymphoma, not myeloma. Lenalidomide, Bortezomib, Dexamethasone is the correct answer.'},\n {id:71,stem:'Which of the following can be used in the initial management of heparin induced thrombocytopenia?\\n1. Fondaparinux\\n2. Rivaroxaban\\n3. Lepirudin\\n4. Warfarin',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'HIT requires immediate heparin cessation and substitution with a non-heparin anticoagulant. Fondaparinux (synthetic pentasaccharide) does not cross-react with HIT antibodies. Lepirudin (recombinant hirudin, direct thrombin inhibitor) is a parenteral agent approved for HIT. Warfarin can be cautiously introduced once platelet count recovers to >150\u00d710\u2079\/L (early warfarin risks warfarin-induced skin necrosis from protein C depletion). Rivaroxaban is an emerging option but not yet first-line standard of care for HIT in the classical UPSC CMS teaching. Statements 1, 3, and 4 are correct.'},\n {id:72,stem:'Red cell protoporphyrin levels will be raised in which of the following conditions?\\n1. Absolute iron deficiency\\n2. Relative iron deficiency\\n3. Lead poisoning',correct:'1, 2 and 3',options:['1 and 3 only','1 and 2 only','2 and 3 only','1, 2 and 3'],exp:'Free erythrocyte protoporphyrin (FEP) accumulates when iron is unavailable for haem synthesis. This occurs in: (1) Absolute iron deficiency anaemia \u2014 iron stores depleted; (2) Relative (functional) iron deficiency \u2014 iron trapped in reticuloendothelial stores; FEP rises because iron cannot be mobilised fast enough; (3) Lead poisoning \u2014 lead directly inhibits ferrochelatase (the enzyme inserting Fe\u00b2\u207a into protoporphyrin IX), causing protoporphyrin accumulation irrespective of iron availability. All three are correct.'},\n {id:73,stem:'Negative Iron Balance is the first stage in the progression to Iron Deficiency Anaemia. Which of the following laboratory investigations will be found deranged in this stage, thereby pointing to early iron-store depletion?',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Stage 1 (negative iron balance \/ pre-latent iron deficiency): iron stores are being depleted but haemoglobin and serum iron are still normal. Investigations deranged at this stage: (1) Bone marrow iron stores (Prussian blue stain) \u2014 the first and most sensitive indicator of iron depletion; (2) Percent transferrin saturation \u2014 begins to fall as stores diminish; (3) Serum ferritin \u2014 the best single indicator of total body iron stores; falls early. TIBC (statement 4) rises in later stages (Stage 2 onwards). Statements 1, 2, and 3 are deranged at Stage 1.'},\n {id:74,stem:'Which of the following drugs carry a definite risk of causing clinical haemolysis in persons suffering from Glucose-6 phosphate dehydrogenase deficiency?',correct:'1, 2, 3 and 4',options:['1, 3 and 4','1 and 2 only','2, 3 and 4 only','1, 2, 3 and 4'],exp:'G6PD deficiency causes haemolytic anaemia when RBCs are exposed to oxidative stress. All four listed drugs are oxidising agents with definite haemolytic risk: Primaquine (antimalarial) \u2014 the prototype drug causing haemolysis in G6PD deficiency. Dapsone (antileprosy, PCP prophylaxis) \u2014 causes haemolysis even at therapeutic doses. Cotrimoxazole (TMP-SMX) \u2014 the sulfonamide component is the oxidant. Nitrofurantoin (urinary antiseptic) \u2014 definite haemolytic risk. All four are correct.'},\n {id:75,stem:'A 40 year old male presented with complaints of generalised weakness, weight loss, abdominal discomfort and decreased appetite. On examination Splenomegaly (massive) was present. On investigation it was found that haemoglobin was 7\u00b70 g\/dL, platelet count \u2013 8 lakh per cubic mm, WBC-90000 per cubic mm. Most probably this is the case of',correct:'Chronic myeloid leukemia',options:['Chronic lymphocytic leukemia','Chronic myeloid leukemia','Acute lymphoblastic leukemia','Acute myeloid leukemia'],exp:'The combination of massive splenomegaly + markedly elevated WBC (~90,000\/\u03bcL) + elevated platelet count (800,000\/\u03bcL thrombocytosis) + moderate anaemia in a middle-aged patient is the classic presentation of CML. CML is caused by BCR-ABL1 fusion gene (Philadelphia chromosome, t(9;22)) producing a constitutively active tyrosine kinase. Massive splenomegaly from extramedullary haematopoiesis is the hallmark. Treatment: imatinib.'},\n {id:76,stem:'Which of the following are risk factors for type 2 diabetes mellitus?\\n1. Family history of diabetes\\n2. Underweight\\n3. Physical inactivity\\n4. Polycystic ovary syndrome',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Risk factors for T2DM: (1) Family history \u2014 first-degree relative with T2DM confers 3\u20135\u00d7 increased risk. (3) Physical inactivity \u2014 reduces glucose uptake in skeletal muscle and worsens insulin resistance. (4) PCOS \u2014 characterised by hyperinsulinaemia and insulin resistance; women with PCOS have 5\u20137\u00d7 higher lifetime risk. Underweight (statement 2) is a PROTECTIVE factor \u2014 obesity and central adiposity are the major modifiable risk factors. Statements 1, 3, and 4 are correct.'},\n {id:77,stem:'Which of the following statements with regard to gestational diabetes mellitus (GDM) are correct?\\n1. Most women revert to normal glucose tolerance post partum\\n2. Children born to a GDM mother have no increased risk of diabetes mellitus later in life\\n3. Glucose intolerance develops during second and third trimesters\\n4. Insulin resistance is related to metabolic changes of pregnancy',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Statement 1 is correct \u2014 approximately 90% of GDM women revert to normal glucose tolerance after delivery, though retaining 50% lifetime risk of T2DM. Statement 2 is false \u2014 offspring of GDM mothers have significantly increased risk of obesity, metabolic syndrome, and T2DM (intrauterine programming). Statement 3 is correct \u2014 placental hormones peak in 2nd and 3rd trimesters causing progressive insulin resistance, the window when GDM manifests (OGTT screening at 24\u201328 weeks). Statement 4 is correct \u2014 the physiological insulin resistance of pregnancy unmasks GDM in susceptible women. Statements 1, 3, and 4 are correct.'},\n {id:78,stem:'A Thyroid Function Test report shows the following results: TSH-Undetectable, T3-Raised, T4-Raised. Which one of the following will be the most likely interpretation on the basis of the above report?',correct:'Primary thyrotoxicosis',options:['Hypothyroidism secondary to pituitary disease','Transient thyroiditis in evolution','Primary thyrotoxicosis','Overtreatment of hypothyroidism with Liothyronine'],exp:\"TSH undetectable (suppressed) + raised T3 and T4 = primary thyrotoxicosis. In primary thyrotoxicosis (Graves' disease, toxic multinodular goitre, toxic adenoma), excess thyroid hormones directly suppress TSH via negative feedback on pituitary thyrotrophs. Secondary hypothyroidism would show low TSH with LOW T3\/T4. The straightforward pattern of suppressed TSH + raised both T3 and T4 is primary thyrotoxicosis.\"},\n {id:79,stem:'Which of the following biochemical abnormality is seen in severe hypertriglyceridaemia?',correct:'Pseudohyponatremia',options:['Pseudohyponatremia','Metabolic alkalosis','Hyperuricemia','Hyperkalemia'],exp:'In severe hypertriglyceridaemia (triglycerides typically >1000 mg\/dL), large lipid particles displace water in a given volume of plasma, reducing the water fraction. Since sodium is distributed in the aqueous phase only, but older dilution-based methods measure Na\u207a in total plasma volume, the measured serum sodium appears falsely low \u2014 pseudohyponatremia. The true tonicity is normal. This is a laboratory artefact and does not require treatment.'},\n {id:80,stem:'Which of the following statements are correct about treatment with Vitamin D supplement?\\n1. Serum calcium levels improve earlier than serum PTH levels.\\n2. Patients should be closely observed with serial vitamin D levels in blood as vitamin D toxicity occurs frequently\\n3. Vitamin D supplementation should always be in conjunction with calcium supplementation.\\n4. Nephrolithiasis is a known complication',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Statement 1 is correct \u2014 serum calcium normalises relatively quickly (within weeks), while PTH normalisation takes several months. Statement 2 is false \u2014 vitamin D toxicity is actually rare with standard supplementation doses; routine serial 25(OH)D monitoring is not required unless high-dose regimens are used. Statement 3 is correct \u2014 for osteoporosis and osteomalacia treatment, vitamin D should generally be co-prescribed with calcium supplements. Statement 4 is correct \u2014 nephrolithiasis (calcium oxalate and calcium phosphate stones) is a recognised complication of excessive vitamin D-mediated hypercalciuria. Statements 1, 3, and 4 are correct.'}\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,quizSubmitted=false;\n function shuffle(arr){const a=arr.slice();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]];}return a;}\n function fmtTime(s){const m=Math.floor(s\/60),sec=s%60;return(m<10?'0':'')+m+':'+(sec<10?'0':'')+sec;}\n function startTimer(){\n if(timerRunning||quizSubmitted)return;timerRunning=true;\n const btn=document.getElementById(NS+'-timer-btn');btn.textContent='\u23f1 '+fmtTime(timerRemaining);btn.classList.add('running');\n document.getElementById(NS+'-timer-item').classList.add('active');\n timerInterval=setInterval(function(){\n timerRemaining--;const disp=fmtTime(timerRemaining);\n document.getElementById(NS+'-timer-display').textContent=disp;document.getElementById(NS+'-timer-btn').textContent='\u23f1 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.cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms22p1b .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms22p1b .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms22p1b .cq-retry-btn{margin-top:22px;background:transparent;border:2px solid var(--ter);color:var(--ter);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#cms22p1b .cq-retry-btn:hover{background:var(--ter);color:var(--white)}\n@media(max-width:480px){#cms22p1b .cq-header h1{font-size:1.15rem}#cms22p1b .cq-qtext{font-size:0.88rem}#cms22p1b .cq-opt-text{font-size:0.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms22p1b\">\n <div class=\"cq-sentinel\" id=\"cms22p1b-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms22p1b-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms22p1b-timer-item\">\u23f1 <strong id=\"cms22p1b-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms22p1b-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms22p1b-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms22p1b-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms22p1b-sn\">0<\/strong> \/ <strong id=\"cms22p1b-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms22p1b-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms22p1b-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms22p1b-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms22p1b-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2022<br>General Medicine & Paediatrics \u00b7 Paper I \u00b7 Part B<\/h1>\n <p>Endocrinology \u00b7 Rheumatology \u00b7 Nephrology \u00b7 Emergency Medicine \u00b7 Haematology \u00b7 Infectious Disease<\/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=\"cms22p1b-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms22p1b-questions\"><\/div>\n <div class=\"cq-submit-wrap\"><button class=\"cq-btn\" id=\"cms22p1b-submit\">Submit Answers<\/button><\/div>\n <div class=\"cq-score\" id=\"cms22p1b-score\">\n <div class=\"cq-score-ring\" id=\"cms22p1b-ring\"><div class=\"cq-ring-inner\"><span class=\"cq-ring-pct\" id=\"cms22p1b-ring-pct\">0%<\/span><span class=\"cq-ring-sub\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms22p1b-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms22p1b-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms22p1b-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms22p1b-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms22p1b-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms22p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms22p1b',TOTAL=40,MAX=160,TIMER_SECS=2400,GRACE_SECS=10;\n const QUESTIONS=[\n {id:41,stem:'Which of the following are useful for the treatment of Hirsutism?\\n1. Amiloride\\n2. Oestrogen\\n3. Finasteride\\n4. Spironolactone',correct:'2, 3 and 4',options:['1, 2 and 3','1, 2 and 4','3 and 4 only','2, 3 and 4'],exp:'Oestrogen (via OCP) raises SHBG, reducing free testosterone. Finasteride (5\u03b1-reductase type II inhibitor) blocks conversion of testosterone to DHT at the hair follicle. Spironolactone has significant anti-androgen activity \u2014 the most widely used pharmacological treatment for hirsutism. Amiloride is a potassium-sparing diuretic with no meaningful anti-androgen effect. Statements 2, 3, and 4 are correct.'},\n {id:42,stem:'Which of the following is a long acting insulin?',correct:'Glargine',options:['Aspart','Glargine','Lispro','Regular'],exp:'Insulin glargine (Lantus) is a long-acting basal insulin analogue with ~20\u201324 hours duration and a peakless (flat) pharmacokinetic profile \u2014 ideal for once-daily basal coverage with low hypoglycaemia risk. Aspart and lispro are rapid-acting analogues (onset 10\u201315 min, duration 3\u20135 h). Regular (soluble) insulin is short-acting (onset 30\u201360 min, duration 6\u20138 h). Other long-acting analogues: detemir and degludec (~42 h).'},\n {id:43,stem:'A 15 year girl presents to the hospital with severe abdominal pain, vomiting and cold extremities. She has tachycardia and hypotension. Lab investigations show blood glucose 400 mg\/dL, blood pH 6\u00b79, urine ketones +++ and serum creatinine of 1\u00b74 mg\/dL. She is promptly administered IV fluids and insulin. After 4 hours, she complains of inability to lift her limbs. What is the next step to be considered in her management?',correct:'Potassium repletion',options:['Intravenous normal saline','Intravenous sodium bicarbonate','Urine sample for ketones','Potassium repletion'],exp:'This is DKA. After 4 hours of insulin and IV fluid therapy, new limb weakness is caused by hypokalaemia. Insulin drives potassium into cells (K\u207a-Na\u207a-ATPase activation) and correction of acidosis shifts K\u207a intracellularly, rapidly lowering serum potassium. Total body K\u207a is severely depleted in DKA. Hypokalaemic paralysis is a well-recognised complication during DKA treatment. Potassium repletion (IV KCl) is urgently required. Sodium bicarbonate is not routinely indicated even at pH 6.9.'},\n {id:44,stem:'Composition of oral rehydration solution (WHO) is',correct:'Na\u201390 m mol\/L, K\u201320 m mol\/L, Cl\u201380 m mol\/L, Energy\u201354 kca\/L',options:['Na\u201390 m mol\/L, K\u201320 m mol\/L, Cl\u201380 m mol\/L, Energy\u201354 kca\/L','Na\u201380 m mol\/L, K\u201320 m mol\/L, Cl\u201370 m mol\/L, Energy\u201354 kca\/L','Na\u201390 m mol\/L, K\u201340 m mol\/L, Cl\u201380 m mol\/L, Energy\u201327 kca\/L','Na\u201380 m mol\/L, K\u201320 m mol\/L, Cl\u201370 m mol\/L, Energy\u201354 kca\/L'],exp:'WHO standard ORS: sodium 90 mmol\/L, potassium 20 mmol\/L, chloride 80 mmol\/L, glucose 111 mmol\/L (20 g\/L), energy approximately 54 kcal\/L, total osmolarity ~311 mOsm\/L. This is the standard formulation taught for cholera and severe dehydration and remains the standard answer in this examination context.'},\n {id:45,stem:'Which of the following are correct regarding tuberculous meningitis?\\n1. Acid-Fast Bacilli are infrequently seen on direct smear of CSF\\n2. CSF culture for MTB is the gold standard for diagnosis\\n3. Xpert MTB\/RIF assay is a preferred initial diagnostic option',correct:'1, 2 and 3',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'All three are correct. (1) AFB are seen on direct ZN smear of CSF in only 10\u201340% of TBM cases \u2014 sensitivity is low; multiple large-volume samples improve yield. (2) Mycobacterial culture (MGIT liquid culture) remains the gold standard with >80% sensitivity, though requiring 4\u20138 weeks. (3) WHO recommends Xpert MTB\/RIF as the preferred initial rapid test for TBM \u2014 same-day results with ~80% sensitivity and rifampicin resistance detection. All three are correct.'},\n {id:46,stem:'Which one of the following is a subcutaneous preparation useful for treatment of osteoporosis?',correct:'Denosumab',options:['Denosumab','Alendronate','Zoledronic acid','Raloxifene'],exp:'Denosumab (Prolia) is a fully human monoclonal antibody against RANK-L. By blocking RANK-L it prevents osteoclast differentiation and bone resorption. It is administered as a subcutaneous injection of 60 mg every 6 months. Alendronate is an oral bisphosphonate. Zoledronic acid is an intravenous bisphosphonate (annual infusion). Raloxifene is an oral SERM.'},\n {id:47,stem:'Which of the following are correct with regard to osteoporosis?\\n1. It does not cause symptoms until a fracture occurs\\n2. Vertebral fracture can present with loss of height, in absence of pain\\n3. Smoking is protective\\n4. It sometimes presents incidentally as radiological osteopenia',correct:'1, 2 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:\"Osteoporosis is a silent disease until fracture occurs \u2014 statement 1 is correct. Vertebral compression fractures frequently occur without acute pain and manifest as progressive loss of height and kyphosis ('dowager's hump') \u2014 statement 2 is correct. Smoking is a well-established RISK FACTOR for osteoporosis \u2014 statement 3 (smoking is protective) is false. Osteoporosis is often an incidental finding on plain radiographs as osteopenia \u2014 statement 4 is correct. Statements 1, 2, and 4 are correct.\"},\n {id:48,stem:'Which of the following are correct with regard to Ankylosing spondylitis?\\n1. Bamboo spine may be seen\\n2. Early morning back pain is rare\\n3. Uveitis is most common extra-articular feature\\n4. It is more common in males',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Bamboo spine (complete vertebral fusion with syndesmophytes) is the pathognomonic radiological finding in advanced AS \u2014 statement 1 is correct. Early morning back stiffness and pain that IMPROVES with exercise (not rest) is the hallmark of inflammatory back pain in AS; it is characteristic and NOT rare \u2014 statement 2 (rare) is false. Acute anterior uveitis (iritis) is the most common extra-articular manifestation occurring in 25\u201330% of patients \u2014 statement 3 is correct. AS is 2\u20133 times more common in males \u2014 statement 4 is correct. Statements 1, 3, and 4 are correct.'},\n {id:49,stem:'Carpal Tunnel Syndrome is associated with which of the following features?\\n1. Pain and tingling in hands at night\\n2. Weakness of thumb abduction\\n3. Loss of sensation over lateral half of the palm\\n4. Atrophy of hypothenar eminence',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Carpal tunnel syndrome results from compression of the median nerve at the wrist. Features: (1) Nocturnal pain and paraesthesiae in median nerve distribution \u2014 classic presenting symptom; (2) Weakness of thumb abduction (abductor pollicis brevis) \u2014 correct; (3) Loss of sensation over the lateral palm (palmar cutaneous branch) \u2014 correct. Hypothenar atrophy (statement 4) indicates ulnar nerve pathology \u2014 thenar atrophy is the CTS finding. Statements 1, 2, and 3 are correct.'},\n {id:50,stem:'Which of the following can be used to monitor disease activity in rheumatoid arthritis?\\n1. Pain (visual analogue scale)\\n2. X-Ray of hands and wrists\\n3. DAS 28 score\\n4. ESR',correct:'2, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'DAS28 is the gold standard composite measure of RA disease activity incorporating tender joint count, swollen joint count, ESR (or CRP), and patient global assessment. ESR is a validated acute-phase reactant used independently and within DAS28. X-ray of hands and wrists tracks erosive structural damage over time. Pain VAS alone is a subjective patient-reported outcome and not a validated standalone measure of objective RA disease activity. Statements 2, 3, and 4 are correct.'},\n {id:51,stem:'Which one of the following HIV-associated infections is least likely with CD4 count > 100 cells\/mm\u00b3?',correct:'Cerebral toxoplasmosis',options:['Cerebral toxoplasmosis','Tuberculosis','Herpes zoster','Pneumocystis jirovecii pneumonia'],exp:'Cerebral toxoplasmosis almost exclusively occurs when CD4 falls below 100 cells\/mm\u00b3, typically <50 \u2014 it is the OI least likely at CD4 >100. PCP typically occurs at CD4 <200 but can occur up to 200. Herpes zoster can reactivate at CD4 up to 500. TB can occur at any CD4 level. Cerebral toxoplasmosis is least likely with CD4 >100 cells\/mm\u00b3.'},\n {id:52,stem:'Tests for graphesthesia and stereognosis are used clinically to assess',correct:'Cortical sensation',options:['Cortical sensation','Posterior column','Cerebellar function','Lateral spinothalamic tract'],exp:'Graphesthesia (identifying numbers or letters traced on skin) and stereognosis (identifying objects by touch alone) are tests of cortical sensory integration \u2014 they require intact primary sensory input AND parietal cortex processing. These are examples of discriminative (cortical) sensation, processed in the contralateral somatosensory cortex (postcentral gyrus). They are impaired in parietal lobe lesions even when basic primary sensations are intact.'},\n {id:53,stem:'A blast victim is brought to the emergency. Victim is unconscious. BP is 80\/50 mm Hg. Pulse is 110 per minute and thready and SpO\u2082 is 70%. Victim has rapid shallow breathing and signs of external blood loss are present. JVP is raised and heart sounds are absent on auscultation. Which one of the following is the next single most immediate step in the management, after securing airway, breathing and circulation?',correct:'Urgent pericardiocentesis',options:['Chest X-ray PA and lateral view','Urgent needle thoracostomy','Urgent pericardiocentesis','Blood for cross match followed by blood transfusion'],exp:\"The clinical triad of hypotension + raised JVP + absent heart sounds = Beck's triad of cardiac tamponade. In a blast injury, haemopericardium causes tamponade. After ABC is secured, the next immediate life-saving step is urgent pericardiocentesis. A chest X-ray would delay definitive treatment. Needle thoracostomy treats tension pneumothorax (absent breath sounds, tracheal deviation). Blood transfusion addresses hypovolaemia but will not relieve tamponade.\"},\n {id:54,stem:'A 21 year young female was brought to Emergency Department with history of unknown substance ingestion. She was having vomiting, profuse diarrhoea, bronchorrhoea and excessive sweating. On examination miosis and muscular fasciculations were present. What is the most likely diagnosis?',correct:'Organophosphorus poisoning',options:['Corrosive substance poisoning','Aluminium phosphide poisoning','Zinc phosphide poisoning','Organophosphorus poisoning'],exp:'This is the classic SLUDGE\/DUMBELS toxidrome of cholinergic excess: Salivation, Lacrimation, Urination, Defaecation, GI distress, Emesis, Bronchospasm\/Bronchorrhoea, Bradycardia, Sweating + miosis and muscular fasciculations (nicotinic effect). All features point to organophosphorus poisoning \u2014 irreversible acetylcholinesterase inhibition causing ACh accumulation. Management: atropine (muscarinic reversal) + pralidoxime + benzodiazepines for seizures.'},\n {id:55,stem:'A young female of 22 year old presented to the medical emergency with complaints of nausea, vomiting, abdominal pain, diarrhoea, and convulsions along with methaemoglobinaemia. What is the likely diagnosis?',correct:'Copper sulphate poisoning',options:['Aluminium phosphide poisoning','Zinc phosphide poisoning','Copper sulphate poisoning','Lead poisoning'],exp:'Copper sulphate poisoning classically causes: GI symptoms (nausea, vomiting, diarrhoea, abdominal pain), neurological features (convulsions), and characteristically methaemoglobinaemia \u2014 copper oxidises haemoglobin Fe\u00b2\u207a to Fe\u00b3\u207a. The blue-green vomitus is another clue. Treatment: gastric lavage, IV fluids, D-penicillamine (chelation), and methylene blue for methaemoglobinaemia. Aluminium and zinc phosphide cause phosphine gas toxicity. Lead poisoning causes chronic encephalopathy.'},\n {id:56,stem:'Which of the following are the components of the SOFA (Sequential Organ Failure Assessment)?\\n1. Serum bilirubin\\n2. Platelet count\\n3. Leucocyte count\\n4. Serum Creatinine',correct:'1, 2 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'The SOFA score assesses six organ systems: Respiratory (PaO\u2082\/FiO\u2082), Coagulation (platelet count), Liver (serum bilirubin), Cardiovascular (MAP or vasopressor), CNS (GCS), Renal (serum creatinine or urine output). Leucocyte count is NOT a SOFA component (it is part of SIRS criteria). Serum bilirubin (1), platelet count (2), and serum creatinine (4) are all SOFA components. Statements 1, 2, and 4 are correct.'},\n {id:57,stem:\"Purtscher's retinopathy may be associated with\",correct:'Acute pancreatitis',options:['Acute fulminant hepatic failure','Acute pancreatitis','Acute peritonitis','Acute cholecystitis'],exp:\"Purtscher's retinopathy is a traumatic occlusive microangiopathy of the retinal vasculature characterised by cotton-wool spots, haemorrhages, and sudden visual loss. It classically occurs with severe crush injuries but is also a recognised complication of acute pancreatitis (Purtscher-like retinopathy) \u2014 thought to be caused by complement activation, granulocyte aggregation, and fat emboli to retinal arterioles from pancreatic lipase-mediated fat necrosis. Acute pancreatitis is the classic non-traumatic association tested in examinations.\"},\n {id:58,stem:'Which of the following may constitute the characteristic triad of Zollinger-Ellison syndrome?\\n1. Severe peptic ulceration\\n2. Gastric acid hyposecretion\\n3. Gastrinoma\\n4. Pancreatic Neuro-endocrine tumour',correct:'1, 3 and 4',options:['1 and 3 only','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'ZES is caused by a gastrin-secreting tumour (gastrinoma), typically arising in the pancreas or duodenum. The triad: (1) Severe, recurrent, often multiple peptic ulcers in unusual locations; (3) A gastrin-secreting gastrinoma; (4) The tumour is a pancreatic or duodenal neuroendocrine tumour. Statement 2 is the opposite of the truth \u2014 ZES is characterised by gastric acid HYPERsecretion (not hyposecretion). Statements 1, 3, and 4 are correct.'},\n {id:59,stem:'In a healthy young adult, what proportion of sleep time is comprised Rapid Eye Movement (REM) sleep?',correct:'20-25%',options:['5-10%','20-25%','45-50%','70-75%'],exp:'In a healthy young adult, total sleep time is divided into approximately 75\u201380% NREM sleep and 20\u201325% REM sleep. REM sleep occurs in 4\u20135 cycles per night with each cycle lasting ~90 minutes and REM periods becoming longer towards morning. REM sleep is characterised by rapid eye movements, muscle atonia, vivid dreaming, and desynchronised EEG. REM decreases with age. The 20\u201325% figure is the standard examination answer for healthy young adults.'},\n {id:60,stem:'Which of the following drugs can cause Idiopathic Intracranial Hypertension?\\n1. Tetracycline\\n2. Retinoid\\n3. Vitamin A\\n4. Sulfonamides',correct:'1, 2 and 3',options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'IIH (formerly pseudotumour cerebri) presents with headache, papilloedema, and raised CSF pressure without a space-occupying lesion. Drug causes: tetracyclines (and doxycycline, minocycline) \u2014 most commonly implicated antibiotics; retinoids (isotretinoin) \u2014 significant side effect requiring ophthalmological monitoring; vitamin A (excess\/toxicity) \u2014 shares the retinoid mechanism. Sulfonamides are a much weaker association. Statements 1, 2, and 3 represent the three firmly established drug causes.'},\n {id:61,stem:\"As per the Gell and Coombs classification, Farmer's lung is which type of hypersensitivity disease?\",correct:'Type-III',options:['Type-I','Type-II','Type-III','Type-IV'],exp:\"Farmer's lung is a hypersensitivity pneumonitis (extrinsic allergic alveolitis) caused by inhalation of thermophilic actinomycetes (Saccharopolyspora rectivirgula) from mouldy hay. It is a Type III (immune complex-mediated) hypersensitivity reaction \u2014 IgG antibody-antigen immune complexes activate complement causing alveolar inflammation. Type I = IgE-mediated immediate hypersensitivity (asthma, urticaria). Type II = cytotoxic antibody-mediated (haemolytic anaemia). Type IV = delayed T-cell-mediated (tuberculin test, contact dermatitis).\"},\n {id:62,stem:'Hormonal regulation of salt and water balance in a nephron occurs at',correct:'Collecting Ducts',options:['Proximal Convoluted Tubule (PCT)','Loop of Henle','Distal Convoluted Tubule (DCT)','Collecting Ducts'],exp:'The primary site of hormonal regulation is the collecting duct. Aldosterone acts on principal cells of the cortical collecting duct, upregulating ENaC (epithelial Na\u207a channels) and ROMK (K\u207a channels), increasing Na\u207a reabsorption and K\u207a secretion. ADH\/vasopressin acts on V2 receptors of principal cells in the medullary collecting duct, inserting aquaporin-2 (AQP2) water channels to maximise water reabsorption. The collecting duct is the principal site where both aldosterone and ADH exert their integrated regulatory effects.'},\n {id:63,stem:'Which one of the following parameters suggests pre-renal azotemia?',correct:'Hyaline casts in urine sediment',options:['Renal tubular epithelial cell casts','Granular casts in urine sediment','Hyaline casts in urine sediment','Fractional excretion of sodium > 1%'],exp:'Pre-renal azotemia arises from renal hypoperfusion with intact tubular function. Urine is concentrated (high specific gravity) with sodium retention (FENa <1%). Urine sediment in pre-renal failure is bland \u2014 hyaline casts (formed from Tamm-Horsfall protein, seen in normal individuals and concentrated urine) are consistent with pre-renal aetiology. Renal tubular epithelial cell casts and muddy-brown granular casts are characteristic of acute tubular necrosis. FENa >1% suggests intrinsic renal disease.'},\n {id:64,stem:'Most common cause of Chronic Kidney Disease (CKD) is',correct:'Diabetic nephropathy',options:['Hypertension associated CKD','Autosomal Dominant Polycystic Kidney Disease (ADPKD)','Diabetic nephropathy','Glomerulonephritis'],exp:'Diabetic nephropathy (diabetic kidney disease) is the single most common cause of CKD and ESRD worldwide, accounting for approximately 40\u201345% of new cases requiring renal replacement therapy. Hypertensive nephrosclerosis is the second most common cause (~25\u201330%). Glomerulonephritis accounts for ~10\u201315%. ADPKD is the most common hereditary kidney disease but accounts for only ~5\u20138% of ESRD. For UPSC CMS, diabetic nephropathy is the correct answer.'},\n {id:65,stem:'Which of the following statements regarding contrast induced nephrotoxicity are correct?\\n1. Diabetes Mellitus is a risk factor.\\n2. N-acetylcysteine can fully reverse the renal injury.\\n3. Hydration is necessary.\\n4. Omit Metformin if nephrotoxicity occurs.',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','2, 3 and 4','1, 3 and 4'],exp:'Statement 1 is correct \u2014 DM (especially with pre-existing diabetic nephropathy) is a major CIN risk factor. Statement 2 is false \u2014 NAC may help prevent CIN but cannot fully reverse established renal injury; its benefit has been questioned in large trials. Statement 3 is correct \u2014 adequate IV hydration (isotonic saline) before and after contrast is the most effective preventive measure. Statement 4 is correct \u2014 metformin must be withheld at the time of contrast and for 48 hours after, because CIN-induced renal impairment can lead to metformin accumulation and fatal lactic acidosis. Statements 1, 3, and 4 are correct.'},\n {id:66,stem:'Which component of auto-regulation of glomerular filtration acts on the efferent arteriole?',correct:'Angiotensin II mediated vasoconstriction',options:['Autonomous myogenic reflex','Tubuloglomerular feedback','Angiotensin II mediated vasoconstriction','None of the above'],exp:'GFR autoregulation: (1) The myogenic reflex acts on the AFFERENT arteriole \u2014 stretch-activated calcium channels cause afferent vasoconstriction limiting GFR rise. (2) Tubuloglomerular feedback: macula densa senses NaCl concentration; at high NaCl, adenosine causes AFFERENT arteriolar constriction. Angiotensin II predominantly constricts the EFFERENT arteriole (higher AT1 receptor density), maintaining glomerular filtration pressure when systemic pressure falls. ACE inhibitors\/ARBs blunt this efferent vasoconstriction \u2014 hence their care in bilateral RAS.'},\n {id:67,stem:'Which of the following are consequences of nephrotic syndrome?\\n1. Increased lipoprotein synthesis\\n2. Low serum globulin levels\\n3. Increased serum aldosterone levels\\n4. Increased serum Antithrombin III levels',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2 and 3 only'],exp:'In nephrotic syndrome: (1) The liver compensates for low oncotic pressure by synthesising more lipoproteins (VLDL, LDL) causing hyperlipidaemia \u2014 correct. (2) Small immunoglobulins (IgG) are lost in urine, lowering serum globulins and predisposing to infections \u2014 correct. (3) Hypoalbuminaemia reduces plasma oncotic pressure causing effective volume depletion which activates RAAS, elevating aldosterone \u2014 correct. (4) Antithrombin III is LOST in urine (small protein ~58 kDa) \u2014 statement 4 (increased AT III) is false. Statements 1, 2, and 3 are correct.'},\n {id:68,stem:'Sickle cell syndromes are caused by a mutation in the \u03b2-globin gene. Which one of the following correctly describes the change?',correct:'Sixth amino acid-glutamic acid is replaced by valine.',options:['Sixth amino acid-glutamic acid is replaced by valine.','Twenty-sixth amino acid-glutamic acid is replaced by lysine.','Sixth amino acid-glutamic acid is replaced by lysine','Ninety eighth amino acid-valine is replaced by methionine.'],exp:'Sickle cell disease results from a point mutation in codon 6 of the \u03b2-globin gene (HBB): GAG \u2192 GTG, causing substitution of glutamic acid (hydrophilic, negatively charged) by valine (hydrophobic, uncharged) at the 6th amino acid position. This creates HbS. Under deoxygenated conditions, valine at position 6 docks into a complementary hydrophobic pocket on an adjacent HbS molecule, initiating polymerisation and sickling. The 26th amino acid substitution (Glu \u2192 Lys) characterises HbE.'},\n {id:69,stem:'In which of the following a high reticulocyte production index is seen?\\n1. Sickle cell disease\\n2. Vitamin B-12 deficiency\\n3. Glucose-6-phosphate dehydrogenase deficiency\\n4. Blood loss',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'High RPI (>2\u20133) indicates a hyperproliferative marrow responding to peripheral RBC destruction or loss. Sickle cell disease causes chronic haemolytic anaemia \u2014 the marrow is in compensated hyperplasia producing reticulocytes at a high rate (1 correct). G6PD deficiency causes acute haemolytic episodes during which RPI is markedly elevated (3 correct). Blood loss triggers erythropoietin release and compensatory reticulocytosis (4 correct). Vitamin B12 deficiency causes megaloblastic anaemia \u2014 a hypoproliferative state with a LOW reticulocyte index (2 incorrect). Statements 1, 3, and 4 are correct.'},\n {id:70,stem:'Which one of the following combinations of drugs can be used for treatment of relapsed myeloma?',correct:'Lenalidomide, Bortezomib, Dexamethasone',options:['Infliximab, Methotrexate, Dexamethasone','Lenalidomide, Bortezomib, Dexamethasone','Rituximab, Vincristine, Cytarabine','Methotrexate, Doxorubicin, Prednisone'],exp:'The VRd regimen \u2014 Bortezomib (proteasome inhibitor) + Lenalidomide (IMiD) + Dexamethasone \u2014 is a standard, guideline-recommended regimen for relapsed myeloma. Infliximab is an anti-TNF biologic for RA and IBD. Rituximab + Vincristine + Cytarabine are used in lymphomas (myeloma cells lack CD20). Methotrexate + Doxorubicin + Prednisone is for lymphoma, not myeloma. Lenalidomide, Bortezomib, Dexamethasone is the correct answer.'},\n {id:71,stem:'Which of the following can be used in the initial management of heparin induced thrombocytopenia?\\n1. Fondaparinux\\n2. Rivaroxaban\\n3. Lepirudin\\n4. Warfarin',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'HIT requires immediate heparin cessation and substitution with a non-heparin anticoagulant. Fondaparinux (synthetic pentasaccharide) does not cross-react with HIT antibodies. Lepirudin (recombinant hirudin, direct thrombin inhibitor) is a parenteral agent approved for HIT. Warfarin can be cautiously introduced once platelet count recovers to >150\u00d710\u2079\/L (early warfarin risks warfarin-induced skin necrosis from protein C depletion). Rivaroxaban is an emerging option but not yet first-line standard of care for HIT in the classical UPSC CMS teaching. Statements 1, 3, and 4 are correct.'},\n {id:72,stem:'Red cell protoporphyrin levels will be raised in which of the following conditions?\\n1. Absolute iron deficiency\\n2. Relative iron deficiency\\n3. Lead poisoning',correct:'1, 2 and 3',options:['1 and 3 only','1 and 2 only','2 and 3 only','1, 2 and 3'],exp:'Free erythrocyte protoporphyrin (FEP) accumulates when iron is unavailable for haem synthesis. This occurs in: (1) Absolute iron deficiency anaemia \u2014 iron stores depleted; (2) Relative (functional) iron deficiency \u2014 iron trapped in reticuloendothelial stores; FEP rises because iron cannot be mobilised fast enough; (3) Lead poisoning \u2014 lead directly inhibits ferrochelatase (the enzyme inserting Fe\u00b2\u207a into protoporphyrin IX), causing protoporphyrin accumulation irrespective of iron availability. All three are correct.'},\n {id:73,stem:'Negative Iron Balance is the first stage in the progression to Iron Deficiency Anaemia. Which of the following laboratory investigations will be found deranged in this stage, thereby pointing to early iron-store depletion?',correct:'1, 2 and 3',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Stage 1 (negative iron balance \/ pre-latent iron deficiency): iron stores are being depleted but haemoglobin and serum iron are still normal. Investigations deranged at this stage: (1) Bone marrow iron stores (Prussian blue stain) \u2014 the first and most sensitive indicator of iron depletion; (2) Percent transferrin saturation \u2014 begins to fall as stores diminish; (3) Serum ferritin \u2014 the best single indicator of total body iron stores; falls early. TIBC (statement 4) rises in later stages (Stage 2 onwards). Statements 1, 2, and 3 are deranged at Stage 1.'},\n {id:74,stem:'Which of the following drugs carry a definite risk of causing clinical haemolysis in persons suffering from Glucose-6 phosphate dehydrogenase deficiency?',correct:'1, 2, 3 and 4',options:['1, 3 and 4','1 and 2 only','2, 3 and 4 only','1, 2, 3 and 4'],exp:'G6PD deficiency causes haemolytic anaemia when RBCs are exposed to oxidative stress. All four listed drugs are oxidising agents with definite haemolytic risk: Primaquine (antimalarial) \u2014 the prototype drug causing haemolysis in G6PD deficiency. Dapsone (antileprosy, PCP prophylaxis) \u2014 causes haemolysis even at therapeutic doses. Cotrimoxazole (TMP-SMX) \u2014 the sulfonamide component is the oxidant. Nitrofurantoin (urinary antiseptic) \u2014 definite haemolytic risk. All four are correct.'},\n {id:75,stem:'A 40 year old male presented with complaints of generalised weakness, weight loss, abdominal discomfort and decreased appetite. On examination Splenomegaly (massive) was present. On investigation it was found that haemoglobin was 7\u00b70 g\/dL, platelet count \u2013 8 lakh per cubic mm, WBC-90000 per cubic mm. Most probably this is the case of',correct:'Chronic myeloid leukemia',options:['Chronic lymphocytic leukemia','Chronic myeloid leukemia','Acute lymphoblastic leukemia','Acute myeloid leukemia'],exp:'The combination of massive splenomegaly + markedly elevated WBC (~90,000\/\u03bcL) + elevated platelet count (800,000\/\u03bcL thrombocytosis) + moderate anaemia in a middle-aged patient is the classic presentation of CML. CML is caused by BCR-ABL1 fusion gene (Philadelphia chromosome, t(9;22)) producing a constitutively active tyrosine kinase. Massive splenomegaly from extramedullary haematopoiesis is the hallmark. Treatment: imatinib.'},\n {id:76,stem:'Which of the following are risk factors for type 2 diabetes mellitus?\\n1. Family history of diabetes\\n2. Underweight\\n3. Physical inactivity\\n4. Polycystic ovary syndrome',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Risk factors for T2DM: (1) Family history \u2014 first-degree relative with T2DM confers 3\u20135\u00d7 increased risk. (3) Physical inactivity \u2014 reduces glucose uptake in skeletal muscle and worsens insulin resistance. (4) PCOS \u2014 characterised by hyperinsulinaemia and insulin resistance; women with PCOS have 5\u20137\u00d7 higher lifetime risk. Underweight (statement 2) is a PROTECTIVE factor \u2014 obesity and central adiposity are the major modifiable risk factors. Statements 1, 3, and 4 are correct.'},\n {id:77,stem:'Which of the following statements with regard to gestational diabetes mellitus (GDM) are correct?\\n1. Most women revert to normal glucose tolerance post partum\\n2. Children born to a GDM mother have no increased risk of diabetes mellitus later in life\\n3. Glucose intolerance develops during second and third trimesters\\n4. Insulin resistance is related to metabolic changes of pregnancy',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Statement 1 is correct \u2014 approximately 90% of GDM women revert to normal glucose tolerance after delivery, though retaining 50% lifetime risk of T2DM. Statement 2 is false \u2014 offspring of GDM mothers have significantly increased risk of obesity, metabolic syndrome, and T2DM (intrauterine programming). Statement 3 is correct \u2014 placental hormones peak in 2nd and 3rd trimesters causing progressive insulin resistance, the window when GDM manifests (OGTT screening at 24\u201328 weeks). Statement 4 is correct \u2014 the physiological insulin resistance of pregnancy unmasks GDM in susceptible women. Statements 1, 3, and 4 are correct.'},\n {id:78,stem:'A Thyroid Function Test report shows the following results: TSH-Undetectable, T3-Raised, T4-Raised. Which one of the following will be the most likely interpretation on the basis of the above report?',correct:'Primary thyrotoxicosis',options:['Hypothyroidism secondary to pituitary disease','Transient thyroiditis in evolution','Primary thyrotoxicosis','Overtreatment of hypothyroidism with Liothyronine'],exp:\"TSH undetectable (suppressed) + raised T3 and T4 = primary thyrotoxicosis. In primary thyrotoxicosis (Graves' disease, toxic multinodular goitre, toxic adenoma), excess thyroid hormones directly suppress TSH via negative feedback on pituitary thyrotrophs. Secondary hypothyroidism would show low TSH with LOW T3\/T4. The straightforward pattern of suppressed TSH + raised both T3 and T4 is primary thyrotoxicosis.\"},\n {id:79,stem:'Which of the following biochemical abnormality is seen in severe hypertriglyceridaemia?',correct:'Pseudohyponatremia',options:['Pseudohyponatremia','Metabolic alkalosis','Hyperuricemia','Hyperkalemia'],exp:'In severe hypertriglyceridaemia (triglycerides typically >1000 mg\/dL), large lipid particles displace water in a given volume of plasma, reducing the water fraction. Since sodium is distributed in the aqueous phase only, but older dilution-based methods measure Na\u207a in total plasma volume, the measured serum sodium appears falsely low \u2014 pseudohyponatremia. The true tonicity is normal. This is a laboratory artefact and does not require treatment.'},\n {id:80,stem:'Which of the following statements are correct about treatment with Vitamin D supplement?\\n1. Serum calcium levels improve earlier than serum PTH levels.\\n2. Patients should be closely observed with serial vitamin D levels in blood as vitamin D toxicity occurs frequently\\n3. Vitamin D supplementation should always be in conjunction with calcium supplementation.\\n4. Nephrolithiasis is a known complication',correct:'1, 3 and 4',options:['1, 2 and 3','1, 2 and 4','1, 3 and 4','2, 3 and 4'],exp:'Statement 1 is correct \u2014 serum calcium normalises relatively quickly (within weeks), while PTH normalisation takes several months. Statement 2 is false \u2014 vitamin D toxicity is actually rare with standard supplementation doses; routine serial 25(OH)D monitoring is not required unless high-dose regimens are used. Statement 3 is correct \u2014 for osteoporosis and osteomalacia treatment, vitamin D should generally be co-prescribed with calcium supplements. Statement 4 is correct \u2014 nephrolithiasis (calcium oxalate and calcium phosphate stones) is a recognised complication of excessive vitamin D-mediated hypercalciuria. 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2022 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! Submitting in 10 Submit Now Combined Medical Services Examination 2022General Medicine & Paediatrics \u00b7 Paper I \u00b7 Part B Endocrinology \u00b7 Rheumatology \u00b7 Nephrology \u00b7 Emergency Medicine \u00b7 Haematology \u00b7 Infectious Disease Questions 41 \u2013 80 Options reshuffled \u23f1 Start… <\/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-36636","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2022 P2 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\/04\/20\/cms-2022-p2-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2022 P2 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2022 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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