CMS 2025 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#cms25p1a*,#cms25p1a *::before,#cms25p1a *::after{box-sizing:border-box;margin:0;padding:0}\n#cms25p1a{--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#cms25p1a .sen{height:1px}\n#cms25p1a .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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0%,var(--line) 0%);display:flex;align-items:center;justify-content:center;margin:0 auto 20px;position:relative}\n#cms25p1a .ring::before{content:'';position:absolute;width:86px;height:86px;border-radius:50%;background:var(--white)}\n#cms25p1a .ri{position:relative;display:flex;flex-direction:column;align-items:center;line-height:1.2}\n#cms25p1a .rp{font-family:'Playfair Display',serif;font-size:1.3rem;font-weight:700;color:var(--teal)}\n#cms25p1a .rs{font-size:.6rem;color:var(--ink-soft);text-transform:uppercase;letter-spacing:.05em}\n#cms25p1a .sc h2{font-family:'Playfair Display',serif;font-size:1.2rem;color:var(--ink);margin-bottom:8px}\n#cms25p1a .nl{font-size:1rem;color:var(--teal);font-weight:600;margin-bottom:6px}\n#cms25p1a .vd{font-size:.85rem;color:var(--ink-soft);margin-bottom:20px}\n#cms25p1a .bands{display:flex;justify-content:center;gap:10px;flex-wrap:wrap;font-size:.8rem}\n#cms25p1a .band{padding:4px 12px;border-radius:16px;font-weight:600}\n#cms25p1a 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id=\"cms25p1a-td\">40:00<\/strong><\/div>\n <div class=\"sb-it\">\u2705 <strong id=\"cms25p1a-sc\">0<\/strong><\/div>\n <div class=\"sb-it\">\u274c <strong id=\"cms25p1a-sw\">0<\/strong><\/div>\n <div class=\"sb-it\">\u23f3 <strong id=\"cms25p1a-sr\">40<\/strong> left<\/div>\n <div class=\"sb-sep\"><\/div>\n <div class=\"sb-it\">Net <strong id=\"cms25p1a-sn\">0.00<\/strong> \/ <strong id=\"cms25p1a-sm\">40<\/strong><\/div>\n <\/div>\n <div class=\"sb-bar\"><div class=\"sb-fill\" id=\"cms25p1a-fill\"><\/div><\/div>\n<\/div>\n<div class=\"grace\" id=\"cms25p1a-grace\">\n <div class=\"gb\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"gc\" id=\"cms25p1a-gc\">10<\/div>\n <button class=\"gnow\" id=\"cms25p1a-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n<div class=\"hdr\">\n <h1>Combined Medical Services Examination 2025<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine (Q1 \u2013 Q40)<\/p>\n <div class=\"meta\">\n <span class=\"bdg\">Questions 1 \u2013 40<\/span>\n <span class=\"bdg\">+1 correct \u00b7 \u2212\u2153 wrong<\/span>\n <button class=\"tbtn\" id=\"cms25p1a-tbtn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"body\">\n <div class=\"note\">Scoring: +1 for correct \u00b7 \u22120.33 for wrong \u00b7 0 for skipped (CMS 2025 scheme)<\/div>\n <div id=\"cms25p1a-qs\"><\/div>\n <div class=\"sw\"><button class=\"btn\" id=\"cms25p1a-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms25p1a-sc-box\">\n <div class=\"ring\" id=\"cms25p1a-ring\"><div class=\"ri\"><span class=\"rp\" id=\"cms25p1a-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms25p1a-nl\"><\/div>\n <div class=\"vd\" id=\"cms25p1a-vd\"><\/div>\n <div class=\"bands\">\n <span class=\"band bc\" id=\"cms25p1a-bc\"><\/span>\n <span class=\"band bw\" id=\"cms25p1a-bw\"><\/span>\n <span class=\"band bs\" id=\"cms25p1a-bs\"><\/span>\n <\/div>\n <button class=\"rbtn\" id=\"cms25p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms25p1a',TOTAL=40,MAX=40,TSECS=2400,GSECS=10;\n\/\/ Scoring: correct=+100 units, wrong=-33 units; display divides by 100\nvar CU=100,WU=33;\nvar QS=[\n{id:1,stem:'Which of the following heart sounds are best heard with the bell of stethoscope?\\nI. Opening snap\\nII. Systolic click\\nIII. Third heart sound\\nIV. Mid diastolic murmur\\nSelect the correct answer using the code given below:',correct:'III and IV',options:['I and IV','II and III only','III and IV','I, II and III'],exp:'The BELL of the stethoscope is used to auscultate LOW-FREQUENCY sounds. LOW-PITCH sounds: S3 (Third heart sound) \u2714 \u2014 low-pitched, best heard at apex with bell; produced by rapid ventricular filling in early diastole. Mid-diastolic murmur \u2714 \u2014 e.g., mitral stenosis rumble; low-pitched, heard at apex with bell, patient in left lateral decubitus. HIGH-PITCH sounds (use DIAPHRAGM): Opening snap \u2014 high-pitched snap heard with diaphragm. Systolic click \u2014 high-pitched sound (prolapse, ejection click); diaphragm. S1, S2, aortic\/pulmonary murmurs \u2014 diaphragm. Mnemonic: Bell = 3Ms (S3, Mitral stenosis murmur, and low-freq sounds). Answer: III and IV.'},\n{id:2,stem:'Consider the following statements for diagnosing ventricular aneurysm in a patient with recent myocardial infarction:\\nI. Paradoxical impulse on chest wall\\nII. Persistent ST elevation on ECG\\nIII. Unusual bulge from cardiac silhouette on X-ray\\nIV. Presence of pulsus paradoxsus\\nWhich of the above are correct?',correct:'I, II and III',options:['I and II only','I and IV','I, II and III','II, III and IV'],exp:'Ventricular aneurysm post-MI \u2014 diagnostic features: PARADOXICAL IMPULSE \u2714 \u2014 a systolic outward bulge at an unusual location (outside the normal apex); the aneurysmal segment balloons outward during systole while normal myocardium contracts inward. PERSISTENT ST ELEVATION \u2714 \u2014 classic ECG hallmark; ST elevation persisting >6 weeks post-MI (without ongoing chest pain) strongly suggests left ventricular aneurysm. CARDIAC SILHOUETTE BULGE \u2714 \u2014 CXR may show a localised bulge on the left heart border. PULSUS PARADOXUS \u2717 \u2014 this is a sign of cardiac tamponade or severe obstructive lung disease; NOT a feature of ventricular aneurysm. Answer: I, II and III.'},\n{id:3,stem:'Which one of the following statements is correct for subcutaneous nodules in Rheumatic fever?',correct:'They typically appear more than 3 weeks after onset of other clinical manifestations',options:['They are present over flexor aspect of forearm','They are painful tender nodules','The usual size of these nodules is 3-5 cm','They typically appear more than 3 weeks after onset of other clinical manifestations'],exp:'Subcutaneous nodules in Rheumatic fever (Jones major criterion): Location: over EXTENSOR (bony) surfaces \u2014 elbows, wrists, knuckles, knees, ankles, occiput, spine; NOT flexor aspect. Character: PAINLESS, firm, non-tender (option b incorrect). Size: 0.5\u20132 cm (pea-sized to marble); NOT 3\u20135 cm (option c incorrect). Timing: appear 2\u20133 WEEKS AFTER the onset of other manifestations \u2714; closely associated with carditis (present in ~70\u201380% with severe carditis). Evanescent, lasting 1\u20132 weeks. Answer: They typically appear more than 3 weeks after onset of other clinical manifestations.'},\n{id:4,stem:'Which one of the following is correct with regard to Carey Coombs murmur?',correct:'Soft mid-diastolic murmur due to mitral valvulitis',options:['Soft systolic murmur due to mitral regurgitation','Soft mid-diastolic murmur due to mitral valvulitis','Harsh early diastolic murmur due to aortic regurgitation','Blowing late systolic murmur due to aortic stenosis'],exp:'Carey Coombs murmur: a soft, short MID-DIASTOLIC murmur heard at the apex in ACUTE RHEUMATIC FEVER. Caused by: MITRAL VALVULITIS \u2014 inflammatory oedema and thickening of the mitral valve leaflets; the swollen, rough leaflet edges cause turbulent blood flow during rapid ventricular filling \u2192 mid-diastolic murmur. It is TRANSIENT (disappears when active carditis resolves) \u2014 distinguishing it from the established mitral stenosis murmur (which also has a mid-diastolic murmur but due to structural leaflet fusion). It is NOT due to mitral regurgitation (which gives a pansystolic murmur). Answer: Soft mid-diastolic murmur due to mitral valvulitis.'},\n{id:5,stem:'Which of the following statements is correct regarding the Opening Snap (OS) in a patient of mitral stenosis?',correct:'OS moves closer to the second sound (S2) as the stenosis becomes more severe',options:['OS is best heard with the bell of stethoscope','Intensity of OS becomes louder when the valve is calcified','OS moves closer to the second sound (S2) as the stenosis becomes more severe','OS is best heard at the second left intercostal space'],exp:'Opening Snap (OS) in Mitral Stenosis: BEST HEARD: with DIAPHRAGM (high-pitched sound), medial to apex \/ lower left sternal border (NOT bell, NOT 2nd LICS \u2014 option a and d incorrect). INTENSITY: OS becomes SOFTER when valve is calcified\/immobile (calcified leaflets cannot snap; option b incorrect). S2-OS INTERVAL \u2714: The S2-OS interval DECREASES (OS moves CLOSER to S2) as stenosis WORSENS. Reason: In severe MS, LA pressure is very high; even before the mitral valve \"opens\" the LA-LV pressure gradient is large \u2192 mitral valve snaps open EARLIER after S2. Short S2-OS interval (<0.07s) = severe MS. Answer: OS moves closer to the second sound (S2) as the stenosis becomes more severe.'},\n{id:6,stem:'Which one of the following responses to intravenous adenosine is correctly matched?\\n(a) Atrial fibrillation \u2013 Termination\\n(b) Atrio-ventricular nodal reentrant tachycardia \u2013 Termination\\n(c) Ventricular tachycardia \u2013 Termination and complete recovery\\n(d) Atrial flutter \u2013 Termination and complete recovery',correct:'Atrio-ventricular nodal reentrant tachycardia \u2013 Termination',options:['Atrial fibrillation \u2013 Termination','Atrio-ventricular nodal reentrant tachycardia \u2013 Termination','Ventricular tachycardia \u2013 Termination and complete recovery','Atrial flutter \u2013 Termination and complete recovery'],exp:'Adenosine (IV) \u2014 mechanism: transiently blocks AV nodal conduction (opens K+ channels, hyperpolarises AV node). AVNRT \u2714 \u2014 the reentry circuit depends on the AV node; adenosine TERMINATES AVNRT completely and the patient recovers sinus rhythm. Also terminates: AVRT (WPW), AV nodal tachycardias. ATRIAL FIBRILLATION \u2717 \u2014 adenosine does NOT terminate AF; it may transiently slow ventricular rate (by AV block) but the atrial fibrillation continues. ATRIAL FLUTTER \u2717 \u2014 adenosine transiently increases AV block (unmasks the flutter waves) but does NOT terminate flutter; the flutter continues. VENTRICULAR TACHYCARDIA \u2717 \u2014 adenosine is generally INEFFECTIVE for VT (VT circuit does not involve the AV node); only some outflow tract VTs (cAMP-mediated) respond. Answer: AVNRT \u2013 Termination.'},\n{id:7,stem:'Consider the following steps for using a metered dose inhaler (MDI):\\nI. Incline the head backward to minimize oropharyngeal deposition\\nII. Remove the cap and shake the inhaler\\nIII. Breathe out gently and place the mouthpiece into the mouth\\nIV. Hold the breath for 10 seconds\\nV. Simultaneously, begin a slow deep inspiration, depress the canister and continue to inhale\\nWhich one of the following is the correct sequence of using MDI?',correct:'II, III, I, V, IV',options:['III, II, I, V, IV','II, I, IV, III, V','II, III, I, V, IV','III, I, II, IV, V'],exp:'Correct MDI technique sequence: Step 1 \u2014 Remove cap, SHAKE the inhaler (II). Step 2 \u2014 Breathe out gently (exhale), place mouthpiece in mouth (III). Step 3 \u2014 Tilt head slightly back\/incline backward (I) \u2014 minimises oropharyngeal deposition by opening the airway. Step 4 \u2014 Begin SLOW DEEP INSPIRATION and simultaneously depress the canister (V) \u2014 coordination is key. Step 5 \u2014 Hold breath for 10 seconds (IV) \u2014 allows drug to settle in airways. Correct sequence: II \u2192 III \u2192 I \u2192 V \u2192 IV. Answer: II, III, I, V, IV.'},\n{id:8,stem:'Under the Stepwise Approach to the management of Bronchial Asthma, which one of the following is the correct initial treatment at Step 1 for a patient diagnosed with Asthma?',correct:'Low dose inhaled corticosteroid plus leukotriene antagonist',options:['Low dose inhaled corticosteroid only','Low dose inhaled corticosteroid plus oral corticosteroid','Low dose inhaled corticosteroid plus long acting anti-muscarinic agents','Low dose inhaled corticosteroid plus leukotriene antagonist'],exp:'GINA 2023 Stepwise Asthma Management: STEP 1 (mild intermittent): As-needed low-dose ICS-formoterol (preferred) OR low-dose ICS taken whenever SABA is taken. In older classifications (BTS\/SIGN): Step 1 = SABA alone. However, in the current GINA\/CMS context, the \"Step 1 preferred controller\" option among those listed is Low dose ICS + LTRA (leukotriene receptor antagonist), as the question presents options in the context of what is recommended as initial\/preferred treatment. Note: Step 2 = low-dose ICS alone; Step 3 = low-dose ICS + LABA or medium ICS. Among the options, low dose ICS + leukotriene antagonist represents a valid Step 1\u20132 approach. Answer (per official key): Low dose inhaled corticosteroid plus leukotriene antagonist.'},\n{id:9,stem:'A 62-year-old male chronic smoker has been diagnosed with COPD. On pulmonary function testing, FEV1\/FVC was 0\u00b76 and FEV1 was 70% of predicted. What is the severity of airflow obstruction as per GOLD criteria?',correct:'Stage II \u2013 Moderate',options:['Stage I \u2013 Mild','Stage II \u2013 Moderate','Stage III \u2013 Severe','Stage IV \u2013 Very severe'],exp:'GOLD (Global Initiative for Chronic Obstructive Lung Disease) COPD staging: Requirement for COPD: post-bronchodilator FEV1\/FVC < 0.70 \u2714 (here 0.6). GOLD stages based on FEV1 % predicted (post-bronchodilator): GOLD 1 (Mild): FEV1 \u226580%. GOLD 2 (Moderate): 50% \u2264 FEV1 < 80%. GOLD 3 (Severe): 30% \u2264 FEV1 < 50%. GOLD 4 (Very Severe): FEV1 < 30%. This patient: FEV1 = 70% of predicted \u2192 GOLD Stage II (Moderate). Answer: Stage II \u2013 Moderate.'},\n{id:10,stem:'Which one of the following correctly denotes the inheritance pattern of cystic fibrosis?',correct:'Autosomal Recessive',options:['Autosomal Dominant','Autosomal Recessive','X-linked Dominant','X-linked Recessive'],exp:'Cystic Fibrosis (CF): Gene: CFTR (Cystic Fibrosis Transmembrane conductance Regulator) on chromosome 7q31. Most common mutation: \u0394F508 (deletion of phenylalanine at position 508). Inheritance: AUTOSOMAL RECESSIVE \u2714 \u2014 both copies of CFTR must be defective for disease expression; carriers (one defective copy) are unaffected. Most common lethal autosomal recessive disease in Caucasians. Affects: lungs (mucous plugging, bronchiectasis), pancreas (exocrine insufficiency), gut (meconium ileus), sweat glands (elevated sweat chloride). Answer: Autosomal Recessive.'},\n{id:11,stem:'Which of the following conditions are contraindications for noninvasive positive-pressure ventilation in patients with respiratory failure?\\nI. Craniofacial abnormalities\\nII. Significant burns\\nIII. Respiratory failure with PaCO\u2082 of 60 mm Hg\\nIV. Cardiovascular instability\\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:'Contraindications to Non-Invasive Positive Pressure Ventilation (NIPPV\/BiPAP\/CPAP): Absolute: Respiratory\/cardiac arrest, inability to protect airway, uncooperative patient, facial trauma\/burns\/craniofacial abnormalities \u2714, recent upper GI\/oesophageal surgery, excessive secretions. CRANIOFACIAL ABNORMALITIES \u2714 \u2014 mask cannot be fitted. SIGNIFICANT BURNS \u2714 \u2014 facial burns preclude mask application. CARDIOVASCULAR INSTABILITY \u2714 \u2014 haemodynamic compromise (hypotension, arrhythmias) requires invasive support; NIPPV may worsen cardiac output. RESPIRATORY FAILURE WITH HIGH PaCO\u2082 \u2717 \u2014 High PaCO\u2082 (hypercapnic failure, PaCO\u2082 60 mmHg) is actually an INDICATION for NIPPV (BiPAP), not a contraindication; NIPPV is very effective in type II respiratory failure. Answer: I, II and IV.'},\n{id:12,stem:'Which one of the following terms denotes the extensive sclerosis of the skin of the chest wall which restricts chest wall movement and is seen as a rare complication of systemic sclerosis?',correct:'Hidebound Chest',options:['Flail Chest','Hidebound Chest','Barrel Chest','Pigeon Chest'],exp:'Hidebound chest: a RARE complication of SYSTEMIC SCLEROSIS (scleroderma) \u2014 extensive fibrosis and sclerosis of the skin of the chest wall \u2192 the skin becomes adherent, tethered, and board-like \u2192 severely restricts chest wall expansion \u2192 restrictive ventilatory defect. \"Hidebound\" = skin bound tightly like a hide (animal skin). Other chest deformities: Flail chest: multiple rib fractures \u2192 paradoxical movement during respiration (trauma). Barrel chest: hyperinflation (COPD) \u2192 horizontal ribs, increased AP diameter. Pigeon chest (pectus carinatum): protrusion of sternum anteriorly. Answer: Hidebound Chest.'},\n{id:13,stem:'Consider the following pleural fluid analysis:\\npH 7\u00b76, Pleural fluid protein 0\u00b75 g\/dL, Serum total protein 6\u00b75 g\/dL, Pleural fluid LDH 100 U\/L, Serum LDH 300 U\/L\\nWhat is the most likely diagnosis?',correct:'Myxedema',options:['Pancreatitis','Myxedema','Sarcoidosis','Rheumatoid arthritis'],exp:'Light\\'s criteria for transudate vs exudate: Protein ratio (PF\/serum): 0.5\/6.5 = 0.077 < 0.5 \u2192 TRANSUDATE. LDH ratio (PF\/serum): 100\/300 = 0.33 < 0.6 \u2192 TRANSUDATE. pH 7.6 = alkaline (normal\/transudate). This is a TRANSUDATE. Causes of transudate: heart failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia, hypothyroidism (MYXOEDEMA), peritoneal dialysis, Meigs syndrome. Of the options: PANCREATITIS \u2192 exudate (high amylase). SARCOIDOSIS \u2192 exudate\/lymphocytic. RHEUMATOID ARTHRITIS \u2192 exudate (very low glucose, low pH). MYXOEDEMA (hypothyroidism) \u2714 \u2192 classic cause of transudate (lymphatic\/protein leak due to glycosaminoglycan accumulation). Answer: Myxedema.'},\n{id:14,stem:'\\'Masson Bodies\\' formed due to proliferation of immature collagen are a characteristic histopathological finding seen in which of the following conditions?',correct:'Cryptogenic Organizing Pneumonia',options:['Lymphocytic Interstitial Pneumonia','Cryptogenic Organizing Pneumonia','Desquamative Interstitial Pneumonia','Respiratory Bronchiolitis'],exp:'Masson bodies (intraluminal fibroblastic plugs \/ polypoid plugs of granulation tissue composed of immature collagen\/myofibroblasts): CRYPTOGENIC ORGANIZING PNEUMONIA (COP) \u2714 \u2014 formerly called BOOP (Bronchiolitis Obliterans Organizing Pneumonia). Pathology: plugs of organising fibrous tissue (Masson bodies) fill the distal airspaces, alveolar ducts and bronchioles. Masson bodies are the HALLMARK of COP on biopsy. COP: subacute presentation; bilateral patchy consolidation on CT; responds well to corticosteroids. LIP: lymphocytic infiltration of alveolar walls. DIP: macrophage accumulation in alveoli (smokers). Respiratory bronchiolitis: pigmented macrophages in respiratory bronchioles. Answer: Cryptogenic Organizing Pneumonia.'},\n{id:15,stem:'Consider the following statements regarding respiratory function in old age:\\nI. There is increasing ventilation-perfusion mismatch\\nII. There is increased ventilatory response to hypoxia and hypercapnia\\nIII. There is a decline in maximum oxygen uptake leading to reduction in cardiorespiratory reserve\\nIV. There is decline in the Forced Expiratory Volume to Forced Vital Capacity ratio (FEV1\/FVC) by around 0\u00b72% per year after the forties\\nWhich of the statements given above are correct?',correct:'I, III and IV',options:['I, II and III','I, II and IV','II, III and IV','I, III and IV'],exp:'Respiratory changes in ageing: Statement I \u2714 \u2014 V\/Q MISMATCH INCREASES with age: reduced elastic recoil \u2192 small airways close at higher lung volumes (increased closing capacity) \u2192 dependent zones underventilated \u2192 V\/Q mismatch \u2192 progressive fall in PaO\u2082 with age. Statement II \u2717 \u2014 DECREASED (not increased) ventilatory response to hypoxia and hypercapnia in the elderly; chemoreceptor sensitivity declines; blunted respiratory drive. Statement III \u2714 \u2014 Maximum O\u2082 uptake (VO\u2082 max) DECLINES ~1% per year after age 30; cardiorespiratory reserve decreases. Statement IV \u2714 \u2014 FEV1\/FVC ratio declines at approximately 0.2% per year after age 40 (FEV1 declines faster than FVC). Correct: I, III, IV. Answer: I, III and IV.'},\n{id:16,stem:'Which one of the following statements is correct in respect of pulmonary involvement in rheumatoid disease?',correct:'Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging',options:['Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging','Rheumatoid pulmonary nodules are often solitary and located near hilum','Pleural effusion in these patients is transudative and usually bilateral','Combination of pleural effusion and pneumoconiosis in these patients is known as Caplan syndrome'],exp:'Pulmonary manifestations of RA: RHEUMATOID NODULES \u2714 \u2014 usually ASYMPTOMATIC, detected incidentally on CXR\/CT; peripheral subpleural location (not hilar); usually multiple (not solitary). Option b incorrect (solitary + hilar). PLEURAL EFFUSION: EXUDATE (very LOW glucose <30 mg\/dL, low pH, low complement) and usually UNILATERAL (left or right); NOT transudative bilateral. Option c incorrect. CAPLAN SYNDROME: combination of RA with PNEUMOCONIOSIS (coal\/silica dust exposure) + multiple large nodules \u2014 NOT pleural effusion + pneumoconiosis. Option d incorrect. Answer: Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging.'},\n{id:17,stem:'Which one of the following conditions is a complication of bacterial pharyngitis involving extension of infection into the internal jugular veins leading to thrombosis and metastatic dispersal of the organism?',correct:'Lemierre syndrome',options:['Cystic Fibrosis','Chronic Pulmonary Aspergillosis','Lemierre syndrome','Wegener\\'s granulomatosis'],exp:'Lemierre syndrome (postanginal sepsis \/ \"forgotten disease\"): caused by Fusobacterium necrophorum (anaerobic gram-negative rod); follows oropharyngeal infection (tonsillitis\/pharyngitis). Pathophysiology: peritonsillar abscess \u2192 spreads to parapharyngeal space \u2192 lateral pharyngeal space \u2192 infection of the INTERNAL JUGULAR VEIN wall \u2192 septic thrombophlebitis of the IJV \u2192 septic emboli to lungs (cavitating pneumonia), joints, liver, brain. Key features: young adults, recent sore throat, fever, neck stiffness\/swelling (IJV), bilateral pulmonary infiltrates\/cavities. Answer: Lemierre syndrome.'},\n{id:18,stem:'A 42-year-old man with history of alcohol dependency presents with progressive abdominal distension. Abdominal examination reveals a shifting dullness. Which one of the following is the most appropriate drug to relieve this abdominal distension?',correct:'Spironolactone',options:['Octreotide','Propranolol','Lactulose','Spironolactone'],exp:'Ascites in alcoholic liver disease management: SPIRONOLACTONE \u2714 \u2014 FIRST-LINE diuretic for cirrhotic ascites. Mechanism: aldosterone antagonist (K+-sparing diuretic); cirrhosis \u2192 secondary hyperaldosteronism \u2192 sodium and water retention \u2192 ascites. Spironolactone 100\u2013400 mg\/day \u00b1 furosemide 40\u2013160 mg\/day. Octreotide: for variceal bleeding (reduces portal pressure). Propranolol: non-selective beta-blocker for primary\/secondary prophylaxis of variceal bleeding. Lactulose: for hepatic encephalopathy (reduces ammonia production). The question asks about ABDOMINAL DISTENSION from ascites \u2192 diuretic therapy. Answer: Spironolactone.'},\n{id:19,stem:'Which one of the following is the investigation of choice for diagnosing the presence of stones in the gall-bladder?',correct:'Transabdominal ultrasound',options:['Transabdominal ultrasound','Erect X ray of abdomen','Capsule endoscopy','Computed Tomography'],exp:'Investigation of choice for gallstones: TRANSABDOMINAL ULTRASOUND \u2714 \u2014 sensitivity >95% for gallstones \u22652 mm; detects acoustic shadowing; non-invasive, no radiation, cheap, widely available; also assesses gallbladder wall, CBD diameter. Erect X-ray abdomen: only 10\u201315% of gallstones are radio-opaque (calcium-containing); misses 85% \u2192 NOT investigation of choice. CT: better than X-ray but less sensitive than USG for cholesterol stones (iso-dense); expensive. Capsule endoscopy: for small bowel imaging; no role for gallstones. Ultrasound is the GOLD STANDARD first-line investigation for cholelithiasis. Answer: Transabdominal ultrasound.'},\n{id:20,stem:'Which one of the following biologic agents used in the treatment of inflammatory bowel disease acts by inhibiting the enzyme \"Janus Kinase\"?',correct:'Tofacitinib',options:['Infliximab','Adalimumab','Vedolizumab','Tofacitinib'],exp:'IBD biologics by mechanism: INFLIXIMAB\/ADALIMUMAB: anti-TNF-\u03b1 monoclonal antibodies. VEDOLIZUMAB: anti-integrin (anti-\u03b14\u03b27) \u2014 prevents gut-specific lymphocyte trafficking. TOFACITINIB \u2714 \u2014 JAK inhibitor (Janus Kinase inhibitor); inhibits JAK1 and JAK3 \u2192 blocks downstream cytokine signalling (IL-6, IL-12, IL-23 pathways); oral small molecule; approved for moderate-to-severe ulcerative colitis. Other JAK inhibitors for IBD: upadacitinib (JAK1-selective), filgotinib. \"Janus Kinase\" = JAK enzymes (JAK1, JAK2, JAK3, TYK2) \u2014 tofacitinib is the prototype JAK inhibitor in IBD. Answer: Tofacitinib.'},\n{id:21,stem:'Melanosis coli, which occurs due to long term consumption of stimulant laxatives, presents as brown discolouration of colonic mucosa due to deposition of which one of the following pigments?',correct:'Lipofuscin',options:['Melanin','Haemosiderin','Lipofuscin','Haemoglobin'],exp:'Melanosis coli: a benign, reversible condition caused by long-term use of ANTHRAQUINONE laxatives (senna, cascara, rhubarb, aloe). Brown\/black discolouration of colonic mucosa. Pigment: LIPOFUSCIN \u2714 \u2014 NOT melanin (despite the misleading name \"melanosis\"). The anthraquinone laxatives cause apoptosis of colonic epithelial cells \u2192 phagocytosed by macrophages \u2192 lipofuscin-laden macrophages accumulate in the lamina propria \u2192 brown discolouration. Lipofuscin = \"wear and tear\" pigment; a brownish residue of lipid peroxidation and cellular digestion. Haemosiderin: iron-storage pigment (haemorrhage). Haemoglobin: oxygen-carrying protein. Answer: Lipofuscin.'},\n{id:22,stem:'Consider the following with regard to Gilbert Syndrome:\\nI. Autosomal recessive trait of a mutation in gene for UDP-glucuronyl transferase enzyme\\nII. Elevation of unconjugated bilirubin\\nIII. No stigmata of chronic liver disease other than jaundice\\nIV. Early Liver biopsy recommended in patients with possible Gilbert Syndrome\\nWhich of the above are correct?',correct:'II and III only',options:['I and II only','II and III only','I, II and III','III and IV'],exp:'Gilbert Syndrome: GENETICS: AUTOSOMAL RECESSIVE inheritance of a TA repeat polymorphism in the UGT1A1 gene promoter (TATAA box) \u2192 reduced UDP-glucuronosyltransferase activity \u2192 reduced conjugation. Statement I \u2717 \u2014 the inheritance is correct (AR) but the description as \"mutation in gene for UDP-glucuronyl transferase\" is slightly imprecise (it is a PROMOTER polymorphism); more importantly in the context of the answer choices: Statement II \u2714 \u2014 unconjugated (indirect) hyperbilirubinaemia; no haemolysis; no liver disease. Statement III \u2714 \u2014 NO stigmata of chronic liver disease; only fluctuating jaundice (exacerbated by fasting, stress, illness, exercise). Statement IV \u2717 \u2014 liver biopsy is NOT recommended; Gilbert syndrome is diagnosed clinically\/biochemically; biopsy would show normal or mildly increased lipofuscin. Correct: II and III. Answer: II and III only.'},\n{id:23,stem:'The single most important treatment and prognostic factor in alcohol-related liver disease is',correct:'Cessation of alcohol consumption',options:['N-acetyl cysteine','Cessation of alcohol consumption','Liver transplantation','High dose vitamin E'],exp:'Alcohol-related liver disease (ARLD) \u2014 steatosis, alcoholic hepatitis, cirrhosis: CESSATION OF ALCOHOL \u2714 \u2014 the SINGLE MOST IMPORTANT intervention; even in advanced cirrhosis, abstinence improves portal hypertension, liver function, and survival; prevents progression from steatosis to hepatitis to cirrhosis; improves prognosis at every stage. N-acetylcysteine: used in paracetamol toxicity; limited evidence in severe alcoholic hepatitis. Liver transplantation: reserved for selected patients with end-stage disease; requires 6 months of abstinence. Vitamin E: antioxidant; role in NASH, not primarily in ARLD. No pharmacological intervention surpasses abstinence in impact. Answer: Cessation of alcohol consumption.'},\n{id:24,stem:'A 40-year-old man with a known case of chronic pancreatitis presents to OPD with complaint of skin pigmentation over the abdomen. The patient gives a history of chronic use of a hot water bottle to relieve the abdominal discomfort. Which one of the following is the most appropriate diagnosis?',correct:'Erythema ab igne',options:['Erythema infectiosum','Erythema marginatum','Erythema nodosum','Erythema ab igne'],exp:'ERYTHEMA AB IGNE (EAI): Latin = \"redness from fire.\" Caused by prolonged, repeated exposure to RADIANT HEAT (not sufficient to cause burns): hot water bottles, heating pads, laptops on lap. Presentation: RETICULATE (lace-like\/net-like), MOTTLED, BROWNISH pigmentation at the site of heat application \u2014 abdomen in this case. Chronic use of a hot water bottle for abdominal pain (chronic pancreatitis) \u2714. Histology: epidermal atrophy, dermal elastosis, melanin deposition. Caution: chronic EAI can rarely progress to Merkel cell carcinoma or SCC. Erythema nodosum: tender red nodules on shins (panniculitis). Erythema marginatum: RF feature (gyrate erythema). Erythema infectiosum: viral rash (parvovirus B19). Answer: Erythema ab igne.'},\n{id:25,stem:'Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?',correct:'It is an oral drug',options:['It is useful in hypovolemic hyponatremia','It antagonises the V\u2081 receptor','It should be used for at least 1 year','It is an oral drug'],exp:'Tolvaptan (Samsca\/Jynarque): VAPTANS class \u2014 selective vasopressin V2 receptor antagonists (aquaretics). It is an ORAL drug \u2714 \u2014 taken once daily orally; unlike conivaptan (IV only). V2 receptor antagonist \u2717 \u2014 it antagonises V2 receptors (NOT V1); V2 blockade prevents aquaporin-2 insertion \u2192 free water excretion \u2192 raises serum sodium. INDICATION: EUVOLAEMIC or HYPERVOLAEMIC hyponatraemia (SIADH, cirrhosis, heart failure); CONTRAINDICATED in HYPOVOLAEMIC hyponatraemia (would worsen volume depletion). Duration: limited to \u226430 days typically; NOT for \u22651 year. Answer: It is an oral drug.'},\n{id:26,stem:'Which one of the following conditions is caused by mutations in the gene that encodes the sodium-potassium-2-chloride cotransporter (NKCC2), and presents with sodium wasting, hypokalaemia, hypomagnesaemia and hypercalciuria?',correct:'Bartter syndrome',options:['Alport syndrome','Bartter syndrome','Fanconi syndrome','Gitelman syndrome'],exp:'Tubular transport disorders: BARTTER SYNDROME \u2714 \u2014 mutation in NKCC2 (SLC12A1) on thick ascending limb of loop of Henle; similar effect to furosemide (loop diuretic); features: sodium\/potassium\/chloride wasting, hyponatraemia, hypokalaemia, metabolic alkalosis, HYPERCALCIURIA, normal\/low blood pressure, hyperreninaemia. GITELMAN SYNDROME: mutation in NCCT (thiazide-sensitive NaCl cotransporter in DCT); HYPOCALCIURIA + hypomagnesaemia + hypokalaemia (mimics thiazide). Alport: collagen IV mutation \u2192 glomerulonephritis + deafness. Fanconi: proximal tubule generalised dysfunction. Mnemonic: Bartter = Loop (NKCC2); Gitelman = Distal (NCC). Answer: Bartter syndrome.'},\n{id:27,stem:'A 52-year-old male has uncontrolled diabetes. Which one of the following tests will help in early detection of nephropathy?',correct:'Urine albumin',options:['Blood urea level','Serum creatinine level','Ultrasonography','Urine albumin'],exp:'Diabetic nephropathy screening: URINE ALBUMIN (microalbuminuria) \u2714 \u2014 EARLIEST marker of diabetic nephropathy. Microalbuminuria: 30\u2013300 mg\/24h (or ACR 30\u2013300 mg\/g); appears BEFORE any rise in serum creatinine or fall in GFR. Blood urea: insensitive early marker; rises only when GFR is significantly reduced. Serum creatinine: also a late marker; rises only when ~50% of nephrons are lost. Ultrasonography: detects structural changes (size, echogenicity) \u2014 later finding; not early screening. Screening protocol: Annual urine ACR (albumin:creatinine ratio) in all diabetic patients from 5 years post-diagnosis (Type 1) or at diagnosis (Type 2). Answer: Urine albumin.'},\n{id:28,stem:'Autosomal dominant mutations in which one of the following genes may cause focal segmental glomerulosclerosis associated with abnormal genitalia, Wilm\\'s tumour and mental retardation?',correct:'WT1',options:['WT1','INF2','LMX1B','APOL1'],exp:'WT1 gene (Wilms Tumour suppressor gene 1) on chromosome 11p13: WT1 mutations cause: DENYS-DRASH SYNDROME (DDS): diffuse mesangial sclerosis \u2192 nephrotic syndrome, WILMS TUMOUR, genital anomalies. FRASIER SYNDROME: FSGS, gonadal dysgenesis (streak gonads), Wilms tumour (less common). Also WAGR syndrome (Wilms tumour, Aniridia, GU anomalies, intellectual disability) with 11p deletion. AD mutations in WT1 \u2192 FSGS + abnormal genitalia + Wilms tumour + intellectual disability \u2714. INF2: AD FSGS without extrarenal features. LMX1B: Nail-Patella syndrome (NPS) + FSGS. APOL1: AD susceptibility to FSGS in African populations. Answer: WT1.'},\n{id:29,stem:'Kidney damage and Glomerular Filtration Rate (GFR) value between 15-29 mL\/min\/1\u00b773 m\u00b2 are found in which stage of Chronic Kidney Disease?',correct:'Stage 4 (severe)',options:['Stage 2 (mild)','Stage 3A (mild to moderate)','Stage 4 (severe)','Stage 5 (kidney failure)'],exp:'KDIGO CKD staging by GFR: G1: \u226590 (normal\/high). G2: 60\u201389 (mildly decreased). G3a: 45\u201359 (mildly to moderately decreased). G3b: 30\u201344 (moderately to severely decreased). G4: 15\u201329 (severely decreased) \u2714. G5: <15 or on dialysis (kidney failure). GFR 15\u201329 = Stage G4 (Severe CKD). This is the stage at which preparation for renal replacement therapy (dialysis, transplant workup) should begin. Answer: Stage 4 (severe).'},\n{id:30,stem:'Which one of the following hereditary tubulo-interstitial kidney diseases has an autosomal recessive mode of inheritance?',correct:'Nephronophthisis',options:['Medullary cystic kidney disease type 1','Medullary cystic kidney disease type 2','Nephronophthisis','Juvenile hyperuricaemic nephropathy'],exp:'Hereditary tubulointerstitial kidney diseases: NEPHRONOPHTHISIS (NPHP) \u2714 \u2014 AUTOSOMAL RECESSIVE; most common genetic cause of end-stage renal disease in children and young adults; NPHP1 gene mutation; presents with polyuria\/polydipsia, anaemia, growth retardation; small, echogenic kidneys with corticomedullary cysts; may associate with retinal dystrophy (Senior-L\u00f8ken syndrome). MEDULLARY CYSTIC KIDNEY DISEASE type 1 and 2 (MCKD1, MCKD2): AUTOSOMAL DOMINANT. JUVENILE HYPERURICAEMIC NEPHROPATHY: AUTOSOMAL DOMINANT (UMOD mutation, same group as MCKD2). Answer: Nephronophthisis.'},\n{id:31,stem:'Which of the following findings in a patient are suggestive of acute nephritis?\\nI. Hematuria\\nII. Oliguria\\nIII. Reduced size of both kidneys\\nIV. Edema\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I and III','III and IV','I and II only','I, II and IV'],exp:'Acute nephritic syndrome features: HAEMATURIA \u2714 \u2014 hallmark; RBC casts (pathognomonic), dysmorphic RBCs; smoky brown urine. OLIGURIA \u2714 \u2014 reduced urine output due to glomerular inflammation \u2192 reduced GFR \u2192 fluid retention. OEDEMA \u2714 \u2014 sodium and water retention (periorbital oedema, leg oedema, hypertension). Also: hypertension, proteinuria (usually sub-nephrotic <3.5g\/day), azotaemia. REDUCED SIZE OF KIDNEYS \u2717 \u2014 ACUTE nephritis: kidneys are NORMAL or ENLARGED (swollen, inflamed). Small kidneys suggest CHRONIC kidney disease (contracted, scarred). Correct: I, II, IV. Answer: I, II and IV.'},\n{id:32,stem:'A 35-year-old male presents with increased urine output. On evaluation, his urinary output was around 4L\/day; urinary osmolality was 200 mosmol\/L. Which of the following are various differential diagnoses?\\nI. Psychogenic polydipsia\\nII. Solute diuresis\\nIII. Central diabetes insipidus\\nIV. Nephrogenic diabetes insipidus\\nSelect the correct answer using the code given below:',correct:'I, III and IV',options:['I, III and IV','I and III only','II and IV','I and IV only'],exp:'Polyuria (>3L\/day) with URINE OSMOLALITY 200 mosmol\/L (hypotonic urine = <300 mosmol\/L): This indicates WATER DIURESIS (dilute urine) \u2014 insufficient ADH effect. PSYCHOGENIC POLYDIPSIA \u2714 \u2014 primary polydipsia \u2192 excessive water intake \u2192 dilute urine; urine osmolality low. CENTRAL DI \u2714 \u2014 ADH deficiency \u2192 inability to concentrate urine \u2192 dilute polyuria. NEPHROGENIC DI \u2714 \u2014 renal resistance to ADH \u2192 dilute urine. SOLUTE DIURESIS \u2717 \u2014 e.g., hyperglycaemia, mannitol, high protein feeds \u2192 urine osmolality is HIGH (>300 mosmol\/L) due to osmotically active solutes; the urine is NOT hypotonic; solute diuresis produces high-osmolality urine. Urine osm 200 mosmol\/L rules out solute diuresis. Answer: I, III and IV.'},\n{id:33,stem:'Contralateral Homonymous upper quadrantanopia is the type of visual loss seen when the lesion is located at which one of the following anatomical locations?',correct:'Temporal lobe',options:['Frontal lobe','Temporal lobe','Parietal lobe','Occipital lobe'],exp:'Visual field defects by lesion site: Optic nerve: monocular blindness. Optic chiasm: bitemporal hemianopia. Optic tract (post-chiasm): contralateral homonymous hemianopia. TEMPORAL LOBE \u2714 \u2014 Meyer\\'s loop (inferior fibres of optic radiation carry visual information from superior visual field) loops through temporal lobe \u2192 lesion \u2192 \"pie in the sky\" = contralateral HOMONYMOUS UPPER QUADRANTANOPIA. PARIETAL LOBE: superior fibres of optic radiation \u2192 lesion \u2192 contralateral homonymous LOWER quadrantanopia (\"pie on the floor\"). OCCIPITAL LOBE: complete contralateral homonymous hemianopia with macular sparing. Frontal lobe: no primary visual field defect (eye movement control). Answer: Temporal lobe.'},\n{id:34,stem:'Which of the following are clinical features of migraine?\\nI. It is associated with dilatation of extracranial vessels\\nII. Common migraine is seen without Aura\\nIII. Aura is most often visual\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I and II only','II and III only','I and III only'],exp:'Migraine features: Statement I \u2714 \u2014 Migraine involves DILATATION of extracranial (and intracranial) blood vessels; calcitonin gene-related peptide (CGRP) and other mediators cause vasodilation and neurogenic inflammation of meningeal vessels \u2192 pain. Statement II \u2714 \u2014 COMMON MIGRAINE (migraine WITHOUT aura) = 70\u201380% of cases; most frequent type; no aura precedes headache. Statement III \u2714 \u2014 AURA: typically VISUAL (most common aura ~90% of cases with aura): positive phenomena (scintillating scotoma, fortification spectra\/zigzag lines) or negative (scotoma); lasts 20\u201360 minutes before headache. All three correct. Answer: I, II and III.'},\n{id:35,stem:'A 50-year-old man presents with brief episodes of lancinating unilateral facial pain, involving the buccal distribution. Pain is triggered by washing face with cold water. What is the most likely diagnosis?',correct:'Trigeminal neuralgia',options:['Migraine','Medication overuse headache','Chronic paroxysmal hemicrania','Trigeminal neuralgia'],exp:'TRIGEMINAL NEURALGIA (Tic douloureux): Classic features \u2714: LANCINATING (electric shock-like, stabbing) pain. UNILATERAL \u2014 in the distribution of a trigeminal nerve branch; V2 (maxillary\/buccal) or V3 (mandibular) most common. TRIGGER FACTORS: light touch \u2014 washing face, eating, talking, cold wind. BRIEF episodes (seconds); pain-free between attacks. Migraine: throbbing hemicranial, hours duration, no triggers from light touch. Medication overuse: chronic daily headache. Chronic paroxysmal hemicrania: periorbital pain, autonomic features, responds to indomethacin. Triggering by washing face = classic TN. Answer: Trigeminal neuralgia.'},\n{id:36,stem:'Which of the following are trigger factors for seizures?\\nI. Sleep deprivation\\nII. Missed doses of antiepileptic drugs\\nIII. Recreational drug misuse\\nIV. Physical exhaustion\\nSelect the correct answer using the code given below:',correct:'I, II, III and IV',options:['II and III only','I and IV only','I, II and III only','I, II, III and IV'],exp:'Seizure trigger factors \u2014 all four are well-recognised: SLEEP DEPRIVATION \u2714 \u2014 one of the most potent triggers; reduces seizure threshold; used in provoked sleep EEG. MISSED ANTIEPILEPTIC DOSES \u2714 \u2014 subtherapeutic drug levels \u2192 breakthrough seizures; commonest precipitant in known epileptics. RECREATIONAL DRUG MISUSE \u2714 \u2014 cocaine, amphetamines, alcohol (especially alcohol withdrawal) lower seizure threshold. PHYSICAL EXHAUSTION \u2714 \u2014 fatigue, systemic illness, fever can precipitate seizures. Other triggers: photosensitive stimuli, hyperventilation, hormonal changes (catamenial epilepsy), stress. All four are correct triggers. Answer: I, II, III and IV.'},\n{id:37,stem:'Which one of the following childhood epileptic disorders often needs long term treatment with anti-epileptic drugs?',correct:'Juvenile myoclonic epilepsy',options:['Benign neonatal seizures','Febrile seizures','Benign rolandic epilepsy','Juvenile myoclonic epilepsy'],exp:'Childhood epilepsy syndromes \u2014 prognosis and treatment: BENIGN NEONATAL SEIZURES: self-limiting; usually do not require long-term AED. FEBRILE SEIZURES: NOT epilepsy; do not require long-term AED treatment in most cases; only prophylaxis for complex\/recurrent febrile seizures. BENIGN ROLANDIC EPILEPSY (BECTS): self-limiting; resolves by mid-adolescence; most children do NOT require long-term AEDs. JUVENILE MYOCLONIC EPILEPSY (JME) \u2714 \u2014 lifelong\/long-term AED treatment required; JME has a high relapse rate on stopping medication (>90% relapse); valproate is drug of choice; condition persists into adulthood despite excellent seizure control on medication. Answer: Juvenile myoclonic epilepsy.'},\n{id:38,stem:'Which of the following are clinical features of Parkinson\\'s disease?\\nI. Reduced eye blinking\\nII. Drooling of saliva\\nIII. Soft voice\\nIV. Macrographia\\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:'Parkinson\\'s disease features: REDUCED EYE BLINKING \u2714 \u2014 reduced blink rate (normal ~15\u201320\/min; PD ~5\u201310\/min); mask-like facies. DROOLING OF SALIVA \u2714 \u2014 sialorrhoea; not from increased production but from IMPAIRED SWALLOWING (dysphagia, reduced automatic swallowing frequency). SOFT VOICE (HYPOPHONIA) \u2714 \u2014 reduced vocal volume; monotone speech; dysarthria. MACROGRAPHIA \u2717 \u2014 FALSE. PD causes MICROGRAPHIA (small, cramped handwriting) \u2014 a classic early sign; writing becomes progressively smaller. Macrographia (large writing) is NOT a PD feature. Correct: I, II, III. Answer: I, II and III.'},\n{id:39,stem:'A 35-year-old female presents with easy fatigability. Investigations show that Hb is 6 g%; Red cell morphology is normocytic normochromic; and reticulocyte production index is 5\u00b75. Which one of the following conditions favours this abnormality?',correct:'Intravascular hemolysis',options:['Iron deficiency anemia','Sideroblastic anemia','Folate deficiency','Intravascular hemolysis'],exp:'Interpretation: Normocytic normochromic anaemia + RETICULOCYTE PRODUCTION INDEX (RPI) = 5.5 (MARKEDLY ELEVATED, normal <2). High RPI = hyperproliferative anaemia = adequate bone marrow response = peripheral destruction or acute blood loss. With normocytic morphology and very high RPI = HAEMOLYTIC ANAEMIA. INTRAVASCULAR HAEMOLYSIS \u2714 \u2014 intravascular destruction of RBCs \u2192 release of Hb into plasma \u2192 haemoglobinaemia, haemoglobinuria; brisk reticulocyte response (RPI >3); normocytic normochromic (or slight macrocytosis due to reticulocytes). Iron deficiency: microcytic hypochromic, low reticulocytes. Sideroblastic: microcytic\/dimorphic. Folate deficiency: macrocytic, megaloblastic. Answer: Intravascular hemolysis.'},\n{id:40,stem:'A 46-year-old lady on vegan diet for a decade presents with tingling and numbness in lower limbs for two months and a history of swaying while walking through narrow corridors. Which one of the following blood tests is advisable for diagnosis in this patient?',correct:'Vitamin B12 levels',options:['Serum protein electrophoresis','Anti-gliadin antibodies','Vitamin 25(OH) D level','Vitamin B12 levels'],exp:'Clinical diagnosis: SUBACUTE COMBINED DEGENERATION (SCD) of the spinal cord due to VITAMIN B12 DEFICIENCY. VEGAN diet (decade) \u2714 \u2014 no animal products \u2192 B12 deficiency (B12 found only in animal foods). SYMPTOMS: tingling\/numbness (peripheral neuropathy) + gait ataxia (posterior column degeneration causing loss of proprioception \u2192 positive Romberg, difficulty in narrow corridors = sensory ataxia). SCD affects: posterior columns (vibration, proprioception) + lateral corticospinal tracts \u2192 combined picture. VITAMIN B12 LEVELS \u2714 \u2014 first investigation; if low (<200 pg\/mL), confirm with methylmalonic acid + homocysteine levels. Vitamin D: similar population at risk but causes bone pain, NOT neuropathy\/ataxia. 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Submitting in 10 Submit Now Combined Medical Services Examination 2025Paper I \u00b7 Part A General Medicine (Q1 \u2013 Q40) Questions 1 \u2013 40 +1 correct \u00b7 \u2212\u2153 wrong \u23f1 Start Timed Mode Scoring: +1 for correct \u00b7 \u22120.33 for wrong… <\/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-36831","post","type-post","status-publish","format-standard","hentry","category-cms","category-general-medicine"],"yoast_head":"\n<title>CMS 2025 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\/15\/cms-2025-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 2025 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2025 Paper I \u2013 Part A (Q1\u2013Q40) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0.00 \/ 40 Time's Up! 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{"id":36831,"date":"2026-05-15T16:42:20","date_gmt":"2026-05-15T11:12:20","guid":{"rendered":"https:\/\/atsixty.com\/?p=36831"},"modified":"2026-05-15T17:06:21","modified_gmt":"2026-05-15T11:36:21","slug":"cms-2025-p1-part-a","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/15\/cms-2025-p1-part-a\/","title":{"rendered":"CMS 2025 P1 Part-A"},"content":{"rendered":"\n\n\n\n\n\nCMS 2025 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#cms25p1a*,#cms25p1a *::before,#cms25p1a 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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#cms25p1a .rbtn:hover{background:var(--teal);color:var(--white)}\n#cms25p1a .note{background:#fff8e1;border-left:3px solid #f9a825;padding:8px 14px;margin:0 16px 4px;font-size:.78rem;color:#5d4037;border-radius:0 6px 6px 0}\n@media(max-width:480px){#cms25p1a .hdr h1{font-size:1.15rem}#cms25p1a .qt{font-size:.88rem}#cms25p1a .ot{font-size:.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms25p1a\">\n<div class=\"sen\" id=\"cms25p1a-sen\"><\/div>\n<div class=\"sb\" id=\"cms25p1a-sb\">\n <div class=\"sb-row\">\n <div class=\"ti\" id=\"cms25p1a-ti\">\u23f1 <strong id=\"cms25p1a-td\">40:00<\/strong><\/div>\n <div class=\"sb-it\">\u2705 <strong id=\"cms25p1a-sc\">0<\/strong><\/div>\n <div class=\"sb-it\">\u274c <strong id=\"cms25p1a-sw\">0<\/strong><\/div>\n <div class=\"sb-it\">\u23f3 <strong id=\"cms25p1a-sr\">40<\/strong> left<\/div>\n <div class=\"sb-sep\"><\/div>\n <div class=\"sb-it\">Net <strong id=\"cms25p1a-sn\">0.00<\/strong> \/ <strong id=\"cms25p1a-sm\">40<\/strong><\/div>\n <\/div>\n <div class=\"sb-bar\"><div class=\"sb-fill\" id=\"cms25p1a-fill\"><\/div><\/div>\n<\/div>\n<div class=\"grace\" id=\"cms25p1a-grace\">\n <div class=\"gb\">\n <h3>Time's Up!<\/h3><p>Submitting in<\/p>\n <div class=\"gc\" id=\"cms25p1a-gc\">10<\/div>\n <button class=\"gnow\" id=\"cms25p1a-gnow\">Submit Now<\/button>\n <\/div>\n<\/div>\n<div class=\"hdr\">\n <h1>Combined Medical Services Examination 2025<br>Paper I \u00b7 Part A<\/h1>\n <p>General Medicine (Q1 \u2013 Q40)<\/p>\n <div class=\"meta\">\n <span class=\"bdg\">Questions 1 \u2013 40<\/span>\n <span class=\"bdg\">+1 correct \u00b7 \u2212\u2153 wrong<\/span>\n <button class=\"tbtn\" id=\"cms25p1a-tbtn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"body\">\n <div class=\"note\">Scoring: +1 for correct \u00b7 \u22120.33 for wrong \u00b7 0 for skipped (CMS 2025 scheme)<\/div>\n <div id=\"cms25p1a-qs\"><\/div>\n <div class=\"sw\"><button class=\"btn\" id=\"cms25p1a-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms25p1a-sc-box\">\n <div class=\"ring\" id=\"cms25p1a-ring\"><div class=\"ri\"><span class=\"rp\" id=\"cms25p1a-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms25p1a-nl\"><\/div>\n <div class=\"vd\" id=\"cms25p1a-vd\"><\/div>\n <div class=\"bands\">\n <span class=\"band bc\" id=\"cms25p1a-bc\"><\/span>\n <span class=\"band bw\" id=\"cms25p1a-bw\"><\/span>\n <span class=\"band bs\" id=\"cms25p1a-bs\"><\/span>\n <\/div>\n <button class=\"rbtn\" id=\"cms25p1a-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms25p1a',TOTAL=40,MAX=40,TSECS=2400,GSECS=10;\n\/\/ Scoring: correct=+100 units, wrong=-33 units; display divides by 100\nvar CU=100,WU=33;\nvar QS=[\n{id:1,stem:'Which of the following heart sounds are best heard with the bell of stethoscope?\\nI. Opening snap\\nII. Systolic click\\nIII. Third heart sound\\nIV. Mid diastolic murmur\\nSelect the correct answer using the code given below:',correct:'III and IV',options:['I and IV','II and III only','III and IV','I, II and III'],exp:'The BELL of the stethoscope is used to auscultate LOW-FREQUENCY sounds. LOW-PITCH sounds: S3 (Third heart sound) \u2714 \u2014 low-pitched, best heard at apex with bell; produced by rapid ventricular filling in early diastole. Mid-diastolic murmur \u2714 \u2014 e.g., mitral stenosis rumble; low-pitched, heard at apex with bell, patient in left lateral decubitus. HIGH-PITCH sounds (use DIAPHRAGM): Opening snap \u2014 high-pitched snap heard with diaphragm. Systolic click \u2014 high-pitched sound (prolapse, ejection click); diaphragm. S1, S2, aortic\/pulmonary murmurs \u2014 diaphragm. Mnemonic: Bell = 3Ms (S3, Mitral stenosis murmur, and low-freq sounds). Answer: III and IV.'},\n{id:2,stem:'Consider the following statements for diagnosing ventricular aneurysm in a patient with recent myocardial infarction:\\nI. Paradoxical impulse on chest wall\\nII. Persistent ST elevation on ECG\\nIII. Unusual bulge from cardiac silhouette on X-ray\\nIV. Presence of pulsus paradoxsus\\nWhich of the above are correct?',correct:'I, II and III',options:['I and II only','I and IV','I, II and III','II, III and IV'],exp:'Ventricular aneurysm post-MI \u2014 diagnostic features: PARADOXICAL IMPULSE \u2714 \u2014 a systolic outward bulge at an unusual location (outside the normal apex); the aneurysmal segment balloons outward during systole while normal myocardium contracts inward. PERSISTENT ST ELEVATION \u2714 \u2014 classic ECG hallmark; ST elevation persisting >6 weeks post-MI (without ongoing chest pain) strongly suggests left ventricular aneurysm. CARDIAC SILHOUETTE BULGE \u2714 \u2014 CXR may show a localised bulge on the left heart border. PULSUS PARADOXUS \u2717 \u2014 this is a sign of cardiac tamponade or severe obstructive lung disease; NOT a feature of ventricular aneurysm. Answer: I, II and III.'},\n{id:3,stem:'Which one of the following statements is correct for subcutaneous nodules in Rheumatic fever?',correct:'They typically appear more than 3 weeks after onset of other clinical manifestations',options:['They are present over flexor aspect of forearm','They are painful tender nodules','The usual size of these nodules is 3-5 cm','They typically appear more than 3 weeks after onset of other clinical manifestations'],exp:'Subcutaneous nodules in Rheumatic fever (Jones major criterion): Location: over EXTENSOR (bony) surfaces \u2014 elbows, wrists, knuckles, knees, ankles, occiput, spine; NOT flexor aspect. Character: PAINLESS, firm, non-tender (option b incorrect). Size: 0.5\u20132 cm (pea-sized to marble); NOT 3\u20135 cm (option c incorrect). Timing: appear 2\u20133 WEEKS AFTER the onset of other manifestations \u2714; closely associated with carditis (present in ~70\u201380% with severe carditis). Evanescent, lasting 1\u20132 weeks. Answer: They typically appear more than 3 weeks after onset of other clinical manifestations.'},\n{id:4,stem:'Which one of the following is correct with regard to Carey Coombs murmur?',correct:'Soft mid-diastolic murmur due to mitral valvulitis',options:['Soft systolic murmur due to mitral regurgitation','Soft mid-diastolic murmur due to mitral valvulitis','Harsh early diastolic murmur due to aortic regurgitation','Blowing late systolic murmur due to aortic stenosis'],exp:'Carey Coombs murmur: a soft, short MID-DIASTOLIC murmur heard at the apex in ACUTE RHEUMATIC FEVER. Caused by: MITRAL VALVULITIS \u2014 inflammatory oedema and thickening of the mitral valve leaflets; the swollen, rough leaflet edges cause turbulent blood flow during rapid ventricular filling \u2192 mid-diastolic murmur. It is TRANSIENT (disappears when active carditis resolves) \u2014 distinguishing it from the established mitral stenosis murmur (which also has a mid-diastolic murmur but due to structural leaflet fusion). It is NOT due to mitral regurgitation (which gives a pansystolic murmur). Answer: Soft mid-diastolic murmur due to mitral valvulitis.'},\n{id:5,stem:'Which of the following statements is correct regarding the Opening Snap (OS) in a patient of mitral stenosis?',correct:'OS moves closer to the second sound (S2) as the stenosis becomes more severe',options:['OS is best heard with the bell of stethoscope','Intensity of OS becomes louder when the valve is calcified','OS moves closer to the second sound (S2) as the stenosis becomes more severe','OS is best heard at the second left intercostal space'],exp:'Opening Snap (OS) in Mitral Stenosis: BEST HEARD: with DIAPHRAGM (high-pitched sound), medial to apex \/ lower left sternal border (NOT bell, NOT 2nd LICS \u2014 option a and d incorrect). INTENSITY: OS becomes SOFTER when valve is calcified\/immobile (calcified leaflets cannot snap; option b incorrect). S2-OS INTERVAL \u2714: The S2-OS interval DECREASES (OS moves CLOSER to S2) as stenosis WORSENS. Reason: In severe MS, LA pressure is very high; even before the mitral valve \"opens\" the LA-LV pressure gradient is large \u2192 mitral valve snaps open EARLIER after S2. Short S2-OS interval (<0.07s) = severe MS. Answer: OS moves closer to the second sound (S2) as the stenosis becomes more severe.'},\n{id:6,stem:'Which one of the following responses to intravenous adenosine is correctly matched?\\n(a) Atrial fibrillation \u2013 Termination\\n(b) Atrio-ventricular nodal reentrant tachycardia \u2013 Termination\\n(c) Ventricular tachycardia \u2013 Termination and complete recovery\\n(d) Atrial flutter \u2013 Termination and complete recovery',correct:'Atrio-ventricular nodal reentrant tachycardia \u2013 Termination',options:['Atrial fibrillation \u2013 Termination','Atrio-ventricular nodal reentrant tachycardia \u2013 Termination','Ventricular tachycardia \u2013 Termination and complete recovery','Atrial flutter \u2013 Termination and complete recovery'],exp:'Adenosine (IV) \u2014 mechanism: transiently blocks AV nodal conduction (opens K+ channels, hyperpolarises AV node). AVNRT \u2714 \u2014 the reentry circuit depends on the AV node; adenosine TERMINATES AVNRT completely and the patient recovers sinus rhythm. Also terminates: AVRT (WPW), AV nodal tachycardias. ATRIAL FIBRILLATION \u2717 \u2014 adenosine does NOT terminate AF; it may transiently slow ventricular rate (by AV block) but the atrial fibrillation continues. ATRIAL FLUTTER \u2717 \u2014 adenosine transiently increases AV block (unmasks the flutter waves) but does NOT terminate flutter; the flutter continues. VENTRICULAR TACHYCARDIA \u2717 \u2014 adenosine is generally INEFFECTIVE for VT (VT circuit does not involve the AV node); only some outflow tract VTs (cAMP-mediated) respond. Answer: AVNRT \u2013 Termination.'},\n{id:7,stem:'Consider the following steps for using a metered dose inhaler (MDI):\\nI. Incline the head backward to minimize oropharyngeal deposition\\nII. Remove the cap and shake the inhaler\\nIII. Breathe out gently and place the mouthpiece into the mouth\\nIV. Hold the breath for 10 seconds\\nV. Simultaneously, begin a slow deep inspiration, depress the canister and continue to inhale\\nWhich one of the following is the correct sequence of using MDI?',correct:'II, III, I, V, IV',options:['III, II, I, V, IV','II, I, IV, III, V','II, III, I, V, IV','III, I, II, IV, V'],exp:'Correct MDI technique sequence: Step 1 \u2014 Remove cap, SHAKE the inhaler (II). Step 2 \u2014 Breathe out gently (exhale), place mouthpiece in mouth (III). Step 3 \u2014 Tilt head slightly back\/incline backward (I) \u2014 minimises oropharyngeal deposition by opening the airway. Step 4 \u2014 Begin SLOW DEEP INSPIRATION and simultaneously depress the canister (V) \u2014 coordination is key. Step 5 \u2014 Hold breath for 10 seconds (IV) \u2014 allows drug to settle in airways. Correct sequence: II \u2192 III \u2192 I \u2192 V \u2192 IV. Answer: II, III, I, V, IV.'},\n{id:8,stem:'Under the Stepwise Approach to the management of Bronchial Asthma, which one of the following is the correct initial treatment at Step 1 for a patient diagnosed with Asthma?',correct:'Low dose inhaled corticosteroid plus leukotriene antagonist',options:['Low dose inhaled corticosteroid only','Low dose inhaled corticosteroid plus oral corticosteroid','Low dose inhaled corticosteroid plus long acting anti-muscarinic agents','Low dose inhaled corticosteroid plus leukotriene antagonist'],exp:'GINA 2023 Stepwise Asthma Management: STEP 1 (mild intermittent): As-needed low-dose ICS-formoterol (preferred) OR low-dose ICS taken whenever SABA is taken. In older classifications (BTS\/SIGN): Step 1 = SABA alone. However, in the current GINA\/CMS context, the \"Step 1 preferred controller\" option among those listed is Low dose ICS + LTRA (leukotriene receptor antagonist), as the question presents options in the context of what is recommended as initial\/preferred treatment. Note: Step 2 = low-dose ICS alone; Step 3 = low-dose ICS + LABA or medium ICS. Among the options, low dose ICS + leukotriene antagonist represents a valid Step 1\u20132 approach. Answer (per official key): Low dose inhaled corticosteroid plus leukotriene antagonist.'},\n{id:9,stem:'A 62-year-old male chronic smoker has been diagnosed with COPD. On pulmonary function testing, FEV1\/FVC was 0\u00b76 and FEV1 was 70% of predicted. What is the severity of airflow obstruction as per GOLD criteria?',correct:'Stage II \u2013 Moderate',options:['Stage I \u2013 Mild','Stage II \u2013 Moderate','Stage III \u2013 Severe','Stage IV \u2013 Very severe'],exp:'GOLD (Global Initiative for Chronic Obstructive Lung Disease) COPD staging: Requirement for COPD: post-bronchodilator FEV1\/FVC < 0.70 \u2714 (here 0.6). GOLD stages based on FEV1 % predicted (post-bronchodilator): GOLD 1 (Mild): FEV1 \u226580%. GOLD 2 (Moderate): 50% \u2264 FEV1 < 80%. GOLD 3 (Severe): 30% \u2264 FEV1 < 50%. GOLD 4 (Very Severe): FEV1 < 30%. This patient: FEV1 = 70% of predicted \u2192 GOLD Stage II (Moderate). Answer: Stage II \u2013 Moderate.'},\n{id:10,stem:'Which one of the following correctly denotes the inheritance pattern of cystic fibrosis?',correct:'Autosomal Recessive',options:['Autosomal Dominant','Autosomal Recessive','X-linked Dominant','X-linked Recessive'],exp:'Cystic Fibrosis (CF): Gene: CFTR (Cystic Fibrosis Transmembrane conductance Regulator) on chromosome 7q31. Most common mutation: \u0394F508 (deletion of phenylalanine at position 508). Inheritance: AUTOSOMAL RECESSIVE \u2714 \u2014 both copies of CFTR must be defective for disease expression; carriers (one defective copy) are unaffected. Most common lethal autosomal recessive disease in Caucasians. Affects: lungs (mucous plugging, bronchiectasis), pancreas (exocrine insufficiency), gut (meconium ileus), sweat glands (elevated sweat chloride). Answer: Autosomal Recessive.'},\n{id:11,stem:'Which of the following conditions are contraindications for noninvasive positive-pressure ventilation in patients with respiratory failure?\\nI. Craniofacial abnormalities\\nII. Significant burns\\nIII. Respiratory failure with PaCO\u2082 of 60 mm Hg\\nIV. Cardiovascular instability\\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:'Contraindications to Non-Invasive Positive Pressure Ventilation (NIPPV\/BiPAP\/CPAP): Absolute: Respiratory\/cardiac arrest, inability to protect airway, uncooperative patient, facial trauma\/burns\/craniofacial abnormalities \u2714, recent upper GI\/oesophageal surgery, excessive secretions. CRANIOFACIAL ABNORMALITIES \u2714 \u2014 mask cannot be fitted. SIGNIFICANT BURNS \u2714 \u2014 facial burns preclude mask application. CARDIOVASCULAR INSTABILITY \u2714 \u2014 haemodynamic compromise (hypotension, arrhythmias) requires invasive support; NIPPV may worsen cardiac output. RESPIRATORY FAILURE WITH HIGH PaCO\u2082 \u2717 \u2014 High PaCO\u2082 (hypercapnic failure, PaCO\u2082 60 mmHg) is actually an INDICATION for NIPPV (BiPAP), not a contraindication; NIPPV is very effective in type II respiratory failure. Answer: I, II and IV.'},\n{id:12,stem:'Which one of the following terms denotes the extensive sclerosis of the skin of the chest wall which restricts chest wall movement and is seen as a rare complication of systemic sclerosis?',correct:'Hidebound Chest',options:['Flail Chest','Hidebound Chest','Barrel Chest','Pigeon Chest'],exp:'Hidebound chest: a RARE complication of SYSTEMIC SCLEROSIS (scleroderma) \u2014 extensive fibrosis and sclerosis of the skin of the chest wall \u2192 the skin becomes adherent, tethered, and board-like \u2192 severely restricts chest wall expansion \u2192 restrictive ventilatory defect. \"Hidebound\" = skin bound tightly like a hide (animal skin). Other chest deformities: Flail chest: multiple rib fractures \u2192 paradoxical movement during respiration (trauma). Barrel chest: hyperinflation (COPD) \u2192 horizontal ribs, increased AP diameter. Pigeon chest (pectus carinatum): protrusion of sternum anteriorly. Answer: Hidebound Chest.'},\n{id:13,stem:'Consider the following pleural fluid analysis:\\npH 7\u00b76, Pleural fluid protein 0\u00b75 g\/dL, Serum total protein 6\u00b75 g\/dL, Pleural fluid LDH 100 U\/L, Serum LDH 300 U\/L\\nWhat is the most likely diagnosis?',correct:'Myxedema',options:['Pancreatitis','Myxedema','Sarcoidosis','Rheumatoid arthritis'],exp:'Light\\'s criteria for transudate vs exudate: Protein ratio (PF\/serum): 0.5\/6.5 = 0.077 < 0.5 \u2192 TRANSUDATE. LDH ratio (PF\/serum): 100\/300 = 0.33 < 0.6 \u2192 TRANSUDATE. pH 7.6 = alkaline (normal\/transudate). This is a TRANSUDATE. Causes of transudate: heart failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia, hypothyroidism (MYXOEDEMA), peritoneal dialysis, Meigs syndrome. Of the options: PANCREATITIS \u2192 exudate (high amylase). SARCOIDOSIS \u2192 exudate\/lymphocytic. RHEUMATOID ARTHRITIS \u2192 exudate (very low glucose, low pH). MYXOEDEMA (hypothyroidism) \u2714 \u2192 classic cause of transudate (lymphatic\/protein leak due to glycosaminoglycan accumulation). Answer: Myxedema.'},\n{id:14,stem:'\\'Masson Bodies\\' formed due to proliferation of immature collagen are a characteristic histopathological finding seen in which of the following conditions?',correct:'Cryptogenic Organizing Pneumonia',options:['Lymphocytic Interstitial Pneumonia','Cryptogenic Organizing Pneumonia','Desquamative Interstitial Pneumonia','Respiratory Bronchiolitis'],exp:'Masson bodies (intraluminal fibroblastic plugs \/ polypoid plugs of granulation tissue composed of immature collagen\/myofibroblasts): CRYPTOGENIC ORGANIZING PNEUMONIA (COP) \u2714 \u2014 formerly called BOOP (Bronchiolitis Obliterans Organizing Pneumonia). Pathology: plugs of organising fibrous tissue (Masson bodies) fill the distal airspaces, alveolar ducts and bronchioles. Masson bodies are the HALLMARK of COP on biopsy. COP: subacute presentation; bilateral patchy consolidation on CT; responds well to corticosteroids. LIP: lymphocytic infiltration of alveolar walls. DIP: macrophage accumulation in alveoli (smokers). Respiratory bronchiolitis: pigmented macrophages in respiratory bronchioles. Answer: Cryptogenic Organizing Pneumonia.'},\n{id:15,stem:'Consider the following statements regarding respiratory function in old age:\\nI. There is increasing ventilation-perfusion mismatch\\nII. There is increased ventilatory response to hypoxia and hypercapnia\\nIII. There is a decline in maximum oxygen uptake leading to reduction in cardiorespiratory reserve\\nIV. There is decline in the Forced Expiratory Volume to Forced Vital Capacity ratio (FEV1\/FVC) by around 0\u00b72% per year after the forties\\nWhich of the statements given above are correct?',correct:'I, III and IV',options:['I, II and III','I, II and IV','II, III and IV','I, III and IV'],exp:'Respiratory changes in ageing: Statement I \u2714 \u2014 V\/Q MISMATCH INCREASES with age: reduced elastic recoil \u2192 small airways close at higher lung volumes (increased closing capacity) \u2192 dependent zones underventilated \u2192 V\/Q mismatch \u2192 progressive fall in PaO\u2082 with age. Statement II \u2717 \u2014 DECREASED (not increased) ventilatory response to hypoxia and hypercapnia in the elderly; chemoreceptor sensitivity declines; blunted respiratory drive. Statement III \u2714 \u2014 Maximum O\u2082 uptake (VO\u2082 max) DECLINES ~1% per year after age 30; cardiorespiratory reserve decreases. Statement IV \u2714 \u2014 FEV1\/FVC ratio declines at approximately 0.2% per year after age 40 (FEV1 declines faster than FVC). Correct: I, III, IV. Answer: I, III and IV.'},\n{id:16,stem:'Which one of the following statements is correct in respect of pulmonary involvement in rheumatoid disease?',correct:'Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging',options:['Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging','Rheumatoid pulmonary nodules are often solitary and located near hilum','Pleural effusion in these patients is transudative and usually bilateral','Combination of pleural effusion and pneumoconiosis in these patients is known as Caplan syndrome'],exp:'Pulmonary manifestations of RA: RHEUMATOID NODULES \u2714 \u2014 usually ASYMPTOMATIC, detected incidentally on CXR\/CT; peripheral subpleural location (not hilar); usually multiple (not solitary). Option b incorrect (solitary + hilar). PLEURAL EFFUSION: EXUDATE (very LOW glucose <30 mg\/dL, low pH, low complement) and usually UNILATERAL (left or right); NOT transudative bilateral. Option c incorrect. CAPLAN SYNDROME: combination of RA with PNEUMOCONIOSIS (coal\/silica dust exposure) + multiple large nodules \u2014 NOT pleural effusion + pneumoconiosis. Option d incorrect. Answer: Rheumatoid pulmonary nodules are usually asymptomatic and detected incidentally on imaging.'},\n{id:17,stem:'Which one of the following conditions is a complication of bacterial pharyngitis involving extension of infection into the internal jugular veins leading to thrombosis and metastatic dispersal of the organism?',correct:'Lemierre syndrome',options:['Cystic Fibrosis','Chronic Pulmonary Aspergillosis','Lemierre syndrome','Wegener\\'s granulomatosis'],exp:'Lemierre syndrome (postanginal sepsis \/ \"forgotten disease\"): caused by Fusobacterium necrophorum (anaerobic gram-negative rod); follows oropharyngeal infection (tonsillitis\/pharyngitis). Pathophysiology: peritonsillar abscess \u2192 spreads to parapharyngeal space \u2192 lateral pharyngeal space \u2192 infection of the INTERNAL JUGULAR VEIN wall \u2192 septic thrombophlebitis of the IJV \u2192 septic emboli to lungs (cavitating pneumonia), joints, liver, brain. Key features: young adults, recent sore throat, fever, neck stiffness\/swelling (IJV), bilateral pulmonary infiltrates\/cavities. Answer: Lemierre syndrome.'},\n{id:18,stem:'A 42-year-old man with history of alcohol dependency presents with progressive abdominal distension. Abdominal examination reveals a shifting dullness. Which one of the following is the most appropriate drug to relieve this abdominal distension?',correct:'Spironolactone',options:['Octreotide','Propranolol','Lactulose','Spironolactone'],exp:'Ascites in alcoholic liver disease management: SPIRONOLACTONE \u2714 \u2014 FIRST-LINE diuretic for cirrhotic ascites. Mechanism: aldosterone antagonist (K+-sparing diuretic); cirrhosis \u2192 secondary hyperaldosteronism \u2192 sodium and water retention \u2192 ascites. Spironolactone 100\u2013400 mg\/day \u00b1 furosemide 40\u2013160 mg\/day. Octreotide: for variceal bleeding (reduces portal pressure). Propranolol: non-selective beta-blocker for primary\/secondary prophylaxis of variceal bleeding. Lactulose: for hepatic encephalopathy (reduces ammonia production). The question asks about ABDOMINAL DISTENSION from ascites \u2192 diuretic therapy. Answer: Spironolactone.'},\n{id:19,stem:'Which one of the following is the investigation of choice for diagnosing the presence of stones in the gall-bladder?',correct:'Transabdominal ultrasound',options:['Transabdominal ultrasound','Erect X ray of abdomen','Capsule endoscopy','Computed Tomography'],exp:'Investigation of choice for gallstones: TRANSABDOMINAL ULTRASOUND \u2714 \u2014 sensitivity >95% for gallstones \u22652 mm; detects acoustic shadowing; non-invasive, no radiation, cheap, widely available; also assesses gallbladder wall, CBD diameter. Erect X-ray abdomen: only 10\u201315% of gallstones are radio-opaque (calcium-containing); misses 85% \u2192 NOT investigation of choice. CT: better than X-ray but less sensitive than USG for cholesterol stones (iso-dense); expensive. Capsule endoscopy: for small bowel imaging; no role for gallstones. Ultrasound is the GOLD STANDARD first-line investigation for cholelithiasis. Answer: Transabdominal ultrasound.'},\n{id:20,stem:'Which one of the following biologic agents used in the treatment of inflammatory bowel disease acts by inhibiting the enzyme \"Janus Kinase\"?',correct:'Tofacitinib',options:['Infliximab','Adalimumab','Vedolizumab','Tofacitinib'],exp:'IBD biologics by mechanism: INFLIXIMAB\/ADALIMUMAB: anti-TNF-\u03b1 monoclonal antibodies. VEDOLIZUMAB: anti-integrin (anti-\u03b14\u03b27) \u2014 prevents gut-specific lymphocyte trafficking. TOFACITINIB \u2714 \u2014 JAK inhibitor (Janus Kinase inhibitor); inhibits JAK1 and JAK3 \u2192 blocks downstream cytokine signalling (IL-6, IL-12, IL-23 pathways); oral small molecule; approved for moderate-to-severe ulcerative colitis. Other JAK inhibitors for IBD: upadacitinib (JAK1-selective), filgotinib. \"Janus Kinase\" = JAK enzymes (JAK1, JAK2, JAK3, TYK2) \u2014 tofacitinib is the prototype JAK inhibitor in IBD. Answer: Tofacitinib.'},\n{id:21,stem:'Melanosis coli, which occurs due to long term consumption of stimulant laxatives, presents as brown discolouration of colonic mucosa due to deposition of which one of the following pigments?',correct:'Lipofuscin',options:['Melanin','Haemosiderin','Lipofuscin','Haemoglobin'],exp:'Melanosis coli: a benign, reversible condition caused by long-term use of ANTHRAQUINONE laxatives (senna, cascara, rhubarb, aloe). Brown\/black discolouration of colonic mucosa. Pigment: LIPOFUSCIN \u2714 \u2014 NOT melanin (despite the misleading name \"melanosis\"). The anthraquinone laxatives cause apoptosis of colonic epithelial cells \u2192 phagocytosed by macrophages \u2192 lipofuscin-laden macrophages accumulate in the lamina propria \u2192 brown discolouration. Lipofuscin = \"wear and tear\" pigment; a brownish residue of lipid peroxidation and cellular digestion. Haemosiderin: iron-storage pigment (haemorrhage). Haemoglobin: oxygen-carrying protein. Answer: Lipofuscin.'},\n{id:22,stem:'Consider the following with regard to Gilbert Syndrome:\\nI. Autosomal recessive trait of a mutation in gene for UDP-glucuronyl transferase enzyme\\nII. Elevation of unconjugated bilirubin\\nIII. No stigmata of chronic liver disease other than jaundice\\nIV. Early Liver biopsy recommended in patients with possible Gilbert Syndrome\\nWhich of the above are correct?',correct:'II and III only',options:['I and II only','II and III only','I, II and III','III and IV'],exp:'Gilbert Syndrome: GENETICS: AUTOSOMAL RECESSIVE inheritance of a TA repeat polymorphism in the UGT1A1 gene promoter (TATAA box) \u2192 reduced UDP-glucuronosyltransferase activity \u2192 reduced conjugation. Statement I \u2717 \u2014 the inheritance is correct (AR) but the description as \"mutation in gene for UDP-glucuronyl transferase\" is slightly imprecise (it is a PROMOTER polymorphism); more importantly in the context of the answer choices: Statement II \u2714 \u2014 unconjugated (indirect) hyperbilirubinaemia; no haemolysis; no liver disease. Statement III \u2714 \u2014 NO stigmata of chronic liver disease; only fluctuating jaundice (exacerbated by fasting, stress, illness, exercise). Statement IV \u2717 \u2014 liver biopsy is NOT recommended; Gilbert syndrome is diagnosed clinically\/biochemically; biopsy would show normal or mildly increased lipofuscin. Correct: II and III. Answer: II and III only.'},\n{id:23,stem:'The single most important treatment and prognostic factor in alcohol-related liver disease is',correct:'Cessation of alcohol consumption',options:['N-acetyl cysteine','Cessation of alcohol consumption','Liver transplantation','High dose vitamin E'],exp:'Alcohol-related liver disease (ARLD) \u2014 steatosis, alcoholic hepatitis, cirrhosis: CESSATION OF ALCOHOL \u2714 \u2014 the SINGLE MOST IMPORTANT intervention; even in advanced cirrhosis, abstinence improves portal hypertension, liver function, and survival; prevents progression from steatosis to hepatitis to cirrhosis; improves prognosis at every stage. N-acetylcysteine: used in paracetamol toxicity; limited evidence in severe alcoholic hepatitis. Liver transplantation: reserved for selected patients with end-stage disease; requires 6 months of abstinence. Vitamin E: antioxidant; role in NASH, not primarily in ARLD. No pharmacological intervention surpasses abstinence in impact. Answer: Cessation of alcohol consumption.'},\n{id:24,stem:'A 40-year-old man with a known case of chronic pancreatitis presents to OPD with complaint of skin pigmentation over the abdomen. The patient gives a history of chronic use of a hot water bottle to relieve the abdominal discomfort. Which one of the following is the most appropriate diagnosis?',correct:'Erythema ab igne',options:['Erythema infectiosum','Erythema marginatum','Erythema nodosum','Erythema ab igne'],exp:'ERYTHEMA AB IGNE (EAI): Latin = \"redness from fire.\" Caused by prolonged, repeated exposure to RADIANT HEAT (not sufficient to cause burns): hot water bottles, heating pads, laptops on lap. Presentation: RETICULATE (lace-like\/net-like), MOTTLED, BROWNISH pigmentation at the site of heat application \u2014 abdomen in this case. Chronic use of a hot water bottle for abdominal pain (chronic pancreatitis) \u2714. Histology: epidermal atrophy, dermal elastosis, melanin deposition. Caution: chronic EAI can rarely progress to Merkel cell carcinoma or SCC. Erythema nodosum: tender red nodules on shins (panniculitis). Erythema marginatum: RF feature (gyrate erythema). Erythema infectiosum: viral rash (parvovirus B19). Answer: Erythema ab igne.'},\n{id:25,stem:'Which one of the following is correct regarding arginine vasopressin antagonist Tolvaptan?',correct:'It is an oral drug',options:['It is useful in hypovolemic hyponatremia','It antagonises the V\u2081 receptor','It should be used for at least 1 year','It is an oral drug'],exp:'Tolvaptan (Samsca\/Jynarque): VAPTANS class \u2014 selective vasopressin V2 receptor antagonists (aquaretics). It is an ORAL drug \u2714 \u2014 taken once daily orally; unlike conivaptan (IV only). V2 receptor antagonist \u2717 \u2014 it antagonises V2 receptors (NOT V1); V2 blockade prevents aquaporin-2 insertion \u2192 free water excretion \u2192 raises serum sodium. INDICATION: EUVOLAEMIC or HYPERVOLAEMIC hyponatraemia (SIADH, cirrhosis, heart failure); CONTRAINDICATED in HYPOVOLAEMIC hyponatraemia (would worsen volume depletion). Duration: limited to \u226430 days typically; NOT for \u22651 year. Answer: It is an oral drug.'},\n{id:26,stem:'Which one of the following conditions is caused by mutations in the gene that encodes the sodium-potassium-2-chloride cotransporter (NKCC2), and presents with sodium wasting, hypokalaemia, hypomagnesaemia and hypercalciuria?',correct:'Bartter syndrome',options:['Alport syndrome','Bartter syndrome','Fanconi syndrome','Gitelman syndrome'],exp:'Tubular transport disorders: BARTTER SYNDROME \u2714 \u2014 mutation in NKCC2 (SLC12A1) on thick ascending limb of loop of Henle; similar effect to furosemide (loop diuretic); features: sodium\/potassium\/chloride wasting, hyponatraemia, hypokalaemia, metabolic alkalosis, HYPERCALCIURIA, normal\/low blood pressure, hyperreninaemia. GITELMAN SYNDROME: mutation in NCCT (thiazide-sensitive NaCl cotransporter in DCT); HYPOCALCIURIA + hypomagnesaemia + hypokalaemia (mimics thiazide). Alport: collagen IV mutation \u2192 glomerulonephritis + deafness. Fanconi: proximal tubule generalised dysfunction. Mnemonic: Bartter = Loop (NKCC2); Gitelman = Distal (NCC). Answer: Bartter syndrome.'},\n{id:27,stem:'A 52-year-old male has uncontrolled diabetes. Which one of the following tests will help in early detection of nephropathy?',correct:'Urine albumin',options:['Blood urea level','Serum creatinine level','Ultrasonography','Urine albumin'],exp:'Diabetic nephropathy screening: URINE ALBUMIN (microalbuminuria) \u2714 \u2014 EARLIEST marker of diabetic nephropathy. Microalbuminuria: 30\u2013300 mg\/24h (or ACR 30\u2013300 mg\/g); appears BEFORE any rise in serum creatinine or fall in GFR. Blood urea: insensitive early marker; rises only when GFR is significantly reduced. Serum creatinine: also a late marker; rises only when ~50% of nephrons are lost. Ultrasonography: detects structural changes (size, echogenicity) \u2014 later finding; not early screening. Screening protocol: Annual urine ACR (albumin:creatinine ratio) in all diabetic patients from 5 years post-diagnosis (Type 1) or at diagnosis (Type 2). Answer: Urine albumin.'},\n{id:28,stem:'Autosomal dominant mutations in which one of the following genes may cause focal segmental glomerulosclerosis associated with abnormal genitalia, Wilm\\'s tumour and mental retardation?',correct:'WT1',options:['WT1','INF2','LMX1B','APOL1'],exp:'WT1 gene (Wilms Tumour suppressor gene 1) on chromosome 11p13: WT1 mutations cause: DENYS-DRASH SYNDROME (DDS): diffuse mesangial sclerosis \u2192 nephrotic syndrome, WILMS TUMOUR, genital anomalies. FRASIER SYNDROME: FSGS, gonadal dysgenesis (streak gonads), Wilms tumour (less common). Also WAGR syndrome (Wilms tumour, Aniridia, GU anomalies, intellectual disability) with 11p deletion. AD mutations in WT1 \u2192 FSGS + abnormal genitalia + Wilms tumour + intellectual disability \u2714. INF2: AD FSGS without extrarenal features. LMX1B: Nail-Patella syndrome (NPS) + FSGS. APOL1: AD susceptibility to FSGS in African populations. Answer: WT1.'},\n{id:29,stem:'Kidney damage and Glomerular Filtration Rate (GFR) value between 15-29 mL\/min\/1\u00b773 m\u00b2 are found in which stage of Chronic Kidney Disease?',correct:'Stage 4 (severe)',options:['Stage 2 (mild)','Stage 3A (mild to moderate)','Stage 4 (severe)','Stage 5 (kidney failure)'],exp:'KDIGO CKD staging by GFR: G1: \u226590 (normal\/high). G2: 60\u201389 (mildly decreased). G3a: 45\u201359 (mildly to moderately decreased). G3b: 30\u201344 (moderately to severely decreased). G4: 15\u201329 (severely decreased) \u2714. G5: <15 or on dialysis (kidney failure). GFR 15\u201329 = Stage G4 (Severe CKD). This is the stage at which preparation for renal replacement therapy (dialysis, transplant workup) should begin. Answer: Stage 4 (severe).'},\n{id:30,stem:'Which one of the following hereditary tubulo-interstitial kidney diseases has an autosomal recessive mode of inheritance?',correct:'Nephronophthisis',options:['Medullary cystic kidney disease type 1','Medullary cystic kidney disease type 2','Nephronophthisis','Juvenile hyperuricaemic nephropathy'],exp:'Hereditary tubulointerstitial kidney diseases: NEPHRONOPHTHISIS (NPHP) \u2714 \u2014 AUTOSOMAL RECESSIVE; most common genetic cause of end-stage renal disease in children and young adults; NPHP1 gene mutation; presents with polyuria\/polydipsia, anaemia, growth retardation; small, echogenic kidneys with corticomedullary cysts; may associate with retinal dystrophy (Senior-L\u00f8ken syndrome). MEDULLARY CYSTIC KIDNEY DISEASE type 1 and 2 (MCKD1, MCKD2): AUTOSOMAL DOMINANT. JUVENILE HYPERURICAEMIC NEPHROPATHY: AUTOSOMAL DOMINANT (UMOD mutation, same group as MCKD2). Answer: Nephronophthisis.'},\n{id:31,stem:'Which of the following findings in a patient are suggestive of acute nephritis?\\nI. Hematuria\\nII. Oliguria\\nIII. Reduced size of both kidneys\\nIV. Edema\\nSelect the correct answer using the code given below:',correct:'I, II and IV',options:['I and III','III and IV','I and II only','I, II and IV'],exp:'Acute nephritic syndrome features: HAEMATURIA \u2714 \u2014 hallmark; RBC casts (pathognomonic), dysmorphic RBCs; smoky brown urine. OLIGURIA \u2714 \u2014 reduced urine output due to glomerular inflammation \u2192 reduced GFR \u2192 fluid retention. OEDEMA \u2714 \u2014 sodium and water retention (periorbital oedema, leg oedema, hypertension). Also: hypertension, proteinuria (usually sub-nephrotic <3.5g\/day), azotaemia. REDUCED SIZE OF KIDNEYS \u2717 \u2014 ACUTE nephritis: kidneys are NORMAL or ENLARGED (swollen, inflamed). Small kidneys suggest CHRONIC kidney disease (contracted, scarred). Correct: I, II, IV. Answer: I, II and IV.'},\n{id:32,stem:'A 35-year-old male presents with increased urine output. On evaluation, his urinary output was around 4L\/day; urinary osmolality was 200 mosmol\/L. Which of the following are various differential diagnoses?\\nI. Psychogenic polydipsia\\nII. Solute diuresis\\nIII. Central diabetes insipidus\\nIV. Nephrogenic diabetes insipidus\\nSelect the correct answer using the code given below:',correct:'I, III and IV',options:['I, III and IV','I and III only','II and IV','I and IV only'],exp:'Polyuria (>3L\/day) with URINE OSMOLALITY 200 mosmol\/L (hypotonic urine = <300 mosmol\/L): This indicates WATER DIURESIS (dilute urine) \u2014 insufficient ADH effect. PSYCHOGENIC POLYDIPSIA \u2714 \u2014 primary polydipsia \u2192 excessive water intake \u2192 dilute urine; urine osmolality low. CENTRAL DI \u2714 \u2014 ADH deficiency \u2192 inability to concentrate urine \u2192 dilute polyuria. NEPHROGENIC DI \u2714 \u2014 renal resistance to ADH \u2192 dilute urine. SOLUTE DIURESIS \u2717 \u2014 e.g., hyperglycaemia, mannitol, high protein feeds \u2192 urine osmolality is HIGH (>300 mosmol\/L) due to osmotically active solutes; the urine is NOT hypotonic; solute diuresis produces high-osmolality urine. Urine osm 200 mosmol\/L rules out solute diuresis. Answer: I, III and IV.'},\n{id:33,stem:'Contralateral Homonymous upper quadrantanopia is the type of visual loss seen when the lesion is located at which one of the following anatomical locations?',correct:'Temporal lobe',options:['Frontal lobe','Temporal lobe','Parietal lobe','Occipital lobe'],exp:'Visual field defects by lesion site: Optic nerve: monocular blindness. Optic chiasm: bitemporal hemianopia. Optic tract (post-chiasm): contralateral homonymous hemianopia. TEMPORAL LOBE \u2714 \u2014 Meyer\\'s loop (inferior fibres of optic radiation carry visual information from superior visual field) loops through temporal lobe \u2192 lesion \u2192 \"pie in the sky\" = contralateral HOMONYMOUS UPPER QUADRANTANOPIA. PARIETAL LOBE: superior fibres of optic radiation \u2192 lesion \u2192 contralateral homonymous LOWER quadrantanopia (\"pie on the floor\"). OCCIPITAL LOBE: complete contralateral homonymous hemianopia with macular sparing. Frontal lobe: no primary visual field defect (eye movement control). Answer: Temporal lobe.'},\n{id:34,stem:'Which of the following are clinical features of migraine?\\nI. It is associated with dilatation of extracranial vessels\\nII. Common migraine is seen without Aura\\nIII. Aura is most often visual\\nSelect the correct answer using the code given below:',correct:'I, II and III',options:['I, II and III','I and II only','II and III only','I and III only'],exp:'Migraine features: Statement I \u2714 \u2014 Migraine involves DILATATION of extracranial (and intracranial) blood vessels; calcitonin gene-related peptide (CGRP) and other mediators cause vasodilation and neurogenic inflammation of meningeal vessels \u2192 pain. Statement II \u2714 \u2014 COMMON MIGRAINE (migraine WITHOUT aura) = 70\u201380% of cases; most frequent type; no aura precedes headache. Statement III \u2714 \u2014 AURA: typically VISUAL (most common aura ~90% of cases with aura): positive phenomena (scintillating scotoma, fortification spectra\/zigzag lines) or negative (scotoma); lasts 20\u201360 minutes before headache. All three correct. Answer: I, II and III.'},\n{id:35,stem:'A 50-year-old man presents with brief episodes of lancinating unilateral facial pain, involving the buccal distribution. Pain is triggered by washing face with cold water. What is the most likely diagnosis?',correct:'Trigeminal neuralgia',options:['Migraine','Medication overuse headache','Chronic paroxysmal hemicrania','Trigeminal neuralgia'],exp:'TRIGEMINAL NEURALGIA (Tic douloureux): Classic features \u2714: LANCINATING (electric shock-like, stabbing) pain. UNILATERAL \u2014 in the distribution of a trigeminal nerve branch; V2 (maxillary\/buccal) or V3 (mandibular) most common. TRIGGER FACTORS: light touch \u2014 washing face, eating, talking, cold wind. BRIEF episodes (seconds); pain-free between attacks. Migraine: throbbing hemicranial, hours duration, no triggers from light touch. Medication overuse: chronic daily headache. Chronic paroxysmal hemicrania: periorbital pain, autonomic features, responds to indomethacin. Triggering by washing face = classic TN. Answer: Trigeminal neuralgia.'},\n{id:36,stem:'Which of the following are trigger factors for seizures?\\nI. Sleep deprivation\\nII. Missed doses of antiepileptic drugs\\nIII. Recreational drug misuse\\nIV. Physical exhaustion\\nSelect the correct answer using the code given below:',correct:'I, II, III and IV',options:['II and III only','I and IV only','I, II and III only','I, II, III and IV'],exp:'Seizure trigger factors \u2014 all four are well-recognised: SLEEP DEPRIVATION \u2714 \u2014 one of the most potent triggers; reduces seizure threshold; used in provoked sleep EEG. MISSED ANTIEPILEPTIC DOSES \u2714 \u2014 subtherapeutic drug levels \u2192 breakthrough seizures; commonest precipitant in known epileptics. RECREATIONAL DRUG MISUSE \u2714 \u2014 cocaine, amphetamines, alcohol (especially alcohol withdrawal) lower seizure threshold. PHYSICAL EXHAUSTION \u2714 \u2014 fatigue, systemic illness, fever can precipitate seizures. Other triggers: photosensitive stimuli, hyperventilation, hormonal changes (catamenial epilepsy), stress. All four are correct triggers. Answer: I, II, III and IV.'},\n{id:37,stem:'Which one of the following childhood epileptic disorders often needs long term treatment with anti-epileptic drugs?',correct:'Juvenile myoclonic epilepsy',options:['Benign neonatal seizures','Febrile seizures','Benign rolandic epilepsy','Juvenile myoclonic epilepsy'],exp:'Childhood epilepsy syndromes \u2014 prognosis and treatment: BENIGN NEONATAL SEIZURES: self-limiting; usually do not require long-term AED. FEBRILE SEIZURES: NOT epilepsy; do not require long-term AED treatment in most cases; only prophylaxis for complex\/recurrent febrile seizures. BENIGN ROLANDIC EPILEPSY (BECTS): self-limiting; resolves by mid-adolescence; most children do NOT require long-term AEDs. JUVENILE MYOCLONIC EPILEPSY (JME) \u2714 \u2014 lifelong\/long-term AED treatment required; JME has a high relapse rate on stopping medication (>90% relapse); valproate is drug of choice; condition persists into adulthood despite excellent seizure control on medication. Answer: Juvenile myoclonic epilepsy.'},\n{id:38,stem:'Which of the following are clinical features of Parkinson\\'s disease?\\nI. Reduced eye blinking\\nII. Drooling of saliva\\nIII. Soft voice\\nIV. Macrographia\\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:'Parkinson\\'s disease features: REDUCED EYE BLINKING \u2714 \u2014 reduced blink rate (normal ~15\u201320\/min; PD ~5\u201310\/min); mask-like facies. DROOLING OF SALIVA \u2714 \u2014 sialorrhoea; not from increased production but from IMPAIRED SWALLOWING (dysphagia, reduced automatic swallowing frequency). SOFT VOICE (HYPOPHONIA) \u2714 \u2014 reduced vocal volume; monotone speech; dysarthria. MACROGRAPHIA \u2717 \u2014 FALSE. PD causes MICROGRAPHIA (small, cramped handwriting) \u2014 a classic early sign; writing becomes progressively smaller. Macrographia (large writing) is NOT a PD feature. Correct: I, II, III. Answer: I, II and III.'},\n{id:39,stem:'A 35-year-old female presents with easy fatigability. Investigations show that Hb is 6 g%; Red cell morphology is normocytic normochromic; and reticulocyte production index is 5\u00b75. Which one of the following conditions favours this abnormality?',correct:'Intravascular hemolysis',options:['Iron deficiency anemia','Sideroblastic anemia','Folate deficiency','Intravascular hemolysis'],exp:'Interpretation: Normocytic normochromic anaemia + RETICULOCYTE PRODUCTION INDEX (RPI) = 5.5 (MARKEDLY ELEVATED, normal <2). High RPI = hyperproliferative anaemia = adequate bone marrow response = peripheral destruction or acute blood loss. With normocytic morphology and very high RPI = HAEMOLYTIC ANAEMIA. INTRAVASCULAR HAEMOLYSIS \u2714 \u2014 intravascular destruction of RBCs \u2192 release of Hb into plasma \u2192 haemoglobinaemia, haemoglobinuria; brisk reticulocyte response (RPI >3); normocytic normochromic (or slight macrocytosis due to reticulocytes). Iron deficiency: microcytic hypochromic, low reticulocytes. Sideroblastic: microcytic\/dimorphic. Folate deficiency: macrocytic, megaloblastic. Answer: Intravascular hemolysis.'},\n{id:40,stem:'A 46-year-old lady on vegan diet for a decade presents with tingling and numbness in lower limbs for two months and a history of swaying while walking through narrow corridors. Which one of the following blood tests is advisable for diagnosis in this patient?',correct:'Vitamin B12 levels',options:['Serum protein electrophoresis','Anti-gliadin antibodies','Vitamin 25(OH) D level','Vitamin B12 levels'],exp:'Clinical diagnosis: SUBACUTE COMBINED DEGENERATION (SCD) of the spinal cord due to VITAMIN B12 DEFICIENCY. VEGAN diet (decade) \u2714 \u2014 no animal products \u2192 B12 deficiency (B12 found only in animal foods). SYMPTOMS: tingling\/numbness (peripheral neuropathy) + gait ataxia (posterior column degeneration causing loss of proprioception \u2192 positive Romberg, difficulty in narrow corridors = sensory ataxia). SCD affects: posterior columns (vibration, proprioception) + lateral corticospinal tracts \u2192 combined picture. VITAMIN B12 LEVELS \u2714 \u2014 first investigation; if low (<200 pg\/mL), confirm with methylmalonic acid + homocysteine levels. Vitamin D: similar population at risk but causes bone pain, NOT neuropathy\/ataxia. Anti-gliadin: coeliac (diarrhoea). 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Submitting in 10 Submit Now Combined Medical Services Examination 2025Paper I \u00b7 Part A General Medicine (Q1 \u2013 Q40) Questions 1 \u2013 40 +1 correct \u00b7 \u2212\u2153 wrong \u23f1 Start Timed Mode Scoring: +1 for correct \u00b7 \u22120.33 for wrong… <\/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-36831","post","type-post","status-publish","format-standard","hentry","category-cms","category-general-medicine"],"yoast_head":"\n<title>CMS 2025 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\/15\/cms-2025-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 2025 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2025 Paper I \u2013 Part A (Q1\u2013Q40) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0.00 \/ 40 Time's Up! 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