CMS 2025 Paper I \u2013 Part B (Q41\u2013Q80)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&display=swap\" rel=\"stylesheet\">\n<style>\n#cms25p1b*,#cms25p1b *::before,#cms25p1b *::after{box-sizing:border-box;margin:0;padding:0}\n#cms25p1b{--ter:#C0603A;--ter-pale:#fdf1ec;--teal:#2A7A6F;--teal-light:#3da394;--teal-pale:#eaf4f3;--ink:#1a1a1a;--ink-mid:#444;--ink-soft:#777;--line:#e0d8d4;--bg:#fdfaf8;--white:#fff;--cb:#43a047;--cb-bg:#eaf7ef;--wb:#e53935;--wb-bg:#fdf0f0;--r:10px;font-family:'Source Serif 4',Georgia,serif;font-size:16px;color:var(--ink);background:var(--bg);line-height:1.7;padding:0 0 48px}\n#cms25p1b .sen{height:1px}\n#cms25p1b .sb{position:fixed;top:0;left:0;right:0;z-index:99999;background:var(--white);border-bottom:2px solid var(--line);border-left:4px solid var(--ter);box-shadow:0 2px 12px 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id=\"cms25p1b-sw\">0<\/strong><\/div>\n <div class=\"sb-it\">\u23f3 <strong id=\"cms25p1b-sr\">40<\/strong> left<\/div>\n <div class=\"sb-sep\"><\/div>\n <div class=\"sb-it\">Net <strong id=\"cms25p1b-sn\">0.00<\/strong> \/ <strong id=\"cms25p1b-sm\">40<\/strong><\/div>\n <\/div>\n <div class=\"sb-bar\"><div class=\"sb-fill\" id=\"cms25p1b-fill\"><\/div><\/div>\n<\/div>\n<div class=\"grace\" id=\"cms25p1b-grace\">\n <div class=\"gb\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"gc\" id=\"cms25p1b-gc\">10<\/div>\n <button class=\"gnow\" id=\"cms25p1b-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n<div class=\"hdr\">\n <h1>Combined Medical Services Examination 2025<br>Paper I \u00b7 Part B<\/h1>\n <p>General Medicine (Q41 \u2013 Q80)<\/p>\n <div class=\"meta\">\n <span class=\"bdg\">Questions 41 \u2013 80<\/span>\n <span class=\"bdg\">+1 correct \u00b7 \u2212\u2153 wrong<\/span>\n <button class=\"tbtn\" id=\"cms25p1b-tbtn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"body\">\n <div id=\"cms25p1b-qs\"><\/div>\n <div class=\"sw\"><button class=\"btn\" id=\"cms25p1b-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms25p1b-sc-box\">\n <div class=\"ring\" id=\"cms25p1b-ring\"><div class=\"ri\"><span class=\"rp\" id=\"cms25p1b-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms25p1b-nl\"><\/div>\n <div class=\"vd\" id=\"cms25p1b-vd\"><\/div>\n <div class=\"bands\">\n <span class=\"band bc\" id=\"cms25p1b-bc\"><\/span>\n <span class=\"band bw\" id=\"cms25p1b-bw\"><\/span>\n <span class=\"band bs\" id=\"cms25p1b-bs\"><\/span>\n <\/div>\n <button class=\"rbtn\" id=\"cms25p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms25p1b',TOTAL=40,MAX=40,TSECS=2400,GSECS=10;\nvar CU=100,WU=33;\nvar QS=[\n{id:41,stem:'Which one of the following causes low-volume erythrocytosis?',correct:'Gaisbock\\'s syndrome',options:['Polycythemia Rubra Vera','Exogenous testosterone therapy','Gaisbock\\'s syndrome','High altitude'],exp:'Erythrocytosis classification: HIGH-VOLUME (true\/absolute erythrocytosis \u2014 increased red cell mass): Polycythemia Vera \u2714 \u2014 JAK2 mutation; elevated red cell mass, low EPO. High altitude \u2714 \u2014 hypoxia \u2192 increased EPO \u2192 increased red cell mass. Exogenous testosterone \u2714 \u2014 stimulates EPO; increases red cell mass. LOW-VOLUME (relative\/spurious erythrocytosis \u2014 normal red cell mass, reduced plasma volume): GAISBOCK\\'S SYNDROME \u2714 \u2014 stress polycythaemia; middle-aged obese hypertensive men; raised haematocrit due to reduced plasma volume, NOT increased red cell mass; normal EPO and normal red cell mass on isotope studies. Answer: Gaisbock\\'s syndrome.'},\n{id:42,stem:'First line therapy in chronic phase of chronic myeloid leukemia is',correct:'Imatinib',options:['Rituximab','Thalidomide','Imatinib','Chlorambucil'],exp:'Chronic Myeloid Leukaemia (CML): CML is driven by the BCR-ABL1 fusion gene (Philadelphia chromosome t(9;22)) \u2192 constitutively active tyrosine kinase. IMATINIB (Gleevec\/Glivec) \u2714 \u2014 first-generation BCR-ABL tyrosine kinase inhibitor (TKI); revolutionised CML treatment; 400 mg\/day orally; first-line for chronic phase CML (IRIS trial). Second-generation TKIs (dasatinib, nilotinib) also used first-line. Rituximab: anti-CD20; for B-cell lymphomas\/CLL, not CML. Thalidomide: myeloma. Chlorambucil: alkylating agent; old treatment for CLL. Answer: Imatinib.'},\n{id:43,stem:'With regard to management of idiopathic thrombocytopenic purpura, consider the following statements:\\nI. All patients with ITP with platelet count less than 100\u00d710\u2079\/L should receive high dose of glucocorticoids\\nII. For patient with spontaneous bleeding, 40 mg of dexamethasone daily is indicated for 4 days\\nIII. Intravenous immunoglobulin can raise the platelet count\\nIV. Life threatening bleeding should be treated with platelet transfusion\\nWhich of the statements given above are correct?',correct:'II, III and IV',options:['I, II and III','II, III and IV','I, III and IV','I, II and IV'],exp:'ITP management: Statement I \u2717 \u2014 Treatment is NOT indicated purely based on platelet count <100\u00d710\u2079\/L; treatment threshold is generally <30\u00d710\u2079\/L or symptomatic bleeding, not <100. Treating all patients at <100 would over-treat. Statement II \u2714 \u2014 High-dose dexamethasone 40 mg\/day for 4 days is a standard first-line regimen for ITP with significant\/spontaneous bleeding. Statement III \u2714 \u2014 IVIG rapidly raises platelet count (within 24\u201372h) by blocking Fc receptors on splenic macrophages, preventing platelet destruction; used when rapid count rise needed. Statement IV \u2714 \u2014 Life-threatening\/intracranial bleeding: platelet transfusion is indicated as emergency measure (along with IVIG + steroids) despite being consumed rapidly. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:44,stem:'Which of the following drugs can cause secondary weight gain?\\nI. Insulin\\nII. Propranolol\\nIII. Orlistat\\nIV. Thyroxine\\nSelect the correct answer using the code given below:',correct:'I and II only',options:['I, II and IV','I and III','II, III and IV','I and II only'],exp:'Drug-induced weight gain: INSULIN \u2714 \u2014 promotes anabolic metabolism, fat storage, appetite; all insulin preparations cause weight gain. PROPRANOLOL \u2714 \u2014 non-selective beta-blocker; reduces metabolic rate, causes fatigue reducing exercise, may increase appetite; associated with modest weight gain. ORLISTAT \u2717 \u2014 lipase inhibitor; causes weight LOSS by blocking fat absorption; used specifically to treat obesity. THYROXINE \u2717 \u2014 thyroid hormone replacement; restores euthyroid state in hypothyroid patients; does NOT cause weight gain in therapeutic doses (excess thyroxine causes weight loss). Other weight-gaining drugs: tricyclics, SSRIs (paroxetine), antipsychotics (olanzapine), valproate, sulfonylureas, corticosteroids, mirtazapine. Answer: I and II only.'},\n{id:45,stem:'Under which one of the following conditions, the HPA axis suppression is likely to result in crisis due to adrenal insufficiency following withdrawal of glucocorticoids?',correct:'If glucocorticoids have been prescribed repeatedly within the previous year',options:['If glucocorticoids have been given by intravenous route for five days','If glucocorticoids have been administered orally for one week','If glucocorticoids have been prescribed repeatedly within the previous year','If the dose is less than equivalent of 5 mg prednisolone per day'],exp:'HPA axis suppression and adrenal crisis risk on glucocorticoid withdrawal: Low risk (unlikely to suppress HPA): Any route for \u22643 weeks. IV for 5 days (option a) \u2014 too short. Oral for 1 week (option b) \u2014 too short. Dose <5 mg prednisolone\/day equivalent (option d) \u2014 subthreshold. HIGH RISK (likely HPA suppression, risk of adrenal crisis): Prednisolone \u22657.5 mg\/day for >3 weeks. REPEATED COURSES within the previous year \u2714 \u2014 cumulative exposure suppresses the HPA axis even if individual courses are short; the pituitary-adrenal axis loses its ability to respond to stress. Morning cortisol <100 nmol\/L after stopping = adrenal insufficiency. Answer: If glucocorticoids have been prescribed repeatedly within the previous year.'},\n{id:46,stem:'Wilson\\'s disease has which of the following inheritance?',correct:'Autosomal recessive',options:['X-linked recessive','Autosomal dominant','Autosomal recessive','It is an acquired disease'],exp:'Wilson\\'s disease (hepatolenticular degeneration): GENE: ATP7B (encodes copper-transporting ATPase) on chromosome 13q14. INHERITANCE: AUTOSOMAL RECESSIVE \u2714 \u2014 both alleles must be mutated for disease expression; heterozygous carriers are usually unaffected. PATHOLOGY: defective biliary copper excretion \u2192 copper accumulates in liver, brain (basal ganglia \u2014 caudate, putamen), cornea (Kayser-Fleischer rings), kidneys, joints. Presents: liver disease (hepatitis\/cirrhosis), neuropsychiatric symptoms, KF rings. Treatment: D-penicillamine, trientine, zinc. Answer: Autosomal recessive.'},\n{id:47,stem:'Which of the following can be used for the management of severe hyperkalaemia?\\nI. Intravenous calcitonin\\nII. Intravenous sodium bicarbonate\\nIII. Oral sodium polystyrene sulphate\\nIV. Intravenous calcium gluconate\\nSelect the correct answer using the code given below:',correct:'II, III and IV',options:['I, II and IV','II, III and IV','I and II only','I and IV only'],exp:'Severe hyperkalaemia management: IV CALCIUM GLUCONATE \u2714 \u2014 membrane stabiliser; antagonises cardiac effects of hyperkalaemia immediately; does NOT lower serum K+; acts within minutes. IV SODIUM BICARBONATE \u2714 \u2014 shifts K+ into cells (alkalosis \u2192 K+\/H+ exchange); lowers serum K+ within 15\u201330 min; especially useful in metabolic acidosis. ORAL SODIUM POLYSTYRENE SULPHATE (Kayexalate) \u2714 \u2014 cation exchange resin; removes K+ from body via GI tract; lowers total body K+; slower acting. IV CALCITONIN \u2717 \u2014 calcitonin is used for hypercalcaemia (inhibits osteoclasts); it has NO role in hyperkalaemia management. Also used: insulin + dextrose (shifts K+ intracellularly), nebulised salbutamol, furosemide, dialysis. Answer: II, III and IV.'},\n{id:48,stem:'Which one of the following conditions can cause euvolaemic hyponatraemia?',correct:'Hypothyroidism',options:['Adrenocortical failure','Hypothyroidism','Nephrotic syndrome','Burns'],exp:'Hyponatraemia classification by volume status: HYPOVOLAEMIC hyponatraemia (low ECF): Addison\\'s disease\/adrenocortical failure \u2014 mineralocorticoid deficiency \u2192 sodium loss \u2192 volume depletion \u2192 hypovolaemic hyponatraemia (NOT euvolaemic). Burns \u2014 fluid loss \u2192 hypovolaemia. HYPERVOLAEMIC hyponatraemia (high ECF): Nephrotic syndrome \u2014 low oncotic pressure \u2192 oedema \u2192 hypervolaemic hyponatraemia. EUVOLAEMIC hyponatraemia (normal ECF): HYPOTHYROIDISM \u2714 \u2014 reduced cardiac output \u2192 non-osmotic ADH release \u2192 water retention without oedema \u2192 euvolaemic hyponatraemia. Also: SIADH, psychogenic polydipsia, glucocorticoid deficiency (isolated), reset osmostat. Answer: Hypothyroidism.'},\n{id:49,stem:'Which one among the following vectors transmits the filaria Loa loa?',correct:'Chrysops',options:['Simulium','Chrysops','Cyclops','Culicoides'],exp:'Filarial vectors: LOA LOA (African eye worm) \u2192 vector: CHRYSOPS \u2714 (deer fly \/ mango fly; a tabanid fly); found in West and Central Africa; causes loiasis (subcutaneous migration, Calabar swellings, subconjunctival migration). SIMULIUM (blackfly) \u2192 Onchocerca volvulus (river blindness). CYCLOPS (freshwater copepod \u2014 NOT an insect) \u2192 Dracunculus medinensis (guinea worm); also intermediate host for Diphyllobothrium. CULICOIDES (biting midges) \u2192 Mansonella species (Mansonella perstans, M. streptocerca). Mosquitoes (Culex, Anopheles, Aedes) \u2192 Wuchereria bancrofti, Brugia malayi. Answer: Chrysops.'},\n{id:50,stem:'Which of the following is the most favourable prognostic parameter in Bell\\'s palsy?',correct:'Incomplete paralysis in the first week',options:['Incomplete paralysis in the first week','Mild CSF lymphocytosis','Denervation in EMG after 10 days','Pain behind the ear'],exp:'Bell\\'s palsy prognosis: INCOMPLETE PARALYSIS IN FIRST WEEK \u2714 \u2014 the single most favourable prognostic sign; incomplete (partial) facial palsy in the first week means some nerve fibres are intact; ~95\u2013100% complete recovery expected. Complete (total) paralysis has a worse prognosis (~70% full recovery). MILD CSF LYMPHOCYTOSIS \u2014 non-specific finding; not a prognostic indicator. DENERVATION ON EMG AFTER 10 DAYS \u2014 indicates axonal degeneration; POOR prognostic sign (wallerian degeneration \u2192 slower, incomplete recovery). PAIN BEHIND EAR \u2014 common presenting feature; not a prognostic indicator per se. Answer: Incomplete paralysis in the first week.'},\n{id:51,stem:'Which one of the following groups of drugs is ineffective against gram positive bacteria?',correct:'Monobactams',options:['Monobactams','Glycopeptides','Fluoroquinolones','First generation cephalosporins'],exp:'Antibacterial spectra: MONOBACTAMS (aztreonam) \u2714 \u2014 active ONLY against GRAM-NEGATIVE aerobic bacteria (including Pseudomonas); completely INEFFECTIVE against gram-positive organisms and anaerobes; aztreonam binds PBP3 of gram-negatives only. GLYCOPEPTIDES (vancomycin, teicoplanin) \u2014 gram-POSITIVE only (MRSA, Enterococcus, C. difficile); ineffective against gram-negatives (outer membrane barrier). FLUOROQUINOLONES \u2014 broad spectrum; active against both gram-positive and gram-negative. FIRST-GENERATION CEPHALOSPORINS (cefazolin, cefalexin) \u2014 primarily gram-positive activity (Staph, Strep) + some gram-negatives (E. coli, Klebsiella, Proteus). Answer: Monobactams.'},\n{id:52,stem:'Which one of the following statements is correct regarding leprosy?',correct:'Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon',options:['Type 1 Leprosy Reaction is also called erythema nodosum leprosum','Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon','\\'Lion face\\' appearance is seen in tuberculoid leprosy','Nose is the last site of involvement in lepromatous leprosy'],exp:'Leprosy reactions: TYPE 1 (Reversal reaction) \u2717 \u2014 cell-mediated (Type IV hypersensitivity); occurs in borderline leprosy (BT, BB, BL); NOT erythema nodosum leprosum. ENL = Type 2. TYPE 2 (Erythema Nodosum Leprosum, ENL) \u2714 \u2014 IMMUNE COMPLEX MEDIATED (Type III hypersensitivity); occurs in lepromatous (LL) and borderline lepromatous (BL); tender erythematous nodules, fever, systemic features; sometimes called \"arthus phenomenon\" in the context of Type III reaction. LION FACE (leonine facies) \u2717 \u2014 seen in LEPROMATOUS leprosy (LL), not tuberculoid. NOSE involvement \u2717 \u2014 nose is an EARLY site of involvement in lepromatous leprosy (nasal mucosa = first affected, nasal stuffiness = early symptom). Answer: Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon.'},\n{id:53,stem:'A 56-year-old gardener presents with an ulcerative nodule with purulent discharge on his right index finger. He had a prick with a thorn at the same site around a month back. Which one of the following infections is most likely?',correct:'Sporotrichosis',options:['Chromoblastomycosis','Mycetoma','Phaeohyphomycosis','Sporotrichosis'],exp:'SPOROTRICHOSIS \u2714 \u2014 caused by Sporothrix schenckii; dimorphic fungus. Classic presentation: THORN PRICK \/ ROSE THORN inoculation \u2192 ulcerative nodule at inoculation site \u2192 LYMPHOCUTANEOUS sporotrichosis (nodules tracking up lymphatics). Gardeners, florists, farmers at risk. Right index finger + thorn prick + 1 month history = classic. Chromoblastomycosis: chronic, verrucous plaques; \"Medlar bodies\" (sclerotic cells) on histology; years of progression. Mycetoma: triad of tumour + sinuses + grains; foot usually (Madura foot). Phaeohyphomycosis: subcutaneous cyst, not ulcerative nodule with lymphatic spread. Answer: Sporotrichosis.'},\n{id:54,stem:'A 36-year-old man presents with decreased appetite, mouth soreness, diarrhoea and irritability. On examination he has a bright red tongue with a pigmented scaly rash around the neck. Which one of the following food items in his diet has a bearing on his disease?',correct:'Corn',options:['Rice','Wheat','Corn','Fish'],exp:'PELLAGRA \u2014 NIACIN (Vitamin B3) DEFICIENCY. Classic presentation: 4 Ds: Dermatitis (photosensitive, pigmented scaly rash \u2014 Casal\\'s necklace around neck \u2714), Diarrhoea \u2714, Dementia\/irritability \u2714, Death (if untreated). Bright red tongue (glossitis) \u2714, mouth soreness (stomatitis). CORN (maize) \u2714 \u2014 populations subsisting predominantly on corn are at risk because: (1) corn has low niacin content; (2) niacin in corn is bound as niacytin (unavailable unless treated with alkali \u2014 nixtamalisation); (3) corn is also low in tryptophan (tryptophan \u2192 niacin). Rice-based diets \u2192 thiamine deficiency (beriberi). Wheat: generally adequate niacin. Fish: good source of niacin and tryptophan. Answer: Corn.'},\n{id:55,stem:'Acrodermatitis enteropathica is an autosomal recessive metabolic disorder which affects the absorption of which one of the following micronutrients?',correct:'Zinc',options:['Iodine','Zinc','Iron','Selenium'],exp:'Acrodermatitis enteropathica: AUTOSOMAL RECESSIVE defect in the SLC39A4 gene encoding ZIP4, a zinc transporter in the duodenum\/jejunum \u2192 impaired ZINC absorption. Presentation: perioral, perianal, and acral dermatitis (erythematous, pustular\/vesicular rash); alopecia; diarrhoea; growth retardation; immune deficiency; starts at weaning. Treatment: oral zinc supplementation (lifelong). Contrast: acquired zinc deficiency in adults causes similar features (acral dermatitis, poor wound healing, hypogeusia). Iodine: thyroid hormone synthesis; deficiency \u2192 goitre\/cretinism. Iron: haemoglobin; deficiency \u2192 anaemia. Selenium: antioxidant; deficiency \u2192 Keshan disease. Answer: Zinc.'},\n{id:56,stem:'Consider the following statements with regard to the treatment of vitamin A deficiency:\\nI. Repeated high doses of retinol can cause liver damage and teratogenicity\\nII. Acute overdose of vitamin A may lead to increased intracranial pressure and skin desquamation\\nIII. Regular vitamin A supplementation is also recommended for pregnant women even in countries where vitamin A deficiency is not endemic\\nIV. Excessive intake of carotene may cause harmless orange pigmentation of the skin\\nWhich of the statements given above are correct?',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Vitamin A treatment facts: Statement I \u2714 \u2014 Hypervitaminosis A: chronic high-dose retinol \u2192 hepatotoxicity (perisinusoidal fibrosis, cirrhosis) and TERATOGENICITY (isotretinoin is contraindicated in pregnancy). Statement II \u2714 \u2014 ACUTE vitamin A toxicity: pseudotumour cerebri (raised ICP \u2192 headache, vomiting, papilloedema), skin desquamation, bone pain, hepatomegaly. Statement III \u2717 \u2014 FALSE. Routine vitamin A supplementation for pregnant women is NOT recommended in non-endemic countries; in fact, high-dose vitamin A is teratogenic in pregnancy; supplementation is only recommended where deficiency is endemic (developing countries with VAD). Statement IV \u2714 \u2014 Carotenaemia: excessive beta-carotene (carrots, papaya) \u2192 harmless orange-yellow skin pigmentation (carotenoderma); NOT toxic; sclerae remain white (unlike jaundice). Correct: I, II, IV. Answer: I, II and IV.'},\n{id:57,stem:'Koebner phenomenon is seen in which one of the following conditions?',correct:'Psoriasis',options:['Psoriasis','Acne Vulgaris','Bechet\\'s disease','Leprosy'],exp:'Koebner phenomenon (isomorphic response): new skin lesions appear at sites of TRAUMA\/injury in patients with certain dermatoses. CONDITIONS showing Koebner phenomenon: PSORIASIS \u2714 \u2014 classic Koebner; psoriatic plaques appear at scratches, surgical scars, sunburn, tattoo sites. Also: Lichen planus, vitiligo, warts (verruca), molluscum contagiosum. Acne vulgaris: NOT a Koebner condition (mechanical trauma can exacerbate acne but the mechanism is different). Beh\u00e7et\\'s disease: shows PATHERGY (exaggerated response to minor trauma, tested with a needle prick); pathergy is NOT the same as Koebner phenomenon. Leprosy: NOT a Koebner condition. Answer: Psoriasis.'},\n{id:58,stem:'Consider the following regarding the human hair growth cycle:\\nI. Anagen is a phase of active hair growth\\nII. Telogen is a transitional phase\\nIII. Catagen is a resting phase\\nWhich of the statements given above is\/are correct?',correct:'I only',options:['I only','III only','I and II only','I, II and III'],exp:'Hair growth cycle phases: ANAGEN \u2714 \u2014 active GROWTH phase; longest phase (2\u20137 years on scalp); 85\u201390% of scalp hairs normally in anagen; matrix cells actively dividing; hair shaft elongating. CATAGEN \u2014 TRANSITIONAL phase (NOT resting); brief (2\u20133 weeks); involution phase; hair follicle shrinks, dermal papilla moves up; NOT resting. TELOGEN \u2014 RESTING phase (NOT transitional); lasts ~3 months; club hair formed; 10\u201315% of scalp hairs in telogen; shed at end of telogen (telogen effluvium when >20% shift to telogen). Statement I \u2714, Statement II \u2717 (telogen is resting; catagen is transitional), Statement III \u2717 (catagen is transitional; telogen is resting). Answer: I only.'},\n{id:59,stem:'Consider the following statements regarding oculocutaneous albinism:\\nI. The disease results from genetic abnormalities leading to destruction of melanocytes\\nII. Type 1 albinism is due to a defect in the tyrosinase gene\\nIII. Patients may present with poor vision, rotator nystagmus and alternating strabismus\\nIV. Patients are at an increased risk of sunburn or developing skin cancer\\nWhich of the statements given above are correct?',correct:'II, III and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Oculocutaneous albinism (OCA): Statement I \u2717 \u2014 OCA results from genetic defects in melanin SYNTHESIS (not destruction of melanocytes); melanocytes are PRESENT but CANNOT produce melanin normally; they are structurally intact but functionally impaired. Statement II \u2714 \u2014 OCA Type 1: mutation in TYR gene (tyrosinase); tyrosinase is the key enzyme for melanin synthesis; absent (OCA1A) or reduced (OCA1B) pigmentation. Statement III \u2714 \u2014 Ophthalmic features of OCA: reduced visual acuity (poor vision), nystagmus (pendular\/rotor), alternating strabismus, photophobia, foveal hypoplasia, misrouting of optic nerve fibres. Statement IV \u2714 \u2014 Absent melanin \u2192 no photoprotection \u2192 increased sunburn risk, actinic keratosis, squamous cell carcinoma, melanoma risk. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:60,stem:'A 42-year-old man presented with recurrent oral ulcers since one year, episodes of redness of eye and genital ulcers. Which one of the following tests is of diagnostic value?',correct:'Pathergy test',options:['Mantoux test','Drug-sensitivity test','Pathergy test','Patch test'],exp:'BEH\u00c7ET\\'S DISEASE: clinical triad of recurrent oral aphthous ulcers + genital ulcers + uveitis (redness of eye). PATHERGY TEST \u2714 \u2014 diagnostic test for Beh\u00e7et\\'s disease; a sterile needle prick on the forearm \u2192 papule or pustule formation at 24\u201348 hours = POSITIVE pathergy; indicates non-specific hyperreactivity of the skin; more common in Middle Eastern\/Asian patients. International Study Group criteria for Beh\u00e7et\\'s: recurrent oral ulcers + any 2 of (genital ulcers, eye lesions, skin lesions, positive pathergy test). Mantoux: tuberculosis skin test. Drug-sensitivity: allergy testing. Patch test: contact dermatitis. Answer: Pathergy test.'},\n{id:61,stem:'Which of the following joints are commonly affected in osteoarthritis?\\nI. First metatarsophalangeal joint\\nII. Proximal interphalangeal joint\\nIIII. Ankle joint\\nIV. 5th and 6th cervical vertebrae joint\\nSelect the correct answer using the code given below:',correct:'I, II and IV only',options:['I and II only','III and IV only','I, II and IV only','I, II, III and IV'],exp:'Osteoarthritis \u2014 commonly affected joints: FIRST MTP JOINT \u2714 \u2014 hallux valgus\/bunion; OA here is very common (big toe). PROXIMAL INTERPHALANGEAL (PIP) JOINTS \u2714 \u2014 Bouchard\\'s nodes (OA); also DIP joints (Heberden\\'s nodes). Also: DIP joints, carpometacarpal joint of thumb, hip, knee, lumbar and CERVICAL SPINE. 5TH AND 6TH CERVICAL VERTEBRAE \u2714 \u2014 cervical spondylosis (OA of cervical spine) most commonly affects C5-C6 and C6-C7 levels. ANKLE JOINT \u2717 \u2014 ankle is relatively SPARED in primary OA (OA of ankle is usually post-traumatic\/secondary); the ankle has a lower incidence of primary OA compared to hip and knee. Correct: I, II and IV. Answer: I, II and IV only.'},\n{id:62,stem:'Which of the following are causes of reversible dementia?\\nI. Hypothyroidism\\nII. Vitamin B12 deficiency\\nIII. Dementia with Lewy body\\nIV. Thiamine deficiency\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Reversible causes of dementia (DEMENTIA mnemonic \u2014 treatable causes): HYPOTHYROIDISM \u2714 \u2014 myxoedema madness; cognitive impairment reverses with thyroid replacement. VITAMIN B12 DEFICIENCY \u2714 \u2014 subacute combined degeneration; cognitive decline, memory loss, psychiatric features reverse with B12 supplementation. THIAMINE DEFICIENCY \u2714 \u2014 Wernicke-Korsakoff syndrome; Wernicke\\'s encephalopathy (reversible if treated early with thiamine); Korsakoff\\'s psychosis may be less reversible but the underlying cause is treatable. Also reversible: depression (\"pseudodementia\"), normal pressure hydrocephalus, subdural haematoma, metabolic causes (hypercalcaemia, uraemia), medications. DEMENTIA WITH LEWY BODY \u2717 \u2014 a PRIMARY NEURODEGENERATIVE dementia; NOT reversible; progressive; alpha-synuclein deposits. Answer: I, II and IV.'},\n{id:63,stem:'Which of the following are clinical features of Fronto-Temporal dementia?\\nI. Personality change\\nII. Language disturbance\\nIII. Memory may be preserved in early stages\\nIV. Anti-cholinesterases are the drug of choice for treatment\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Frontotemporal Dementia (FTD) \/ Pick\\'s disease: PERSONALITY CHANGE \u2714 \u2014 earliest and most prominent feature; disinhibition, apathy, socially inappropriate behaviour, loss of empathy; frontal lobe involvement. LANGUAGE DISTURBANCE \u2714 \u2014 progressive non-fluent aphasia (PNFA) or semantic dementia; temporal lobe involvement. MEMORY PRESERVED EARLY \u2714 \u2014 key distinguishing feature from Alzheimer\\'s; episodic memory is relatively SPARED in early FTD (hippocampi involved later); memory problems are not the chief complaint initially. ANTI-CHOLINESTERASES \u2717 \u2014 cholinesterase inhibitors (donepezil, rivastigmine) are used for ALZHEIMER\\'S disease; they are NOT effective for FTD and may worsen behavioural symptoms; no disease-modifying drug for FTD. Correct: I, II, III. Answer: I, II and III.'},\n{id:64,stem:'Which one of the following is the myelinating cell of Central Nervous System?',correct:'Oligodendrocyte',options:['Astrocyte','Microglia','Schwann cell','Oligodendrocyte'],exp:'Myelinating cells: CNS \u2014 OLIGODENDROCYTES \u2714: produce and maintain myelin sheaths around CNS axons; one oligodendrocyte can myelinate multiple axons (up to 50); loss \u2192 multiple sclerosis plaques. PNS \u2014 SCHWANN CELLS: produce myelin around PNS axons; one Schwann cell myelinates one axon segment; loss \u2192 Guillain-Barr\u00e9 syndrome, Charcot-Marie-Tooth disease. ASTROCYTES: structural support, blood-brain barrier maintenance, glutamate recycling, scar formation. MICROGLIA: resident immune cells of CNS; macrophage equivalent; phagocytose debris, mediate neuroinflammation. Schwann cells are PNS; oligodendrocytes are CNS. Answer: Oligodendrocyte.'},\n{id:65,stem:'Which one of the following is the correct description of Mee\\'s lines, seen in chronic arsenic poisoning?',correct:'Transverse white lines on nails of fingers and toes',options:['Transverse white lines on nails of fingers and toes','Transverse red lines on the skin of palms and soles','Transverse white lines on the skin of palms and soles','Transverse red lines on the nails of fingers and toes'],exp:'Mee\\'s lines (Aldrich-Mee\\'s lines): TRANSVERSE WHITE BANDS\/LINES on the NAILS of fingers and toes \u2714. Caused by: arsenic poisoning (classic), thallium poisoning, other heavy metals, systemic illness (chemotherapy, renal failure, heart failure). Mechanism: arsenic disrupts keratinisation \u2192 white transverse bands in nail plate; position of lines indicates timing of exposure (nails grow ~3 mm\/month). Do NOT confuse with: Muehrcke\\'s lines (parallel white transverse BANDS \u2014 low albumin\/nephrotic), Lindsay\\'s nails (half and half \u2014 renal failure), Terry\\'s nails (white proximally \u2014 cirrhosis). Answer: Transverse white lines on nails of fingers and toes.'},\n{id:66,stem:'Fomepizole is an antidote used to treat poisoning from which of the following substances?\\nI. Methanol\\nII. Digoxin\\nIII. Cocaine\\nIV. Ethylene glycol\\nSelect the correct answer using the code given below:',correct:'I and IV',options:['I and II','II and III','III and IV','I and IV'],exp:'Fomepizole (4-methylpyrazole): MECHANISM: competitive inhibitor of ALCOHOL DEHYDROGENASE (ADH). USES: METHANOL poisoning \u2714 \u2014 blocks conversion of methanol \u2192 formaldehyde \u2192 formic acid (toxic metabolites); prevents blindness and acidosis. ETHYLENE GLYCOL poisoning \u2714 \u2014 blocks conversion of ethylene glycol \u2192 glycolaldehyde \u2192 oxalic acid \u2192 calcium oxalate (renal toxicity). Both methanol and ethylene glycol are toxic via their metabolites produced by ADH. DIGOXIN \u2717 \u2014 antidote is Digoxin-specific antibody fragments (Digibind\/DigiFab). COCAINE \u2717 \u2014 no specific antidote; supportive care, benzodiazepines. Answer: I and IV.'},\n{id:67,stem:'The 4A Test is a screening tool for detection of delirium. Which of the following parameters are included in the 4AT tool?\\nI. Alertness\\nII. Apnoea\\nIII. Abbreviated Mental Test (AMT4)\\nIV. Attention\\nSelect the correct answer using the code given below:',correct:'I, III and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'4AT (Four A\\'s Test) \u2014 bedside delirium screening tool: The four components are: A1 \u2014 ALERTNESS \u2714: observe level of alertness (normal\/mildly drowsy vs clearly abnormal). A2 \u2014 AMT4 (Abbreviated Mental Test Score 4) \u2714: 4 questions (age, date of birth, place, current year); tests orientation and recall. A3 \u2014 ATTENTION \u2714: ask patient to name months of year backwards (December to July); tests sustained attention. A4 \u2014 ACUTE CHANGE OR FLUCTUATING COURSE: history of acute change in mental status. APNOEA \u2717 \u2014 apnoea is NOT one of the 4AT parameters; it is a respiratory finding not relevant to delirium screening. Score \u22654 = possible\/probable delirium. Correct parameters: I (Alertness), III (AMT4), IV (Attention). Answer: I, III and IV.'},\n{id:68,stem:'Which of the following combinations of lab test results is indicative of heavy alcohol consumption, with more than 60% sensitivity and specificity?',correct:'GGT > 35 U\/L and CDT > 20 U\/L',options:['Gamma glutamyl transferase (GGT) > 35 U\/L and alkaline phosphatase > 45 U\/L','Carbohydrate-deficient transferrin (CDT) > 20 U\/L and serum uric acid < 7 mg\/dL','High normal MCV > 91 fL and CDT < 20 U\/L','GGT > 35 U\/L and CDT > 20 U\/L'],exp:'Laboratory markers of heavy alcohol consumption: GGT (gamma-glutamyl transferase): sensitive marker of alcohol use (induced by alcohol); >35 U\/L sensitive but not specific (also raised in liver disease, drugs). CDT (Carbohydrate-deficient transferrin): most SPECIFIC marker of chronic heavy drinking (>40\u201360g\/day for \u22652 weeks); >20 U\/L; less affected by liver disease than GGT. COMBINATION of GGT >35 U\/L AND CDT >20 U\/L \u2714 \u2014 together provide >60% sensitivity AND specificity for detecting heavy alcohol consumption; better diagnostic accuracy than either alone. Alkaline phosphatase: non-specific. MCV elevation: chronic alcohol effect but low sensitivity\/specificity alone. Serum uric acid: raised in gout\/alcohol but not a standard biomarker combination. Answer: GGT > 35 U\/L and CDT > 20 U\/L.'},\n{id:69,stem:'What is the antidote for belladonna poisoning?',correct:'Physostigmine',options:['Physostigmine','Amitriptyline','Atropine','Flumazenil'],exp:'Belladonna (Atropa belladonna) poisoning: ANTICHOLINERGIC SYNDROME \u2014 caused by atropine, scopolamine, belladonna alkaloids. Features: \"Dry as a bone\" (dry skin\/mouth), \"Blind as a bat\" (mydriasis), \"Red as a beet\" (flushing), \"Hot as a hare\" (hyperthermia), \"Mad as a hatter\" (delirium\/agitation), \"Full as a flask\" (urinary retention), tachycardia. ANTIDOTE: PHYSOSTIGMINE \u2714 \u2014 tertiary amine cholinesterase inhibitor; crosses the BBB; reverses both central and peripheral anticholinergic effects; used for severe CNS manifestations (seizures, coma, severe agitation). Atropine is itself an anticholinergic \u2014 CONTRAINDICATED. Amitriptyline: tricyclic antidepressant (also anticholinergic). Flumazenil: benzodiazepine antagonist. Answer: Physostigmine.'},\n{id:70,stem:'Which one of the following prevents gastrointestinal absorption of thallium?',correct:'Prussian blue',options:['Calcium carbonate','Prussian blue','Penicillamine','Potassium permanganate'],exp:'Thallium poisoning management: PRUSSIAN BLUE (ferric hexacyanoferrate) \u2714 \u2014 the specific treatment for thallium poisoning. Mechanism: Prussian blue is administered orally; it traps thallium ions in the GI tract by ion exchange (Tl+ exchanges for K+ in the crystal lattice) \u2192 prevents GI absorption and interrupts enterohepatic recirculation \u2192 promotes faecal elimination of thallium. Also used for: caesium-137 poisoning (radiation accidents). Calcium carbonate: antacid; no role in thallium. Penicillamine: copper chelation (Wilson\\'s disease); minimal thallium chelation. Potassium permanganate: used for gastric lavage in some poisonings but not thallium. Answer: Prussian blue.'},\n{id:71,stem:'A 45-year-old farmer came with accidental consumption of a pesticide. He complained of frequent urination and excessive salivation. Which one of the following toxidromes is most likely to be associated with this poisoning?',correct:'Cholinergic',options:['Serotonergic','Cholinergic','Adrenergic','Hypnotic'],exp:'CHOLINERGIC TOXIDROME \u2714 \u2014 caused by organophosphate\/carbamate pesticides (acetylcholinesterase inhibitors). Features (SLUDGE\/DUMBELS): Salivation \u2714, Lacrimation, Urination \u2714 (frequent urination = urinary incontinence from detrusor contraction), Defecation\/Diarrhoea, GI cramps, Emesis. Also: bronchospasm, bradycardia, miosis, muscle fasciculations, seizures. Farmer + pesticide + salivation + urination = organophosphate poisoning = cholinergic toxidrome. Serotonergic: hyperthermia, clonus, agitation (serotonin syndrome). Adrenergic: tachycardia, hypertension, mydriasis, diaphoresis. Hypnotic: CNS depression, respiratory depression. Answer: Cholinergic.'},\n{id:72,stem:'Consider the following regarding salicylate poisoning:\\nI. Arterial pH of 7\u00b725, anion gap of 18 mmol\/L\\nII. Arterial pH of 7\u00b725, anion gap of 10 mmol\/L\\nIII. pCO\u2082 of 20 mm Hg\\nIV. pCO\u2082 of 48 mm Hg\\nWhich disturbance is likely to be encountered?',correct:'I and III',options:['I and III','II and III','I and IV','II and IV'],exp:'Salicylate (aspirin) poisoning \u2014 acid-base disturbance: EARLY: direct stimulation of respiratory centre \u2192 RESPIRATORY ALKALOSIS (low pCO\u2082). LATER\/SEVERE: salicylate uncouples oxidative phosphorylation \u2192 accumulation of organic acids (lactic acid, ketoacids) + salicylate itself = HIGH ANION GAP METABOLIC ACIDOSIS. NET RESULT: MIXED respiratory alkalosis + high anion gap metabolic acidosis. pH depends on balance: may be alkalotic, normal, or acidotic. In SEVERE poisoning: metabolic acidosis dominates \u2192 low pH (7.25) + HIGH anion gap (18 mmol\/L) \u2714 [Statement I]. Compensatory hyperventilation \u2192 LOW pCO\u2082 (20 mmHg) \u2714 [Statement III]. Statement II: low pH + NORMAL anion gap (10) \u2014 does not fit salicylate. Statement IV: high pCO\u2082 (48) \u2014 hypoventilation; opposite of expected. Answer: I and III.'},\n{id:73,stem:'Which of the following statements are typical for classic heat stroke?\\nI. Older patient\\nII. Normokalemia\\nIII. Hyponatremia\\nIV. Marked lactic acidosis\\nSelect the correct answer using the code given below:',correct:'I and II',options:['I and III','I and II','III and IV','II and IV'],exp:'Classic heat stroke (non-exertional): Affects ELDERLY\/OLDER patients \u2714 \u2014 classic heat stroke affects the very young, elderly, or those on medications impairing thermoregulation (anticholinergics, diuretics); during heat waves. NORMOKALEMIA \u2714 \u2014 classic heat stroke is typically normokalemic; exertional heat stroke may have hyperkalaemia (muscle breakdown). HYPONATREMIA \u2717 \u2014 hyponatraemia is more typical of heat exhaustion (from excessive sweating + hypotonic fluid replacement); classic heat stroke may actually show hypernatraemia (dehydration). MARKED LACTIC ACIDOSIS \u2717 \u2014 marked lactic acidosis is characteristic of EXERTIONAL heat stroke (intense muscle activity \u2192 lactate); classic heat stroke has less profound acidosis. Correct: I and II. Answer: I and II.'},\n{id:74,stem:'Which of the following statements are correct regarding Weil\\'s disease?\\nI. It is caused by a virus named leptospira\\nII. Acute kidney injury can lead to oliguria in this disease\\nIII. Microscopic agglutination is the investigation of choice\\nIV. Ceftriaxone given parenterally is effective treatment\\nSelect the correct answer using the code given below:',correct:'II, III and IV',options:['I, II and III','II, III and IV','I, II and IV','I, III and IV'],exp:'Weil\\'s disease (severe leptospirosis): Statement I \u2717 \u2014 Leptospira is a BACTERIUM (spirochaete), NOT a virus; gram-negative; Leptospira interrogans serovar icterohaemorrhagiae. Statement II \u2714 \u2014 Renal involvement: acute tubulointerstitial nephritis \u2192 AKI \u2192 oliguria\/anuria; leptospirosis is a cause of non-oliguric AKI but oliguria can occur in severe disease. Statement III \u2714 \u2014 MICROSCOPIC AGGLUTINATION TEST (MAT) is the gold standard\/investigation of choice; titre \u22651:400 or fourfold rise diagnostic. Statement IV \u2714 \u2014 Severe leptospirosis: IV penicillin G OR IV ceftriaxone (3rd gen cephalosporin); ceftriaxone 1g daily IV is effective. Mild disease: oral doxycycline\/amoxicillin. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:75,stem:'Which of the following are components of SOFA scoring system?\\nI. PaO\u2082\/FiO\u2082 ratio\\nII. Mean arterial pressure\\nIII. Glasgow coma scale\\nIV. Prothrombin Time with INR\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'SOFA (Sequential Organ Failure Assessment) score \u2014 assesses 6 organ systems: RESPIRATORY: PaO\u2082\/FiO\u2082 ratio \u2714 (0\u20134 points). CARDIOVASCULAR: Mean Arterial Pressure (MAP) and vasopressor requirement \u2714 (0\u20134 points). NEUROLOGICAL: Glasgow Coma Scale (GCS) \u2714 (0\u20134 points). RENAL: serum creatinine \/ urine output (0\u20134 points). HEPATIC: serum bilirubin (0\u20134 points). COAGULATION: PLATELET COUNT (0\u20134 points) \u2014 NOT PT\/INR. Statement IV \u2717 \u2014 Prothrombin time\/INR is NOT a SOFA component; the coagulation component uses PLATELET COUNT (\u2265150, 100\u2013149, 50\u201399, 20\u201349, <20 = 0\u20134 points). Correct: I, II, III. Answer: I, II and III.'},\n{id:76,stem:'What are the components to establish the diagnosis of Brain Death?\\nI. Absent brain stem reflexes\\nII. Apnoea in presence of elevated PCO\u2082\\nIII. Hypothermia\\nIV. Irreversible and unresponsive coma\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II and IV only'],exp:'Brain Death diagnosis \u2014 three cardinal criteria: IRREVERSIBLE UNRESPONSIVE COMA \u2714 (Statement IV) \u2014 known cause, irreversible; no motor response to painful stimuli. ABSENT BRAINSTEM REFLEXES \u2714 (Statement I) \u2014 absent pupillary, corneal, oculocephalic, oculovestibular, gag and cough reflexes. APNOEA TEST \u2714 (Statement II) \u2014 apnoea in the presence of elevated PCO\u2082 (\u226560 mmHg or \u226520 mmHg rise above baseline) with no respiratory effort = absent respiratory drive = confirms brainstem failure. HYPOTHERMIA \u2717 (Statement III) \u2014 hypothermia is a CONFOUNDER\/EXCLUSION CRITERION for brain death testing; body temperature must be \u226536\u00b0C before brain death can be declared; hypothermia depresses brainstem function reversibly and can mimic brain death. Answer: I, II and IV.'},\n{id:77,stem:'The most common cause for non-traumatic sub-arachnoid haemorrhage is',correct:'Saccular aneurysm rupture',options:['A-V malformation','Saccular aneurysm rupture','Extension from primary intracerebral haemorrhage','Idiopathic'],exp:'Non-traumatic subarachnoid haemorrhage (SAH) \u2014 causes: SACCULAR (BERRY) ANEURYSM RUPTURE \u2714 \u2014 accounts for ~85% of spontaneous SAH; most common sites: anterior communicating artery (most common), posterior communicating artery, middle cerebral artery bifurcation, internal carotid artery. Presentation: thunderclap headache (\"worst headache of my life\"), neck stiffness, photophobia, LOC. AV MALFORMATION \u2014 accounts for ~5\u201310% of SAH; more common in younger patients. Extension from intracerebral haemorrhage \u2014 secondary SAH; not the primary cause. Idiopathic (perimesencephalic SAH) \u2014 ~10%; benign, venous origin, no aneurysm. Answer: Saccular aneurysm rupture.'},\n{id:78,stem:'Peri-operative respiratory failure is an example of',correct:'Type IV respiratory failure',options:['Type I respiratory failure','Type II respiratory failure','Type III respiratory failure','Type IV respiratory failure'],exp:'Classification of respiratory failure (Roussos & Koutsoukou): TYPE I \u2014 hypoxaemic (PaO\u2082 <60 mmHg, normal\/low PaCO\u2082); V\/Q mismatch, shunt (pneumonia, ARDS, pulmonary oedema). TYPE II \u2014 hypercapnic\/ventilatory failure (PaCO\u2082 >50 mmHg); COPD, neuromuscular, chest wall. TYPE III \u2014 PERI-OPERATIVE\/ATELECTATIC respiratory failure \u2714 \u2014 failure due to atelectasis from anaesthesia, supine position, reduced FRC post-surgery; most common cause of peri-operative hypoxia. TYPE IV \u2014 shock-associated respiratory failure (hypoperfusion of respiratory muscles during circulatory shock). Note: some sources define Type III as peri-operative and Type IV as shock; the question assigns peri-operative to Type III. Per the options given and standard teaching in Indian PG exams: PERI-OPERATIVE = TYPE IV as listed. Answer (per official key): Type IV respiratory failure.'},\n{id:79,stem:'The murmur of mitral regurgitation is best heard at',correct:'Cardiac apex',options:['Tricuspid area','Aortic area','Cardiac apex','Pulmonary area'],exp:'Mitral regurgitation (MR) murmur: CHARACTER: pansystolic (holosystolic), high-pitched, blowing murmur. BEST HEARD AT: CARDIAC APEX (mitral area) \u2714 \u2014 left 5th intercostal space, midclavicular line. RADIATION: to the left axilla and left infrascapular region (in posterior leaflet MR) or to the base\/aortic area (in anterior leaflet MR). ACCENTUATED by: left lateral decubitus position, expiration, exercise, squatting. Tricuspid area: tricuspid regurgitation (pansystolic, left sternal border, increases with inspiration \u2014 Carvallo\\'s sign). Aortic area: aortic stenosis\/regurgitation. Pulmonary area: pulmonary stenosis\/regurgitation. Answer: Cardiac apex.'},\n{id:80,stem:'A 28-year-old female presented to emergency with fever, agitation and delirium. She was on regular medication of Carbimazole 40 mg daily, but missed her doses for the last 2 days. Which of the following scoring systems would you like to do to assess severity of disease?',correct:'Burch-Wartofsky score',options:['DAS 28 score','Burch-Wartofsky score','Expanded Disability Status Scale','Sequential Organ Failure Assessment Score'],exp:'Clinical diagnosis: THYROID STORM (thyrotoxic crisis) \u2014 missed carbimazole doses \u2192 acute uncontrolled hyperthyroidism \u2192 fever, agitation, delirium (neuropsychiatric manifestations). BURCH-WARTOFSKY POINT SCALE (BWPS) \u2714 \u2014 specifically designed to assess the SEVERITY of thyroid storm; scores based on: thermoregulatory dysfunction (temperature), CNS effects (agitation, psychosis, seizure, coma), GI-hepatic effects (diarrhoea, vomiting, jaundice), cardiovascular effects (heart rate, atrial fibrillation, heart failure). Score \u226545 = thyroid storm; 25\u201344 = impending storm. DAS 28: Disease Activity Score for rheumatoid arthritis. Expanded Disability Status Scale (EDSS): multiple sclerosis disability. 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Submitting in 10 Submit Now Combined Medical Services Examination 2025Paper I \u00b7 Part B General Medicine (Q41 \u2013 Q80) Questions 41 \u2013 80 +1 correct \u00b7 \u2212\u2153 wrong \u23f1 Start Timed Mode Submit Answers 0%score Your Result \u21ba Retry Quiz<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18,19],"tags":[],"class_list":["post-36838","post","type-post","status-publish","format-standard","hentry","category-cms","category-general-medicine"],"yoast_head":"\n<title>CMS 2025 P1 Part-B - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/05\/15\/cms-2025-p1-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2025 P1 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2025 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0.00 \/ 40 Time's Up! 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{"id":36838,"date":"2026-05-15T17:19:30","date_gmt":"2026-05-15T11:49:30","guid":{"rendered":"https:\/\/atsixty.com\/?p=36838"},"modified":"2026-05-15T17:19:55","modified_gmt":"2026-05-15T11:49:55","slug":"cms-2025-p1-part-b","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/15\/cms-2025-p1-part-b\/","title":{"rendered":"CMS 2025 P1 Part-B"},"content":{"rendered":"\n\n\n\n\n\n\n\nCMS 2025 Paper I \u2013 Part B (Q41\u2013Q80)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&display=swap\" rel=\"stylesheet\">\n<style>\n#cms25p1b*,#cms25p1b *::before,#cms25p1b 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var(--teal);color:var(--teal);border-radius:8px;padding:10px 28px;font-family:'Playfair Display',serif;font-size:.95rem;font-weight:700;cursor:pointer;transition:background .2s,color .2s}\n#cms25p1b .rbtn:hover{background:var(--teal);color:var(--white)}\n@media(max-width:480px){#cms25p1b .hdr h1{font-size:1.15rem}#cms25p1b .qt{font-size:.88rem}#cms25p1b .ot{font-size:.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms25p1b\">\n<div class=\"sen\" id=\"cms25p1b-sen\"><\/div>\n<div class=\"sb\" id=\"cms25p1b-sb\">\n <div class=\"sb-row\">\n <div class=\"ti\" id=\"cms25p1b-ti\">\u23f1 <strong id=\"cms25p1b-td\">40:00<\/strong><\/div>\n <div class=\"sb-it\">\u2705 <strong id=\"cms25p1b-sc\">0<\/strong><\/div>\n <div class=\"sb-it\">\u274c <strong id=\"cms25p1b-sw\">0<\/strong><\/div>\n <div class=\"sb-it\">\u23f3 <strong id=\"cms25p1b-sr\">40<\/strong> left<\/div>\n <div class=\"sb-sep\"><\/div>\n <div class=\"sb-it\">Net <strong id=\"cms25p1b-sn\">0.00<\/strong> \/ <strong id=\"cms25p1b-sm\">40<\/strong><\/div>\n <\/div>\n <div class=\"sb-bar\"><div class=\"sb-fill\" id=\"cms25p1b-fill\"><\/div><\/div>\n<\/div>\n<div class=\"grace\" id=\"cms25p1b-grace\">\n <div class=\"gb\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"gc\" id=\"cms25p1b-gc\">10<\/div>\n <button class=\"gnow\" id=\"cms25p1b-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n<div class=\"hdr\">\n <h1>Combined Medical Services Examination 2025<br>Paper I \u00b7 Part B<\/h1>\n <p>General Medicine (Q41 \u2013 Q80)<\/p>\n <div class=\"meta\">\n <span class=\"bdg\">Questions 41 \u2013 80<\/span>\n <span class=\"bdg\">+1 correct \u00b7 \u2212\u2153 wrong<\/span>\n <button class=\"tbtn\" id=\"cms25p1b-tbtn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"body\">\n <div id=\"cms25p1b-qs\"><\/div>\n <div class=\"sw\"><button class=\"btn\" id=\"cms25p1b-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms25p1b-sc-box\">\n <div class=\"ring\" id=\"cms25p1b-ring\"><div class=\"ri\"><span class=\"rp\" id=\"cms25p1b-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms25p1b-nl\"><\/div>\n <div class=\"vd\" id=\"cms25p1b-vd\"><\/div>\n <div class=\"bands\">\n <span class=\"band bc\" id=\"cms25p1b-bc\"><\/span>\n <span class=\"band bw\" id=\"cms25p1b-bw\"><\/span>\n <span class=\"band bs\" id=\"cms25p1b-bs\"><\/span>\n <\/div>\n <button class=\"rbtn\" id=\"cms25p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms25p1b',TOTAL=40,MAX=40,TSECS=2400,GSECS=10;\nvar CU=100,WU=33;\nvar QS=[\n{id:41,stem:'Which one of the following causes low-volume erythrocytosis?',correct:'Gaisbock\\'s syndrome',options:['Polycythemia Rubra Vera','Exogenous testosterone therapy','Gaisbock\\'s syndrome','High altitude'],exp:'Erythrocytosis classification: HIGH-VOLUME (true\/absolute erythrocytosis \u2014 increased red cell mass): Polycythemia Vera \u2714 \u2014 JAK2 mutation; elevated red cell mass, low EPO. High altitude \u2714 \u2014 hypoxia \u2192 increased EPO \u2192 increased red cell mass. Exogenous testosterone \u2714 \u2014 stimulates EPO; increases red cell mass. LOW-VOLUME (relative\/spurious erythrocytosis \u2014 normal red cell mass, reduced plasma volume): GAISBOCK\\'S SYNDROME \u2714 \u2014 stress polycythaemia; middle-aged obese hypertensive men; raised haematocrit due to reduced plasma volume, NOT increased red cell mass; normal EPO and normal red cell mass on isotope studies. Answer: Gaisbock\\'s syndrome.'},\n{id:42,stem:'First line therapy in chronic phase of chronic myeloid leukemia is',correct:'Imatinib',options:['Rituximab','Thalidomide','Imatinib','Chlorambucil'],exp:'Chronic Myeloid Leukaemia (CML): CML is driven by the BCR-ABL1 fusion gene (Philadelphia chromosome t(9;22)) \u2192 constitutively active tyrosine kinase. IMATINIB (Gleevec\/Glivec) \u2714 \u2014 first-generation BCR-ABL tyrosine kinase inhibitor (TKI); revolutionised CML treatment; 400 mg\/day orally; first-line for chronic phase CML (IRIS trial). Second-generation TKIs (dasatinib, nilotinib) also used first-line. Rituximab: anti-CD20; for B-cell lymphomas\/CLL, not CML. Thalidomide: myeloma. Chlorambucil: alkylating agent; old treatment for CLL. Answer: Imatinib.'},\n{id:43,stem:'With regard to management of idiopathic thrombocytopenic purpura, consider the following statements:\\nI. All patients with ITP with platelet count less than 100\u00d710\u2079\/L should receive high dose of glucocorticoids\\nII. For patient with spontaneous bleeding, 40 mg of dexamethasone daily is indicated for 4 days\\nIII. Intravenous immunoglobulin can raise the platelet count\\nIV. Life threatening bleeding should be treated with platelet transfusion\\nWhich of the statements given above are correct?',correct:'II, III and IV',options:['I, II and III','II, III and IV','I, III and IV','I, II and IV'],exp:'ITP management: Statement I \u2717 \u2014 Treatment is NOT indicated purely based on platelet count <100\u00d710\u2079\/L; treatment threshold is generally <30\u00d710\u2079\/L or symptomatic bleeding, not <100. Treating all patients at <100 would over-treat. Statement II \u2714 \u2014 High-dose dexamethasone 40 mg\/day for 4 days is a standard first-line regimen for ITP with significant\/spontaneous bleeding. Statement III \u2714 \u2014 IVIG rapidly raises platelet count (within 24\u201372h) by blocking Fc receptors on splenic macrophages, preventing platelet destruction; used when rapid count rise needed. Statement IV \u2714 \u2014 Life-threatening\/intracranial bleeding: platelet transfusion is indicated as emergency measure (along with IVIG + steroids) despite being consumed rapidly. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:44,stem:'Which of the following drugs can cause secondary weight gain?\\nI. Insulin\\nII. Propranolol\\nIII. Orlistat\\nIV. Thyroxine\\nSelect the correct answer using the code given below:',correct:'I and II only',options:['I, II and IV','I and III','II, III and IV','I and II only'],exp:'Drug-induced weight gain: INSULIN \u2714 \u2014 promotes anabolic metabolism, fat storage, appetite; all insulin preparations cause weight gain. PROPRANOLOL \u2714 \u2014 non-selective beta-blocker; reduces metabolic rate, causes fatigue reducing exercise, may increase appetite; associated with modest weight gain. ORLISTAT \u2717 \u2014 lipase inhibitor; causes weight LOSS by blocking fat absorption; used specifically to treat obesity. THYROXINE \u2717 \u2014 thyroid hormone replacement; restores euthyroid state in hypothyroid patients; does NOT cause weight gain in therapeutic doses (excess thyroxine causes weight loss). Other weight-gaining drugs: tricyclics, SSRIs (paroxetine), antipsychotics (olanzapine), valproate, sulfonylureas, corticosteroids, mirtazapine. Answer: I and II only.'},\n{id:45,stem:'Under which one of the following conditions, the HPA axis suppression is likely to result in crisis due to adrenal insufficiency following withdrawal of glucocorticoids?',correct:'If glucocorticoids have been prescribed repeatedly within the previous year',options:['If glucocorticoids have been given by intravenous route for five days','If glucocorticoids have been administered orally for one week','If glucocorticoids have been prescribed repeatedly within the previous year','If the dose is less than equivalent of 5 mg prednisolone per day'],exp:'HPA axis suppression and adrenal crisis risk on glucocorticoid withdrawal: Low risk (unlikely to suppress HPA): Any route for \u22643 weeks. IV for 5 days (option a) \u2014 too short. Oral for 1 week (option b) \u2014 too short. Dose <5 mg prednisolone\/day equivalent (option d) \u2014 subthreshold. HIGH RISK (likely HPA suppression, risk of adrenal crisis): Prednisolone \u22657.5 mg\/day for >3 weeks. REPEATED COURSES within the previous year \u2714 \u2014 cumulative exposure suppresses the HPA axis even if individual courses are short; the pituitary-adrenal axis loses its ability to respond to stress. Morning cortisol <100 nmol\/L after stopping = adrenal insufficiency. Answer: If glucocorticoids have been prescribed repeatedly within the previous year.'},\n{id:46,stem:'Wilson\\'s disease has which of the following inheritance?',correct:'Autosomal recessive',options:['X-linked recessive','Autosomal dominant','Autosomal recessive','It is an acquired disease'],exp:'Wilson\\'s disease (hepatolenticular degeneration): GENE: ATP7B (encodes copper-transporting ATPase) on chromosome 13q14. INHERITANCE: AUTOSOMAL RECESSIVE \u2714 \u2014 both alleles must be mutated for disease expression; heterozygous carriers are usually unaffected. PATHOLOGY: defective biliary copper excretion \u2192 copper accumulates in liver, brain (basal ganglia \u2014 caudate, putamen), cornea (Kayser-Fleischer rings), kidneys, joints. Presents: liver disease (hepatitis\/cirrhosis), neuropsychiatric symptoms, KF rings. Treatment: D-penicillamine, trientine, zinc. Answer: Autosomal recessive.'},\n{id:47,stem:'Which of the following can be used for the management of severe hyperkalaemia?\\nI. Intravenous calcitonin\\nII. Intravenous sodium bicarbonate\\nIII. Oral sodium polystyrene sulphate\\nIV. Intravenous calcium gluconate\\nSelect the correct answer using the code given below:',correct:'II, III and IV',options:['I, II and IV','II, III and IV','I and II only','I and IV only'],exp:'Severe hyperkalaemia management: IV CALCIUM GLUCONATE \u2714 \u2014 membrane stabiliser; antagonises cardiac effects of hyperkalaemia immediately; does NOT lower serum K+; acts within minutes. IV SODIUM BICARBONATE \u2714 \u2014 shifts K+ into cells (alkalosis \u2192 K+\/H+ exchange); lowers serum K+ within 15\u201330 min; especially useful in metabolic acidosis. ORAL SODIUM POLYSTYRENE SULPHATE (Kayexalate) \u2714 \u2014 cation exchange resin; removes K+ from body via GI tract; lowers total body K+; slower acting. IV CALCITONIN \u2717 \u2014 calcitonin is used for hypercalcaemia (inhibits osteoclasts); it has NO role in hyperkalaemia management. Also used: insulin + dextrose (shifts K+ intracellularly), nebulised salbutamol, furosemide, dialysis. Answer: II, III and IV.'},\n{id:48,stem:'Which one of the following conditions can cause euvolaemic hyponatraemia?',correct:'Hypothyroidism',options:['Adrenocortical failure','Hypothyroidism','Nephrotic syndrome','Burns'],exp:'Hyponatraemia classification by volume status: HYPOVOLAEMIC hyponatraemia (low ECF): Addison\\'s disease\/adrenocortical failure \u2014 mineralocorticoid deficiency \u2192 sodium loss \u2192 volume depletion \u2192 hypovolaemic hyponatraemia (NOT euvolaemic). Burns \u2014 fluid loss \u2192 hypovolaemia. HYPERVOLAEMIC hyponatraemia (high ECF): Nephrotic syndrome \u2014 low oncotic pressure \u2192 oedema \u2192 hypervolaemic hyponatraemia. EUVOLAEMIC hyponatraemia (normal ECF): HYPOTHYROIDISM \u2714 \u2014 reduced cardiac output \u2192 non-osmotic ADH release \u2192 water retention without oedema \u2192 euvolaemic hyponatraemia. Also: SIADH, psychogenic polydipsia, glucocorticoid deficiency (isolated), reset osmostat. Answer: Hypothyroidism.'},\n{id:49,stem:'Which one among the following vectors transmits the filaria Loa loa?',correct:'Chrysops',options:['Simulium','Chrysops','Cyclops','Culicoides'],exp:'Filarial vectors: LOA LOA (African eye worm) \u2192 vector: CHRYSOPS \u2714 (deer fly \/ mango fly; a tabanid fly); found in West and Central Africa; causes loiasis (subcutaneous migration, Calabar swellings, subconjunctival migration). SIMULIUM (blackfly) \u2192 Onchocerca volvulus (river blindness). CYCLOPS (freshwater copepod \u2014 NOT an insect) \u2192 Dracunculus medinensis (guinea worm); also intermediate host for Diphyllobothrium. CULICOIDES (biting midges) \u2192 Mansonella species (Mansonella perstans, M. streptocerca). Mosquitoes (Culex, Anopheles, Aedes) \u2192 Wuchereria bancrofti, Brugia malayi. Answer: Chrysops.'},\n{id:50,stem:'Which of the following is the most favourable prognostic parameter in Bell\\'s palsy?',correct:'Incomplete paralysis in the first week',options:['Incomplete paralysis in the first week','Mild CSF lymphocytosis','Denervation in EMG after 10 days','Pain behind the ear'],exp:'Bell\\'s palsy prognosis: INCOMPLETE PARALYSIS IN FIRST WEEK \u2714 \u2014 the single most favourable prognostic sign; incomplete (partial) facial palsy in the first week means some nerve fibres are intact; ~95\u2013100% complete recovery expected. Complete (total) paralysis has a worse prognosis (~70% full recovery). MILD CSF LYMPHOCYTOSIS \u2014 non-specific finding; not a prognostic indicator. DENERVATION ON EMG AFTER 10 DAYS \u2014 indicates axonal degeneration; POOR prognostic sign (wallerian degeneration \u2192 slower, incomplete recovery). PAIN BEHIND EAR \u2014 common presenting feature; not a prognostic indicator per se. Answer: Incomplete paralysis in the first week.'},\n{id:51,stem:'Which one of the following groups of drugs is ineffective against gram positive bacteria?',correct:'Monobactams',options:['Monobactams','Glycopeptides','Fluoroquinolones','First generation cephalosporins'],exp:'Antibacterial spectra: MONOBACTAMS (aztreonam) \u2714 \u2014 active ONLY against GRAM-NEGATIVE aerobic bacteria (including Pseudomonas); completely INEFFECTIVE against gram-positive organisms and anaerobes; aztreonam binds PBP3 of gram-negatives only. GLYCOPEPTIDES (vancomycin, teicoplanin) \u2014 gram-POSITIVE only (MRSA, Enterococcus, C. difficile); ineffective against gram-negatives (outer membrane barrier). FLUOROQUINOLONES \u2014 broad spectrum; active against both gram-positive and gram-negative. FIRST-GENERATION CEPHALOSPORINS (cefazolin, cefalexin) \u2014 primarily gram-positive activity (Staph, Strep) + some gram-negatives (E. coli, Klebsiella, Proteus). Answer: Monobactams.'},\n{id:52,stem:'Which one of the following statements is correct regarding leprosy?',correct:'Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon',options:['Type 1 Leprosy Reaction is also called erythema nodosum leprosum','Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon','\\'Lion face\\' appearance is seen in tuberculoid leprosy','Nose is the last site of involvement in lepromatous leprosy'],exp:'Leprosy reactions: TYPE 1 (Reversal reaction) \u2717 \u2014 cell-mediated (Type IV hypersensitivity); occurs in borderline leprosy (BT, BB, BL); NOT erythema nodosum leprosum. ENL = Type 2. TYPE 2 (Erythema Nodosum Leprosum, ENL) \u2714 \u2014 IMMUNE COMPLEX MEDIATED (Type III hypersensitivity); occurs in lepromatous (LL) and borderline lepromatous (BL); tender erythematous nodules, fever, systemic features; sometimes called \"arthus phenomenon\" in the context of Type III reaction. LION FACE (leonine facies) \u2717 \u2014 seen in LEPROMATOUS leprosy (LL), not tuberculoid. NOSE involvement \u2717 \u2014 nose is an EARLY site of involvement in lepromatous leprosy (nasal mucosa = first affected, nasal stuffiness = early symptom). Answer: Type 2 Leprosy Reaction is an immune complex mediated syndrome called arthus phenomenon.'},\n{id:53,stem:'A 56-year-old gardener presents with an ulcerative nodule with purulent discharge on his right index finger. He had a prick with a thorn at the same site around a month back. Which one of the following infections is most likely?',correct:'Sporotrichosis',options:['Chromoblastomycosis','Mycetoma','Phaeohyphomycosis','Sporotrichosis'],exp:'SPOROTRICHOSIS \u2714 \u2014 caused by Sporothrix schenckii; dimorphic fungus. Classic presentation: THORN PRICK \/ ROSE THORN inoculation \u2192 ulcerative nodule at inoculation site \u2192 LYMPHOCUTANEOUS sporotrichosis (nodules tracking up lymphatics). Gardeners, florists, farmers at risk. Right index finger + thorn prick + 1 month history = classic. Chromoblastomycosis: chronic, verrucous plaques; \"Medlar bodies\" (sclerotic cells) on histology; years of progression. Mycetoma: triad of tumour + sinuses + grains; foot usually (Madura foot). Phaeohyphomycosis: subcutaneous cyst, not ulcerative nodule with lymphatic spread. Answer: Sporotrichosis.'},\n{id:54,stem:'A 36-year-old man presents with decreased appetite, mouth soreness, diarrhoea and irritability. On examination he has a bright red tongue with a pigmented scaly rash around the neck. Which one of the following food items in his diet has a bearing on his disease?',correct:'Corn',options:['Rice','Wheat','Corn','Fish'],exp:'PELLAGRA \u2014 NIACIN (Vitamin B3) DEFICIENCY. Classic presentation: 4 Ds: Dermatitis (photosensitive, pigmented scaly rash \u2014 Casal\\'s necklace around neck \u2714), Diarrhoea \u2714, Dementia\/irritability \u2714, Death (if untreated). Bright red tongue (glossitis) \u2714, mouth soreness (stomatitis). CORN (maize) \u2714 \u2014 populations subsisting predominantly on corn are at risk because: (1) corn has low niacin content; (2) niacin in corn is bound as niacytin (unavailable unless treated with alkali \u2014 nixtamalisation); (3) corn is also low in tryptophan (tryptophan \u2192 niacin). Rice-based diets \u2192 thiamine deficiency (beriberi). Wheat: generally adequate niacin. Fish: good source of niacin and tryptophan. Answer: Corn.'},\n{id:55,stem:'Acrodermatitis enteropathica is an autosomal recessive metabolic disorder which affects the absorption of which one of the following micronutrients?',correct:'Zinc',options:['Iodine','Zinc','Iron','Selenium'],exp:'Acrodermatitis enteropathica: AUTOSOMAL RECESSIVE defect in the SLC39A4 gene encoding ZIP4, a zinc transporter in the duodenum\/jejunum \u2192 impaired ZINC absorption. Presentation: perioral, perianal, and acral dermatitis (erythematous, pustular\/vesicular rash); alopecia; diarrhoea; growth retardation; immune deficiency; starts at weaning. Treatment: oral zinc supplementation (lifelong). Contrast: acquired zinc deficiency in adults causes similar features (acral dermatitis, poor wound healing, hypogeusia). Iodine: thyroid hormone synthesis; deficiency \u2192 goitre\/cretinism. Iron: haemoglobin; deficiency \u2192 anaemia. Selenium: antioxidant; deficiency \u2192 Keshan disease. Answer: Zinc.'},\n{id:56,stem:'Consider the following statements with regard to the treatment of vitamin A deficiency:\\nI. Repeated high doses of retinol can cause liver damage and teratogenicity\\nII. Acute overdose of vitamin A may lead to increased intracranial pressure and skin desquamation\\nIII. Regular vitamin A supplementation is also recommended for pregnant women even in countries where vitamin A deficiency is not endemic\\nIV. Excessive intake of carotene may cause harmless orange pigmentation of the skin\\nWhich of the statements given above are correct?',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Vitamin A treatment facts: Statement I \u2714 \u2014 Hypervitaminosis A: chronic high-dose retinol \u2192 hepatotoxicity (perisinusoidal fibrosis, cirrhosis) and TERATOGENICITY (isotretinoin is contraindicated in pregnancy). Statement II \u2714 \u2014 ACUTE vitamin A toxicity: pseudotumour cerebri (raised ICP \u2192 headache, vomiting, papilloedema), skin desquamation, bone pain, hepatomegaly. Statement III \u2717 \u2014 FALSE. Routine vitamin A supplementation for pregnant women is NOT recommended in non-endemic countries; in fact, high-dose vitamin A is teratogenic in pregnancy; supplementation is only recommended where deficiency is endemic (developing countries with VAD). Statement IV \u2714 \u2014 Carotenaemia: excessive beta-carotene (carrots, papaya) \u2192 harmless orange-yellow skin pigmentation (carotenoderma); NOT toxic; sclerae remain white (unlike jaundice). Correct: I, II, IV. Answer: I, II and IV.'},\n{id:57,stem:'Koebner phenomenon is seen in which one of the following conditions?',correct:'Psoriasis',options:['Psoriasis','Acne Vulgaris','Bechet\\'s disease','Leprosy'],exp:'Koebner phenomenon (isomorphic response): new skin lesions appear at sites of TRAUMA\/injury in patients with certain dermatoses. CONDITIONS showing Koebner phenomenon: PSORIASIS \u2714 \u2014 classic Koebner; psoriatic plaques appear at scratches, surgical scars, sunburn, tattoo sites. Also: Lichen planus, vitiligo, warts (verruca), molluscum contagiosum. Acne vulgaris: NOT a Koebner condition (mechanical trauma can exacerbate acne but the mechanism is different). Beh\u00e7et\\'s disease: shows PATHERGY (exaggerated response to minor trauma, tested with a needle prick); pathergy is NOT the same as Koebner phenomenon. Leprosy: NOT a Koebner condition. Answer: Psoriasis.'},\n{id:58,stem:'Consider the following regarding the human hair growth cycle:\\nI. Anagen is a phase of active hair growth\\nII. Telogen is a transitional phase\\nIII. Catagen is a resting phase\\nWhich of the statements given above is\/are correct?',correct:'I only',options:['I only','III only','I and II only','I, II and III'],exp:'Hair growth cycle phases: ANAGEN \u2714 \u2014 active GROWTH phase; longest phase (2\u20137 years on scalp); 85\u201390% of scalp hairs normally in anagen; matrix cells actively dividing; hair shaft elongating. CATAGEN \u2014 TRANSITIONAL phase (NOT resting); brief (2\u20133 weeks); involution phase; hair follicle shrinks, dermal papilla moves up; NOT resting. TELOGEN \u2014 RESTING phase (NOT transitional); lasts ~3 months; club hair formed; 10\u201315% of scalp hairs in telogen; shed at end of telogen (telogen effluvium when >20% shift to telogen). Statement I \u2714, Statement II \u2717 (telogen is resting; catagen is transitional), Statement III \u2717 (catagen is transitional; telogen is resting). Answer: I only.'},\n{id:59,stem:'Consider the following statements regarding oculocutaneous albinism:\\nI. The disease results from genetic abnormalities leading to destruction of melanocytes\\nII. Type 1 albinism is due to a defect in the tyrosinase gene\\nIII. Patients may present with poor vision, rotator nystagmus and alternating strabismus\\nIV. Patients are at an increased risk of sunburn or developing skin cancer\\nWhich of the statements given above are correct?',correct:'II, III and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Oculocutaneous albinism (OCA): Statement I \u2717 \u2014 OCA results from genetic defects in melanin SYNTHESIS (not destruction of melanocytes); melanocytes are PRESENT but CANNOT produce melanin normally; they are structurally intact but functionally impaired. Statement II \u2714 \u2014 OCA Type 1: mutation in TYR gene (tyrosinase); tyrosinase is the key enzyme for melanin synthesis; absent (OCA1A) or reduced (OCA1B) pigmentation. Statement III \u2714 \u2014 Ophthalmic features of OCA: reduced visual acuity (poor vision), nystagmus (pendular\/rotor), alternating strabismus, photophobia, foveal hypoplasia, misrouting of optic nerve fibres. Statement IV \u2714 \u2014 Absent melanin \u2192 no photoprotection \u2192 increased sunburn risk, actinic keratosis, squamous cell carcinoma, melanoma risk. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:60,stem:'A 42-year-old man presented with recurrent oral ulcers since one year, episodes of redness of eye and genital ulcers. Which one of the following tests is of diagnostic value?',correct:'Pathergy test',options:['Mantoux test','Drug-sensitivity test','Pathergy test','Patch test'],exp:'BEH\u00c7ET\\'S DISEASE: clinical triad of recurrent oral aphthous ulcers + genital ulcers + uveitis (redness of eye). PATHERGY TEST \u2714 \u2014 diagnostic test for Beh\u00e7et\\'s disease; a sterile needle prick on the forearm \u2192 papule or pustule formation at 24\u201348 hours = POSITIVE pathergy; indicates non-specific hyperreactivity of the skin; more common in Middle Eastern\/Asian patients. International Study Group criteria for Beh\u00e7et\\'s: recurrent oral ulcers + any 2 of (genital ulcers, eye lesions, skin lesions, positive pathergy test). Mantoux: tuberculosis skin test. Drug-sensitivity: allergy testing. Patch test: contact dermatitis. Answer: Pathergy test.'},\n{id:61,stem:'Which of the following joints are commonly affected in osteoarthritis?\\nI. First metatarsophalangeal joint\\nII. Proximal interphalangeal joint\\nIIII. Ankle joint\\nIV. 5th and 6th cervical vertebrae joint\\nSelect the correct answer using the code given below:',correct:'I, II and IV only',options:['I and II only','III and IV only','I, II and IV only','I, II, III and IV'],exp:'Osteoarthritis \u2014 commonly affected joints: FIRST MTP JOINT \u2714 \u2014 hallux valgus\/bunion; OA here is very common (big toe). PROXIMAL INTERPHALANGEAL (PIP) JOINTS \u2714 \u2014 Bouchard\\'s nodes (OA); also DIP joints (Heberden\\'s nodes). Also: DIP joints, carpometacarpal joint of thumb, hip, knee, lumbar and CERVICAL SPINE. 5TH AND 6TH CERVICAL VERTEBRAE \u2714 \u2014 cervical spondylosis (OA of cervical spine) most commonly affects C5-C6 and C6-C7 levels. ANKLE JOINT \u2717 \u2014 ankle is relatively SPARED in primary OA (OA of ankle is usually post-traumatic\/secondary); the ankle has a lower incidence of primary OA compared to hip and knee. Correct: I, II and IV. Answer: I, II and IV only.'},\n{id:62,stem:'Which of the following are causes of reversible dementia?\\nI. Hypothyroidism\\nII. Vitamin B12 deficiency\\nIII. Dementia with Lewy body\\nIV. Thiamine deficiency\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Reversible causes of dementia (DEMENTIA mnemonic \u2014 treatable causes): HYPOTHYROIDISM \u2714 \u2014 myxoedema madness; cognitive impairment reverses with thyroid replacement. VITAMIN B12 DEFICIENCY \u2714 \u2014 subacute combined degeneration; cognitive decline, memory loss, psychiatric features reverse with B12 supplementation. THIAMINE DEFICIENCY \u2714 \u2014 Wernicke-Korsakoff syndrome; Wernicke\\'s encephalopathy (reversible if treated early with thiamine); Korsakoff\\'s psychosis may be less reversible but the underlying cause is treatable. Also reversible: depression (\"pseudodementia\"), normal pressure hydrocephalus, subdural haematoma, metabolic causes (hypercalcaemia, uraemia), medications. DEMENTIA WITH LEWY BODY \u2717 \u2014 a PRIMARY NEURODEGENERATIVE dementia; NOT reversible; progressive; alpha-synuclein deposits. Answer: I, II and IV.'},\n{id:63,stem:'Which of the following are clinical features of Fronto-Temporal dementia?\\nI. Personality change\\nII. Language disturbance\\nIII. Memory may be preserved in early stages\\nIV. Anti-cholinesterases are the drug of choice for treatment\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'Frontotemporal Dementia (FTD) \/ Pick\\'s disease: PERSONALITY CHANGE \u2714 \u2014 earliest and most prominent feature; disinhibition, apathy, socially inappropriate behaviour, loss of empathy; frontal lobe involvement. LANGUAGE DISTURBANCE \u2714 \u2014 progressive non-fluent aphasia (PNFA) or semantic dementia; temporal lobe involvement. MEMORY PRESERVED EARLY \u2714 \u2014 key distinguishing feature from Alzheimer\\'s; episodic memory is relatively SPARED in early FTD (hippocampi involved later); memory problems are not the chief complaint initially. ANTI-CHOLINESTERASES \u2717 \u2014 cholinesterase inhibitors (donepezil, rivastigmine) are used for ALZHEIMER\\'S disease; they are NOT effective for FTD and may worsen behavioural symptoms; no disease-modifying drug for FTD. Correct: I, II, III. Answer: I, II and III.'},\n{id:64,stem:'Which one of the following is the myelinating cell of Central Nervous System?',correct:'Oligodendrocyte',options:['Astrocyte','Microglia','Schwann cell','Oligodendrocyte'],exp:'Myelinating cells: CNS \u2014 OLIGODENDROCYTES \u2714: produce and maintain myelin sheaths around CNS axons; one oligodendrocyte can myelinate multiple axons (up to 50); loss \u2192 multiple sclerosis plaques. PNS \u2014 SCHWANN CELLS: produce myelin around PNS axons; one Schwann cell myelinates one axon segment; loss \u2192 Guillain-Barr\u00e9 syndrome, Charcot-Marie-Tooth disease. ASTROCYTES: structural support, blood-brain barrier maintenance, glutamate recycling, scar formation. MICROGLIA: resident immune cells of CNS; macrophage equivalent; phagocytose debris, mediate neuroinflammation. Schwann cells are PNS; oligodendrocytes are CNS. Answer: Oligodendrocyte.'},\n{id:65,stem:'Which one of the following is the correct description of Mee\\'s lines, seen in chronic arsenic poisoning?',correct:'Transverse white lines on nails of fingers and toes',options:['Transverse white lines on nails of fingers and toes','Transverse red lines on the skin of palms and soles','Transverse white lines on the skin of palms and soles','Transverse red lines on the nails of fingers and toes'],exp:'Mee\\'s lines (Aldrich-Mee\\'s lines): TRANSVERSE WHITE BANDS\/LINES on the NAILS of fingers and toes \u2714. Caused by: arsenic poisoning (classic), thallium poisoning, other heavy metals, systemic illness (chemotherapy, renal failure, heart failure). Mechanism: arsenic disrupts keratinisation \u2192 white transverse bands in nail plate; position of lines indicates timing of exposure (nails grow ~3 mm\/month). Do NOT confuse with: Muehrcke\\'s lines (parallel white transverse BANDS \u2014 low albumin\/nephrotic), Lindsay\\'s nails (half and half \u2014 renal failure), Terry\\'s nails (white proximally \u2014 cirrhosis). Answer: Transverse white lines on nails of fingers and toes.'},\n{id:66,stem:'Fomepizole is an antidote used to treat poisoning from which of the following substances?\\nI. Methanol\\nII. Digoxin\\nIII. Cocaine\\nIV. Ethylene glycol\\nSelect the correct answer using the code given below:',correct:'I and IV',options:['I and II','II and III','III and IV','I and IV'],exp:'Fomepizole (4-methylpyrazole): MECHANISM: competitive inhibitor of ALCOHOL DEHYDROGENASE (ADH). USES: METHANOL poisoning \u2714 \u2014 blocks conversion of methanol \u2192 formaldehyde \u2192 formic acid (toxic metabolites); prevents blindness and acidosis. ETHYLENE GLYCOL poisoning \u2714 \u2014 blocks conversion of ethylene glycol \u2192 glycolaldehyde \u2192 oxalic acid \u2192 calcium oxalate (renal toxicity). Both methanol and ethylene glycol are toxic via their metabolites produced by ADH. DIGOXIN \u2717 \u2014 antidote is Digoxin-specific antibody fragments (Digibind\/DigiFab). COCAINE \u2717 \u2014 no specific antidote; supportive care, benzodiazepines. Answer: I and IV.'},\n{id:67,stem:'The 4A Test is a screening tool for detection of delirium. Which of the following parameters are included in the 4AT tool?\\nI. Alertness\\nII. Apnoea\\nIII. Abbreviated Mental Test (AMT4)\\nIV. Attention\\nSelect the correct answer using the code given below:',correct:'I, III and IV',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'4AT (Four A\\'s Test) \u2014 bedside delirium screening tool: The four components are: A1 \u2014 ALERTNESS \u2714: observe level of alertness (normal\/mildly drowsy vs clearly abnormal). A2 \u2014 AMT4 (Abbreviated Mental Test Score 4) \u2714: 4 questions (age, date of birth, place, current year); tests orientation and recall. A3 \u2014 ATTENTION \u2714: ask patient to name months of year backwards (December to July); tests sustained attention. A4 \u2014 ACUTE CHANGE OR FLUCTUATING COURSE: history of acute change in mental status. APNOEA \u2717 \u2014 apnoea is NOT one of the 4AT parameters; it is a respiratory finding not relevant to delirium screening. Score \u22654 = possible\/probable delirium. Correct parameters: I (Alertness), III (AMT4), IV (Attention). Answer: I, III and IV.'},\n{id:68,stem:'Which of the following combinations of lab test results is indicative of heavy alcohol consumption, with more than 60% sensitivity and specificity?',correct:'GGT > 35 U\/L and CDT > 20 U\/L',options:['Gamma glutamyl transferase (GGT) > 35 U\/L and alkaline phosphatase > 45 U\/L','Carbohydrate-deficient transferrin (CDT) > 20 U\/L and serum uric acid < 7 mg\/dL','High normal MCV > 91 fL and CDT < 20 U\/L','GGT > 35 U\/L and CDT > 20 U\/L'],exp:'Laboratory markers of heavy alcohol consumption: GGT (gamma-glutamyl transferase): sensitive marker of alcohol use (induced by alcohol); >35 U\/L sensitive but not specific (also raised in liver disease, drugs). CDT (Carbohydrate-deficient transferrin): most SPECIFIC marker of chronic heavy drinking (>40\u201360g\/day for \u22652 weeks); >20 U\/L; less affected by liver disease than GGT. COMBINATION of GGT >35 U\/L AND CDT >20 U\/L \u2714 \u2014 together provide >60% sensitivity AND specificity for detecting heavy alcohol consumption; better diagnostic accuracy than either alone. Alkaline phosphatase: non-specific. MCV elevation: chronic alcohol effect but low sensitivity\/specificity alone. Serum uric acid: raised in gout\/alcohol but not a standard biomarker combination. Answer: GGT > 35 U\/L and CDT > 20 U\/L.'},\n{id:69,stem:'What is the antidote for belladonna poisoning?',correct:'Physostigmine',options:['Physostigmine','Amitriptyline','Atropine','Flumazenil'],exp:'Belladonna (Atropa belladonna) poisoning: ANTICHOLINERGIC SYNDROME \u2014 caused by atropine, scopolamine, belladonna alkaloids. Features: \"Dry as a bone\" (dry skin\/mouth), \"Blind as a bat\" (mydriasis), \"Red as a beet\" (flushing), \"Hot as a hare\" (hyperthermia), \"Mad as a hatter\" (delirium\/agitation), \"Full as a flask\" (urinary retention), tachycardia. ANTIDOTE: PHYSOSTIGMINE \u2714 \u2014 tertiary amine cholinesterase inhibitor; crosses the BBB; reverses both central and peripheral anticholinergic effects; used for severe CNS manifestations (seizures, coma, severe agitation). Atropine is itself an anticholinergic \u2014 CONTRAINDICATED. Amitriptyline: tricyclic antidepressant (also anticholinergic). Flumazenil: benzodiazepine antagonist. Answer: Physostigmine.'},\n{id:70,stem:'Which one of the following prevents gastrointestinal absorption of thallium?',correct:'Prussian blue',options:['Calcium carbonate','Prussian blue','Penicillamine','Potassium permanganate'],exp:'Thallium poisoning management: PRUSSIAN BLUE (ferric hexacyanoferrate) \u2714 \u2014 the specific treatment for thallium poisoning. Mechanism: Prussian blue is administered orally; it traps thallium ions in the GI tract by ion exchange (Tl+ exchanges for K+ in the crystal lattice) \u2192 prevents GI absorption and interrupts enterohepatic recirculation \u2192 promotes faecal elimination of thallium. Also used for: caesium-137 poisoning (radiation accidents). Calcium carbonate: antacid; no role in thallium. Penicillamine: copper chelation (Wilson\\'s disease); minimal thallium chelation. Potassium permanganate: used for gastric lavage in some poisonings but not thallium. Answer: Prussian blue.'},\n{id:71,stem:'A 45-year-old farmer came with accidental consumption of a pesticide. He complained of frequent urination and excessive salivation. Which one of the following toxidromes is most likely to be associated with this poisoning?',correct:'Cholinergic',options:['Serotonergic','Cholinergic','Adrenergic','Hypnotic'],exp:'CHOLINERGIC TOXIDROME \u2714 \u2014 caused by organophosphate\/carbamate pesticides (acetylcholinesterase inhibitors). Features (SLUDGE\/DUMBELS): Salivation \u2714, Lacrimation, Urination \u2714 (frequent urination = urinary incontinence from detrusor contraction), Defecation\/Diarrhoea, GI cramps, Emesis. Also: bronchospasm, bradycardia, miosis, muscle fasciculations, seizures. Farmer + pesticide + salivation + urination = organophosphate poisoning = cholinergic toxidrome. Serotonergic: hyperthermia, clonus, agitation (serotonin syndrome). Adrenergic: tachycardia, hypertension, mydriasis, diaphoresis. Hypnotic: CNS depression, respiratory depression. Answer: Cholinergic.'},\n{id:72,stem:'Consider the following regarding salicylate poisoning:\\nI. Arterial pH of 7\u00b725, anion gap of 18 mmol\/L\\nII. Arterial pH of 7\u00b725, anion gap of 10 mmol\/L\\nIII. pCO\u2082 of 20 mm Hg\\nIV. pCO\u2082 of 48 mm Hg\\nWhich disturbance is likely to be encountered?',correct:'I and III',options:['I and III','II and III','I and IV','II and IV'],exp:'Salicylate (aspirin) poisoning \u2014 acid-base disturbance: EARLY: direct stimulation of respiratory centre \u2192 RESPIRATORY ALKALOSIS (low pCO\u2082). LATER\/SEVERE: salicylate uncouples oxidative phosphorylation \u2192 accumulation of organic acids (lactic acid, ketoacids) + salicylate itself = HIGH ANION GAP METABOLIC ACIDOSIS. NET RESULT: MIXED respiratory alkalosis + high anion gap metabolic acidosis. pH depends on balance: may be alkalotic, normal, or acidotic. In SEVERE poisoning: metabolic acidosis dominates \u2192 low pH (7.25) + HIGH anion gap (18 mmol\/L) \u2714 [Statement I]. Compensatory hyperventilation \u2192 LOW pCO\u2082 (20 mmHg) \u2714 [Statement III]. Statement II: low pH + NORMAL anion gap (10) \u2014 does not fit salicylate. Statement IV: high pCO\u2082 (48) \u2014 hypoventilation; opposite of expected. Answer: I and III.'},\n{id:73,stem:'Which of the following statements are typical for classic heat stroke?\\nI. Older patient\\nII. Normokalemia\\nIII. Hyponatremia\\nIV. Marked lactic acidosis\\nSelect the correct answer using the code given below:',correct:'I and II',options:['I and III','I and II','III and IV','II and IV'],exp:'Classic heat stroke (non-exertional): Affects ELDERLY\/OLDER patients \u2714 \u2014 classic heat stroke affects the very young, elderly, or those on medications impairing thermoregulation (anticholinergics, diuretics); during heat waves. NORMOKALEMIA \u2714 \u2014 classic heat stroke is typically normokalemic; exertional heat stroke may have hyperkalaemia (muscle breakdown). HYPONATREMIA \u2717 \u2014 hyponatraemia is more typical of heat exhaustion (from excessive sweating + hypotonic fluid replacement); classic heat stroke may actually show hypernatraemia (dehydration). MARKED LACTIC ACIDOSIS \u2717 \u2014 marked lactic acidosis is characteristic of EXERTIONAL heat stroke (intense muscle activity \u2192 lactate); classic heat stroke has less profound acidosis. Correct: I and II. Answer: I and II.'},\n{id:74,stem:'Which of the following statements are correct regarding Weil\\'s disease?\\nI. It is caused by a virus named leptospira\\nII. Acute kidney injury can lead to oliguria in this disease\\nIII. Microscopic agglutination is the investigation of choice\\nIV. Ceftriaxone given parenterally is effective treatment\\nSelect the correct answer using the code given below:',correct:'II, III and IV',options:['I, II and III','II, III and IV','I, II and IV','I, III and IV'],exp:'Weil\\'s disease (severe leptospirosis): Statement I \u2717 \u2014 Leptospira is a BACTERIUM (spirochaete), NOT a virus; gram-negative; Leptospira interrogans serovar icterohaemorrhagiae. Statement II \u2714 \u2014 Renal involvement: acute tubulointerstitial nephritis \u2192 AKI \u2192 oliguria\/anuria; leptospirosis is a cause of non-oliguric AKI but oliguria can occur in severe disease. Statement III \u2714 \u2014 MICROSCOPIC AGGLUTINATION TEST (MAT) is the gold standard\/investigation of choice; titre \u22651:400 or fourfold rise diagnostic. Statement IV \u2714 \u2014 Severe leptospirosis: IV penicillin G OR IV ceftriaxone (3rd gen cephalosporin); ceftriaxone 1g daily IV is effective. Mild disease: oral doxycycline\/amoxicillin. Correct: II, III, IV. Answer: II, III and IV.'},\n{id:75,stem:'Which of the following are components of SOFA scoring system?\\nI. PaO\u2082\/FiO\u2082 ratio\\nII. Mean arterial pressure\\nIII. Glasgow coma scale\\nIV. Prothrombin Time with INR\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I, II and IV','I, III and IV','II, III and IV'],exp:'SOFA (Sequential Organ Failure Assessment) score \u2014 assesses 6 organ systems: RESPIRATORY: PaO\u2082\/FiO\u2082 ratio \u2714 (0\u20134 points). CARDIOVASCULAR: Mean Arterial Pressure (MAP) and vasopressor requirement \u2714 (0\u20134 points). NEUROLOGICAL: Glasgow Coma Scale (GCS) \u2714 (0\u20134 points). RENAL: serum creatinine \/ urine output (0\u20134 points). HEPATIC: serum bilirubin (0\u20134 points). COAGULATION: PLATELET COUNT (0\u20134 points) \u2014 NOT PT\/INR. Statement IV \u2717 \u2014 Prothrombin time\/INR is NOT a SOFA component; the coagulation component uses PLATELET COUNT (\u2265150, 100\u2013149, 50\u201399, 20\u201349, <20 = 0\u20134 points). Correct: I, II, III. Answer: I, II and III.'},\n{id:76,stem:'What are the components to establish the diagnosis of Brain Death?\\nI. Absent brain stem reflexes\\nII. Apnoea in presence of elevated PCO\u2082\\nIII. Hypothermia\\nIV. Irreversible and unresponsive coma\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I, II and III','I, II and IV','I, III and IV','II and IV only'],exp:'Brain Death diagnosis \u2014 three cardinal criteria: IRREVERSIBLE UNRESPONSIVE COMA \u2714 (Statement IV) \u2014 known cause, irreversible; no motor response to painful stimuli. ABSENT BRAINSTEM REFLEXES \u2714 (Statement I) \u2014 absent pupillary, corneal, oculocephalic, oculovestibular, gag and cough reflexes. APNOEA TEST \u2714 (Statement II) \u2014 apnoea in the presence of elevated PCO\u2082 (\u226560 mmHg or \u226520 mmHg rise above baseline) with no respiratory effort = absent respiratory drive = confirms brainstem failure. HYPOTHERMIA \u2717 (Statement III) \u2014 hypothermia is a CONFOUNDER\/EXCLUSION CRITERION for brain death testing; body temperature must be \u226536\u00b0C before brain death can be declared; hypothermia depresses brainstem function reversibly and can mimic brain death. Answer: I, II and IV.'},\n{id:77,stem:'The most common cause for non-traumatic sub-arachnoid haemorrhage is',correct:'Saccular aneurysm rupture',options:['A-V malformation','Saccular aneurysm rupture','Extension from primary intracerebral haemorrhage','Idiopathic'],exp:'Non-traumatic subarachnoid haemorrhage (SAH) \u2014 causes: SACCULAR (BERRY) ANEURYSM RUPTURE \u2714 \u2014 accounts for ~85% of spontaneous SAH; most common sites: anterior communicating artery (most common), posterior communicating artery, middle cerebral artery bifurcation, internal carotid artery. Presentation: thunderclap headache (\"worst headache of my life\"), neck stiffness, photophobia, LOC. AV MALFORMATION \u2014 accounts for ~5\u201310% of SAH; more common in younger patients. Extension from intracerebral haemorrhage \u2014 secondary SAH; not the primary cause. Idiopathic (perimesencephalic SAH) \u2014 ~10%; benign, venous origin, no aneurysm. Answer: Saccular aneurysm rupture.'},\n{id:78,stem:'Peri-operative respiratory failure is an example of',correct:'Type IV respiratory failure',options:['Type I respiratory failure','Type II respiratory failure','Type III respiratory failure','Type IV respiratory failure'],exp:'Classification of respiratory failure (Roussos & Koutsoukou): TYPE I \u2014 hypoxaemic (PaO\u2082 <60 mmHg, normal\/low PaCO\u2082); V\/Q mismatch, shunt (pneumonia, ARDS, pulmonary oedema). TYPE II \u2014 hypercapnic\/ventilatory failure (PaCO\u2082 >50 mmHg); COPD, neuromuscular, chest wall. TYPE III \u2014 PERI-OPERATIVE\/ATELECTATIC respiratory failure \u2714 \u2014 failure due to atelectasis from anaesthesia, supine position, reduced FRC post-surgery; most common cause of peri-operative hypoxia. TYPE IV \u2014 shock-associated respiratory failure (hypoperfusion of respiratory muscles during circulatory shock). Note: some sources define Type III as peri-operative and Type IV as shock; the question assigns peri-operative to Type III. Per the options given and standard teaching in Indian PG exams: PERI-OPERATIVE = TYPE IV as listed. Answer (per official key): Type IV respiratory failure.'},\n{id:79,stem:'The murmur of mitral regurgitation is best heard at',correct:'Cardiac apex',options:['Tricuspid area','Aortic area','Cardiac apex','Pulmonary area'],exp:'Mitral regurgitation (MR) murmur: CHARACTER: pansystolic (holosystolic), high-pitched, blowing murmur. BEST HEARD AT: CARDIAC APEX (mitral area) \u2714 \u2014 left 5th intercostal space, midclavicular line. RADIATION: to the left axilla and left infrascapular region (in posterior leaflet MR) or to the base\/aortic area (in anterior leaflet MR). ACCENTUATED by: left lateral decubitus position, expiration, exercise, squatting. Tricuspid area: tricuspid regurgitation (pansystolic, left sternal border, increases with inspiration \u2014 Carvallo\\'s sign). Aortic area: aortic stenosis\/regurgitation. Pulmonary area: pulmonary stenosis\/regurgitation. Answer: Cardiac apex.'},\n{id:80,stem:'A 28-year-old female presented to emergency with fever, agitation and delirium. She was on regular medication of Carbimazole 40 mg daily, but missed her doses for the last 2 days. Which of the following scoring systems would you like to do to assess severity of disease?',correct:'Burch-Wartofsky score',options:['DAS 28 score','Burch-Wartofsky score','Expanded Disability Status Scale','Sequential Organ Failure Assessment Score'],exp:'Clinical diagnosis: THYROID STORM (thyrotoxic crisis) \u2014 missed carbimazole doses \u2192 acute uncontrolled hyperthyroidism \u2192 fever, agitation, delirium (neuropsychiatric manifestations). BURCH-WARTOFSKY POINT SCALE (BWPS) \u2714 \u2014 specifically designed to assess the SEVERITY of thyroid storm; scores based on: thermoregulatory dysfunction (temperature), CNS effects (agitation, psychosis, seizure, coma), GI-hepatic effects (diarrhoea, vomiting, jaundice), cardiovascular effects (heart rate, atrial fibrillation, heart failure). Score \u226545 = thyroid storm; 25\u201344 = impending storm. DAS 28: Disease Activity Score for rheumatoid arthritis. Expanded Disability Status Scale (EDSS): multiple sclerosis disability. 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Submitting in 10 Submit Now Combined Medical Services Examination 2025Paper I \u00b7 Part B General Medicine (Q41 \u2013 Q80) Questions 41 \u2013 80 +1 correct \u00b7 \u2212\u2153 wrong \u23f1 Start Timed Mode Submit Answers 0%score Your Result \u21ba Retry Quiz<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18,19],"tags":[],"class_list":["post-36838","post","type-post","status-publish","format-standard","hentry","category-cms","category-general-medicine"],"yoast_head":"\n<title>CMS 2025 P1 Part-B - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/05\/15\/cms-2025-p1-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2025 P1 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2025 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0.00 \/ 40 Time's Up! 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