CMS 2018 Paper I \u2013 Part C (Q81\u2013Q120)<\/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: cms18p1c \u2500\u2500 *\/\n#cms18p1c *,#cms18p1c *::before,#cms18p1c *::after{box-sizing:border-box;margin:0;padding:0}\n#cms18p1c{\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#cms18p1c .cq-sentinel{height:1px}\n#cms18p1c .cq-statusbar{\n 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.cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms18p1c\">\n <div class=\"cq-sentinel\" id=\"cms18p1c-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms18p1c-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms18p1c-timer-item\">\u23f1 <strong id=\"cms18p1c-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms18p1c-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms18p1c-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms18p1c-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms18p1c-sn\">0<\/strong> \/ <strong id=\"cms18p1c-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms18p1c-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms18p1c-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=\"cms18p1c-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms18p1c-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2018<br>Paper I \u00b7 Part C<\/h1>\n <p>Dermatology \u00b7 Nephrology \u00b7 Neurology \u00b7 Endocrinology \u00b7 Cardiology \u00b7 Paediatrics \u00b7 Obstetrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 81 \u2013 120<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms18p1c-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms18p1c-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms18p1c-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms18p1c-score\">\n <div class=\"cq-score-ring\" id=\"cms18p1c-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms18p1c-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=\"cms18p1c-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms18p1c-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms18p1c-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms18p1c-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms18p1c-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms18p1c-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms18p1c', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60, GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:81,\n stem:'Corkscrew hairs are seen due to deficiency of:',\n correct:'Vitamin C',\n options:['Vitamin A','Vitamin E','Vitamin K','Vitamin C'],\n exp:'Corkscrew (coiled\/twisted) hairs are a hallmark of VITAMIN C (Ascorbic acid) deficiency \u2014 SCURVY. Mechanism: Vitamin C is essential for hydroxylation of proline and lysine residues in collagen synthesis (cofactor for prolyl hydroxylase and lysyl hydroxylase). Deficiency \u2192 defective collagen \u2192 weakened perifollicular connective tissue \u2192 hair follicles cannot keep hairs straight \u2192 hairs coil and twist into corkscrew shapes. Other features of scurvy: perifollicular haemorrhages, swollen\/bleeding gums (gingivitis), poor wound healing, periosteal haemorrhages, \"woody\" oedema of legs. Vitamin A deficiency: night blindness, Bitot spots, follicular hyperkeratosis (toad skin) \u2014 NOT corkscrew hairs. Vitamin E: haemolytic anaemia in neonates, peripheral neuropathy. Vitamin K: coagulopathy. Corkscrew hairs = pathognomonic of Vitamin C deficiency (scurvy).'\n },\n {\n id:82,\n stem:'Which of the following are the indications of Renal biopsy?\\n1. Chronic Kidney disease with normal sized kidney\\n2. Nephrotic syndrome in adults\\n3. Nephrotic syndrome in children with atypical features\\n\\nSelect the correct answer using the code given below:',\n correct:'2 and 3 only',\n options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],\n exp:'Indications for renal biopsy: (1) CKD with NORMAL SIZED kidneys \u2714 \u2014 small kidneys in CKD = end-stage fibrosis\/scarring \u2192 biopsy unhelpful and risky; normal-sized kidneys suggest a potentially reversible or treatable cause worth biopsying. However, this statement is somewhat debated \u2014 biopsy is indicated when the cause of CKD is UNKNOWN and the kidneys are still normal-sized, as fibrosis has not yet dominated. (2) Nephrotic syndrome in ADULTS \u2714 \u2014 mandatory (multiple possible causes: MCD, FSGS, membranous nephropathy, MPGN, amyloid \u2014 treatment differs). (3) Nephrotic syndrome in CHILDREN with ATYPICAL features \u2714 \u2014 typical childhood NS (age 1\u20138, no haematuria, no hypertension, normal complement) is empirically treated as MCD without biopsy. Atypical features (age <1 or >8, haematuria, hypertension, low complement, steroid resistance) mandate biopsy. Standard teaching: statements 2 and 3 are the most straightforward indications. Statement 1 (CKD with normal kidneys) is also correct per many guidelines, making the intended answer 2 and 3 per UPSC convention.'\n },\n {\n id:83,\n stem:'Which of the following are common risk factors for contrast Induced Nephrotoxicity?\\n1. Use of high osmolality, ionic contrast media\\n2. Diabetes Mellitus\\n3. Myeloma\\n\\nSelect the correct answer using the code given below:',\n correct:'1, 2 and 3',\n options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],\n exp:'Contrast-Induced Nephropathy (CIN) \/ Contrast-Associated AKI \u2014 risk factors: Patient-related: Pre-existing CKD (most important risk factor), Diabetes mellitus \u2714 (especially with nephropathy \u2014 reduced renal reserve, tubular vulnerability), Dehydration\/volume depletion, Heart failure, Myeloma \u2714 (multiple myeloma \u2014 Bence-Jones proteins precipitate in tubules causing cast nephropathy; myeloma kidney is exquisitely sensitive to contrast), Advanced age, Concurrent nephrotoxins (NSAIDs, aminoglycosides). Contrast-related: High osmolality ionic contrast media \u2714 (e.g., diatrizoate \u2014 osmolality ~2000 mOsm\/kg vs iso-osmolar iodixanol ~290 mOsm\/kg); high osmolality causes direct tubular toxicity and vasoconstriction. Large contrast volume. All three statements are risk factors \u2192 answer: 1, 2 and 3.'\n },\n {\n id:84,\n stem:'Presence of Dysmorphic Erythrocytes in urine analysis is suggestive of:',\n correct:'Nephritis',\n options:['Pyelonephritis','Nephritis','Renal stone disease','Renal tract infection'],\n exp:'DYSMORPHIC ERYTHROCYTES (acanthocytes, G1 cells \u2014 RBCs with membrane blebs and irregular contours) in urine microscopy indicate GLOMERULAR haematuria \u2014 the RBCs are deformed as they squeeze through damaged glomerular basement membrane and are subjected to osmotic and shear stresses in the tubules. Dysmorphic RBCs (>5% acanthocytes or >80% dysmorphic RBCs) = GLOMERULONEPHRITIS (NEPHRITIS). Associated with: IgA nephropathy, post-infectious GN, RPGN, lupus nephritis, ANCA vasculitis, Goodpasture syndrome. Isomorphic (normal-shaped) RBCs = non-glomerular haematuria (stones, infection, tumour, trauma). Pyelonephritis: WBC casts, pyuria, bacteria \u2014 not dysmorphic RBCs. Renal stone disease: isomorphic RBCs. Renal tract infection: pyuria, bacteriuria. Dysmorphic RBCs = glomerular origin = nephritis.'\n },\n {\n id:85,\n stem:'Syndrome of Inappropriate ADH secretion (SIADH) is usually associated with:',\n correct:'Small cell lung cancer',\n options:['Small cell lung cancer','Squamous cell lung cancer','Large cell lung cancer','Adenocarcinoma lung cancer'],\n exp:'SIADH \u2014 paraneoplastic syndrome from ectopic ADH (vasopressin) secretion. SMALL CELL LUNG CANCER (SCLC) is the most common cause of paraneoplastic SIADH. SCLC is a neuroendocrine tumour arising from Kulchitsky cells \u2014 it has unique capability to synthesise and secrete numerous peptide hormones and hormone-like substances: ADH \u2192 SIADH (hyponatraemia, euvolaemia, concentrated urine). ACTH \u2192 Ectopic Cushing syndrome. Anti-Hu, anti-Ri antibodies \u2192 paraneoplastic encephalomyelitis. Lambert-Eaton Myasthenic Syndrome (LEMS \u2014 anti-VGCC). Squamous cell carcinoma: PTHrP \u2192 hypercalcaemia (most common cause of humoral hypercalcaemia of malignancy). Large cell: gynecomastia (hCG), less specific. Adenocarcinoma: brain\/liver metastases more typical. SIADH = SCLC.'\n },\n {\n id:86,\n stem:'A silent, resonant Hemithorax on examination is suggestive of:',\n correct:'Pneumothorax',\n options:['Large Pleural effusion','Pneumothorax','Bronchial asthma','Consolidation'],\n exp:'Clinical signs of a SILENT (absent breath sounds) + RESONANT (hyperresonant on percussion) hemithorax: PNEUMOTHORAX \u2014 air in the pleural space causes: Hyperresonance\/tympanism on percussion (air between the chest wall and lung). Absent\/reduced breath sounds (lung collapsed away from chest wall). Tracheal deviation AWAY from affected side (tension pneumothorax). Reduced chest expansion on affected side. Large pleural effusion: STONY DULL on percussion + absent breath sounds + tracheal deviation away (massive). Bronchial asthma: bilateral hyperresonance + bilateral wheeze (not silent or unilateral). Consolidation: DULL on percussion + bronchial breath sounds + increased vocal resonance. The combination of SILENCE + RESONANCE on one side = PNEUMOTHORAX until proven otherwise \u2014 a medical emergency if tension pneumothorax.'\n },\n {\n id:87,\n stem:'Gower\\'s sign is positive in:',\n correct:'Duchenne\\'s dystrophy',\n options:['Peroneal muscle atrophy','Duchenne\\'s dystrophy','Friedreich ataxia','Cerebellar disease'],\n exp:'GOWER\\'S SIGN: the child uses hands to \"walk up\" the thighs to stand from a supine\/floor position \u2014 a manoeuvre used to compensate for severe proximal lower limb muscle weakness (glutei, quadriceps). Caused by inability to extend the hips and knees against gravity without arm support. Classic in DUCHENNE MUSCULAR DYSTROPHY (DMD): X-linked recessive, dystrophin gene mutation (Xp21), males affected, onset age 2\u20135 years. Features: progressive proximal muscle weakness (Gower\\'s sign by age 3\u20135), pseudohypertrophy of calves (fibrofatty replacement), cardiomyopathy, learning difficulties, elevated CPK (often >10\u00d7 normal). Gower\\'s sign is PATHOGNOMONIC of proximal muscle weakness \u2014 especially DMD. Peroneal muscle atrophy (Charcot-Marie-Tooth): distal weakness, foot drop. Friedreich ataxia: cerebellar + proprioceptive ataxia \u2014 no proximal limb weakness. Cerebellar disease: ataxia, not proximal weakness.'\n },\n {\n id:88,\n stem:'All of the following are the indications of renal replacement therapy EXCEPT:',\n correct:'Hypercalcemia',\n options:['Metabolic Acidosis (pH < 7.25)','Hypercalcemia','Hyperkalemia (K\u207a > 6 mmol\/L)','Fluid overload'],\n exp:'AEIOU mnemonic for Indications of Renal Replacement Therapy (RRT\/Dialysis): A \u2014 Acidosis (metabolic, pH <7.2 or <7.25 refractory to treatment) \u2714. E \u2014 Electrolyte imbalances (Hyperkalaemia K\u207a >6.5 mmol\/L, or >6 with ECG changes) \u2714. I \u2014 Intoxication (dialysable drugs: methanol, ethylene glycol, salicylates, lithium, theophylline). O \u2014 Overload (fluid overload\/pulmonary oedema refractory to diuretics) \u2714. U \u2014 Uraemia (uraemic encephalopathy, pericarditis, bleeding). HYPERCALCAEMIA is NOT an indication for RRT. Hypercalcaemia is treated with: IV fluids (0.9% saline \u2014 volume expansion and calciuresis), Furosemide (after hydration), Bisphosphonates (zoledronic acid, pamidronate), Calcitonin, Corticosteroids (vitamin D-mediated hypercalcaemia), Cinacalcet (primary hyperparathyroidism). Dialysis is rarely used for hypercalcaemia and is NOT a standard indication. Hypercalcaemia = the EXCEPT.'\n },\n {\n id:89,\n stem:'All of the bacterial diseases are exotoxin-mediated EXCEPT:',\n correct:'Typhoid',\n options:['Botulism','Diphtheria','Typhoid','Tetanus'],\n exp:'Exotoxin-mediated bacterial diseases: BOTULISM \u2714 \u2014 Clostridium botulinum produces botulinum toxin (most potent known biological toxin) \u2014 inhibits ACh release at NMJ \u2192 flaccid paralysis. DIPHTHERIA \u2714 \u2014 Corynebacterium diphtheriae produces diphtheria toxin (ADP-ribosylates EF-2 \u2192 inhibits protein synthesis) \u2192 pseudomembrane, myocarditis, neuropathy. TETANUS \u2714 \u2014 Clostridium tetani produces tetanospasmin (inhibits glycine\/GABA release at inhibitory interneurons) \u2192 spastic paralysis. TYPHOID: caused by Salmonella typhi \u2014 it is primarily an INVASIVE\/BACTERAEMIC disease, not exotoxin-mediated. S. typhi invades through Peyer\\'s patches, survives within macrophages, and causes systemic disease through cell invasion and LPS endotoxin (not a classic exotoxin). The pathogenesis involves intracellular survival and bacteraemia \u2014 not a single dominant exotoxin. Typhoid = NOT primarily exotoxin-mediated.'\n },\n {\n id:90,\n stem:'The following substances can cause dilated pupils EXCEPT:',\n correct:'Clonidine',\n options:['Tricyclic Antidepressants','Cocaine','Clonidine','Amphetamines'],\n exp:'MYDRIASIS (dilated pupils) \u2014 caused by sympathetic stimulation or parasympathetic blockade: Tricyclic Antidepressants (TCAs) \u2714 \u2014 anticholinergic effects (muscarinic blockade) \u2192 block constrictor pupillae \u2192 mydriasis. Also cause: dry mouth, urinary retention, tachycardia, ileus. Cocaine \u2714 \u2014 sympathomimetic (blocks catecholamine reuptake) \u2192 mydriasis, tachycardia, hypertension. Amphetamines \u2714 \u2014 sympathomimetic (catecholamine release) \u2192 mydriasis. Other mydriatics: atropine, antihistamines, phenylephrine, MAO inhibitors, LSD. CLONIDINE: \u03b12-adrenergic agonist \u2192 CENTRAL sympatholytic \u2192 reduces sympathetic outflow \u2192 MIOSIS (small pupils), bradycardia, hypotension. Clonidine causes MIOSIS, not mydriasis. It is used to treat hypertension and ADHD. Clonidine poisoning: miosis + bradycardia + hypotension \u2014 mimics opioid toxidrome. Clonidine is the EXCEPT.'\n },\n {\n id:91,\n stem:'Which one of the following drugs can cause Pulmonary Eosinophilia?',\n correct:'Nitrofurantoin',\n options:['Nitrofurantoin','Valproate','Enalapril','Amoxycillin'],\n exp:'Drug-induced Pulmonary Eosinophilia (L\u00f6ffler-like syndrome): NITROFURANTOIN is the classic drug causing pulmonary eosinophilia \u2014 both acute (within hours to weeks \u2014 fever, dyspnoea, eosinophilia, bilateral pulmonary infiltrates) and chronic (insidious, fibrosis). Mechanism: immune-mediated hypersensitivity. Other drugs causing pulmonary eosinophilia: Sulfonamides, NSAIDs (aspirin), Methotrexate, Bleomycin, Amiodarone, Carbamazepine, Phenytoin, Minocycline, Para-aminosalicylic acid. VALPROATE: hepatotoxicity, teratogenicity, pancreatitis \u2014 not pulmonary eosinophilia. ENALAPRIL (ACE inhibitor): dry cough (bradykinin-mediated) \u2014 not pulmonary eosinophilia. AMOXYCILLIN: rare hypersensitivity reactions, but not a recognised cause of pulmonary eosinophilia. Nitrofurantoin = the classic drug causing pulmonary eosinophilia.'\n },\n {\n id:92,\n stem:'CA 19-9 is a tumour marker used for the diagnosis of:',\n correct:'Pancreatic cancer',\n options:['Lung cancer','Prostate cancer','Ovarian cancer','Pancreatic cancer'],\n exp:'TUMOUR MARKER \u2014 CA 19-9 (Carbohydrate Antigen 19-9 \/ Sialyl-Lewis antigen): PRIMARY ASSOCIATION: Pancreatic adenocarcinoma \u2014 most sensitive and specific tumour marker (sensitivity ~70\u201380%, specificity ~80%). Used for diagnosis, monitoring response to treatment, and detecting recurrence. ALSO elevated in: Cholangiocarcinoma (biliary cancers), Gastric cancer, Colorectal cancer (less than CEA), Hepatocellular carcinoma (sometimes). NON-malignant elevation: pancreatitis, cholestasis, biliary obstruction (any cause). NOT specific for: Lung cancer (CEA, NSE, CYFRA 21-1), Prostate cancer (PSA), Ovarian cancer (CA-125, HE4). Important caveat: CA 19-9 requires Lewis antigen expression \u2014 ~5\u201310% of individuals are Lewis antigen negative and cannot produce CA 19-9 regardless of tumour burden. CA 19-9 = pancreatic cancer marker.'\n },\n {\n id:93,\n stem:'Tinea versicolor is caused by:',\n correct:'Malassezia furfur',\n options:['Candida albicans','Trichophyton','Streptococci','Malassezia furfur'],\n exp:'TINEA VERSICOLOR (Pityriasis versicolor) \u2014 a superficial fungal infection of the skin causing hypo- or hyperpigmented macules, typically on the trunk and upper arms. Causative organism: MALASSEZIA FURFUR (and related species M. globosa, M. sympodialis) \u2014 a lipophilic dimorphic yeast that is part of normal skin flora. Under certain conditions (heat, humidity, oily skin, immunosuppression) it converts to its mycelial form and causes skin infection. Diagnosis: KOH mount shows \"spaghetti and meatballs\" appearance (short hyphae + round spores). Wood\\'s lamp: yellow-green fluorescence. Trichophyton: causes true tinea (tinea pedis, tinea corporis, tinea capitis, tinea unguium \u2014 all dermatophytes). Candida albicans: candidiasis \u2014 oral thrush, vaginal, skin folds. Streptococci: impetigo, cellulitis, erysipelas. Malassezia furfur = tinea versicolor.'\n },\n {\n id:94,\n stem:'Osborn wave in ECG is characteristic of:',\n correct:'Hypothermia',\n options:['Hypothyroidism','Hypovolemia','Hypothermia','Hypocalcemia'],\n exp:'OSBORN WAVE (J wave) \u2014 a distinctive ECG finding: a positive deflection at the J-point (junction of QRS complex and ST segment), appearing as a \"hump\" or \"camel hump\" between the QRS and ST segment, most prominent in leads V3\u2013V6, I, and aVL. HYPOTHERMIA is the classic and most important cause \u2014 Osborn waves appear when core temperature falls below 30\u201332\u00b0C and are virtually pathognomonic of severe hypothermia. Their amplitude correlates inversely with temperature (larger waves = lower temperature). The hypothermic heart is also prone to: sinus bradycardia \u2192 AF \u2192 VF. Other causes: Hypercalcaemia (not hypocalcaemia), Subarachnoid haemorrhage, Early repolarisation syndrome, Brugada syndrome variant. Hypothyroidism: bradycardia, low voltage, prolonged QT \u2014 not Osborn waves. Hypocalcaemia: prolonged QT, not Osborn waves. Hypovolaemia: sinus tachycardia. Osborn wave = hypothermia.'\n },\n {\n id:95,\n stem:'Disease modifying agent of choice for the peripheral manifestations of ankylosing spondylitis is:',\n correct:'Sulfasalazine',\n options:['Methotrexate','Hydroxychloroquine','Sulfasalazine','Leflunomide'],\n exp:'Ankylosing Spondylitis (AS) \u2014 treatment principles: AXIAL (spinal) disease: NSAIDs (first-line), TNF-alpha inhibitors (adalimumab, etanercept, infliximab), IL-17 inhibitors (secukinumab, ixekizumab) \u2014 second-line for NSAID failure. Conventional DMARDs (MTX, SSZ, HCQ) have NO proven benefit for axial disease in AS. PERIPHERAL manifestations (peripheral arthritis, enthesitis, dactylitis): SULFASALAZINE is the DMARD of choice \u2014 evidence supports its efficacy for peripheral joint involvement. Methotrexate: used in peripheral AS but less evidence than SSZ; SSZ is preferred first-line. Hydroxychloroquine: no evidence in AS. Leflunomide: limited evidence in peripheral AS. Per standard teaching (including Harrison\\'s and standard NEET-PG texts): Sulfasalazine = DMARD of choice for peripheral manifestations of AS. For axial disease: biologics (TNF-i or IL-17i) after NSAID failure.'\n },\n {\n id:96,\n stem:'Drug of choice for treating hypertensive emergency in a case of Aortic dissection is:',\n correct:'Nitroprusside',\n options:['Phentolamine','Prazosin','Nitroprusside','Amlodipine'],\n exp:'AORTIC DISSECTION \u2014 hypertensive emergency management goals: Reduce heart rate (\u2193 dp\/dt \u2014 rate of pressure rise) AND reduce systolic BP (target <120 mmHg within 20 minutes). LABETALOL: beta+alpha blocker \u2014 first-line (combines negative chronotropy + afterload reduction). ESMOLOL + NITROPRUSSIDE: combination \u2014 esmolol first to reduce HR (prevent reflex tachycardia from nitroprusside), then nitroprusside for BP reduction. NITROPRUSSIDE (sodium nitroprusside): potent arterial and venous vasodilator \u2014 rapidly titratable IV agent; reduces afterload. Must be combined with a beta-blocker to prevent reflex tachycardia (tachycardia increases dp\/dt and worsens dissection). Among the options listed, NITROPRUSSIDE is the most appropriate for acute BP reduction in aortic dissection. Phentolamine: alpha blocker \u2014 for phaeochromocytoma crisis. Prazosin: oral alpha-blocker \u2014 not for emergencies. Amlodipine: oral CCB \u2014 not for acute emergencies. Nitroprusside = correct answer from given options.'\n },\n {\n id:97,\n stem:'A 5 year old boy is brought to the Emergency Room following a crushing injury. The ECG reveals peaked T waves, prolonged PR interval and widened QRS complexes. What of the following treatments should be administered immediately?',\n correct:'Sodium bicarbonate infusion',\n options:['Sodium bicarbonate infusion','Intravenous bolus procainamide','Insulin infusion','Intravenous magnesium sulphate'],\n exp:'ECG changes: Peaked T waves \u2192 Prolonged PR \u2192 Wide QRS \u2192 Sine wave \u2192 VF\/Asystole = progressive HYPERKALAEMIA. Crushing injury (rhabdomyolysis) \u2192 massive potassium release from damaged muscle cells. Management of severe hyperkalaemia \u2014 sequence: (1) IV Calcium gluconate\/chloride: membrane STABILISATION \u2014 most IMMEDIATE\/urgent action \u2014 prevents cardiac arrhythmia (onset within 1\u20132 min). BUT calcium is not in the options. (2) IV Sodium Bicarbonate \u2714: drives K\u207a into cells (along with H\u207a exchange \u2014 alkalosis shifts K\u207a intracellularly); also available immediately; effective in acidosis (common with rhabdomyolysis). (3) Insulin + Dextrose: shifts K\u207a intracellularly \u2014 effective but onset 15\u201330 min. (4) Salbutamol (nebulised): also shifts K\u207a in. Among the given options, SODIUM BICARBONATE is the most immediately appropriate \u2014 especially given the likely metabolic acidosis from crush injury. Insulin infusion alone (without glucose) risks hypoglycaemia. Procainamide is contraindicated in hyperkalaemia (worsens conduction). Magnesium: for hypomagnesaemia, Torsades \u2014 not primary treatment of hyperkalaemia.'\n },\n {\n id:98,\n stem:'A child with Acute Lymphoblastic Leukaemia is started on chemotherapy. After 2 days he develops vomiting, decreased urine output, abdominal pain and tetanic spasms. The ECG reveals QTc prolongation. Which one of the following therapies will be detrimental to his management?',\n correct:'None of these',\n options:['Normal maintenance intravenous fluid','Oral phosphate binders','Intravenous rasburicase','None of these'],\n exp:'TUMOUR LYSIS SYNDROME (TLS): massive cell death from chemotherapy releases intracellular contents \u2192 Hyperuricaemia, Hyperkalaemia, Hyperphosphataemia, Hypocalcaemia. Features here: Tetanic spasms = Hypocalcaemia (from hyperphosphataemia \u2014 phosphate chelates calcium). QTc prolongation = Hypocalcaemia. Decreased urine output = Urate nephropathy\/AKI. Treatment: (a) IV fluids (normal maintenance) \u2714 \u2014 essential: maintain urine output, flush uric acid, prevent AKI. (b) Oral phosphate binders \u2714 \u2014 sevelamer, calcium carbonate \u2014 bind dietary phosphate, reduce hyperphosphataemia \u2192 correct hypocalcaemia indirectly. (c) IV Rasburicase \u2714 \u2014 recombinant urate oxidase \u2014 converts uric acid to allantoin (more soluble) \u2192 rapidly reduces uric acid levels \u2014 prevents urate nephropathy; superior to allopurinol for established TLS. All three are appropriate. NONE OF THESE is detrimental \u2014 answer is (d) None of these. Note: Calcium supplementation without correcting phosphate first can cause calcium-phosphate precipitation.'\n },\n {\n id:99,\n stem:'Which of the following treatment modalities is NOT recommended for worsening respiratory distress in a child suspected to be suffering from acute croup?',\n correct:'Intravenous antibiotics',\n options:['Sedation','Intravenous antibiotics','Nebulised racemic epinephrine','Intramuscular dexamethasone'],\n exp:'Acute Croup (Laryngotracheobronchitis) \u2014 caused by parainfluenza virus (most common), also RSV, adenovirus, influenza. Management of moderate-severe croup: Nebulised RACEMIC EPINEPHRINE (or L-epinephrine) \u2714 \u2014 causes mucosal vasoconstriction \u2192 reduces subglottic oedema \u2192 rapid symptom relief (onset 10\u201330 min); effect transient (rebound in 2 hours \u2014 observe for 2\u20133 hours post-treatment). DEXAMETHASONE \u2714 (IM, oral, or nebulised budesonide) \u2014 reduces subglottic inflammation; single dose of oral\/IM dexamethasone 0.15\u20130.6 mg\/kg is standard of care \u2014 shown to reduce hospitalisation and severity. SEDATION \u2714 \u2014 careful sedation in intubated\/very severe cases (but listed here as NOT recommended \u2014 SEDATION IS ACTUALLY CONTRAINDICATED in croup as it reduces respiratory drive and can worsen upper airway obstruction; however option (a) says sedation, which in many standard answers is listed as \"not recommended\"). IV ANTIBIOTICS: croup is VIRAL \u2014 antibiotics have NO role. They are not recommended. IV antibiotics = NOT recommended for croup.'\n },\n {\n id:100,\n stem:'Which of the following developmental skills will you expect a child to have acquired by 9 months?',\n correct:'Refers to mother as \\'ma-ma\\'',\n options:['Cruising around the furniture','Mature pincer grasp','Waves \\'bye-bye\\'','Refers to mother as \\'ma-ma\\''],\n exp:'Developmental milestones at 9 months: GROSS MOTOR: Sits without support (6\u20139 months), Pulls to stand (9 months), Cruising (10\u201312 months \u2014 NOT yet at 9 months). FINE MOTOR: Inferior pincer grasp (9 months \u2014 thumb and lateral side of index finger); MATURE (tip-to-tip) pincer grasp: 12 months. LANGUAGE: Non-specific \"mama\", \"dada\" (mama\/dada used non-specifically): 9 months \u2714. Specific use of \"mama\" for mother: 12\u201314 months. However, saying \"ma-ma\" (even non-specifically) in response to seeing mother begins around 9 months. Waves bye-bye: 9\u201310 months (social milestone). Separation anxiety: 8\u20139 months. Cruising: 10\u201312 months \u2014 NOT 9 months. Mature pincer: 12 months. \"Waves bye-bye\" is also around 9\u201310 months, but \"refers to mother as ma-ma\" is the most definitively correct 9-month milestone among the options. Per standard milestone tables: \"ma-ma\/da-da non-specific\" = 9 months.'\n },\n {\n id:101,\n stem:'Which of the following is physiological in a term neonate?',\n correct:'Erythema toxicum',\n options:['Hypotonia','Erythema toxicum','Jaundice at 20 hours of life','Direct serum bilirubin level = 3.0 mg\/dL'],\n exp:'ERYTHEMA TOXICUM NEONATORUM (ETN) is a benign, self-limiting, physiological rash occurring in ~30\u201370% of term neonates. Appears day 2\u20133 of life, resolves by 1\u20132 weeks. Appearance: erythematous macules, papules, and pustules with surrounding erythema \u2014 containing eosinophils (not infection). No treatment needed. Pathophysiology: unknown, possibly immune\/inflammatory. NOT a sign of infection. HYPOTONIA in a neonate: pathological \u2014 causes include hypothyroidism, Down syndrome, hypoxic-ischaemic encephalopathy, inborn errors of metabolism, neuromuscular disease. JAUNDICE at 20 hours: pathological (physiological jaundice appears after 24\u201348 hours); jaundice in first 24 hours = haemolytic disease, infection, sepsis \u2014 always pathological. DIRECT bilirubin 3.0 mg\/dL: pathological (direct\/conjugated bilirubin >1 mg\/dL if total <5 mg\/dL, or >20% of total bilirubin = pathological \u2014 suggests cholestasis). Erythema toxicum = physiological.'\n },\n {\n id:102,\n stem:'A preterm neonate undergoes the initial steps of resuscitation. The clinician observes that the baby is breathing, has a heart rate of 80\/minute and the baby is pink. What will be the next immediate step in management?',\n correct:'Positive pressure ventilation',\n options:['Administering intravenous epinephrine','Chest compressions','Positive pressure ventilation','Supplemental oxygen'],\n exp:'NRP (Neonatal Resuscitation Programme) algorithm: Assess: Breathing \u2714 (breathing present). Heart Rate = 80\/min \u2014 BELOW 100\/min (threshold for PPV). Colour = Pink. HR <100\/min despite initial stimulation and positioning \u2192 POSITIVE PRESSURE VENTILATION (PPV) is the NEXT step, regardless of colour. PPV is initiated at rate of 40\u201360 breaths\/min. Target HR >100 within 30 seconds of PPV. DO NOT give supplemental oxygen alone when HR <100 \u2014 PPV is needed. Chest compressions: only if HR <60 despite 30 seconds of adequate PPV. IV Epinephrine: only if HR <60 despite coordinated PPV + chest compressions for 60 seconds. The critical decision point: HR <100\/min \u2192 PPV immediately. Supplemental oxygen alone is insufficient when HR is <100. PPV is the correct next step.'\n },\n {\n id:103,\n stem:'A child is able to copy a triangle, names 4 colours, dresses and undresses easily and is able to skip. What is the likely age of this child?',\n correct:'60 months',\n options:['30 months','36 months','48 months','60 months'],\n exp:'Developmental milestone analysis: Copy a TRIANGLE: age 5 years (60 months). Sequence: circle (3 years), cross\/plus (4 years), square (4\u20134.5 years), triangle (5 years), diamond (6 years). Names 4 COLOURS: age 5 years (60 months) \u2014 names 4+ colours by 5 years; names 2 colours by 4 years. DRESSES and UNDRESSES easily (with fasteners): 5 years. Undressing: 2 years. Dressing with help: 3\u20134 years. Independent dressing including buttons: 5 years. SKIPPING (alternating feet): 5 years (60 months). Hopping on one foot: 4 years. Galloping: 4 years. Skipping with alternating feet = 5-year milestone. All four milestones converge at 60 months (5 years). Answer: 60 months.'\n },\n {\n id:104,\n stem:'Which of the following will be considered to be a \\'RED FLAG\\' in child development?',\n correct:'No vocalization by 4 months',\n options:['No vocalization by 4 months','Unable to sit without support by 10 months','Unable to walk independently by 15 months','Unable to speak a single word with meaning by 15 months'],\n exp:'RED FLAG developmental warning signs = milestones significantly delayed beyond the expected age, signalling need for urgent evaluation: No vocalization by 4 months \u2714 \u2014 RED FLAG. By 2 months: social smile + cooing; by 4 months: laughs aloud, babbles. No vocalisation at 4 months is a serious developmental red flag (possible hearing loss, autism, neurological disorder). Unable to sit without support by 10 months: Not a red flag \u2014 sits without support is typically achieved by 8\u20139 months, but 10 months is borderline\/within range. Red flag for sitting: not sitting by 12 months. Unable to walk independently by 15 months: Not walking by 18 months is a red flag; 15 months is within normal range (10\u201315 months is normal range for walking). Speaking single words with meaning by 15 months is EXPECTED \u2014 not a red flag. Red flag: no words by 16 months. NO VOCALIZATION by 4 months is the clearest, most definitive red flag among the options.'\n },\n {\n id:105,\n stem:'Gastric lavage is contraindicated in which of the following?\\n1. Corrosive poisoning\\n2. Organophosphorus poisoning\\n3. Iron intoxication\\n4. Turpentine oil ingestion\\n\\nSelect the correct answer using the codes given below:',\n correct:'4 and 1',\n options:['1 and 2','2 and 3','3 and 4','4 and 1'],\n exp:'Gastric Lavage \u2014 contraindications: CORROSIVES (acids, alkalis) \u2714 \u2014 lavage tube passage can perforate oesophagus\/stomach already weakened by corrosive injury; also risks aspiration of caustic material; CONTRAINDICATED. HYDROCARBONS\/VOLATILE SUBSTANCES (petroleum distillates, turpentine oil, kerosene) \u2714 \u2014 lavage risks aspiration of low-viscosity hydrocarbon \u2192 severe aspiration pneumonitis (lipoid pneumonia); CONTRAINDICATED. Loss of airway protective reflexes (unconscious patient \u2014 unless intubated). Sharp objects ingested. ORGANOPHOSPHORUS: lavage is indicated (OP is not corrosive, and removing stomach contents reduces ongoing absorption \u2014 use with airway protection if unconscious). IRON: lavage is relatively indicated in early iron toxicity (though limited efficacy since iron tablets clump; whole bowel irrigation preferred \u2014 but lavage is not absolutely contraindicated). Statements 1 (corrosive) and 4 (turpentine oil) = contraindicated. Answer: 4 and 1.'\n },\n {\n id:106,\n stem:'A 10-year old girl is brought to the emergency following a road traffic accident. The child is comatose with GCS score of 4. She is hypertensive, has bradycardia and extensor posturing. CT imaging reveals comminuted skull fractures and intraparenchymal haemorrhage. The initial management should include all of the following measures EXCEPT:',\n correct:'Intravenous dexamethasone',\n options:['Head of bed elevation','Mechanical ventilation','Intravenous dexamethasone','Hypertonic saline administration'],\n exp:'Severe TBI management with raised ICP (coma GCS 4, Cushing\\'s triad: hypertension + bradycardia + extensor posturing): HEAD OF BED ELEVATION \u2714 (30\u00b0) \u2014 reduces ICP by improving cerebral venous drainage. MECHANICAL VENTILATION \u2714 \u2014 protects airway (GCS 4, unable to protect airway), allows controlled ventilation; moderate hyperventilation (PaCO2 35\u201340 mmHg; avoid aggressive hyperventilation except as bridge). HYPERTONIC SALINE \u2714 \u2014 osmotherapy for raised ICP; draws fluid out of brain parenchyma; increasingly preferred over mannitol in paediatric TBI. IV DEXAMETHASONE: CONTRAINDICATED in traumatic brain injury. Dexamethasone has NO benefit in TBI and is associated with HARM (increased mortality \u2014 CRASH trial). Steroids are indicated for: vasogenic oedema from brain tumours\/abscesses, spinal cord injury (controversial). NOT for TBI or haemorrhagic stroke. Dexamethasone = the EXCEPT (not recommended\/harmful in TBI).'\n },\n {\n id:107,\n stem:'A 3-year old boy is brought with complaints of staying aloof. He also has delayed speech. Rest of the developmental milestones were attained normally. The most likely diagnosis is:',\n correct:'Autism',\n options:['Selective mutism','Attention deficit hyperactivity disorder','Autism','Phonological disorder'],\n exp:'Key features: STAYING ALOOF (social withdrawal, lack of social engagement), DELAYED SPEECH, other milestones normal. AUTISM SPECTRUM DISORDER (ASD): Triad (DSM-IV) \/ Dyad (DSM-5): (1) Social communication and interaction deficits: staying aloof, poor eye contact, not responding to name, lack of joint attention, difficulty with social reciprocity. (2) Restricted, repetitive behaviours. Language delay is common. Other milestones (gross\/fine motor) may be relatively preserved. Typical presentation: noticed by parents at age 18\u201336 months. SELECTIVE MUTISM: child speaks normally in some situations (home) but refuses to speak in others (school) \u2014 NOT aloof from everyone; social interaction not universally impaired. ADHD: hyperactivity, inattention, impulsivity \u2014 NOT social withdrawal or aloofness as primary feature. PHONOLOGICAL DISORDER: articulation difficulties \u2014 specific speech sound errors \u2014 not social withdrawal. Social aloofness + language delay + otherwise normal milestones at age 3 = AUTISM.'\n },\n {\n id:108,\n stem:'Which of the following statements regarding HPV (Human Papilloma Virus) vaccine is NOT true?',\n correct:'It can be safely administered in pregnancy',\n options:['It can be safely administered in pregnancy','The recommended age for initiation of vaccination is 10\u201312 years','Catch up vaccination may be permitted up to 26 years of age, provided the woman is not sexually active','The vaccine is administered intramuscularly in deltoid region'],\n exp:'HPV VACCINE facts: (a) HPV VACCINE IN PREGNANCY: NOT recommended \/ SAFETY NOT ESTABLISHED. Although no adverse outcomes have been documented in inadvertent vaccination during pregnancy, it is DEFERRED until after delivery as a precautionary measure. Available vaccines (Cervarix, Gardasil) are Category B in the US but routinely deferred in pregnancy. \"Can be safely administered in pregnancy\" is NOT TRUE. (b) Recommended age 10\u201312 years \u2714 \u2014 pre-sexual debut, 2 doses (if <15 years); 3 doses (if \u226515 years). (c) Catch-up up to 26 years \u2714 \u2014 if not previously vaccinated; effectiveness highest before sexual activity begins. (d) IM in deltoid \u2714 \u2014 standard route of administration. Statement (a) is NOT true \u2014 HPV vaccine should not be given during pregnancy. This is the correct EXCEPT answer.'\n },\n {\n id:109,\n stem:'A 6-year old boy comes to the immunization clinic having received all vaccines as per schedule till 18 months of age. Which vaccine should be administered now?',\n correct:'DTPw booster',\n options:['DTPw booster','TdaP booster','DT booster','TT booster'],\n exp:'Indian National Immunization Schedule (NIS) \u2014 DTP schedule: Primary series: DTPw at 6 weeks, 10 weeks, 14 weeks. First booster: DTPw at 16\u201318 months. SECOND BOOSTER: DTPw (or DTPa) at 4\u20136 YEARS (school entry) \u2014 this is the vaccine due at age 6. The 6-year-old who received all vaccines including the 18-month DTPw booster is now due for the DTPw SECOND BOOSTER (4\u20136 years). TdaP (reduced antigen Tdap): given at 10\u201312 years (older children\/adolescents). DT (without pertussis): not given as a booster at 6 years in standard NIS. TT (tetanus only): not standard at this age. Per India NIS: Second DTPw booster at 5\u20136 years. Answer: DTPw booster.'\n },\n {\n id:110,\n stem:'\"Time-out\" strategy is used for management of children having:',\n correct:'Temper tantrums',\n options:['Tics','Temper tantrums','Stuttering','Breath holding spells'],\n exp:'\"TIME-OUT\" is a behavioural management technique used for TEMPER TANTRUMS and other oppositional\/disruptive behaviours in children. Technique: when a child has a tantrum or misbehaves, the child is calmly placed in a quiet, non-stimulating area (time-out chair\/room) for a brief period (typically 1 minute per year of age) without attention or reward. Rationale: removes the reinforcing attention that tantrums often attract; teaches self-regulation. Also used for: hitting, biting, non-compliance. Management of other conditions: TICS: habit reversal therapy, clonidine, antipsychotics \u2014 not time-out. STUTTERING: speech therapy (fluency shaping, stuttering modification) \u2014 not time-out. BREATH HOLDING SPELLS: parental reassurance, iron supplementation (if iron-deficient), avoid reinforcing the behaviour \u2014 not time-out. Time-out = behavioural strategy for temper tantrums.'\n },\n {\n id:111,\n stem:'All of the following are included in the \\'Mission Indradhanush\\' EXCEPT:',\n correct:'Hepatitis A vaccine',\n options:['Japanese Encephalitis vaccine','Measles vaccine','Hepatitis A vaccine','Haemophilus influenzae type B vaccine'],\n exp:'MISSION INDRADHANUSH (launched 2014 by Government of India): aimed at achieving full immunisation coverage for children under 2 years and pregnant women. Vaccines included in Mission Indradhanush (original 7, then expanded): Diphtheria (D), Pertussis (P), Tetanus (T) \u2014 DPT. Tuberculosis \u2014 BCG. Polio \u2014 OPV\/IPV. Measles \u2714 (included). Hepatitis B. Subsequently expanded to include: Haemophilus influenzae type B (Hib) \u2714 \u2014 as pentavalent vaccine. Japanese Encephalitis (JE) \u2714 \u2014 in endemic districts. Rotavirus vaccine, PCV (Pneumococcal), IPV (Injectable Polio Vaccine). HEPATITIS A VACCINE: NOT included in Mission Indradhanush or the National Immunization Schedule (as of the time of this question). Hepatitis A is available in the private market but is not part of the government UIP\/Indradhanush programme. Hepatitis A vaccine = the EXCEPT.'\n },\n {\n id:112,\n stem:'Which of the following is the best mode of management of a newborn born to a mother with Hepatitis B infection?',\n correct:'Hepatitis B Immunoglobulin (HBIG) and Hepatitis B vaccine at birth',\n options:['Hepatitis B Immunoglobulin (HBIG) and Hepatitis B vaccine at birth','HBIG and monotherapy with Interferon','HBIG and monotherapy with Lamivudine','HBIG and monotherapy with Adefovir'],\n exp:'Prevention of perinatal (vertical) Hepatitis B transmission: Standard of care: HEPATITIS B IMMUNOGLOBULIN (HBIG) + HEPATITIS B VACCINE \u2014 both given within 12 hours of birth (ideally within 12 hours, at separate sites). HBIG: provides immediate passive immunity (pre-formed anti-HBs antibodies) \u2014 neutralises virus during the window before active immunity develops. Hepatitis B vaccine: provides active immunisation \u2014 long-lasting protection. Combined efficacy: ~95% prevention of perinatal transmission. Antiviral drugs (Lamivudine, Adefovir, Tenofovir, Interferon) are NOT given to the newborn for prophylaxis. Antivirals may be given to the HBeAg-positive MOTHER in 3rd trimester (tenofovir preferred) to reduce maternal viral load and further reduce transmission risk \u2014 but this is adjunctive. The neonate receives HBIG + vaccine ONLY. Monotherapy with any antiviral alone (without HBIG + vaccine) is suboptimal and incorrect. Best mode = HBIG + Hepatitis B vaccine at birth.'\n },\n {\n id:113,\n stem:'At what age should a lateral neck radiograph be done for a child with Down syndrome to rule out atlanto-occipital subluxation?',\n correct:'At 3 years',\n options:['At birth','At 1 year','At 2 years','At 3 years'],\n exp:'Down syndrome (Trisomy 21) is associated with ATLANTOAXIAL INSTABILITY (AAI) \u2014 laxity of the transverse ligament of the atlas allows excessive movement between C1 and C2 \u2192 risk of spinal cord compression with flexion\/extension of the neck. Prevalence of AAI in Down syndrome: ~10\u201330% (radiological); symptomatic: ~1\u20132%. Recommendation: LATERAL NECK X-RAY (flexion, extension, and neutral views) at AGE 3 YEARS (or before starting contact sports, gymnastics, Special Olympics participation). Rationale: done at 3 years because (a) child is old enough to cooperate for proper positioning, (b) ligamentous laxity assessment is meaningful by this age, (c) pre-school physical activity participation requires clearance. Not done at birth or 1\u20132 years as assessment is unreliable and not clinically useful that early. Standard recommendation = 3 years.'\n },\n {\n id:114,\n stem:'Which X-ray will be used to evaluate the bone age (skeletal age) of a term newborn at birth?',\n correct:'Knee',\n options:['Wrist','Shoulder','Knee','Elbow'],\n exp:'BONE AGE ASSESSMENT \u2014 different skeletal sites used at different ages: KNEE X-RAY: used in NEONATES and INFANTS (birth to ~2 years). At birth, the distal femoral epiphysis is typically present (appears around 36 weeks gestation), and the proximal tibial epiphysis appears around 38\u201340 weeks gestation. Presence\/absence and size of these ossification centres at birth assesses skeletal maturity in the neonate. WRIST X-RAY (Greulich-Pyle \/ Tanner-Whitehouse method): used from AGE 2 years onwards through adolescence \u2014 the most common method for bone age in children and adolescents; assesses carpal bones and epiphyses of radius, ulna, metacarpals, and phalanges. SHOULDER\/ELBOW: not standard sites for bone age. At birth, there are no wrist ossification centres visible \u2014 making wrist useless for neonatal bone age. KNEE = standard site for bone age assessment in neonates and premature infants.'\n },\n {\n id:115,\n stem:'Which of the following permanent tooth eruption event has close correlation with menarche?',\n correct:'Second premolar',\n options:['First premolar','First molar','Second premolar','Second molar'],\n exp:'Dental eruption and puberty correlation: SECOND PREMOLAR (permanent) eruption correlates most closely with MENARCHE in girls. The second premolar typically erupts around ages 10\u201312 years in girls \u2014 the same period as menarche. This correlation has been documented in studies showing that girls who experience menarche earlier also tend to have earlier second premolar eruption, reflecting the influence of sex hormones (oestrogen) on dental calcification and eruption timing. The first molar (\"six-year molar\") erupts around age 6 \u2014 well before puberty. The first premolar erupts around age 10\u201311 years \u2014 slightly before menarche on average. The second molar erupts around age 12\u201313 years \u2014 may be after menarche. The second premolar eruption at 10\u201312 years most closely correlates with menarche timing and is the accepted answer in dental and paediatric literature.'\n },\n {\n id:116,\n stem:'Which one of the following is NOT a component of the \\'4 Ds\\' that are the focus of the Rashtriya Bal Suraksha Karyakram (RBSK)?',\n correct:'Developmental delay',\n options:['Deficit','Disease','Deficiency','Developmental delay'],\n exp:'RASHTRIYA BAL SURAKSHA KARYAKRAM (RBSK) \u2014 National Child Health Screening programme launched in 2013 by Government of India under NRHM\/NHM. Aims to screen all children (0\u201318 years) for health conditions requiring early intervention. The 4 Ds of RBSK focus areas: Defects at birth (congenital conditions \u2014 CHD, NTDs, cleft lip\/palate, Down syndrome, etc.). Deficiencies (nutritional deficiencies \u2014 anaemia, vitamin D, rickets, growth faltering). Diseases (childhood diseases \u2014 rheumatic heart disease, reactive airway disease, otitis media, etc.). Development delays (autism, ADHD, learning disability, cerebral palsy, vision\/hearing impairment). DEVELOPMENTAL DELAY is included in RBSK as one of the 4 Ds. \"Deficit\" is NOT one of the 4 Ds \u2014 the 4 Ds are Defects at birth, Deficiencies, Diseases, and Development delays. \"Deficit\" \u2260 \"Defect at birth.\" The EXCEPT is Developmental delay \u2014 wait, re-reading: \"Deficit\" is the odd one out as it is not a standard RBSK category name. The 4 Ds = Defects, Deficiencies, Diseases, Development delays. DEFICIT is NOT one of the official 4 D terms. Answer: Deficit.'\n },\n {\n id:117,\n stem:'In which one of the following age groups is the highest rate of drowning observed, worldwide?',\n correct:'1\u20134 years',\n options:['Less than 1 year','1\u20134 years','4\u201310 years','10\u201315 years'],\n exp:'DROWNING \u2014 epidemiology (WHO data): The highest drowning rates worldwide occur in children aged 1\u20134 YEARS. This age group has: Limited swimming ability \/ inability to swim. Inability to recognise danger. Fascination with water. Unsupervised access to water (bathtubs, pools, ponds, buckets). Inability to escape or call for help. Second highest: 5\u20139 years. The 1\u20134 year age group consistently shows the highest drowning mortality rates globally, particularly in low- and middle-income countries (including India) where open water sources (ponds, rivers, rice paddies) are common. Infants (<1 year): typically drown in bathtubs, usually due to inadequate supervision \u2014 rate is lower than 1\u20134 year group. Older children: better swimming ability and more risk awareness. WHO Global Report on Drowning: 1\u20134 years = highest risk group globally.'\n },\n {\n id:118,\n stem:'Which of the following is the recommended initial intravenous therapy in a 2-year old child with Severe Acute Malnutrition with Severe Dehydration and Shock?',\n correct:'Half-normal saline (N\/2) in 5% dextrose at the rate of 15 mL\/kg over first 60 minutes',\n options:['Ringer Lactate at the rate of 30 mL\/kg over first 30 minutes','Half-normal saline (N\/2) in 5% dextrose at the rate of 15 mL\/kg over first 60 minutes','Normal saline at the rate of 20 mL\/kg over the first 30 minutes','N\/5 saline with 5% dextrose at the rate of 30 mL\/kg over first 60 minutes'],\n exp:'SAM (Severe Acute Malnutrition) with Shock \u2014 special considerations: Children with SAM have impaired cardiac function (myocardial atrophy, reduced cardiac reserve) and abnormal electrolyte handling. Standard ATLS\/PALS fluid resuscitation (20 mL\/kg bolus of NS\/RL) is DANGEROUS in SAM \u2014 risk of fluid overload, cardiac failure, and death. WHO\/IAP recommended IV fluid for SAM with shock: HALF-NORMAL SALINE (N\/2 = 0.45% NaCl) in 5% DEXTROSE at 15 mL\/kg over 60 MINUTES \u2014 much slower and lower volume than standard paediatric resuscitation. Rationale: (1) Glucose prevents hypoglycaemia (common in SAM). (2) Reduced sodium load (SAM patients have total body sodium excess despite low serum Na). (3) Slow rate prevents cardiac overload. (4) Ringer Lactate + large boluses are contraindicated in SAM with shock. This is the IAP\/WHO SAM guideline recommendation. Answer: N\/2 in 5% dextrose at 15 mL\/kg over 60 minutes.'\n },\n {\n id:119,\n stem:'A female carrier for haemophilia A gene gets married to a genetically normal male. What are the chances of her delivering a male offspring with haemophilia?',\n correct:'50%',\n options:['0%','25%','50%','100%'],\n exp:'Haemophilia A (Factor VIII deficiency) \u2014 X-linked recessive inheritance. Mother: carrier (X^H X^h \u2014 one normal X^H, one affected X^h). Father: normal male (X^H Y). Possible offspring: X^H X^H \u2014 normal female (25%). X^H X^h \u2014 carrier female (25%). X^H Y \u2014 normal male (25%). X^h Y \u2014 affected male with haemophilia A (25%). Among ALL offspring: 25% are haemophilic males. Among MALE offspring specifically: 50% of males will have haemophilia (X^h Y). The question asks: \"chances of delivering a MALE OFFSPRING WITH HAEMOPHILIA\" = probability among male offspring = 50%. Among all offspring, 25% will be affected males. But among males only = 50%. Per the question phrasing \"male offspring with haemophilia\" \u2014 this is asking the probability given the offspring is male = 50%.'\n },\n {\n id:120,\n stem:'What is the definition of \\'Cold stress\\' in a newborn as measured by the axillary temperature?',\n correct:'36.0 \u2013 36.4 \u00b0C',\n options:['35.0 \u2013 35.5 \u00b0C','35.0 \u2013 36.0 \u00b0C','35.5 \u2013 36.5 \u00b0C','36.0 \u2013 36.4 \u00b0C'],\n exp:'Neonatal temperature classification (WHO\/NRP \u2014 axillary temperature): NORMAL: 36.5 \u2013 37.5\u00b0C. COLD STRESS (Mild hypothermia): 36.0 \u2013 36.4\u00b0C \u2014 the newborn is mildly hypothermic but not yet severely cold; requires warming interventions (skin-to-skin, warm environment). MODERATE HYPOTHERMIA: 32.0 \u2013 35.9\u00b0C. SEVERE HYPOTHERMIA: <32\u00b0C. Thermal care is critical in neonates as they have: high surface area to volume ratio, limited subcutaneous fat, inability to shiver (rely on non-shivering thermogenesis via brown adipose tissue). Cold stress causes: increased oxygen consumption, hypoglycaemia, metabolic acidosis, poor feeding. Per WHO Thermal Protection guidelines and standard neonatal textbooks: Cold stress = axillary temperature 36.0\u201336.4\u00b0C. Answer: 36.0\u201336.4\u00b0C.'\n }\n ];\n\n function shuffle(arr){\n const a=[...arr];\n for(let i=a.length-1;i>0;i--){const j=Math.floor(Math.random()*(i+1));[a[i],a[j]]=[a[j],a[i]];}\n return a;\n }\n const LETTERS=['A','B','C','D'];\n let userAnswers={},answered=0,shuffledOpts={};\n let timerRunning=false,timerRemaining=TIMER_SECS,timerInterval=null,graceInterval=null;\n let quizSubmitted=false;\n\n function fmtTime(s){const m=Math.floor(s\/60),sec=s%60;return String(m).padStart(2,'0')+':'+String(sec).padStart(2,'0');}\n\n function startTimer(){\n if(timerRunning||quizSubmitted)return;\n timerRunning=true;\n const btn=document.getElementById(NS+'-timer-btn');\n btn.textContent='\u23f1 '+fmtTime(timerRemaining);btn.classList.add('running');\n document.getElementById(NS+'-timer-item').classList.add('active');\n timerInterval=setInterval(function(){\n timerRemaining--;\n const disp=fmtTime(timerRemaining);\n document.getElementById(NS+'-timer-display').textContent=disp;\n 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Submitting in 10 Submit Now Combined Medical Services Examination 2018Paper I \u00b7 Part C Dermatology \u00b7 Nephrology \u00b7 Neurology \u00b7 Endocrinology \u00b7 Cardiology \u00b7 Paediatrics \u00b7 Obstetrics Questions 81 \u2013 120 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0%… <\/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-36807","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2018 P1 Part-C - 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\/10\/cms-2018-p1-part-c\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2018 P1 Part-C - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2018 Paper I \u2013 Part C (Q81\u2013Q120) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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.cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms18p1c .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms18p1c .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms18p1c .cq-retry-btn{margin-top:22px;background:transparent;border:2px solid var(--teal);color:var(--teal);border-radius:8px;padding:10px 28px;font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;cursor:pointer;transition:background 0.2s,color 0.2s;}\n#cms18p1c .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n@media(max-width:480px){\n #cms18p1c .cq-header h1{font-size:1.15rem}\n #cms18p1c .cq-qtext{font-size:0.88rem}\n #cms18p1c .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms18p1c\">\n <div class=\"cq-sentinel\" id=\"cms18p1c-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms18p1c-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms18p1c-timer-item\">\u23f1 <strong id=\"cms18p1c-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms18p1c-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms18p1c-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms18p1c-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms18p1c-sn\">0<\/strong> \/ <strong id=\"cms18p1c-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms18p1c-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms18p1c-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=\"cms18p1c-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms18p1c-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2018<br>Paper I \u00b7 Part C<\/h1>\n <p>Dermatology \u00b7 Nephrology \u00b7 Neurology \u00b7 Endocrinology \u00b7 Cardiology \u00b7 Paediatrics \u00b7 Obstetrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 81 \u2013 120<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms18p1c-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms18p1c-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms18p1c-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms18p1c-score\">\n <div class=\"cq-score-ring\" id=\"cms18p1c-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms18p1c-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=\"cms18p1c-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms18p1c-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms18p1c-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms18p1c-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms18p1c-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms18p1c-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms18p1c', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60, GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:81,\n stem:'Corkscrew hairs are seen due to deficiency of:',\n correct:'Vitamin C',\n options:['Vitamin A','Vitamin E','Vitamin K','Vitamin C'],\n exp:'Corkscrew (coiled\/twisted) hairs are a hallmark of VITAMIN C (Ascorbic acid) deficiency \u2014 SCURVY. Mechanism: Vitamin C is essential for hydroxylation of proline and lysine residues in collagen synthesis (cofactor for prolyl hydroxylase and lysyl hydroxylase). Deficiency \u2192 defective collagen \u2192 weakened perifollicular connective tissue \u2192 hair follicles cannot keep hairs straight \u2192 hairs coil and twist into corkscrew shapes. Other features of scurvy: perifollicular haemorrhages, swollen\/bleeding gums (gingivitis), poor wound healing, periosteal haemorrhages, \"woody\" oedema of legs. Vitamin A deficiency: night blindness, Bitot spots, follicular hyperkeratosis (toad skin) \u2014 NOT corkscrew hairs. Vitamin E: haemolytic anaemia in neonates, peripheral neuropathy. Vitamin K: coagulopathy. Corkscrew hairs = pathognomonic of Vitamin C deficiency (scurvy).'\n },\n {\n id:82,\n stem:'Which of the following are the indications of Renal biopsy?\\n1. Chronic Kidney disease with normal sized kidney\\n2. Nephrotic syndrome in adults\\n3. Nephrotic syndrome in children with atypical features\\n\\nSelect the correct answer using the code given below:',\n correct:'2 and 3 only',\n options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],\n exp:'Indications for renal biopsy: (1) CKD with NORMAL SIZED kidneys \u2714 \u2014 small kidneys in CKD = end-stage fibrosis\/scarring \u2192 biopsy unhelpful and risky; normal-sized kidneys suggest a potentially reversible or treatable cause worth biopsying. However, this statement is somewhat debated \u2014 biopsy is indicated when the cause of CKD is UNKNOWN and the kidneys are still normal-sized, as fibrosis has not yet dominated. (2) Nephrotic syndrome in ADULTS \u2714 \u2014 mandatory (multiple possible causes: MCD, FSGS, membranous nephropathy, MPGN, amyloid \u2014 treatment differs). (3) Nephrotic syndrome in CHILDREN with ATYPICAL features \u2714 \u2014 typical childhood NS (age 1\u20138, no haematuria, no hypertension, normal complement) is empirically treated as MCD without biopsy. Atypical features (age <1 or >8, haematuria, hypertension, low complement, steroid resistance) mandate biopsy. Standard teaching: statements 2 and 3 are the most straightforward indications. Statement 1 (CKD with normal kidneys) is also correct per many guidelines, making the intended answer 2 and 3 per UPSC convention.'\n },\n {\n id:83,\n stem:'Which of the following are common risk factors for contrast Induced Nephrotoxicity?\\n1. Use of high osmolality, ionic contrast media\\n2. Diabetes Mellitus\\n3. Myeloma\\n\\nSelect the correct answer using the code given below:',\n correct:'1, 2 and 3',\n options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],\n exp:'Contrast-Induced Nephropathy (CIN) \/ Contrast-Associated AKI \u2014 risk factors: Patient-related: Pre-existing CKD (most important risk factor), Diabetes mellitus \u2714 (especially with nephropathy \u2014 reduced renal reserve, tubular vulnerability), Dehydration\/volume depletion, Heart failure, Myeloma \u2714 (multiple myeloma \u2014 Bence-Jones proteins precipitate in tubules causing cast nephropathy; myeloma kidney is exquisitely sensitive to contrast), Advanced age, Concurrent nephrotoxins (NSAIDs, aminoglycosides). Contrast-related: High osmolality ionic contrast media \u2714 (e.g., diatrizoate \u2014 osmolality ~2000 mOsm\/kg vs iso-osmolar iodixanol ~290 mOsm\/kg); high osmolality causes direct tubular toxicity and vasoconstriction. Large contrast volume. All three statements are risk factors \u2192 answer: 1, 2 and 3.'\n },\n {\n id:84,\n stem:'Presence of Dysmorphic Erythrocytes in urine analysis is suggestive of:',\n correct:'Nephritis',\n options:['Pyelonephritis','Nephritis','Renal stone disease','Renal tract infection'],\n exp:'DYSMORPHIC ERYTHROCYTES (acanthocytes, G1 cells \u2014 RBCs with membrane blebs and irregular contours) in urine microscopy indicate GLOMERULAR haematuria \u2014 the RBCs are deformed as they squeeze through damaged glomerular basement membrane and are subjected to osmotic and shear stresses in the tubules. Dysmorphic RBCs (>5% acanthocytes or >80% dysmorphic RBCs) = GLOMERULONEPHRITIS (NEPHRITIS). Associated with: IgA nephropathy, post-infectious GN, RPGN, lupus nephritis, ANCA vasculitis, Goodpasture syndrome. Isomorphic (normal-shaped) RBCs = non-glomerular haematuria (stones, infection, tumour, trauma). Pyelonephritis: WBC casts, pyuria, bacteria \u2014 not dysmorphic RBCs. Renal stone disease: isomorphic RBCs. Renal tract infection: pyuria, bacteriuria. Dysmorphic RBCs = glomerular origin = nephritis.'\n },\n {\n id:85,\n stem:'Syndrome of Inappropriate ADH secretion (SIADH) is usually associated with:',\n correct:'Small cell lung cancer',\n options:['Small cell lung cancer','Squamous cell lung cancer','Large cell lung cancer','Adenocarcinoma lung cancer'],\n exp:'SIADH \u2014 paraneoplastic syndrome from ectopic ADH (vasopressin) secretion. SMALL CELL LUNG CANCER (SCLC) is the most common cause of paraneoplastic SIADH. SCLC is a neuroendocrine tumour arising from Kulchitsky cells \u2014 it has unique capability to synthesise and secrete numerous peptide hormones and hormone-like substances: ADH \u2192 SIADH (hyponatraemia, euvolaemia, concentrated urine). ACTH \u2192 Ectopic Cushing syndrome. Anti-Hu, anti-Ri antibodies \u2192 paraneoplastic encephalomyelitis. Lambert-Eaton Myasthenic Syndrome (LEMS \u2014 anti-VGCC). Squamous cell carcinoma: PTHrP \u2192 hypercalcaemia (most common cause of humoral hypercalcaemia of malignancy). Large cell: gynecomastia (hCG), less specific. Adenocarcinoma: brain\/liver metastases more typical. SIADH = SCLC.'\n },\n {\n id:86,\n stem:'A silent, resonant Hemithorax on examination is suggestive of:',\n correct:'Pneumothorax',\n options:['Large Pleural effusion','Pneumothorax','Bronchial asthma','Consolidation'],\n exp:'Clinical signs of a SILENT (absent breath sounds) + RESONANT (hyperresonant on percussion) hemithorax: PNEUMOTHORAX \u2014 air in the pleural space causes: Hyperresonance\/tympanism on percussion (air between the chest wall and lung). Absent\/reduced breath sounds (lung collapsed away from chest wall). Tracheal deviation AWAY from affected side (tension pneumothorax). Reduced chest expansion on affected side. Large pleural effusion: STONY DULL on percussion + absent breath sounds + tracheal deviation away (massive). Bronchial asthma: bilateral hyperresonance + bilateral wheeze (not silent or unilateral). Consolidation: DULL on percussion + bronchial breath sounds + increased vocal resonance. The combination of SILENCE + RESONANCE on one side = PNEUMOTHORAX until proven otherwise \u2014 a medical emergency if tension pneumothorax.'\n },\n {\n id:87,\n stem:'Gower\\'s sign is positive in:',\n correct:'Duchenne\\'s dystrophy',\n options:['Peroneal muscle atrophy','Duchenne\\'s dystrophy','Friedreich ataxia','Cerebellar disease'],\n exp:'GOWER\\'S SIGN: the child uses hands to \"walk up\" the thighs to stand from a supine\/floor position \u2014 a manoeuvre used to compensate for severe proximal lower limb muscle weakness (glutei, quadriceps). Caused by inability to extend the hips and knees against gravity without arm support. Classic in DUCHENNE MUSCULAR DYSTROPHY (DMD): X-linked recessive, dystrophin gene mutation (Xp21), males affected, onset age 2\u20135 years. Features: progressive proximal muscle weakness (Gower\\'s sign by age 3\u20135), pseudohypertrophy of calves (fibrofatty replacement), cardiomyopathy, learning difficulties, elevated CPK (often >10\u00d7 normal). Gower\\'s sign is PATHOGNOMONIC of proximal muscle weakness \u2014 especially DMD. Peroneal muscle atrophy (Charcot-Marie-Tooth): distal weakness, foot drop. Friedreich ataxia: cerebellar + proprioceptive ataxia \u2014 no proximal limb weakness. Cerebellar disease: ataxia, not proximal weakness.'\n },\n {\n id:88,\n stem:'All of the following are the indications of renal replacement therapy EXCEPT:',\n correct:'Hypercalcemia',\n options:['Metabolic Acidosis (pH < 7.25)','Hypercalcemia','Hyperkalemia (K\u207a > 6 mmol\/L)','Fluid overload'],\n exp:'AEIOU mnemonic for Indications of Renal Replacement Therapy (RRT\/Dialysis): A \u2014 Acidosis (metabolic, pH <7.2 or <7.25 refractory to treatment) \u2714. E \u2014 Electrolyte imbalances (Hyperkalaemia K\u207a >6.5 mmol\/L, or >6 with ECG changes) \u2714. I \u2014 Intoxication (dialysable drugs: methanol, ethylene glycol, salicylates, lithium, theophylline). O \u2014 Overload (fluid overload\/pulmonary oedema refractory to diuretics) \u2714. U \u2014 Uraemia (uraemic encephalopathy, pericarditis, bleeding). HYPERCALCAEMIA is NOT an indication for RRT. Hypercalcaemia is treated with: IV fluids (0.9% saline \u2014 volume expansion and calciuresis), Furosemide (after hydration), Bisphosphonates (zoledronic acid, pamidronate), Calcitonin, Corticosteroids (vitamin D-mediated hypercalcaemia), Cinacalcet (primary hyperparathyroidism). Dialysis is rarely used for hypercalcaemia and is NOT a standard indication. Hypercalcaemia = the EXCEPT.'\n },\n {\n id:89,\n stem:'All of the bacterial diseases are exotoxin-mediated EXCEPT:',\n correct:'Typhoid',\n options:['Botulism','Diphtheria','Typhoid','Tetanus'],\n exp:'Exotoxin-mediated bacterial diseases: BOTULISM \u2714 \u2014 Clostridium botulinum produces botulinum toxin (most potent known biological toxin) \u2014 inhibits ACh release at NMJ \u2192 flaccid paralysis. DIPHTHERIA \u2714 \u2014 Corynebacterium diphtheriae produces diphtheria toxin (ADP-ribosylates EF-2 \u2192 inhibits protein synthesis) \u2192 pseudomembrane, myocarditis, neuropathy. TETANUS \u2714 \u2014 Clostridium tetani produces tetanospasmin (inhibits glycine\/GABA release at inhibitory interneurons) \u2192 spastic paralysis. TYPHOID: caused by Salmonella typhi \u2014 it is primarily an INVASIVE\/BACTERAEMIC disease, not exotoxin-mediated. S. typhi invades through Peyer\\'s patches, survives within macrophages, and causes systemic disease through cell invasion and LPS endotoxin (not a classic exotoxin). The pathogenesis involves intracellular survival and bacteraemia \u2014 not a single dominant exotoxin. Typhoid = NOT primarily exotoxin-mediated.'\n },\n {\n id:90,\n stem:'The following substances can cause dilated pupils EXCEPT:',\n correct:'Clonidine',\n options:['Tricyclic Antidepressants','Cocaine','Clonidine','Amphetamines'],\n exp:'MYDRIASIS (dilated pupils) \u2014 caused by sympathetic stimulation or parasympathetic blockade: Tricyclic Antidepressants (TCAs) \u2714 \u2014 anticholinergic effects (muscarinic blockade) \u2192 block constrictor pupillae \u2192 mydriasis. Also cause: dry mouth, urinary retention, tachycardia, ileus. Cocaine \u2714 \u2014 sympathomimetic (blocks catecholamine reuptake) \u2192 mydriasis, tachycardia, hypertension. Amphetamines \u2714 \u2014 sympathomimetic (catecholamine release) \u2192 mydriasis. Other mydriatics: atropine, antihistamines, phenylephrine, MAO inhibitors, LSD. CLONIDINE: \u03b12-adrenergic agonist \u2192 CENTRAL sympatholytic \u2192 reduces sympathetic outflow \u2192 MIOSIS (small pupils), bradycardia, hypotension. Clonidine causes MIOSIS, not mydriasis. It is used to treat hypertension and ADHD. Clonidine poisoning: miosis + bradycardia + hypotension \u2014 mimics opioid toxidrome. Clonidine is the EXCEPT.'\n },\n {\n id:91,\n stem:'Which one of the following drugs can cause Pulmonary Eosinophilia?',\n correct:'Nitrofurantoin',\n options:['Nitrofurantoin','Valproate','Enalapril','Amoxycillin'],\n exp:'Drug-induced Pulmonary Eosinophilia (L\u00f6ffler-like syndrome): NITROFURANTOIN is the classic drug causing pulmonary eosinophilia \u2014 both acute (within hours to weeks \u2014 fever, dyspnoea, eosinophilia, bilateral pulmonary infiltrates) and chronic (insidious, fibrosis). Mechanism: immune-mediated hypersensitivity. Other drugs causing pulmonary eosinophilia: Sulfonamides, NSAIDs (aspirin), Methotrexate, Bleomycin, Amiodarone, Carbamazepine, Phenytoin, Minocycline, Para-aminosalicylic acid. VALPROATE: hepatotoxicity, teratogenicity, pancreatitis \u2014 not pulmonary eosinophilia. ENALAPRIL (ACE inhibitor): dry cough (bradykinin-mediated) \u2014 not pulmonary eosinophilia. AMOXYCILLIN: rare hypersensitivity reactions, but not a recognised cause of pulmonary eosinophilia. Nitrofurantoin = the classic drug causing pulmonary eosinophilia.'\n },\n {\n id:92,\n stem:'CA 19-9 is a tumour marker used for the diagnosis of:',\n correct:'Pancreatic cancer',\n options:['Lung cancer','Prostate cancer','Ovarian cancer','Pancreatic cancer'],\n exp:'TUMOUR MARKER \u2014 CA 19-9 (Carbohydrate Antigen 19-9 \/ Sialyl-Lewis antigen): PRIMARY ASSOCIATION: Pancreatic adenocarcinoma \u2014 most sensitive and specific tumour marker (sensitivity ~70\u201380%, specificity ~80%). Used for diagnosis, monitoring response to treatment, and detecting recurrence. ALSO elevated in: Cholangiocarcinoma (biliary cancers), Gastric cancer, Colorectal cancer (less than CEA), Hepatocellular carcinoma (sometimes). NON-malignant elevation: pancreatitis, cholestasis, biliary obstruction (any cause). NOT specific for: Lung cancer (CEA, NSE, CYFRA 21-1), Prostate cancer (PSA), Ovarian cancer (CA-125, HE4). Important caveat: CA 19-9 requires Lewis antigen expression \u2014 ~5\u201310% of individuals are Lewis antigen negative and cannot produce CA 19-9 regardless of tumour burden. CA 19-9 = pancreatic cancer marker.'\n },\n {\n id:93,\n stem:'Tinea versicolor is caused by:',\n correct:'Malassezia furfur',\n options:['Candida albicans','Trichophyton','Streptococci','Malassezia furfur'],\n exp:'TINEA VERSICOLOR (Pityriasis versicolor) \u2014 a superficial fungal infection of the skin causing hypo- or hyperpigmented macules, typically on the trunk and upper arms. Causative organism: MALASSEZIA FURFUR (and related species M. globosa, M. sympodialis) \u2014 a lipophilic dimorphic yeast that is part of normal skin flora. Under certain conditions (heat, humidity, oily skin, immunosuppression) it converts to its mycelial form and causes skin infection. Diagnosis: KOH mount shows \"spaghetti and meatballs\" appearance (short hyphae + round spores). Wood\\'s lamp: yellow-green fluorescence. Trichophyton: causes true tinea (tinea pedis, tinea corporis, tinea capitis, tinea unguium \u2014 all dermatophytes). Candida albicans: candidiasis \u2014 oral thrush, vaginal, skin folds. Streptococci: impetigo, cellulitis, erysipelas. Malassezia furfur = tinea versicolor.'\n },\n {\n id:94,\n stem:'Osborn wave in ECG is characteristic of:',\n correct:'Hypothermia',\n options:['Hypothyroidism','Hypovolemia','Hypothermia','Hypocalcemia'],\n exp:'OSBORN WAVE (J wave) \u2014 a distinctive ECG finding: a positive deflection at the J-point (junction of QRS complex and ST segment), appearing as a \"hump\" or \"camel hump\" between the QRS and ST segment, most prominent in leads V3\u2013V6, I, and aVL. HYPOTHERMIA is the classic and most important cause \u2014 Osborn waves appear when core temperature falls below 30\u201332\u00b0C and are virtually pathognomonic of severe hypothermia. Their amplitude correlates inversely with temperature (larger waves = lower temperature). The hypothermic heart is also prone to: sinus bradycardia \u2192 AF \u2192 VF. Other causes: Hypercalcaemia (not hypocalcaemia), Subarachnoid haemorrhage, Early repolarisation syndrome, Brugada syndrome variant. Hypothyroidism: bradycardia, low voltage, prolonged QT \u2014 not Osborn waves. Hypocalcaemia: prolonged QT, not Osborn waves. Hypovolaemia: sinus tachycardia. Osborn wave = hypothermia.'\n },\n {\n id:95,\n stem:'Disease modifying agent of choice for the peripheral manifestations of ankylosing spondylitis is:',\n correct:'Sulfasalazine',\n options:['Methotrexate','Hydroxychloroquine','Sulfasalazine','Leflunomide'],\n exp:'Ankylosing Spondylitis (AS) \u2014 treatment principles: AXIAL (spinal) disease: NSAIDs (first-line), TNF-alpha inhibitors (adalimumab, etanercept, infliximab), IL-17 inhibitors (secukinumab, ixekizumab) \u2014 second-line for NSAID failure. Conventional DMARDs (MTX, SSZ, HCQ) have NO proven benefit for axial disease in AS. PERIPHERAL manifestations (peripheral arthritis, enthesitis, dactylitis): SULFASALAZINE is the DMARD of choice \u2014 evidence supports its efficacy for peripheral joint involvement. Methotrexate: used in peripheral AS but less evidence than SSZ; SSZ is preferred first-line. Hydroxychloroquine: no evidence in AS. Leflunomide: limited evidence in peripheral AS. Per standard teaching (including Harrison\\'s and standard NEET-PG texts): Sulfasalazine = DMARD of choice for peripheral manifestations of AS. For axial disease: biologics (TNF-i or IL-17i) after NSAID failure.'\n },\n {\n id:96,\n stem:'Drug of choice for treating hypertensive emergency in a case of Aortic dissection is:',\n correct:'Nitroprusside',\n options:['Phentolamine','Prazosin','Nitroprusside','Amlodipine'],\n exp:'AORTIC DISSECTION \u2014 hypertensive emergency management goals: Reduce heart rate (\u2193 dp\/dt \u2014 rate of pressure rise) AND reduce systolic BP (target <120 mmHg within 20 minutes). LABETALOL: beta+alpha blocker \u2014 first-line (combines negative chronotropy + afterload reduction). ESMOLOL + NITROPRUSSIDE: combination \u2014 esmolol first to reduce HR (prevent reflex tachycardia from nitroprusside), then nitroprusside for BP reduction. NITROPRUSSIDE (sodium nitroprusside): potent arterial and venous vasodilator \u2014 rapidly titratable IV agent; reduces afterload. Must be combined with a beta-blocker to prevent reflex tachycardia (tachycardia increases dp\/dt and worsens dissection). Among the options listed, NITROPRUSSIDE is the most appropriate for acute BP reduction in aortic dissection. Phentolamine: alpha blocker \u2014 for phaeochromocytoma crisis. Prazosin: oral alpha-blocker \u2014 not for emergencies. Amlodipine: oral CCB \u2014 not for acute emergencies. Nitroprusside = correct answer from given options.'\n },\n {\n id:97,\n stem:'A 5 year old boy is brought to the Emergency Room following a crushing injury. The ECG reveals peaked T waves, prolonged PR interval and widened QRS complexes. What of the following treatments should be administered immediately?',\n correct:'Sodium bicarbonate infusion',\n options:['Sodium bicarbonate infusion','Intravenous bolus procainamide','Insulin infusion','Intravenous magnesium sulphate'],\n exp:'ECG changes: Peaked T waves \u2192 Prolonged PR \u2192 Wide QRS \u2192 Sine wave \u2192 VF\/Asystole = progressive HYPERKALAEMIA. Crushing injury (rhabdomyolysis) \u2192 massive potassium release from damaged muscle cells. Management of severe hyperkalaemia \u2014 sequence: (1) IV Calcium gluconate\/chloride: membrane STABILISATION \u2014 most IMMEDIATE\/urgent action \u2014 prevents cardiac arrhythmia (onset within 1\u20132 min). BUT calcium is not in the options. (2) IV Sodium Bicarbonate \u2714: drives K\u207a into cells (along with H\u207a exchange \u2014 alkalosis shifts K\u207a intracellularly); also available immediately; effective in acidosis (common with rhabdomyolysis). (3) Insulin + Dextrose: shifts K\u207a intracellularly \u2014 effective but onset 15\u201330 min. (4) Salbutamol (nebulised): also shifts K\u207a in. Among the given options, SODIUM BICARBONATE is the most immediately appropriate \u2014 especially given the likely metabolic acidosis from crush injury. Insulin infusion alone (without glucose) risks hypoglycaemia. Procainamide is contraindicated in hyperkalaemia (worsens conduction). Magnesium: for hypomagnesaemia, Torsades \u2014 not primary treatment of hyperkalaemia.'\n },\n {\n id:98,\n stem:'A child with Acute Lymphoblastic Leukaemia is started on chemotherapy. After 2 days he develops vomiting, decreased urine output, abdominal pain and tetanic spasms. The ECG reveals QTc prolongation. Which one of the following therapies will be detrimental to his management?',\n correct:'None of these',\n options:['Normal maintenance intravenous fluid','Oral phosphate binders','Intravenous rasburicase','None of these'],\n exp:'TUMOUR LYSIS SYNDROME (TLS): massive cell death from chemotherapy releases intracellular contents \u2192 Hyperuricaemia, Hyperkalaemia, Hyperphosphataemia, Hypocalcaemia. Features here: Tetanic spasms = Hypocalcaemia (from hyperphosphataemia \u2014 phosphate chelates calcium). QTc prolongation = Hypocalcaemia. Decreased urine output = Urate nephropathy\/AKI. Treatment: (a) IV fluids (normal maintenance) \u2714 \u2014 essential: maintain urine output, flush uric acid, prevent AKI. (b) Oral phosphate binders \u2714 \u2014 sevelamer, calcium carbonate \u2014 bind dietary phosphate, reduce hyperphosphataemia \u2192 correct hypocalcaemia indirectly. (c) IV Rasburicase \u2714 \u2014 recombinant urate oxidase \u2014 converts uric acid to allantoin (more soluble) \u2192 rapidly reduces uric acid levels \u2014 prevents urate nephropathy; superior to allopurinol for established TLS. All three are appropriate. NONE OF THESE is detrimental \u2014 answer is (d) None of these. Note: Calcium supplementation without correcting phosphate first can cause calcium-phosphate precipitation.'\n },\n {\n id:99,\n stem:'Which of the following treatment modalities is NOT recommended for worsening respiratory distress in a child suspected to be suffering from acute croup?',\n correct:'Intravenous antibiotics',\n options:['Sedation','Intravenous antibiotics','Nebulised racemic epinephrine','Intramuscular dexamethasone'],\n exp:'Acute Croup (Laryngotracheobronchitis) \u2014 caused by parainfluenza virus (most common), also RSV, adenovirus, influenza. Management of moderate-severe croup: Nebulised RACEMIC EPINEPHRINE (or L-epinephrine) \u2714 \u2014 causes mucosal vasoconstriction \u2192 reduces subglottic oedema \u2192 rapid symptom relief (onset 10\u201330 min); effect transient (rebound in 2 hours \u2014 observe for 2\u20133 hours post-treatment). DEXAMETHASONE \u2714 (IM, oral, or nebulised budesonide) \u2014 reduces subglottic inflammation; single dose of oral\/IM dexamethasone 0.15\u20130.6 mg\/kg is standard of care \u2014 shown to reduce hospitalisation and severity. SEDATION \u2714 \u2014 careful sedation in intubated\/very severe cases (but listed here as NOT recommended \u2014 SEDATION IS ACTUALLY CONTRAINDICATED in croup as it reduces respiratory drive and can worsen upper airway obstruction; however option (a) says sedation, which in many standard answers is listed as \"not recommended\"). IV ANTIBIOTICS: croup is VIRAL \u2014 antibiotics have NO role. They are not recommended. IV antibiotics = NOT recommended for croup.'\n },\n {\n id:100,\n stem:'Which of the following developmental skills will you expect a child to have acquired by 9 months?',\n correct:'Refers to mother as \\'ma-ma\\'',\n options:['Cruising around the furniture','Mature pincer grasp','Waves \\'bye-bye\\'','Refers to mother as \\'ma-ma\\''],\n exp:'Developmental milestones at 9 months: GROSS MOTOR: Sits without support (6\u20139 months), Pulls to stand (9 months), Cruising (10\u201312 months \u2014 NOT yet at 9 months). FINE MOTOR: Inferior pincer grasp (9 months \u2014 thumb and lateral side of index finger); MATURE (tip-to-tip) pincer grasp: 12 months. LANGUAGE: Non-specific \"mama\", \"dada\" (mama\/dada used non-specifically): 9 months \u2714. Specific use of \"mama\" for mother: 12\u201314 months. However, saying \"ma-ma\" (even non-specifically) in response to seeing mother begins around 9 months. Waves bye-bye: 9\u201310 months (social milestone). Separation anxiety: 8\u20139 months. Cruising: 10\u201312 months \u2014 NOT 9 months. Mature pincer: 12 months. \"Waves bye-bye\" is also around 9\u201310 months, but \"refers to mother as ma-ma\" is the most definitively correct 9-month milestone among the options. Per standard milestone tables: \"ma-ma\/da-da non-specific\" = 9 months.'\n },\n {\n id:101,\n stem:'Which of the following is physiological in a term neonate?',\n correct:'Erythema toxicum',\n options:['Hypotonia','Erythema toxicum','Jaundice at 20 hours of life','Direct serum bilirubin level = 3.0 mg\/dL'],\n exp:'ERYTHEMA TOXICUM NEONATORUM (ETN) is a benign, self-limiting, physiological rash occurring in ~30\u201370% of term neonates. Appears day 2\u20133 of life, resolves by 1\u20132 weeks. Appearance: erythematous macules, papules, and pustules with surrounding erythema \u2014 containing eosinophils (not infection). No treatment needed. Pathophysiology: unknown, possibly immune\/inflammatory. NOT a sign of infection. HYPOTONIA in a neonate: pathological \u2014 causes include hypothyroidism, Down syndrome, hypoxic-ischaemic encephalopathy, inborn errors of metabolism, neuromuscular disease. JAUNDICE at 20 hours: pathological (physiological jaundice appears after 24\u201348 hours); jaundice in first 24 hours = haemolytic disease, infection, sepsis \u2014 always pathological. DIRECT bilirubin 3.0 mg\/dL: pathological (direct\/conjugated bilirubin >1 mg\/dL if total <5 mg\/dL, or >20% of total bilirubin = pathological \u2014 suggests cholestasis). Erythema toxicum = physiological.'\n },\n {\n id:102,\n stem:'A preterm neonate undergoes the initial steps of resuscitation. The clinician observes that the baby is breathing, has a heart rate of 80\/minute and the baby is pink. What will be the next immediate step in management?',\n correct:'Positive pressure ventilation',\n options:['Administering intravenous epinephrine','Chest compressions','Positive pressure ventilation','Supplemental oxygen'],\n exp:'NRP (Neonatal Resuscitation Programme) algorithm: Assess: Breathing \u2714 (breathing present). Heart Rate = 80\/min \u2014 BELOW 100\/min (threshold for PPV). Colour = Pink. HR <100\/min despite initial stimulation and positioning \u2192 POSITIVE PRESSURE VENTILATION (PPV) is the NEXT step, regardless of colour. PPV is initiated at rate of 40\u201360 breaths\/min. Target HR >100 within 30 seconds of PPV. DO NOT give supplemental oxygen alone when HR <100 \u2014 PPV is needed. Chest compressions: only if HR <60 despite 30 seconds of adequate PPV. IV Epinephrine: only if HR <60 despite coordinated PPV + chest compressions for 60 seconds. The critical decision point: HR <100\/min \u2192 PPV immediately. Supplemental oxygen alone is insufficient when HR is <100. PPV is the correct next step.'\n },\n {\n id:103,\n stem:'A child is able to copy a triangle, names 4 colours, dresses and undresses easily and is able to skip. What is the likely age of this child?',\n correct:'60 months',\n options:['30 months','36 months','48 months','60 months'],\n exp:'Developmental milestone analysis: Copy a TRIANGLE: age 5 years (60 months). Sequence: circle (3 years), cross\/plus (4 years), square (4\u20134.5 years), triangle (5 years), diamond (6 years). Names 4 COLOURS: age 5 years (60 months) \u2014 names 4+ colours by 5 years; names 2 colours by 4 years. DRESSES and UNDRESSES easily (with fasteners): 5 years. Undressing: 2 years. Dressing with help: 3\u20134 years. Independent dressing including buttons: 5 years. SKIPPING (alternating feet): 5 years (60 months). Hopping on one foot: 4 years. Galloping: 4 years. Skipping with alternating feet = 5-year milestone. All four milestones converge at 60 months (5 years). Answer: 60 months.'\n },\n {\n id:104,\n stem:'Which of the following will be considered to be a \\'RED FLAG\\' in child development?',\n correct:'No vocalization by 4 months',\n options:['No vocalization by 4 months','Unable to sit without support by 10 months','Unable to walk independently by 15 months','Unable to speak a single word with meaning by 15 months'],\n exp:'RED FLAG developmental warning signs = milestones significantly delayed beyond the expected age, signalling need for urgent evaluation: No vocalization by 4 months \u2714 \u2014 RED FLAG. By 2 months: social smile + cooing; by 4 months: laughs aloud, babbles. No vocalisation at 4 months is a serious developmental red flag (possible hearing loss, autism, neurological disorder). Unable to sit without support by 10 months: Not a red flag \u2014 sits without support is typically achieved by 8\u20139 months, but 10 months is borderline\/within range. Red flag for sitting: not sitting by 12 months. Unable to walk independently by 15 months: Not walking by 18 months is a red flag; 15 months is within normal range (10\u201315 months is normal range for walking). Speaking single words with meaning by 15 months is EXPECTED \u2014 not a red flag. Red flag: no words by 16 months. NO VOCALIZATION by 4 months is the clearest, most definitive red flag among the options.'\n },\n {\n id:105,\n stem:'Gastric lavage is contraindicated in which of the following?\\n1. Corrosive poisoning\\n2. Organophosphorus poisoning\\n3. Iron intoxication\\n4. Turpentine oil ingestion\\n\\nSelect the correct answer using the codes given below:',\n correct:'4 and 1',\n options:['1 and 2','2 and 3','3 and 4','4 and 1'],\n exp:'Gastric Lavage \u2014 contraindications: CORROSIVES (acids, alkalis) \u2714 \u2014 lavage tube passage can perforate oesophagus\/stomach already weakened by corrosive injury; also risks aspiration of caustic material; CONTRAINDICATED. HYDROCARBONS\/VOLATILE SUBSTANCES (petroleum distillates, turpentine oil, kerosene) \u2714 \u2014 lavage risks aspiration of low-viscosity hydrocarbon \u2192 severe aspiration pneumonitis (lipoid pneumonia); CONTRAINDICATED. Loss of airway protective reflexes (unconscious patient \u2014 unless intubated). Sharp objects ingested. ORGANOPHOSPHORUS: lavage is indicated (OP is not corrosive, and removing stomach contents reduces ongoing absorption \u2014 use with airway protection if unconscious). IRON: lavage is relatively indicated in early iron toxicity (though limited efficacy since iron tablets clump; whole bowel irrigation preferred \u2014 but lavage is not absolutely contraindicated). Statements 1 (corrosive) and 4 (turpentine oil) = contraindicated. Answer: 4 and 1.'\n },\n {\n id:106,\n stem:'A 10-year old girl is brought to the emergency following a road traffic accident. The child is comatose with GCS score of 4. She is hypertensive, has bradycardia and extensor posturing. CT imaging reveals comminuted skull fractures and intraparenchymal haemorrhage. The initial management should include all of the following measures EXCEPT:',\n correct:'Intravenous dexamethasone',\n options:['Head of bed elevation','Mechanical ventilation','Intravenous dexamethasone','Hypertonic saline administration'],\n exp:'Severe TBI management with raised ICP (coma GCS 4, Cushing\\'s triad: hypertension + bradycardia + extensor posturing): HEAD OF BED ELEVATION \u2714 (30\u00b0) \u2014 reduces ICP by improving cerebral venous drainage. MECHANICAL VENTILATION \u2714 \u2014 protects airway (GCS 4, unable to protect airway), allows controlled ventilation; moderate hyperventilation (PaCO2 35\u201340 mmHg; avoid aggressive hyperventilation except as bridge). HYPERTONIC SALINE \u2714 \u2014 osmotherapy for raised ICP; draws fluid out of brain parenchyma; increasingly preferred over mannitol in paediatric TBI. IV DEXAMETHASONE: CONTRAINDICATED in traumatic brain injury. Dexamethasone has NO benefit in TBI and is associated with HARM (increased mortality \u2014 CRASH trial). Steroids are indicated for: vasogenic oedema from brain tumours\/abscesses, spinal cord injury (controversial). NOT for TBI or haemorrhagic stroke. Dexamethasone = the EXCEPT (not recommended\/harmful in TBI).'\n },\n {\n id:107,\n stem:'A 3-year old boy is brought with complaints of staying aloof. He also has delayed speech. Rest of the developmental milestones were attained normally. The most likely diagnosis is:',\n correct:'Autism',\n options:['Selective mutism','Attention deficit hyperactivity disorder','Autism','Phonological disorder'],\n exp:'Key features: STAYING ALOOF (social withdrawal, lack of social engagement), DELAYED SPEECH, other milestones normal. AUTISM SPECTRUM DISORDER (ASD): Triad (DSM-IV) \/ Dyad (DSM-5): (1) Social communication and interaction deficits: staying aloof, poor eye contact, not responding to name, lack of joint attention, difficulty with social reciprocity. (2) Restricted, repetitive behaviours. Language delay is common. Other milestones (gross\/fine motor) may be relatively preserved. Typical presentation: noticed by parents at age 18\u201336 months. SELECTIVE MUTISM: child speaks normally in some situations (home) but refuses to speak in others (school) \u2014 NOT aloof from everyone; social interaction not universally impaired. ADHD: hyperactivity, inattention, impulsivity \u2014 NOT social withdrawal or aloofness as primary feature. PHONOLOGICAL DISORDER: articulation difficulties \u2014 specific speech sound errors \u2014 not social withdrawal. Social aloofness + language delay + otherwise normal milestones at age 3 = AUTISM.'\n },\n {\n id:108,\n stem:'Which of the following statements regarding HPV (Human Papilloma Virus) vaccine is NOT true?',\n correct:'It can be safely administered in pregnancy',\n options:['It can be safely administered in pregnancy','The recommended age for initiation of vaccination is 10\u201312 years','Catch up vaccination may be permitted up to 26 years of age, provided the woman is not sexually active','The vaccine is administered intramuscularly in deltoid region'],\n exp:'HPV VACCINE facts: (a) HPV VACCINE IN PREGNANCY: NOT recommended \/ SAFETY NOT ESTABLISHED. Although no adverse outcomes have been documented in inadvertent vaccination during pregnancy, it is DEFERRED until after delivery as a precautionary measure. Available vaccines (Cervarix, Gardasil) are Category B in the US but routinely deferred in pregnancy. \"Can be safely administered in pregnancy\" is NOT TRUE. (b) Recommended age 10\u201312 years \u2714 \u2014 pre-sexual debut, 2 doses (if <15 years); 3 doses (if \u226515 years). (c) Catch-up up to 26 years \u2714 \u2014 if not previously vaccinated; effectiveness highest before sexual activity begins. (d) IM in deltoid \u2714 \u2014 standard route of administration. Statement (a) is NOT true \u2014 HPV vaccine should not be given during pregnancy. This is the correct EXCEPT answer.'\n },\n {\n id:109,\n stem:'A 6-year old boy comes to the immunization clinic having received all vaccines as per schedule till 18 months of age. Which vaccine should be administered now?',\n correct:'DTPw booster',\n options:['DTPw booster','TdaP booster','DT booster','TT booster'],\n exp:'Indian National Immunization Schedule (NIS) \u2014 DTP schedule: Primary series: DTPw at 6 weeks, 10 weeks, 14 weeks. First booster: DTPw at 16\u201318 months. SECOND BOOSTER: DTPw (or DTPa) at 4\u20136 YEARS (school entry) \u2014 this is the vaccine due at age 6. The 6-year-old who received all vaccines including the 18-month DTPw booster is now due for the DTPw SECOND BOOSTER (4\u20136 years). TdaP (reduced antigen Tdap): given at 10\u201312 years (older children\/adolescents). DT (without pertussis): not given as a booster at 6 years in standard NIS. TT (tetanus only): not standard at this age. Per India NIS: Second DTPw booster at 5\u20136 years. Answer: DTPw booster.'\n },\n {\n id:110,\n stem:'\"Time-out\" strategy is used for management of children having:',\n correct:'Temper tantrums',\n options:['Tics','Temper tantrums','Stuttering','Breath holding spells'],\n exp:'\"TIME-OUT\" is a behavioural management technique used for TEMPER TANTRUMS and other oppositional\/disruptive behaviours in children. Technique: when a child has a tantrum or misbehaves, the child is calmly placed in a quiet, non-stimulating area (time-out chair\/room) for a brief period (typically 1 minute per year of age) without attention or reward. Rationale: removes the reinforcing attention that tantrums often attract; teaches self-regulation. Also used for: hitting, biting, non-compliance. Management of other conditions: TICS: habit reversal therapy, clonidine, antipsychotics \u2014 not time-out. STUTTERING: speech therapy (fluency shaping, stuttering modification) \u2014 not time-out. BREATH HOLDING SPELLS: parental reassurance, iron supplementation (if iron-deficient), avoid reinforcing the behaviour \u2014 not time-out. Time-out = behavioural strategy for temper tantrums.'\n },\n {\n id:111,\n stem:'All of the following are included in the \\'Mission Indradhanush\\' EXCEPT:',\n correct:'Hepatitis A vaccine',\n options:['Japanese Encephalitis vaccine','Measles vaccine','Hepatitis A vaccine','Haemophilus influenzae type B vaccine'],\n exp:'MISSION INDRADHANUSH (launched 2014 by Government of India): aimed at achieving full immunisation coverage for children under 2 years and pregnant women. Vaccines included in Mission Indradhanush (original 7, then expanded): Diphtheria (D), Pertussis (P), Tetanus (T) \u2014 DPT. Tuberculosis \u2014 BCG. Polio \u2014 OPV\/IPV. Measles \u2714 (included). Hepatitis B. Subsequently expanded to include: Haemophilus influenzae type B (Hib) \u2714 \u2014 as pentavalent vaccine. Japanese Encephalitis (JE) \u2714 \u2014 in endemic districts. Rotavirus vaccine, PCV (Pneumococcal), IPV (Injectable Polio Vaccine). HEPATITIS A VACCINE: NOT included in Mission Indradhanush or the National Immunization Schedule (as of the time of this question). Hepatitis A is available in the private market but is not part of the government UIP\/Indradhanush programme. Hepatitis A vaccine = the EXCEPT.'\n },\n {\n id:112,\n stem:'Which of the following is the best mode of management of a newborn born to a mother with Hepatitis B infection?',\n correct:'Hepatitis B Immunoglobulin (HBIG) and Hepatitis B vaccine at birth',\n options:['Hepatitis B Immunoglobulin (HBIG) and Hepatitis B vaccine at birth','HBIG and monotherapy with Interferon','HBIG and monotherapy with Lamivudine','HBIG and monotherapy with Adefovir'],\n exp:'Prevention of perinatal (vertical) Hepatitis B transmission: Standard of care: HEPATITIS B IMMUNOGLOBULIN (HBIG) + HEPATITIS B VACCINE \u2014 both given within 12 hours of birth (ideally within 12 hours, at separate sites). HBIG: provides immediate passive immunity (pre-formed anti-HBs antibodies) \u2014 neutralises virus during the window before active immunity develops. Hepatitis B vaccine: provides active immunisation \u2014 long-lasting protection. Combined efficacy: ~95% prevention of perinatal transmission. Antiviral drugs (Lamivudine, Adefovir, Tenofovir, Interferon) are NOT given to the newborn for prophylaxis. Antivirals may be given to the HBeAg-positive MOTHER in 3rd trimester (tenofovir preferred) to reduce maternal viral load and further reduce transmission risk \u2014 but this is adjunctive. The neonate receives HBIG + vaccine ONLY. Monotherapy with any antiviral alone (without HBIG + vaccine) is suboptimal and incorrect. Best mode = HBIG + Hepatitis B vaccine at birth.'\n },\n {\n id:113,\n stem:'At what age should a lateral neck radiograph be done for a child with Down syndrome to rule out atlanto-occipital subluxation?',\n correct:'At 3 years',\n options:['At birth','At 1 year','At 2 years','At 3 years'],\n exp:'Down syndrome (Trisomy 21) is associated with ATLANTOAXIAL INSTABILITY (AAI) \u2014 laxity of the transverse ligament of the atlas allows excessive movement between C1 and C2 \u2192 risk of spinal cord compression with flexion\/extension of the neck. Prevalence of AAI in Down syndrome: ~10\u201330% (radiological); symptomatic: ~1\u20132%. Recommendation: LATERAL NECK X-RAY (flexion, extension, and neutral views) at AGE 3 YEARS (or before starting contact sports, gymnastics, Special Olympics participation). Rationale: done at 3 years because (a) child is old enough to cooperate for proper positioning, (b) ligamentous laxity assessment is meaningful by this age, (c) pre-school physical activity participation requires clearance. Not done at birth or 1\u20132 years as assessment is unreliable and not clinically useful that early. Standard recommendation = 3 years.'\n },\n {\n id:114,\n stem:'Which X-ray will be used to evaluate the bone age (skeletal age) of a term newborn at birth?',\n correct:'Knee',\n options:['Wrist','Shoulder','Knee','Elbow'],\n exp:'BONE AGE ASSESSMENT \u2014 different skeletal sites used at different ages: KNEE X-RAY: used in NEONATES and INFANTS (birth to ~2 years). At birth, the distal femoral epiphysis is typically present (appears around 36 weeks gestation), and the proximal tibial epiphysis appears around 38\u201340 weeks gestation. Presence\/absence and size of these ossification centres at birth assesses skeletal maturity in the neonate. WRIST X-RAY (Greulich-Pyle \/ Tanner-Whitehouse method): used from AGE 2 years onwards through adolescence \u2014 the most common method for bone age in children and adolescents; assesses carpal bones and epiphyses of radius, ulna, metacarpals, and phalanges. SHOULDER\/ELBOW: not standard sites for bone age. At birth, there are no wrist ossification centres visible \u2014 making wrist useless for neonatal bone age. KNEE = standard site for bone age assessment in neonates and premature infants.'\n },\n {\n id:115,\n stem:'Which of the following permanent tooth eruption event has close correlation with menarche?',\n correct:'Second premolar',\n options:['First premolar','First molar','Second premolar','Second molar'],\n exp:'Dental eruption and puberty correlation: SECOND PREMOLAR (permanent) eruption correlates most closely with MENARCHE in girls. The second premolar typically erupts around ages 10\u201312 years in girls \u2014 the same period as menarche. This correlation has been documented in studies showing that girls who experience menarche earlier also tend to have earlier second premolar eruption, reflecting the influence of sex hormones (oestrogen) on dental calcification and eruption timing. The first molar (\"six-year molar\") erupts around age 6 \u2014 well before puberty. The first premolar erupts around age 10\u201311 years \u2014 slightly before menarche on average. The second molar erupts around age 12\u201313 years \u2014 may be after menarche. The second premolar eruption at 10\u201312 years most closely correlates with menarche timing and is the accepted answer in dental and paediatric literature.'\n },\n {\n id:116,\n stem:'Which one of the following is NOT a component of the \\'4 Ds\\' that are the focus of the Rashtriya Bal Suraksha Karyakram (RBSK)?',\n correct:'Developmental delay',\n options:['Deficit','Disease','Deficiency','Developmental delay'],\n exp:'RASHTRIYA BAL SURAKSHA KARYAKRAM (RBSK) \u2014 National Child Health Screening programme launched in 2013 by Government of India under NRHM\/NHM. Aims to screen all children (0\u201318 years) for health conditions requiring early intervention. The 4 Ds of RBSK focus areas: Defects at birth (congenital conditions \u2014 CHD, NTDs, cleft lip\/palate, Down syndrome, etc.). Deficiencies (nutritional deficiencies \u2014 anaemia, vitamin D, rickets, growth faltering). Diseases (childhood diseases \u2014 rheumatic heart disease, reactive airway disease, otitis media, etc.). Development delays (autism, ADHD, learning disability, cerebral palsy, vision\/hearing impairment). DEVELOPMENTAL DELAY is included in RBSK as one of the 4 Ds. \"Deficit\" is NOT one of the 4 Ds \u2014 the 4 Ds are Defects at birth, Deficiencies, Diseases, and Development delays. \"Deficit\" \u2260 \"Defect at birth.\" The EXCEPT is Developmental delay \u2014 wait, re-reading: \"Deficit\" is the odd one out as it is not a standard RBSK category name. The 4 Ds = Defects, Deficiencies, Diseases, Development delays. DEFICIT is NOT one of the official 4 D terms. Answer: Deficit.'\n },\n {\n id:117,\n stem:'In which one of the following age groups is the highest rate of drowning observed, worldwide?',\n correct:'1\u20134 years',\n options:['Less than 1 year','1\u20134 years','4\u201310 years','10\u201315 years'],\n exp:'DROWNING \u2014 epidemiology (WHO data): The highest drowning rates worldwide occur in children aged 1\u20134 YEARS. This age group has: Limited swimming ability \/ inability to swim. Inability to recognise danger. Fascination with water. Unsupervised access to water (bathtubs, pools, ponds, buckets). Inability to escape or call for help. Second highest: 5\u20139 years. The 1\u20134 year age group consistently shows the highest drowning mortality rates globally, particularly in low- and middle-income countries (including India) where open water sources (ponds, rivers, rice paddies) are common. Infants (<1 year): typically drown in bathtubs, usually due to inadequate supervision \u2014 rate is lower than 1\u20134 year group. Older children: better swimming ability and more risk awareness. WHO Global Report on Drowning: 1\u20134 years = highest risk group globally.'\n },\n {\n id:118,\n stem:'Which of the following is the recommended initial intravenous therapy in a 2-year old child with Severe Acute Malnutrition with Severe Dehydration and Shock?',\n correct:'Half-normal saline (N\/2) in 5% dextrose at the rate of 15 mL\/kg over first 60 minutes',\n options:['Ringer Lactate at the rate of 30 mL\/kg over first 30 minutes','Half-normal saline (N\/2) in 5% dextrose at the rate of 15 mL\/kg over first 60 minutes','Normal saline at the rate of 20 mL\/kg over the first 30 minutes','N\/5 saline with 5% dextrose at the rate of 30 mL\/kg over first 60 minutes'],\n exp:'SAM (Severe Acute Malnutrition) with Shock \u2014 special considerations: Children with SAM have impaired cardiac function (myocardial atrophy, reduced cardiac reserve) and abnormal electrolyte handling. Standard ATLS\/PALS fluid resuscitation (20 mL\/kg bolus of NS\/RL) is DANGEROUS in SAM \u2014 risk of fluid overload, cardiac failure, and death. WHO\/IAP recommended IV fluid for SAM with shock: HALF-NORMAL SALINE (N\/2 = 0.45% NaCl) in 5% DEXTROSE at 15 mL\/kg over 60 MINUTES \u2014 much slower and lower volume than standard paediatric resuscitation. Rationale: (1) Glucose prevents hypoglycaemia (common in SAM). (2) Reduced sodium load (SAM patients have total body sodium excess despite low serum Na). (3) Slow rate prevents cardiac overload. (4) Ringer Lactate + large boluses are contraindicated in SAM with shock. This is the IAP\/WHO SAM guideline recommendation. Answer: N\/2 in 5% dextrose at 15 mL\/kg over 60 minutes.'\n },\n {\n id:119,\n stem:'A female carrier for haemophilia A gene gets married to a genetically normal male. What are the chances of her delivering a male offspring with haemophilia?',\n correct:'50%',\n options:['0%','25%','50%','100%'],\n exp:'Haemophilia A (Factor VIII deficiency) \u2014 X-linked recessive inheritance. Mother: carrier (X^H X^h \u2014 one normal X^H, one affected X^h). Father: normal male (X^H Y). Possible offspring: X^H X^H \u2014 normal female (25%). X^H X^h \u2014 carrier female (25%). X^H Y \u2014 normal male (25%). X^h Y \u2014 affected male with haemophilia A (25%). Among ALL offspring: 25% are haemophilic males. Among MALE offspring specifically: 50% of males will have haemophilia (X^h Y). The question asks: \"chances of delivering a MALE OFFSPRING WITH HAEMOPHILIA\" = probability among male offspring = 50%. Among all offspring, 25% will be affected males. But among males only = 50%. Per the question phrasing \"male offspring with haemophilia\" \u2014 this is asking the probability given the offspring is male = 50%.'\n },\n {\n id:120,\n stem:'What is the definition of \\'Cold stress\\' in a newborn as measured by the axillary temperature?',\n correct:'36.0 \u2013 36.4 \u00b0C',\n options:['35.0 \u2013 35.5 \u00b0C','35.0 \u2013 36.0 \u00b0C','35.5 \u2013 36.5 \u00b0C','36.0 \u2013 36.4 \u00b0C'],\n exp:'Neonatal temperature classification (WHO\/NRP \u2014 axillary temperature): NORMAL: 36.5 \u2013 37.5\u00b0C. COLD STRESS (Mild hypothermia): 36.0 \u2013 36.4\u00b0C \u2014 the newborn is mildly hypothermic but not yet severely cold; requires warming interventions (skin-to-skin, warm environment). MODERATE HYPOTHERMIA: 32.0 \u2013 35.9\u00b0C. SEVERE HYPOTHERMIA: <32\u00b0C. Thermal care is critical in neonates as they have: high surface area to volume ratio, limited subcutaneous fat, inability to shiver (rely on non-shivering thermogenesis via brown adipose tissue). Cold stress causes: increased oxygen consumption, hypoglycaemia, metabolic acidosis, poor feeding. Per WHO Thermal Protection guidelines and standard neonatal textbooks: Cold stress = axillary temperature 36.0\u201336.4\u00b0C. 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Submitting in 10 Submit Now Combined Medical Services Examination 2018Paper I \u00b7 Part C Dermatology \u00b7 Nephrology \u00b7 Neurology \u00b7 Endocrinology \u00b7 Cardiology \u00b7 Paediatrics \u00b7 Obstetrics Questions 81 \u2013 120 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0%… <\/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-36807","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2018 P1 Part-C - 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\/10\/cms-2018-p1-part-c\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2018 P1 Part-C - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2018 Paper I \u2013 Part C (Q81\u2013Q120) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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