{"id":36786,"date":"2026-05-09T02:51:12","date_gmt":"2026-05-08T21:21:12","guid":{"rendered":"https:\/\/atsixty.com\/?p=36786"},"modified":"2026-05-09T03:16:21","modified_gmt":"2026-05-08T21:46:21","slug":"cms-2018-p1-part-a","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/09\/cms-2018-p1-part-a\/","title":{"rendered":"CMS 2018 P1 Part-A"},"content":{"rendered":"\n\n\n\n\n\nCMS 2018 Paper I \u2013 Part A (Q1\u2013Q40)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&display=swap\" rel=\"stylesheet\">\n<style>\n\/* \u2500\u2500 Namespace: cms18p1a \u2500\u2500 *\/\n#cms18p1a *,#cms18p1a *::before,#cms18p1a *::after{box-sizing:border-box;margin:0;padding:0}\n#cms18p1a{\n --ter:#C0603A;--ter-light:#e8825f;--ter-pale:#fdf1ec;\n --teal:#2A7A6F;--teal-light:#3da394;--teal-pale:#eaf4f3;\n --ink:#1a1a1a;--ink-mid:#444;--ink-soft:#777;\n --line:#e0d8d4;--bg:#fdfaf8;--white:#ffffff;\n --correct:#1e6f46;--correct-bg:#eaf7ef;--correct-border:#43a047;\n --wrong:#b83232;--wrong-bg:#fdf0f0;--wrong-border:#e53935;\n --radius:10px;\n font-family:'Source Serif 4',Georgia,serif;\n font-size:16px;color:var(--ink);background:var(--bg);\n line-height:1.7;padding:0 0 48px;\n}\n#cms18p1a .cq-sentinel{height:1px}\n#cms18p1a .cq-statusbar{\n position:fixed;top:0;left:0;right:0;z-index:99999;\n background:var(--white);border-bottom:2px solid var(--line);\n border-left:4px solid var(--ter);box-shadow:0 2px 12px rgba(0,0,0,0.11);\n opacity:0;pointer-events:none;transform:translateY(-110%);\n transition:opacity 0.22s ease,transform 0.22s ease;\n}\n#cms18p1a .cq-statusbar.visible{opacity:1;pointer-events:auto;transform:translateY(0)}\n#cms18p1a .cq-sb-stats{display:flex;align-items:center;padding:0.38rem 0.7rem;font-size:0.73rem;color:var(--ink-soft);}\n#cms18p1a .cq-sb-item{display:flex;align-items:center;gap:0.18rem;padding:0.1rem 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.cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms18p1a .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms18p1a .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms18p1a .cq-retry-btn{margin-top:22px;background:transparent;border:2px solid var(--teal);color:var(--teal);border-radius:8px;padding:10px 28px;font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;cursor:pointer;transition:background 0.2s,color 0.2s;}\n#cms18p1a .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n@media(max-width:480px){\n #cms18p1a .cq-header h1{font-size:1.15rem}\n #cms18p1a .cq-qtext{font-size:0.88rem}\n #cms18p1a .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms18p1a\">\n <div class=\"cq-sentinel\" id=\"cms18p1a-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms18p1a-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms18p1a-timer-item\">\u23f1 <strong id=\"cms18p1a-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms18p1a-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms18p1a-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms18p1a-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms18p1a-sn\">0<\/strong> \/ <strong id=\"cms18p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms18p1a-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms18p1a-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3>\n <p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms18p1a-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms18p1a-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2018<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine \u00b7 Infectious Diseases \u00b7 Toxicology<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 1 \u2013 40<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms18p1a-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms18p1a-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms18p1a-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms18p1a-score\">\n <div class=\"cq-score-ring\" id=\"cms18p1a-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms18p1a-ring-pct\">0%<\/span>\n <span class=\"cq-ring-sub\">score<\/span>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms18p1a-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms18p1a-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms18p1a-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms18p1a-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms18p1a-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms18p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms18p1a', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60, GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:1,\n stem:'Most common valve involved in Carcinoid syndrome is:',\n correct:'Tricuspid valve',\n options:['Mitral valve','Tricuspid valve','Aortic valve','Pulmonary valve'],\n exp:'Carcinoid syndrome results from serotonin (5-HT) and other vasoactive substances secreted by carcinoid tumours. Because the liver inactivates these amines, cardiac effects occur predominantly on the RIGHT side of the heart (pulmonary circulation has not yet detoxified them). The TRICUSPID valve is the most commonly involved, followed by the pulmonary valve \u2014 causing tricuspid regurgitation and pulmonary stenosis. Left-sided carcinoid heart disease is rare and usually indicates a patent foramen ovale or a primary bronchial carcinoid (bypassing the liver). Carcinoid heart disease = right-sided valvular lesions predominantly affecting the tricuspid valve.'\n },\n {\n id:2,\n stem:'A 70 year old man reports to the emergency with acute chest pain. ECG shows inferior wall Myocardial Infarction (MI). He has recently been discharged 7 days back following thrombolysis with streptokinase for Acute Anterior wall MI. What will be the appropriate management?',\n correct:'Aspirin, Sublingual nitroglycerin, Clopidogrel, Primary PCI',\n options:['Aspirin, Sublingual nitroglycerin, Clopidogrel, Primary PCI','Aspirin, Sublingual nitroglycerin, Clopidogrel, Streptokinase','Aspirin, Sublingual nitroglycerin, Clopidogrel, Heparin','Aspirin, Sublingual nitroglycerin, Clopidogrel, Beta blockers'],\n exp:'Key points: (1) Prior streptokinase use within 5 days\u201312 months is a CONTRAINDICATION to repeat streptokinase \u2014 antibodies develop rapidly and can cause hypersensitivity and reduced efficacy. (2) The patient has a new STEMI (inferior wall) and needs reperfusion. (3) Since streptokinase is contraindicated, the preferred reperfusion strategy is PRIMARY PCI (percutaneous coronary intervention). (4) Antithrombotic therapy: Aspirin + Clopidogrel (dual antiplatelet) + sublingual nitroglycerine are all standard STEMI adjuncts. Primary PCI is the gold-standard reperfusion strategy when available and when thrombolytics are contraindicated.'\n },\n {\n id:3,\n stem:'The presence of a fusion beat on an Electrocardiogram is diagnostic of:',\n correct:'Ventricular Tachycardia',\n options:['Atrial Fibrillation','Ventricular Tachycardia','Supraventricular Tachycardia','Sinus Bradycardia'],\n exp:'A fusion beat occurs when a supraventricular impulse and a ventricular ectopic impulse simultaneously activate the ventricles \u2014 the resulting QRS complex is a \"fusion\" of both (intermediate morphology). Fusion beats are a hallmark of VENTRICULAR TACHYCARDIA and confirm ventricular origin of tachycardia. They are also seen with ventricular pacing and accelerated idioventricular rhythm. Fusion beats (along with capture beats) are among the most reliable ECG criteria for diagnosing VT in wide-complex tachycardia. Atrial fibrillation shows absent P waves and irregularly irregular rhythm. SVT shows narrow QRS (usually). Sinus bradycardia has no fusion beats.'\n },\n {\n id:4,\n stem:'A 64 year old man presents with chest pain of 24 hours duration. His ECG reveals ST elevation, Anterior Wall Myocardial Infarction. The preferred treatment modality for him is:',\n correct:'Primary percutaneous coronary intervention',\n options:['Primary percutaneous coronary intervention','Thrombolysis with Alteplase','Thrombolysis with Streptokinase','Nitroglycerin infusion, Aspirin and Beta blockers'],\n exp:'For STEMI with onset >12 hours but \u226424 hours and ongoing symptoms or haemodynamic instability, revascularisation is still indicated. However, the critical teaching point here: PRIMARY PCI is ALWAYS preferred over thrombolysis when available, especially when (1) door-to-balloon time can be <120 min, (2) there are contraindications to thrombolysis, (3) cardiogenic shock is present, or (4) the patient presents late (>3 hours) when PCI is clearly superior. At 24 hours, thrombolysis is generally not recommended (benefit-risk unfavourable), making primary PCI the only revascularisation option if patient still has pain\/ischaemia. Primary PCI is the preferred modality.'\n },\n {\n id:5,\n stem:'The preferred anti hypertensive drug for a 74 year old male with benign prostatic hypertrophy is:',\n correct:'Prazosin',\n options:['Amlodipine','Hydrochlorothiazide','Prazosin','Atenolol'],\n exp:'Prazosin (and other alpha-1 blockers: terazosin, doxazosin, tamsulosin) serve a DUAL PURPOSE in elderly males: (1) Lower blood pressure by blocking \u03b11-adrenergic receptors in blood vessels \u2192 vasodilation. (2) Relieve BPH symptoms by relaxing smooth muscle in the prostate and bladder neck \u2192 improved urinary flow. This makes \u03b11-blockers the preferred antihypertensive when BPH coexists. Amlodipine is a good antihypertensive but has no benefit in BPH. Hydrochlorothiazide and atenolol are also effective antihypertensives but offer no urinary benefit. Prazosin = preferred in hypertension + BPH.'\n },\n {\n id:6,\n stem:'The treatment of choice for a 32 year old male patient of severe mitral stenosis (Rheumatic) with thickened and calcified valves on echocardiography is:',\n correct:'Mitral valve replacement',\n options:['Balloon valvuloplasty','Mitral valve replacement','Medical management only','Mitral valvotomy'],\n exp:'Balloon mitral valvuloplasty (BMV) is the procedure of choice for rheumatic mitral stenosis when valve morphology is FAVOURABLE (pliable, non-calcified, no significant MR, no LAA thrombus \u2014 assessed by Wilkins score \u22648). THICKENED and CALCIFIED valves = UNFAVOURABLE morphology (high Wilkins score). BMV in calcified valves has poor results and high complication rates. Surgical mitral valvotomy is also suboptimal with calcified valves. MITRAL VALVE REPLACEMENT is the treatment of choice for severe MS with calcified\/thickened valves where BMV is contraindicated or likely to fail. Medical management alone is insufficient for severe MS.'\n },\n {\n id:7,\n stem:'Which one of the following is an example of Type-IV respiratory failure?',\n correct:'Shock',\n options:['Bronchial asthma','Pulmonary embolism','COPD','Shock'],\n exp:'Classification of respiratory failure: Type I (Hypoxaemic) = low PaO\u2082, normal\/low PaCO\u2082 \u2014 examples: pneumonia, PE, ARDS, pulmonary oedema. Type II (Hypercapnic\/Ventilatory) = low PaO\u2082 + high PaCO\u2082 \u2014 examples: COPD, asthma (severe), neuromuscular disease. Type III (Perioperative\/Atelectasis) = postoperative FRC reduction. Type IV = SHOCK \u2014 hypoperfusion of respiratory muscles due to circulatory failure \u2192 respiratory muscles underperfused \u2192 fail to maintain ventilation. In shock, the respiratory muscles themselves receive inadequate cardiac output, leading to ventilatory failure superimposed on cardiovascular collapse. Shock is the classic Type IV respiratory failure.'\n },\n {\n id:8,\n stem:'All of the following are seen in Polyarteritis Nodosa EXCEPT:',\n correct:'Glomerulonephritis',\n options:['Glomerulonephritis','Peripheral Neuropathy','Bowel Infarction','Pericarditis'],\n exp:'Polyarteritis Nodosa (PAN) is a necrotising vasculitis of MEDIUM-SIZED arteries. Features include: peripheral neuropathy (mononeuritis multiplex \u2014 very common), mesenteric vasculitis \u2192 bowel infarction, renal artery involvement \u2192 renovascular hypertension and renal infarction, testicular\/ovarian artery involvement \u2192 testicular pain, skin (livedo, nodules, ulcers), cardiac involvement (coronary arteritis, rarely pericarditis). GLOMERULONEPHRITIS is ABSENT in classic PAN \u2014 because PAN affects medium arteries, NOT small vessels\/capillaries (the glomerular capillaries). GN is a feature of ANCA-associated vasculitis (MPA, GPA) and immune-complex vasculitis. The absence of GN distinguishes PAN from microscopic polyangiitis.'\n },\n {\n id:9,\n stem:'All of the following are pointers to organic cause of psychiatric disease EXCEPT:',\n correct:'Family history of psychiatric illness',\n options:['Late age of onset of psychiatric illness','No previous history of psychiatric illness','Family history of psychiatric illness','No apparent psychological precipitant'],\n exp:'Pointers to an ORGANIC (medical) cause of psychiatric illness: Late age of onset (first psychiatric episode in elderly \u2014 unusual for primary psychiatric disorders). No previous history of psychiatric illness (primary disorders often start earlier). No apparent psychological precipitant (primary psychiatric disorders often have identifiable stressors). Abnormal physical signs, visual hallucinations, cognitive impairment, fluctuating consciousness, focal neurological signs. FAMILY HISTORY of psychiatric illness is a pointer to a PRIMARY (functional\/genetic) psychiatric disorder \u2014 schizophrenia, bipolar disorder, and depression all have strong genetic\/familial components. Family history thus points AWAY from an organic cause. It is not a pointer to organic disease.'\n },\n {\n id:10,\n stem:'All of the following are Long Acting Beta Agonists (LABA) EXCEPT:',\n correct:'Levo salbutamol',\n options:['Levo salbutamol','Salmeterol','Formoterol','Indacaterol'],\n exp:'Long-Acting Beta-2 Agonists (LABA) \u2014 duration \u226512 hours: Salmeterol (12h, slow onset), Formoterol (12h, rapid onset \u2014 can be used for rescue in MART regimen), Indacaterol (24h \u2014 ultra-LABA for COPD once daily), Vilanterol, Olodaterol. SHORT-Acting Beta-2 Agonists (SABA) \u2014 duration 4\u20136 hours: Salbutamol (albuterol), Terbutaline, Levosalbutamol (levalbuterol \u2014 the R-enantiomer of salbutamol). Levosalbutamol is a SABA, not a LABA. It has a slightly longer duration than racemic salbutamol but is still classified as short-acting. Salmeterol, Formoterol, and Indacaterol are all LABAs.'\n },\n {\n id:11,\n stem:'Deficiency of which immune function results in tubercular infections?',\n correct:'Defect in T cell function',\n options:['Defective phagocytic function','Defect in T cell function','Defect in B cell function','Defect in antibody productivity'],\n exp:'Mycobacterium tuberculosis is an INTRACELLULAR pathogen \u2014 it survives and replicates within macrophages. Protection against TB depends critically on CELL-MEDIATED IMMUNITY (CMI), specifically T lymphocytes. CD4+ T helper cells (Th1 subset) produce IFN-\u03b3, which activates macrophages to kill intracellular mycobacteria. CD8+ cytotoxic T cells kill infected macrophages. Granuloma formation (the key defence against TB) requires T cell\u2013macrophage interaction. Defects in T cell function (e.g., HIV\/AIDS \u2014 CD4 depletion) dramatically increase susceptibility to TB. B cell\/antibody defects do not predispose to TB (antibodies are ineffective against intracellular organisms). Phagocytic function is less critical as the bacillus escapes phagolysosome killing.'\n },\n {\n id:12,\n stem:'The most common agent responsible for community acquired pneumonia is:',\n correct:'Streptococcus pneumoniae',\n options:['Streptococcus pneumoniae','Mycoplasma pneumoniae','Staphylococcus aureus','Legionella haemophilia'],\n exp:'Streptococcus pneumoniae (pneumococcus) is the MOST COMMON cause of Community-Acquired Pneumonia (CAP) across all age groups and severity categories worldwide. It accounts for approximately 30\u201350% of bacterial CAP. Other common CAP pathogens: Mycoplasma pneumoniae (common in young adults, atypical pneumonia), Haemophilus influenzae (especially COPD patients), Legionella pneumophila (not Legionella haemophilia \u2014 that is not a species; Legionella causes atypical pneumonia with environmental\/water exposure), Staphylococcus aureus (post-influenza pneumonia, IV drug users). S. pneumoniae remains the \"typical\" pneumonia pathogen and the most common bacterial cause of CAP.'\n },\n {\n id:13,\n stem:'A 26 year old woman presents with fever, arthralgia and erythema nodosum. Her chest X-ray reveals bilateral hilar lymphadenopathy. Her mantoux test is negative. The most likely diagnosis is:',\n correct:'Sarcoidosis',\n options:['Tuberculosis','Allergic bronchopulmonary aspergillosis','Sarcoidosis','Pulmonary thromboembolism'],\n exp:'This is a classic presentation of L\u00d6FGREN SYNDROME \u2014 an acute form of sarcoidosis. The triad: (1) Erythema nodosum (tender red nodules on shins). (2) Bilateral hilar lymphadenopathy (BHL) on CXR. (3) Arthralgia\/periarthritis (ankles most common). Additional: fever, good prognosis. Negative Mantoux: sarcoidosis causes cutaneous anergy (tuberculin negative) because of altered T-cell trafficking to granulomata. Tuberculosis: Mantoux would typically be positive; bilateral symmetric hilar adenopathy is less typical. ABPA: bilateral hilar adenopathy not characteristic; eosinophilia, mucus plugging more typical. Pulmonary embolism: erythema nodosum not a feature. L\u00f6fgren syndrome = sarcoidosis until proven otherwise.'\n },\n {\n id:14,\n stem:'Which of the following are the characteristics of Exudative pleural effusion?\\n1. Pleural fluid protein\/serum protein > 0.5\\n2. Pleural fluid protein\/serum protein < 0.5\\n3. Pleural fluid LDH\/serum LDH > 0.6\\n4. Pleural fluid LDH\/serum LDH < 0.6\\n\\nSelect the correct answer using the code given below:',\n correct:'1 and 3',\n options:['1 and 3','1 and 4','2 and 3','2 and 4'],\n exp:'Light\\'s Criteria distinguish exudate from transudate. An effusion is an EXUDATE if any ONE criterion is met: (1) Pleural fluid protein \/ serum protein > 0.5 \u2714 (exudate). (2) Pleural fluid LDH \/ serum LDH > 0.6 \u2714 (exudate). (3) Pleural fluid LDH > 2\/3 of upper limit of normal serum LDH \u2714. TRANSUDATE: all three criteria are ABSENT (protein ratio <0.5, LDH ratio <0.6). Exudative causes: pneumonia, malignancy, TB, PE, rheumatoid arthritis. Transudative causes: heart failure, nephrotic syndrome, cirrhosis, hypoalbuminaemia. Statements 1 (protein ratio >0.5) and 3 (LDH ratio >0.6) define exudate \u2192 answer is 1 and 3.'\n },\n {\n id:15,\n stem:'All of the following are seen in Whipple\\'s disease EXCEPT:',\n correct:'Hemolytic anemia',\n options:['Weight loss','Migratory arthropathy','Dementia','Hemolytic anemia'],\n exp:'Whipple\\'s disease (Tropheryma whipplei infection) \u2014 classic features: (1) Diarrhoea and malabsorption \u2192 weight loss (almost universal). (2) Migratory\/seronegative arthropathy \u2014 often precedes GI symptoms by years. (3) Neurological: dementia, ophthalmoplegia (oculomasticatory myorhythmia \u2014 pathognomonic), personality change. (4) Fever, hyperpigmentation, lymphadenopathy. (5) Anaemia of chronic disease (normocytic normochromic \u2014 due to malabsorption of iron, B12, folate and chronic inflammation). HAEMOLYTIC ANAEMIA is NOT a feature of Whipple\\'s disease. The anaemia seen is from nutritional deficiency and chronic disease, not haemolysis. Haemolytic anaemia is seen in conditions like autoimmune haemolysis, G6PD deficiency, hereditary spherocytosis \u2014 not Whipple\\'s.'\n },\n {\n id:16,\n stem:'A middle aged patient with chronic liver disease presents with pain abdomen and distension. He also has diarrhoea and fever since one day. Ascitic fluid protein is 0.8 gm%, sugar 100 mg%, total count 500\/mm\u00b3 of which 85% are polymorphonuclear leucocytes and 15% lymphocytes. Most likely diagnosis is:',\n correct:'Spontaneous bacterial peritonitis',\n options:['Spontaneous bacterial peritonitis','Secondary bacterial peritonitis','Perforation peritonitis','TB peritonitis'],\n exp:'Diagnosis: SPONTANEOUS BACTERIAL PERITONITIS (SBP). Key criteria for SBP: Polymorphonuclear (PMN) count \u2265250 cells\/mm\u00b3 in ascitic fluid \u2014 here PMN = 85% of 500 = 425\/mm\u00b3 \u2714. Ascitic fluid protein: in SBP, protein is typically LOW (<1 g\/dL) \u2014 here 0.8 g\/dL \u2714 (consistent with cirrhotic ascites). Glucose: normal (100 mg%) \u2714 \u2014 in secondary peritonitis\/perforation, glucose is typically low. No evidence of hollow viscus perforation. Secondary bacterial peritonitis (bowel perforation) would show: very high cell counts, multiple organisms on culture, low glucose, high protein, LDH elevated. TB peritonitis shows lymphocytic predominance. SBP in cirrhosis = PMN \u2265250\/mm\u00b3 + no surgical source.'\n },\n {\n id:17,\n stem:'Herald patch followed by rash is characteristic of:',\n correct:'Pityriasis rosea',\n options:['Psoriasis','Lichen planus','Pityriasis rosea','Dermatophytosis'],\n exp:'PITYRIASIS ROSEA has a pathognomonic sequence: (1) Herald patch (mother patch) \u2014 a single, oval, salmon-pink scaling plaque (2\u20135 cm) with a collarette of fine scale, appearing 1\u20132 weeks before the generalised eruption. (2) Followed by a generalised rash \u2014 multiple smaller \"daughter\" patches distributed along Langer\\'s lines in a \"Christmas tree\" pattern on the trunk. The rash is self-limiting (6\u20138 weeks), predominantly on the trunk, and follows skin cleavage lines. Psoriasis: well-defined erythematous plaques with silvery scales, no herald patch. Lichen planus: pruritic, polygonal, purple papules \u2014 no herald patch. Dermatophytosis: ringworm pattern, no herald patch sequence. Herald patch = pityriasis rosea.'\n },\n {\n id:18,\n stem:'A young male comes to the OPD with history of jaundice since many years. He has noted that the jaundice may fluctuate but is often aggravated when he is fasting. There is no history of hospitalisation, no drug use, alcoholism or blood transfusion. Family history is not significant. Clinical examination is unremarkable except for mild scleral icterus. What is the likely diagnosis?',\n correct:'Gilbert\\'s syndrome',\n options:['Dubin Johnson syndrome','Crigler Najjar syndrome type-I','Gilbert\\'s syndrome','Rotor syndrome'],\n exp:'GILBERT\\'S SYNDROME \u2014 the most common hereditary hyperbilirubinaemia. Key features: Unconjugated (indirect) hyperbilirubinaemia (mild, <3 mg\/dL). Aggravated by fasting, stress, exercise, intercurrent illness \u2014 classic trigger is fasting. Fluctuating jaundice, often noticed only as mild scleral icterus. Normal liver function tests, no haemolysis, no hepatomegaly. Autosomal recessive (UGT1A1 gene promoter mutation \u2014 reduced glucuronosyltransferase activity by ~30%). Benign, no treatment needed. Crigler-Najjar Type I: severe unconjugated hyperbilirubinaemia from birth, risk of kernicterus, life-threatening \u2014 does not present indolently in a young adult. Dubin-Johnson\/Rotor: conjugated hyperbilirubinaemia (direct). Gilbert\\'s is the answer: mild, fluctuating, unconjugated jaundice worsened by fasting.'\n },\n {\n id:19,\n stem:'All of the following are causes of anemia in a case of chronic kidney disease EXCEPT:',\n correct:'Hemoglobinopathy',\n options:['Decreased red blood cell survival','Hemoglobinopathy','Erythropoietin deficiency','Gastrointestinal blood loss'],\n exp:'Anaemia of Chronic Kidney Disease (CKD) \u2014 multifactorial causes: (1) Erythropoietin (EPO) deficiency \u2014 principal cause; failing kidneys produce insufficient EPO \u2192 reduced RBC production. (2) Decreased RBC survival \u2014 uraemic toxins shorten RBC lifespan (haemolysis). (3) Gastrointestinal blood loss \u2014 uraemic platelet dysfunction \u2192 GI bleeding; also from dialysis circuit losses. (4) Iron deficiency \u2014 from blood loss, reduced absorption, dialysis losses. (5) Folate\/B12 deficiency, bone marrow suppression, aluminium toxicity, hyperparathyroidism (marrow fibrosis). HAEMOGLOBINOPATHY (e.g., sickle cell, thalassaemia) is a PRIMARY genetic condition \u2014 it is NOT caused by CKD. A patient can HAVE both CKD and a haemoglobinopathy, but haemoglobinopathy is not a consequence of CKD. It is the exception in this list.'\n },\n {\n id:20,\n stem:'Characteristic feature of upper motor neuron lesion includes:',\n correct:'Clonus',\n options:['Fasciculations','Hyporeflexia','Clonus','Muscle wasting'],\n exp:'Upper Motor Neuron (UMN) lesion signs (STROKE, cord lesion above anterior horn): Hypertonia (spasticity \u2014 clasp-knife). Hyperreflexia. Clonus (rhythmic involuntary muscle contractions at a joint \u2014 due to loss of descending inhibitory control). Extensor plantar response (Babinski sign). No fasciculations, no significant muscle wasting (atrophy is minimal\/from disuse). Lower Motor Neuron (LMN) lesion signs: Hypotonia, hyporeflexia\/areflexia, fasciculations, significant muscle wasting\/atrophy, no Babinski. Fasciculations = LMN. Hyporeflexia = LMN. Muscle wasting = LMN (prominent). Clonus = UMN. The characteristic UMN feature is CLONUS (along with hyperreflexia and spasticity).'\n },\n {\n id:21,\n stem:'Which one of the following arteries is involved in causation of lateral medullary syndrome?',\n correct:'Posterior inferior cerebellar artery',\n options:['Anterior superior cerebellar artery','Anterior inferior cerebellar artery','Posterior superior cerebellar artery','Posterior inferior cerebellar artery'],\n exp:'Lateral Medullary Syndrome (Wallenberg Syndrome) results from infarction of the lateral medulla, caused by occlusion of the POSTERIOR INFERIOR CEREBELLAR ARTERY (PICA) or its parent vessel the vertebral artery. Clinical features: ipsilateral: facial pain\/numbness (V), Horner\\'s (sympathetic fibres), ataxia (inferior cerebellar peduncle), palatal palsy (IX, X), vestibular nuclei (vertigo, nystagmus, nausea). Contralateral: loss of pain and temperature of body (spinothalamic tract). Dysphagia and hoarseness common. PICA supplies the lateral medulla and inferior cerebellum. AICA supplies the lateral pons (AICA syndrome = different features). Superior cerebellar artery supplies superior cerebellum. PICA = Wallenberg = lateral medullary syndrome.'\n },\n {\n id:22,\n stem:'A right handed 70 year old man has a brain scan which reveals a lesion that has damaged his left angular and supramarginal gyrus. On examination, one would expect the following EXCEPT:',\n correct:'Inappropriate affect',\n options:['Difficulty with left to right discrimination','Inappropriate affect','Finger agnosia','Inability to write'],\n exp:'Left angular gyrus + supramarginal gyrus lesion \u2192 GERSTMANN SYNDROME. The tetrad of Gerstmann syndrome: (1) Agraphia (inability to write) \u2014 angular gyrus involvement. (2) Acalculia (inability to calculate). (3) Finger agnosia (inability to identify fingers). (4) Left-right disorientation (difficulty distinguishing left from right). All four features are components of Gerstmann syndrome following dominant (left) parietal lobe lesions. INAPPROPRIATE AFFECT (e.g., pathological laughing\/crying, disinhibition, emotional lability) is a feature of FRONTAL LOBE lesions or bilateral corticobulbar tract lesions \u2014 NOT parietal lobe lesions. A left angular\/supramarginal lesion does not cause inappropriate affect. The expected EXCEPT answer is inappropriate affect.'\n },\n {\n id:23,\n stem:'Total iron binding capacity of more than 360 \u00b5g\/dl is seen in anemia due to:',\n correct:'Iron deficiency anaemia',\n options:['Chronic inflammation','Hemoglobinopathies','Sideroblastic anemia','Iron deficiency anaemia'],\n exp:'Total Iron Binding Capacity (TIBC) reflects transferrin levels. In IRON DEFICIENCY ANAEMIA: Serum iron \u2193, TIBC \u2191 (>360\u2013400 \u00b5g\/dL), % saturation \u2193 (<20%), Ferritin \u2193. The body upregulates transferrin synthesis (and hence TIBC) to maximise iron capture from the limited available iron. In ANAEMIA OF CHRONIC DISEASE\/INFLAMMATION: Serum iron \u2193, TIBC \u2193 or normal (transferrin is a negative acute-phase reactant), ferritin \u2191 (positive acute-phase reactant). In Sideroblastic anaemia: iron \u2191, TIBC normal or \u2193, ferritin \u2191. In Haemoglobinopathies (thalassaemia): iron studies vary; TIBC not characteristically elevated. Elevated TIBC (>360 \u00b5g\/dL) = iron deficiency anaemia.'\n },\n {\n id:24,\n stem:'Escape behaviour with paroxysmal occurrence is seen in:',\n correct:'Panic disorder',\n options:['Phobic disorder','Anxiety disorder','Obsessive compulsive disorder','Panic disorder'],\n exp:'PANIC DISORDER is characterised by recurrent, unexpected PANIC ATTACKS \u2014 sudden surges of intense fear\/discomfort peaking within minutes (paroxysmal), accompanied by autonomic symptoms (palpitations, sweating, trembling, dyspnoea, chest pain, dizziness, paraesthesiae, derealisation\/depersonalisation). The attacks are paroxysmal (sudden onset, short duration, complete between episodes). ESCAPE BEHAVIOUR: patients actively escape the situation during an attack (leave shops, trains, etc.) and develop agoraphobia (avoidance of situations where escape is difficult). Paroxysmal onset + escape behaviour = Panic disorder. Phobic disorder: fear is situation-specific, not paroxysmal spontaneous attacks. GAD: chronic, persistent worry, not paroxysmal. OCD: obsessions\/compulsions, no paroxysmal escape behaviour.'\n },\n {\n id:25,\n stem:'Which of the following conditions are associated with prolonged prothrombin time?\\n1. Factor VIII deficiency\\n2. Factor VII deficiency\\n3. Heparin anticoagulation\\n4. Warfarin anticoagulation\\n\\nSelect the correct answer using the code given below:',\n correct:'2 and 4',\n options:['1 and 4','1 and 3','2 and 3','2 and 4'],\n exp:'Prothrombin Time (PT) measures the EXTRINSIC pathway + common pathway: Factors VII, X, V, II (prothrombin), fibrinogen. PT is prolonged by: Factor VII deficiency \u2714 (VII is exclusively in extrinsic pathway). Warfarin \u2714 (inhibits Vitamin K-dependent factors II, VII, IX, X \u2014 PT is the most sensitive test for warfarin as VII has the shortest half-life). Liver disease, Vitamin K deficiency (affects II, VII, IX, X). Heparin: primarily prolongs APTT (intrinsic pathway \u2014 affects IIa, Xa, XIIa, XIa via antithrombin). Factor VIII deficiency (haemophilia A): prolongs APTT only (VIII is in intrinsic pathway). PT is NOT significantly prolonged by Factor VIII deficiency or standard heparin doses. Statements 2 (Factor VII deficiency) and 4 (warfarin) are correct.'\n },\n {\n id:26,\n stem:'Syndrome X includes:',\n correct:'Hyperlipidemia, Obesity, Type-2 DM',\n options:['Hyperlipidemia, Obesity, Type-2 DM','Obesity, CAD, COPD','Hyperlipidemia, Hyperuricemia with CAD','Hyponatremia, Hyperlipidemia with type-2 DM'],\n exp:'Syndrome X (Metabolic Syndrome \/ Reaven\\'s Syndrome) is a cluster of cardiovascular risk factors linked by insulin resistance: Central obesity (abdominal), Hyperglycaemia \/ Type-2 DM (or impaired fasting glucose), Dyslipidaemia (\u2191 triglycerides, \u2193 HDL \u2014 sometimes broadly called hyperlipidaemia), Hypertension. The IDF\/NCEP ATP III criteria require central obesity + 2 of the above. Note: In cardiology, \"Syndrome X\" specifically refers to angina with normal coronary arteries (microvascular angina), but in the metabolic context (which this question tests), Syndrome X = metabolic syndrome = Obesity + Hyperlipidaemia + Type-2 DM + Hypertension. The option \"Hyperlipidemia, Obesity, Type-2 DM\" best captures the core metabolic triad.'\n },\n {\n id:27,\n stem:'Growth hormone secretion is inhibited by:',\n correct:'Glucose',\n options:['Arginine','Glucose','Clonidine','L-Dopa'],\n exp:'Growth Hormone (GH) secretion is regulated by GHRH (stimulates) and Somatostatin (inhibits). Stimulators of GH: Hypoglycaemia (insulin-induced), Fasting\/Exercise, Sleep (deep, NREM). Pharmacological stimulators: Arginine, L-Dopa, Clonidine (\u03b12-agonist), Glucagon, Propranolol. These are all used in GH stimulation tests. INHIBITORS of GH: Glucose (hyperglycaemia) \u2014 used in the GH suppression test for acromegaly diagnosis (GH fails to suppress to <1 ng\/mL in acromegaly). Somatostatin analogues (octreotide), IGF-1 (negative feedback), Glucocorticoids (chronic), Obesity. Glucose is the classic INHIBITOR of GH \u2014 hence the glucose tolerance test for acromegaly. Arginine, Clonidine, and L-Dopa are all STIMULATORS.'\n },\n {\n id:28,\n stem:'Which one of the following drugs causes hypercalcemia?',\n correct:'Lithium',\n options:['Phenytoin','Heparin','Lithium','Furosemide'],\n exp:'Lithium causes HYPERCALCAEMIA by impairing the calcium-sensing receptor (CaSR) in the parathyroid glands \u2014 effectively raising the set-point for calcium inhibition of PTH secretion \u2192 inappropriately normal or elevated PTH despite hypercalcaemia (lithium-associated hyperparathyroidism). Other drug causes of hypercalcaemia: Thiazide diuretics (reduce renal calcium excretion), Vitamin D\/A toxicity, Calcium supplements, Teriparatide. Phenytoin: causes hypocalcaemia (increases Vitamin D catabolism via hepatic enzyme induction \u2192 reduced 25-OH Vit D). Heparin: associated with osteoporosis (long-term), hypocalcaemia not a primary effect. Furosemide (loop diuretic): causes HYPOCALCAEMIA (calciuretic effect \u2014 used to treat hypercalcaemia). Lithium = hypercalcaemia via altered CaSR set-point.'\n },\n {\n id:29,\n stem:'All of the following insulins are longer acting EXCEPT:',\n correct:'Glulisine',\n options:['Glargine','Degludec','Glulisine','Detemir'],\n exp:'Insulin classification by duration: RAPID-ACTING (onset 5\u201315 min, duration 4\u20136 h): Lispro, Aspart, GLULISINE. SHORT-ACTING (onset 30 min, duration 6\u20138 h): Regular insulin. INTERMEDIATE-ACTING (duration 12\u201318 h): NPH (Isophane). LONG-ACTING (duration ~24h): Glargine (Lantus), Detemir (Levemir \u2014 ~18\u201324h). ULTRA-LONG-ACTING (duration >42h): DEGLUDEC (Tresiba). Glulisine (Apidra) is a RAPID-ACTING insulin analogue \u2014 it is the shortest-acting of the options. Glargine, Degludec, and Detemir are all long-acting or ultra-long-acting basal insulins. Glulisine is the EXCEPTION \u2014 it is NOT long-acting.'\n },\n {\n id:30,\n stem:'The presence of vitiligo on examination suggests an associated:',\n correct:'Autoimmune disease',\n options:['Autoimmune disease','Degenerative disease','Infection','Malignancy'],\n exp:'Vitiligo is an AUTOIMMUNE condition characterised by destruction of melanocytes by autoreactive T cells. Its presence strongly suggests an underlying autoimmune diathesis. Vitiligo is associated with other organ-specific autoimmune diseases: Thyroid disease (Hashimoto\\'s thyroiditis, Graves\\' disease \u2014 most common association). Type 1 diabetes mellitus. Addison\\'s disease (autoimmune adrenalitis). Pernicious anaemia (autoimmune gastritis). Alopecia areata. Autoimmune polyglandular syndromes (APS type I, II). The clinical lesson: finding vitiligo on examination should prompt screening for associated autoimmune endocrinopathies (TFTs, fasting glucose, morning cortisol). Vitiligo = autoimmune marker.'\n },\n {\n id:31,\n stem:'A mildly elevated TSH (5\u201320 mU\/L) along with a normal T3 and normal T4 levels is suggestive of:',\n correct:'Subclinical hypothyroidism',\n options:['Primary hypothyroidism','Subclinical hypothyroidism','Artefact','Thyroid hormone resistance'],\n exp:'SUBCLINICAL HYPOTHYROIDISM is defined as: TSH elevated (above upper limit of normal, typically >4.0\u20134.5 mU\/L) with NORMAL free T4 and T3. The pituitary is sensing slight inadequacy and compensating (elevated TSH) but peripheral thyroid hormone levels are still maintained. Patients are usually asymptomatic or have subtle symptoms. TSH 5\u201320 mU\/L with normal T4\/T3 = subclinical hypothyroidism. OVERT\/PRIMARY hypothyroidism: TSH elevated + LOW T4 (and possibly T3). Thyroid hormone resistance: TSH normal or elevated, T4 elevated, T3 elevated. Artefact: excluded by repeated testing. The pattern of elevated TSH with normal thyroid hormones defines subclinical hypothyroidism.'\n },\n {\n id:32,\n stem:'Which one of the following suggests patient to be prediabetic?',\n correct:'HbA1c 6.2%, FPG 105 mg\/dL',\n options:['HbA1c 5.6%, FPG 126 mg\/dL','HbA1c 6%, FPG 130 mg\/dL','HbA1c 6.2%, FPG 105 mg\/dL','HbA1c 6.6%, FPG 115 mg\/dL'],\n exp:'ADA diagnostic criteria \u2014 PREDIABETES: HbA1c: 5.7%\u20136.4%. Fasting Plasma Glucose (FPG): 100\u2013125 mg\/dL (Impaired Fasting Glucose). OGTT 2-hour: 140\u2013199 mg\/dL (Impaired Glucose Tolerance). DIABETES: HbA1c \u22656.5%, FPG \u2265126 mg\/dL, OGTT 2h \u2265200, or random \u2265200 with symptoms. Analysis: (a) HbA1c 5.6% (normal) + FPG 126 (diabetic) = discordant; FPG alone suggests DM. (b) HbA1c 6% (prediabetic) + FPG 130 (diabetic) = discordant; FPG suggests DM. (c) HbA1c 6.2% (5.7\u20136.4% \u2714 prediabetes) + FPG 105 (100\u2013125 \u2714 prediabetes) = BOTH criteria in prediabetic range \u2714. (d) HbA1c 6.6% (\u22656.5% = DM) + FPG 115 (prediabetes) = discordant; HbA1c suggests DM. Only option (c) has both values in the prediabetes range.'\n },\n {\n id:33,\n stem:'Cutaneous manifestations of tuberculosis includes:',\n correct:'Erythema nodosum and lupus vulgaris',\n options:['Erythema nodosum and lupus vulgaris','Erythema marginatum and lupus vulgaris','Phyctenular conjunctivitis and erythema multiforme','Pyoderma gangrenosum and Dactylitis'],\n exp:'Cutaneous manifestations of tuberculosis: DIRECT (true TB skin lesions \u2014 from M. tuberculosis infecting skin): Lupus vulgaris (most common \u2014 soft reddish-brown plaques with \"apple jelly\" nodules on diascopy, usually face\/neck), Scrofuloderma (overlying skin breakdown of TB lymph node\/bone), Primary inoculation TB (chancre), TB verrucosa cutis, Miliary TB skin lesions. INDIRECT (tuberculids \u2014 immunological hypersensitivity reactions to TB antigens): Erythema nodosum (panniculitis \u2014 commonest tuberculid). Erythema induratum of Bazin (nodular vasculitis on calves). Papulonecrotic tuberculid. Phyctenular CONJUNCTIVITIS is also a tuberculid (hypersensitivity reaction affecting the eye). Erythema marginatum is associated with RHEUMATIC FEVER. The correct pair: erythema nodosum (tuberculid) + lupus vulgaris (true TB).'\n },\n {\n id:34,\n stem:'Treatment of scrub typhus is:',\n correct:'Azithromycin',\n options:['Ciprofloxacin','Clindamycin','Penicillin','Azithromycin'],\n exp:'Scrub typhus is caused by Orientia tsutsugamushi (formerly Rickettsia tsutsugamushi), transmitted by the chigger mite larva. Treatment: DOXYCYCLINE is the drug of choice (not listed here). AZITHROMYCIN is the preferred alternative, especially in: Children (avoids doxycycline dental staining risk), Pregnant women (doxycycline relatively contraindicated), Areas with doxycycline-resistant strains. Azithromycin has excellent intracellular penetration and has been proven effective in multiple RCTs for scrub typhus. Chloramphenicol is another alternative (used where other drugs unavailable). Ciprofloxacin (fluoroquinolone) \u2014 variable efficacy; NOT first-line. Penicillin and Clindamycin \u2014 NO activity against Orientia. Among the given options, Azithromycin is the correct answer.'\n },\n {\n id:35,\n stem:'Which one of the following is NOT correct regarding Clostridium tetani?',\n correct:'Non motile',\n options:['Anaerobic','Non motile','Gram positive','Spore bearing'],\n exp:'Clostridium tetani characteristics: Anaerobic \u2714 (obligate anaerobe). Gram POSITIVE \u2714 (Gram-positive rod). Spore bearing \u2714 (terminal spores \u2014 \"drumstick\" or \"lollipop\" appearance \u2014 very resistant, can survive boiling). MOTILE \u2014 C. tetani is PERITRICHOUSLY FLAGELLATED and motile. Therefore \"Non motile\" is the INCORRECT statement. Other features: Exotoxin-mediated disease (tetanospasmin = neurotoxin). Found in soil, animal faeces. Produces alpha toxin and tetanolysin. Tetanospasmin inhibits glycine\/GABA release at inhibitory interneurons \u2192 spastic paralysis, trismus (lockjaw), opisthotonus. C. tetani is MOTILE \u2014 the \"non motile\" statement is false and is the correct answer to \"NOT correct\".'\n },\n {\n id:36,\n stem:'All of the following are extrapulmonary manifestations of mycoplasma infection EXCEPT:',\n correct:'Dementia',\n options:['Arthritis','Guillain Barr\u00e9 syndrome','Stevens Johnson syndrome','Dementia'],\n exp:'Mycoplasma pneumoniae extrapulmonary manifestations: HAEMATOLOGICAL: cold agglutinin haemolytic anaemia (most common), thrombocytopenia. NEUROLOGICAL: encephalitis, Guillain-Barr\u00e9 syndrome \u2714, transverse myelitis, cerebellar ataxia, cranial nerve palsies. DERMATOLOGICAL: Stevens-Johnson syndrome \u2714 (erythema multiforme major \u2014 important complication), erythema multiforme. MUSCULOSKELETAL: arthritis \u2714 (polyarthralgia\/arthritis). CARDIAC: myocarditis, pericarditis. EAR: bullous myringitis. DEMENTIA is NOT a recognised extrapulmonary manifestation of mycoplasma infection. Dementia is a chronic neurodegenerative condition (Alzheimer\\'s, vascular, Lewy body, etc.) \u2014 not caused by acute mycoplasma infection. The three correct manifestations are arthritis, GBS, and SJS.'\n },\n {\n id:37,\n stem:'A \\'slapped cheek rash\\' is characteristic of infection with:',\n correct:'Parvovirus B19',\n options:['Rubella','Parvovirus B19','Human herpesvirus 6','Measles'],\n exp:'PARVOVIRUS B19 causes Erythema Infectiosum (Fifth Disease). The classic rash: (1) \"Slapped cheek\" appearance \u2014 fiery red bilateral malar erythema (as if the cheeks were slapped). (2) Followed 1\u20134 days later by a lacy, reticular (fishnet) erythematous rash on the trunk and limbs. In children: usually mild, self-limiting. In adults: polyarthropathy (symmetric small joint arthritis \u2014 can persist). In sickle cell\/haemolytic anaemia: aplastic crisis (parvovirus infects erythroid precursors via P antigen\/globoside receptor). In immunocompromised: chronic anaemia. In pregnancy: hydrops fetalis. Rubella: forchheimer spots (palate), posterior lymphadenopathy. HHV6: roseola infantum (high fever then rash). Measles: Koplik\\'s spots, confluent maculopapular rash starting at hairline. Slapped cheek = Parvovirus B19.'\n },\n {\n id:38,\n stem:'A 34 week pregnant nurse comes in contact with a patient with chickenpox at her workplace. She has never had chickenpox in the past and is unvaccinated. The best option for her is:',\n correct:'Varicella zoster immunoglobulin to be given within 7 days',\n options:['Varicella zoster immunoglobulin to be given within 7 days','Vaccinate for chicken pox','Start oral acyclovir','Wait and watch'],\n exp:'Non-immune pregnant woman + significant VZV exposure = HIGH RISK scenario (risk of severe maternal varicella pneumonia + risk of congenital varicella syndrome if <20 weeks, or neonatal varicella if near term). Management: VARICELLA-ZOSTER IMMUNOGLOBULIN (VZIG) \u2014 passive immunisation providing immediate protection. Given within 96 hours of exposure (some guidelines up to 10 days). VACCINATION is CONTRAINDICATED in pregnancy (live attenuated vaccine \u2014 risk of vaccine strain transmission to foetus). Acyclovir: can be used if varicella disease develops (treatment), but NOT for post-exposure prophylaxis in pregnant women primarily. Wait and watch: unacceptable given high maternal and foetal risk. VZIG within the specified window is the standard of care for susceptible pregnant contacts of chickenpox.'\n },\n {\n id:39,\n stem:'Which one of the following has the maximum diagnostic sensitivity for Leishmaniasis?',\n correct:'Splenic aspirate',\n options:['Splenic aspirate','Bone marrow aspirate','Ascitic fluid aspirate','Lymph node aspirate'],\n exp:'Diagnostic sensitivity for visceral leishmaniasis (Kala-azar) detection of Leishmania donovani bodies (LD bodies): SPLENIC ASPIRATE: Highest sensitivity \u2014 93\u201399% \u2714. The spleen is the primary site of parasite multiplication. However, it carries risk of haemorrhage (contraindicated if PT prolonged, platelets low, uncooperative patient). BONE MARROW ASPIRATE: Sensitivity 53\u201386%. Safer and more commonly used in practice as first-line. LYMPH NODE ASPIRATE: ~53\u201365% sensitivity. LIVER BIOPSY: ~55\u201385%. PERIPHERAL BLOOD BUFFY COAT: lower sensitivity. Although bone marrow is the safer and more practical choice in most settings, the MAXIMUM diagnostic sensitivity is with splenic aspirate. The question asks for maximum diagnostic sensitivity = Splenic aspirate.'\n },\n {\n id:40,\n stem:'Which one of the following statements regarding cryptosporidiosis is NOT correct?',\n correct:'Treatment is with metronidazole',\n options:['Infection is acquired by feco-oral route','It is usually a mild self limiting illness in immunocompetent patient','In HIV infected persons it is a serious opportunistic infection','Treatment is with metronidazole'],\n exp:'Cryptosporidium parvum\/hominis \u2014 key facts: (a) Faeco-oral transmission \u2714 \u2014 oocysts in contaminated water\/food (acid-fast oocysts). (b) Immunocompetent: mild, self-limiting diarrhoea (3\u201312 days) \u2714. (c) HIV\/AIDS: profuse, watery, cholera-like diarrhoea, severe dehydration, AIDS-defining illness \u2714. TREATMENT: Metronidazole has NO activity against Cryptosporidium (it is an antiprotozoal effective against anaerobes, Giardia, Entamoeba, Trichomonas \u2014 not Cryptosporidium). Correct treatment: NITAZOXANIDE (immunocompetent), HAART (immune reconstitution in HIV \u2014 most effective), Paromomycin + Azithromycin (HIV with cryptosporidiosis). Metronidazole treats Giardia, Entamoeba \u2014 not Cryptosporidium. 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Submitting in 10 Submit Now Combined Medical Services Examination 2018Paper I \u00b7 Part A General Medicine \u00b7 Infectious Diseases \u00b7 Toxicology Questions 1 \u2013 40 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0% score Your Result \u21ba Retry Quiz<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18,19],"tags":[],"class_list":["post-36786","post","type-post","status-publish","format-standard","hentry","category-cms","category-general-medicine"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.5 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>CMS 2018 P1 Part-A - 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\/09\/cms-2018-p1-part-a\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2018 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2018 Paper I \u2013 Part A (Q1\u2013Q40) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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