CMS 2019 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#cms19p1a*,#cms19p1a *::before,#cms19p1a *::after{box-sizing:border-box;margin:0;padding:0}\n#cms19p1a{--ter:#C0603A;--tp:#fdf1ec;--teal:#2A7A6F;--tl:#3da394;--tlp:#eaf4f3;--ink:#1a1a1a;--im:#444;--is:#777;--ln:#e0d8d4;--bg:#fdfaf8;--wh:#fff;--cb:#43a047;--cbg:#eaf7ef;--wb:#e53935;--wbg:#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#cms19p1a .sn{height:1px}\n#cms19p1a .sb{position:fixed;top:0;left:0;right:0;z-index:99999;background:var(--wh);border-bottom:2px solid var(--ln);border-left:4px solid var(--ter);box-shadow:0 2px 12px rgba(0,0,0,.11);opacity:0;pointer-events:none;transform:translateY(-110%);transition:opacity .22s,transform 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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#cms19p1a .rb:hover{background:var(--teal);color:var(--wh)}\n@media(max-width:480px){#cms19p1a .hd h1{font-size:1.15rem}#cms19p1a .qt{font-size:.88rem}#cms19p1a .ox{font-size:.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms19p1a\">\n<div class=\"sn\" id=\"cms19p1a-sn\"><\/div>\n<div class=\"sb\" id=\"cms19p1a-sb\">\n <div class=\"sr\">\n <div class=\"ti\" id=\"cms19p1a-ti\">\u23f1 <strong id=\"cms19p1a-td\">40:00<\/strong><\/div>\n <div class=\"si\">\u2705 <strong id=\"cms19p1a-sc\">0<\/strong><\/div>\n <div class=\"si\">\u274c <strong id=\"cms19p1a-sw\">0<\/strong><\/div>\n <div class=\"si\">\u23f3 <strong id=\"cms19p1a-sr\">40<\/strong> left<\/div>\n <div class=\"ss\"><\/div>\n <div class=\"si\">Net <strong id=\"cms19p1a-sn\">0<\/strong> \/ <strong id=\"cms19p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"sp\"><div class=\"sf\" id=\"cms19p1a-sf\"><\/div><\/div>\n<\/div>\n<div class=\"gr\" id=\"cms19p1a-gr\">\n <div class=\"gb\"><h3>Time's Up!<\/h3><p>Submitting in<\/p><div class=\"gc\" id=\"cms19p1a-gc\">10<\/div><button class=\"gn\" id=\"cms19p1a-gn\">Submit Now<\/button><\/div>\n<\/div>\n<div class=\"hd\">\n <h1>Combined Medical Services Examination 2019<br>Paper I \u00b7 Part A<\/h1>\n <p>Cardiology \u00b7 Respiratory \u00b7 Neurology \u00b7 Gastroenterology \u00b7 Haematology \u00b7 Endocrinology<\/p>\n <div class=\"mt\">\n <span class=\"bd\">Questions 1 \u2013 40<\/span>\n <span class=\"bd\">Options reshuffled<\/span>\n <button class=\"tb\" id=\"cms19p1a-tb\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"bd2\">\n <div id=\"cms19p1a-qs\"><\/div>\n <div class=\"sw\"><button class=\"bt\" id=\"cms19p1a-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms19p1a-sc-box\">\n <div class=\"rg\" id=\"cms19p1a-rg\"><div class=\"ri\"><span class=\"rp\" id=\"cms19p1a-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms19p1a-nl\"><\/div>\n <div class=\"vd\" id=\"cms19p1a-vd\"><\/div>\n <div class=\"bs\"><span class=\"bn bc\" id=\"cms19p1a-bc\"><\/span><span class=\"bn bw\" id=\"cms19p1a-bw\"><\/span><span class=\"bn bk\" id=\"cms19p1a-bk\"><\/span><\/div>\n <button class=\"rb\" id=\"cms19p1a-rb\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms19p1a',TOTAL=40,MAX=160,TSECS=2400,GSECS=10;\nvar QS=[\n{id:1,stem:'Austin Flint Murmur occurs in:',correct:'Severe Aortic Regurgitation',options:['Severe Mitral Stenosis','Severe Mitral Regurgitation','Severe Aortic Regurgitation','Severe Aortic Stenosis'],exp:'Austin Flint murmur: a low-pitched, mid-diastolic (or presystolic) rumbling murmur heard at the apex in SEVERE AORTIC REGURGITATION (AR). Mechanism: the regurgitant jet from the aortic valve hits the anterior leaflet of the mitral valve, causing it to partially close \u2192 functional mitral stenosis \u2192 turbulent flow across the mitral valve. It mimics mitral stenosis but has no opening snap, normal S1, and no signs of mitral valve disease. Key distinguishing feature: disappears\/improves with treatment of AR. Austin Flint = AR (not mitral valve disease). Answer: Severe Aortic Regurgitation.'},\n{id:2,stem:'Which amongst the following should be considered in a patient with acute chest pain and ST segment elevation in the precordial leads?\\n1. Acute myocardial infarction\\n2. Acute hyperkalemia\\n3. Pericarditis\\n4. Hypocalcemia\\n5. Oesophagitis\\n6. Pneumothorax\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1, 2 and 3','1, 3 and 4','1, 4 and 5','2, 3 and 6'],exp:'ST elevation in precordial leads \u2014 differential diagnoses: STEMI \u2714 (acute MI \u2014 convex\/tombstone ST elevation, reciprocal changes). Acute hyperkalemia \u2714 \u2014 peaked T waves in early hyperkalaemia, then widening QRS; severe hyperkalemia can cause ST elevation (sine wave). Pericarditis \u2714 \u2014 saddle-shaped diffuse ST elevation, PR depression in most leads. Hypocalcaemia: causes PROLONGED QT interval (not ST elevation). Oesophagitis: can cause chest pain but no ST elevation. Pneumothorax: may cause ECG changes (right heart strain, reduced voltage) but NOT ST elevation in precordial leads typically. Statements 1, 2 and 3 are correct causes of ST elevation. Answer: 1, 2 and 3.'},\n{id:3,stem:'Which amongst the following is the most powerful independent risk factor for atherosclerosis?',correct:'Hypertension',options:['Age','Hypertension','Gender','Physical Activity'],exp:'Atherosclerosis risk factors \u2014 major independent risk factors: Hypertension \u2714, Hyperlipidaemia (elevated LDL), Smoking, Diabetes mellitus, Family history (premature CAD), Age. Among these, HYPERTENSION is consistently identified as the MOST POWERFUL independent risk factor for atherosclerosis and cardiovascular disease in epidemiological studies. It directly damages endothelium (shear stress, turbulent flow), promotes LDL oxidation, smooth muscle proliferation, and plaque formation. While age is a strong risk factor, it is not modifiable and not as powerful as hypertension in direct causal terms. Physical activity is protective. Gender (male sex) is a risk factor but not the most powerful. Answer: Hypertension.'},\n{id:4,stem:'In which of the following SA node dysfunction conditions, permanent pacing may NOT be required?\\n1. Beta blocker drugs\\n2. Narcotic drugs\\n3. Iatrogenic \u2013 Post RT\/Surgery\\n4. Hypothyroidism\\n5. Sick sinus syndrome\\n6. Raised Intracranial tension\\nSelect the correct answer:',correct:'1, 2, 4 and 6',options:['1, 2, 3 and 4','1, 2, 4 and 5','1, 2, 4 and 6','3, 5 and 6'],exp:'Permanent pacing NOT required when SA node dysfunction is REVERSIBLE\/TREATABLE: Beta blocker drugs \u2714 \u2014 drug-induced bradycardia; stop the drug \u2192 normalises. Narcotic drugs \u2714 \u2014 drug-induced; remove\/antagonise the drug. Hypothyroidism \u2714 \u2014 treat with thyroxine \u2192 SA node function normalises. Raised Intracranial tension \u2714 \u2014 Cushing\\'s reflex causes bradycardia; treat the ICP rise. PERMANENT PACING IS REQUIRED FOR: Sick sinus syndrome (intrinsic SA node disease) \u2714 \u2014 permanent structural dysfunction. Post RT\/Surgery iatrogenic damage \u2714 \u2014 irreversible structural damage to SA node. Reversible causes (drugs, metabolic, autonomic) do NOT need permanent pacing \u2014 treat the underlying cause. Irreversible causes (SSS, post-surgical\/RT) require permanent pacing. Answer: 1, 2, 4 and 6.'},\n{id:5,stem:'Kartagener syndrome has the following features EXCEPT:',correct:'Autosomal Dominant',options:['Recurrent Sinusitis','Transposition of Viscera','Autosomal Dominant','Bronchiectasis'],exp:'Kartagener Syndrome (Primary Ciliary Dyskinesia + situs inversus): Features: Bronchiectasis \u2714 (recurrent pulmonary infections from impaired mucociliary clearance), Recurrent Sinusitis \u2714 (same mechanism \u2014 immotile cilia in sinuses), Situs inversus \/ Transposition of viscera \u2714 (dextrocardia + situs inversus \u2014 visceral asymmetry during embryogenesis requires functional cilia; absent ciliary motion causes random lateralisation \u2192 50% get situs inversus), Male infertility (immotile sperm). INHERITANCE: AUTOSOMAL RECESSIVE \u2014 NOT autosomal dominant. Mutations in DNAI1, DNAH5, and other dynein arm genes. \"Autosomal dominant\" is FALSE. Answer: Autosomal Dominant \u2014 the EXCEPT.'},\n{id:6,stem:'Which of the following pulmonary function set is characteristic of COPD?',correct:'FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2191 DLCO Normal',options:['FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2191 DLCO Normal','FEV1\/FVC < 70% ; FEV1 \u2191 ; FVC \u2193 ; TLC \u2193 DLCO \u2193','FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2191 ; TLC \u2191 DLCO \u2191','FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2193 DLCO \u2193'],exp:'COPD (chronic obstructive) PFTs: FEV1\/FVC <70% \u2714 (obstructive pattern \u2014 hallmark). FEV1 \u2193 (airflow obstruction). FVC: typically decreased (air trapping) but less than FEV1 reduction. TLC \u2191 (hyperinflation \u2014 air trapping, barrel chest). RV \u2191, FRC \u2191 (gas trapping). DLCO: Normal in chronic bronchitis (airways disease); DECREASED in emphysema (alveolar destruction reduces gas exchange surface). The option showing TLC \u2191 and DLCO Normal best represents chronic bronchitis-predominant COPD. Note: in emphysema, DLCO would be reduced. For COPD as a category (predominantly chronic bronchitis\/mild emphysema): FEV1\u2193, FVC\u2193, TLC\u2191, DLCO normal. Answer: FEV1\/FVC <70%; FEV1\u2193; FVC\u2193; TLC\u2191; DLCO Normal.'},\n{id:7,stem:'Which of the following drugs causes dry cough as a side effect?',correct:'Ramipril',options:['Fluconazole','Ramipril','Cefixime','Atenolol'],exp:'DRY COUGH is a well-recognised side effect of ACE INHIBITORS \u2014 RAMIPRIL \u2714 (and all other ACE inhibitors: enalapril, lisinopril, captopril, etc.). Mechanism: ACE inhibitors block the degradation of bradykinin and substance P in the pulmonary vasculature \u2192 accumulation of these kinins \u2192 irritation of airway sensory nerve fibres (C-fibres) \u2192 persistent dry, non-productive cough. Incidence: 5\u201320% of patients (more common in Asian populations \u2014 up to 40%). Management: switch to ARB (angiotensin receptor blocker \u2014 e.g., losartan) which does not inhibit bradykinin degradation. Fluconazole: antifungal \u2014 no cough. Cefixime: cephalosporin \u2014 no cough. Atenolol: beta-blocker \u2014 can cause bronchospasm (wheeze) in asthmatics, not dry cough. Answer: Ramipril.'},\n{id:8,stem:'For Acid Fast Bacilli (AFB) to be detected in sputum by direct microscopy, the bacillary burden in sputum typically is:',correct:'5,000\u201310,000 organisms',options:['500\u20131,000 organisms','5,000\u201310,000 organisms','10,000\u201320,000 organisms','Any number of organisms'],exp:'AFB direct smear microscopy detection threshold: Ziehl-Neelsen or fluorescent (auramine-rhodamine) staining of sputum smears requires a MINIMUM BACILLARY BURDEN of approximately 5,000\u201310,000 organisms per mL of sputum to yield a positive result. Below this threshold, smear is typically negative even when culture is positive. This explains why: Smear-negative\/culture-positive cases exist (paucibacillary disease). Sensitivity of smear microscopy is 40\u201370% (depending on technique). Multiple sputum samples improve yield. Culture detects as few as 10\u2013100 organisms\/mL. The 5,000\u201310,000 organisms\/mL threshold is the standard quoted in standard texts (Park\\'s, Harrison\\'s). Answer: 5,000\u201310,000 organisms.'},\n{id:9,stem:'The pleural fluid is considered as empyema if following is present in it:',correct:'All of these',options:['Fluid glucose < 60 mg\/dl','Lactate Dehydrogenase (LDH) of more than 1000 U\/L','Fluid pH of less than 7.0','All of these'],exp:'EMPYEMA THORACIS \u2014 diagnostic criteria for complex\/frank empyema (Light\\'s criteria for complicated parapneumonic effusion\/empyema): Pleural fluid pH <7.0 \u2714 (frank empyema; <7.2 = complicated requiring drainage). Pleural fluid glucose <60 mg\/dL \u2714 (bacterial consumption of glucose). Pleural fluid LDH >1000 U\/L \u2714 (intense inflammatory activity). Grossly purulent fluid (frank pus) = empyema by definition. All three biochemical criteria together are consistent with empyema and indicate the need for chest tube drainage. Any one criterion alone suggests complicated parapneumonic effusion; multiple criteria together = frank empyema. Answer: All of these.'},\n{id:10,stem:'Airway secretions contain all of the following antimicrobial peptides EXCEPT:',correct:'Histidine',options:['Defensins','Immunoglobulin A (IgA)','Lysozyme','Histidine'],exp:'Airway innate immune antimicrobial defence \u2014 constituents of airway surface liquid (ASL): Defensins \u2714 \u2014 alpha and beta defensins; cationic peptides disrupting microbial membranes; secreted by airway epithelium and neutrophils. Secretory IgA \u2714 \u2014 major immunoglobulin of mucosal secretions; neutralises pathogens; produced by submucosal plasma cells and transported across epithelium as secretory IgA. Lysozyme \u2714 \u2014 enzyme cleaving bacterial peptidoglycan (NAM-NAG bonds); abundant in nasal\/airway secretions; from serous cells of submucosal glands. Also: lactoferrin, surfactant proteins (SP-A, SP-D), SLPI (secretory leukocyte protease inhibitor), cathelicidins. HISTIDINE: an amino acid \u2014 not a recognised antimicrobial peptide or immune effector in airway secretions. Histatin (related to histidine) is found in saliva but not a standard airway antimicrobial. Answer: Histidine.'},\n{id:11,stem:'The respiratory motor neuron associated with origin of respiratory cycle is located in:',correct:'Ventral Medulla oblongata',options:['Pons','Posterior Medulla oblongata','Ventral Medulla oblongata','Mid brain'],exp:'Respiratory rhythm generation \u2014 central pattern generator: The primary rhythm-generating centre for breathing is the PRE-B\u00d6TZINGER COMPLEX located in the VENTRAL MEDULLA OBLONGATA (specifically the ventral respiratory group \u2014 VRG). It contains pacemaker neurons that generate the basic inspiratory rhythm. Ventral respiratory group (VRG): expiratory neurons (B\u00f6tzinger complex) and inspiratory neurons (pre-B\u00f6tzinger) in the ventromedial medulla. Dorsal respiratory group (DRG): in the posterior\/dorsal medulla (nucleus tractus solitarius) \u2014 integrates afferent input from chemoreceptors and lung stretch receptors. Pneumotaxic centre (pons): modulates rhythm from the medulla. Apneustic centre (lower pons): prolongs inspiration. The ORIGIN of the respiratory cycle = VENTRAL MEDULLA. Answer: Ventral Medulla oblongata.'},\n{id:12,stem:'Which of the above constitute significant or clinically important weight loss?\\n1. 4.5 kg over 6-12 months\\n2. 10 kg over 6-12 months\\n3. More than 5% over 6-12 months\\n4. More than 10% over 6-12 months',correct:'2 and 4',options:['1 and 3','1 and 4','2 and 3','2 and 4'],exp:'Clinically significant weight loss definition: SIGNIFICANT (clinically important, warrants investigation) weight loss is defined as: >10 kg over 6\u201312 months \u2714 (absolute weight loss). OR >10% of body weight over 6\u201312 months \u2714 (proportional loss). Some sources use >5% as a threshold for \"meaningful\" but 10% is the more commonly cited threshold for \"significant\" requiring investigation for malignancy, chronic illness, etc. 4.5 kg or 5% may be meaningful in obese individuals but are not the standard thresholds for \"significant\" weight loss in clinical\/UPSC exam context. The classic teaching: significant = >10 kg or >10% over 6\u201312 months. Answer: 2 and 4.'},\n{id:13,stem:'Which of the following Ascitic Fluid analysis is most compatible with a diagnosis of Ascites secondary to portal hypertension?',correct:'SAAG > 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl',options:['SAAG < 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl','SAAG < 1.1 g\/dl ; Ascitic Fluid Protein > 2.5 g\/dl','SAAG > 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl','SAAG > 1.1 g\/dl ; Ascitic Fluid Protein > 2.5 g\/dl'],exp:'SAAG (Serum-Ascites Albumin Gradient) = serum albumin \u2013 ascitic fluid albumin. SAAG \u22651.1 g\/dL \u2192 portal hypertension (97% accuracy). SAAG <1.1 g\/dL \u2192 non-portal hypertension (peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome). For LIVER CIRRHOSIS (most common cause of portal hypertension ascites): SAAG >1.1 \u2714 (portal hypertension). Ascitic fluid protein <2.5 g\/dL \u2714 \u2014 cirrhosis causes low-protein ascites (liver makes less albumin; sinusoidal hypertension \u2192 transudative pattern). Contrast: cardiac failure = SAAG >1.1 but protein >2.5 g\/dL (cardiac ascites is high-protein). Cirrhosis = SAAG >1.1 + low protein (<2.5). Answer: SAAG >1.1 g\/dL; Ascitic Fluid Protein <2.5 g\/dL.'},\n{id:14,stem:'All are the causes of Interstitial lung disease EXCEPT:',correct:'Bronchial Asthma',options:['Idiopathic Pulmonary Fibrosis','Granulomatosis with Polyangiitis','Sarcoidosis','Bronchial Asthma'],exp:'Interstitial Lung Diseases (ILD) \u2014 conditions involving the lung interstitium (alveolar walls, peribronchiolar tissue, connective tissue): ILD causes: Idiopathic Pulmonary Fibrosis (IPF) \u2714, Sarcoidosis \u2714, Granulomatosis with Polyangiitis (GPA\/Wegener\\'s) \u2714, Connective tissue diseases (RA, SLE, SSc), Hypersensitivity pneumonitis, Drug-induced (amiodarone, methotrexate, nitrofurantoin), COP, DIP, NSIP, LIP. BRONCHIAL ASTHMA: an obstructive airway disease \u2014 primarily affects the AIRWAYS (bronchi and bronchioles) with reversible airflow obstruction, not the lung interstitium. Asthma is NOT an ILD. Answer: Bronchial Asthma \u2014 EXCEPT.'},\n{id:15,stem:'The rhythmic activity recorded on scalp by EEG in a normal awake adult lying quietly with eyes closed is:',correct:'8 to 13 Hz \u2013 Alpha rhythm',options:['Less than 4Hz \u2013 Delta rhythm','4 to 7 Hz \u2013 Theta rhythm','8 to 13 Hz \u2013 Alpha rhythm','More than 14 Hz \u2013 Beta rhythm'],exp:'EEG frequency bands and states: Delta (<4 Hz): deep sleep (Stage N3\/slow-wave sleep), coma, encephalopathy. Theta (4\u20137 Hz): light sleep, drowsiness, meditation; also seen in some areas normally. ALPHA (8\u201313 Hz) \u2714: NORMAL AWAKE ADULT at rest with EYES CLOSED \u2014 the dominant rhythm over the occipital regions. Disappears (blocks) when eyes open or during mental concentration (alpha block\/alpha attenuation). Beta (>13\u201314 Hz): active thinking, anxious states, eyes open, benzodiazepine administration. Gamma (>30 Hz): sensory processing, cognitive activity. Key fact: the normal waking EEG with eyes closed = ALPHA rhythm (8\u201313 Hz) predominantly in posterior (occipital) leads. Answer: 8\u201313 Hz \u2013 Alpha rhythm.'},\n{id:16,stem:'Transient Monocular blindness may be due to small platelet emboli that occludes:',correct:'Ophthalmic artery',options:['Posterior Cerebellar artery','Posterior Cerebral artery','Ophthalmic artery','Vertebral artery'],exp:'TRANSIENT MONOCULAR BLINDNESS (Amaurosis Fugax): sudden, brief (seconds to minutes), painless loss of vision in ONE eye \u2014 \"like a curtain coming down.\" Mechanism: platelet-fibrin emboli (from carotid artery atherosclerotic plaques, cardiac emboli) travel to the OPHTHALMIC ARTERY (first branch of internal carotid artery) \u2192 occlusion of the central retinal artery or its branches \u2192 transient retinal ischaemia. The ophthalmic artery supplies the retina via the central retinal artery. Clinical importance: a TIA warning sign; requires urgent carotid imaging (US\/CTA) and antiplatelet therapy. Posterior cerebral artery: binocular visual field defects (homonymous hemianopia). Posterior cerebellar, vertebral: brainstem\/cerebellar symptoms. Answer: Ophthalmic artery.'},\n{id:17,stem:'The phenomenon of sparing of macular vision is due to collateral circulation between:',correct:'middle and posterior cerebral artery',options:['middle and posterior cerebral artery','anterior and middle cerebral artery','anterior and posterior cerebral artery','anterior, middle and posterior cerebral artery'],exp:'MACULAR SPARING in occipital lobe lesions: The occipital cortex (primary visual cortex, V1) is supplied by the POSTERIOR CEREBRAL ARTERY (PCA). The occipital pole (representing the macula\/central vision) receives COLLATERAL BLOOD SUPPLY from the MIDDLE CEREBRAL ARTERY (MCA) via anastomoses at the occipital tip. When the PCA is occluded (e.g., in PCA territory stroke): the peripheral visual cortex (representing peripheral vision) is infarcted. The macular cortex (occipital pole) survives due to MCA collaterals \u2192 MACULAR VISION IS SPARED. Result: contralateral homonymous hemianopia with MACULAR SPARING \u2014 the central (foveal\/macular) vision is preserved. Answer: Middle and posterior cerebral artery.'},\n{id:18,stem:'Characteristic features of Horner\\'s Syndrome are:',correct:'partial ptosis, enophthalmos, constricted pupil, decreased sweating',options:['partial ptosis, enophthalmos, constricted pupil, decreased sweating','partial ptosis, exophthalmos, constricted pupil, decreased sweating','partial ptosis, enophthalmos, dilated pupil, decreased sweating','partial ptosis, enophthalmos, constricted pupil, increased sweating'],exp:'HORNER\\'S SYNDROME (oculosympathetic palsy) \u2014 interruption of the sympathetic pathway to the eye (hypothalamus \u2192 ciliospinal centre of Budge \u2192 superior cervical ganglion \u2192 eye): Partial (incomplete) ptosis \u2714 \u2014 loss of sympathetic tone to Muller\\'s muscle (superior tarsal muscle); upper lid drops slightly, lower lid rises (reverse ptosis \u2192 narrowed palpebral fissure). MIOSIS (constricted pupil) \u2714 \u2014 loss of sympathetic dilator pupillae \u2192 parasympathetic sphincter pupillae unopposed. ENOPHTHALMOS \u2714 \u2014 apparent (not true) sinking of the eyeball due to narrowed palpebral fissure; actually pseudo-enophthalmos. ANHIDROSIS (decreased sweating) \u2714 \u2014 on the ipsilateral face (if lesion at or proximal to the superior cervical ganglion). Also: loss of ciliospinal reflex. Answer: Partial ptosis, enophthalmos, constricted pupil, decreased sweating.'},\n{id:19,stem:'All of the following statements are true EXCEPT:',correct:'Spinal cord ends at lower level of 5th lumbar vertebrae',options:['Dorsal column fibres synapse at the cuneate and gracile nuclei','Pain and temperature sensations are carried by lateral spinothalamic tract','Spinal cord ends at lower level of 5th lumbar vertebrae','Dorsal spinocerebellar tract carries fibres from the same side of the body'],exp:'Spinal cord anatomy statements: Dorsal column fibres (posterior columns \u2014 fine touch, proprioception, vibration) synapse at cuneate (upper limb \u2014 from T6 upward, in fasciculus cuneatus) and gracile nuclei (lower limb \u2014 below T6, in fasciculus gracilis) in the medulla \u2714 TRUE. Pain and temperature \u2192 lateral spinothalamic tract \u2714 TRUE (fibres cross within 1\u20132 segments in the anterior commissure then ascend). Dorsal spinocerebellar tract: carries IPSILATERAL proprioceptive information from the same side (uncrossed) to the ipsilateral cerebellum \u2714 TRUE. SPINAL CORD ENDS: at the lower border of L1 or upper border of L2 (conus medullaris) in adults \u2014 NOT at L5. In neonates it ends slightly lower (~L3). \"Lower level of 5th lumbar vertebrae\" is FALSE. Answer: Spinal cord ends at lower level of 5th lumbar \u2014 EXCEPT.'},\n{id:20,stem:'The following conditions usually present with proximal muscle weakness, EXCEPT:',correct:'Myotonia dystrophica',options:['Facio-scapulo-humeral dystrophy','Myotonia dystrophica','Duchenne\\'s muscular dystrophy','Becker muscular dystrophy'],exp:'Proximal muscle weakness (pelvic and shoulder girdle muscles): Duchenne\\'s MD \u2714 PROXIMAL \u2014 hip extensors, quadriceps, shoulder girdle. Becker MD \u2714 PROXIMAL \u2014 same distribution as DMD but milder. Facioscapulohumeral (FSH) dystrophy \u2714 PROXIMAL \u2014 face, shoulder girdle (scapular winging, biceps, triceps); predominantly upper limb proximal + facial. MYOTONIC DYSTROPHY (Myotonia dystrophica\/DM1): DISTAL muscle weakness \u2014 distal limbs (hand intrinsics, foot dorsiflexors, facial and sternocleidomastoid muscles); myotonia (delayed relaxation after contraction). This is the exception \u2014 it presents with DISTAL weakness, unlike most muscular dystrophies which are proximal. Answer: Myotonia dystrophica \u2014 EXCEPT (presents with distal weakness).'},\n{id:21,stem:'Pel-Ebstein fever is seen in:',correct:'Hodgkin\\'s disease',options:['Hodgkin\\'s disease','Malaria','Kalazar','Typhoid fever'],exp:'PEL-EBSTEIN FEVER: a characteristic cyclical fever pattern where periods of high fever (several days to weeks) alternate with afebrile periods of similar duration, then recur. PATHOGNOMONIC of HODGKIN\\'S LYMPHOMA \u2014 seen in ~10\u201335% of patients; associated with cytokine release (IL-1, TNF) from Reed-Sternberg cells and reactive lymphocytes. The cycle repeats every 1\u20132 weeks. Historical note: named after Wilhelm Ebstein and Pieter Pel who described this fever pattern in Hodgkin\\'s disease. Other fever patterns: Malaria \u2014 quotidian (P. falciparum), tertian (P. vivax\/ovale), quartan (P. malariae). Kala-azar \u2014 twice-daily fever spikes. Typhoid \u2014 step-ladder pattern. Answer: Hodgkin\\'s disease.'},\n{id:22,stem:'All of the following are true regarding acute leukaemias, EXCEPT:',correct:'Auer rods suggest acute lymphocytic leukaemia',options:['Promyelocytic leukaemia may present with DIC','Gum hypertrophy is a feature of monocytic leukaemia','Translocation is a common chromosomal abnormality in acute myeloid leukaemia','Auer rods suggest acute lymphocytic leukaemia'],exp:'Acute leukaemia facts: APL (AML-M3) and DIC \u2714 TRUE \u2014 promyelocytic granules contain procoagulant material \u2192 DIC; treated with ATRA. Gum hypertrophy in monocytic (M4\/M5) AML \u2714 TRUE \u2014 monocytic cells infiltrate gingival tissue; characteristic feature. Translocations in AML \u2714 TRUE \u2014 t(15;17) in APL, t(8;21) in M2, inv(16) in M4Eo; translocations are very common. AUER RODS: these are crystallised lysosomal enzymes (myeloperoxidase-positive) appearing as needle-like pink cytoplasmic inclusions. They are found EXCLUSIVELY in MYELOID (AML) blasts \u2014 NEVER in lymphocytic leukaemia (ALL). Auer rods in blasts = AML (NOT ALL). \"Auer rods suggest ALL\" is FALSE. Answer: Auer rods suggest acute lymphocytic leukaemia \u2014 EXCEPT.'},\n{id:23,stem:'All of the following are clinical features of Polycystic Ovarian Syndrome EXCEPT:',correct:'Menorrhagia',options:['Menorrhagia','Hirsutism','Glucose intolerance','Infertility'],exp:'Polycystic Ovarian Syndrome (PCOS) \u2014 clinical features: Hirsutism \u2714 (androgen excess \u2192 male-pattern hair growth \u2014 upper lip, chin, chest, abdomen, thighs). Glucose intolerance \/ Insulin resistance \u2714 \u2014 ~50\u201370% of PCOS; associated with metabolic syndrome, Type 2 DM risk. Infertility \u2714 \u2014 oligo\/anovulation \u2192 difficulty conceiving; most common cause of anovulatory infertility. Acne, obesity (central), acanthosis nigricans. MENSTRUAL PATTERN in PCOS: OLIGOMENORRHOEA (infrequent, scanty periods) or AMENORRHOEA \u2014 NOT menorrhagia. The anovulatory cycles cause prolonged oestrogen exposure WITHOUT progesterone (no corpus luteum) \u2192 endometrial hyperplasia \u2192 irregular\/scanty bleeding or amenorrhoea. Menorrhagia (heavy periods) is NOT typical of PCOS. Answer: Menorrhagia \u2014 EXCEPT.'},\n{id:24,stem:'Clinical features of Turner syndrome include all EXCEPT:',correct:'Narrow carrying angle of Elbow',options:['Webbing of Neck','Narrow carrying angle of Elbow','Coarctation of Aorta','Short stature'],exp:'Turner Syndrome (45,X0) features: Short stature \u2714 (universal \u2014 absent pubertal growth spurt; height 143\u2013147 cm average). Webbing of neck \u2714 (pterygium colli \u2014 redundant neck skin; from fetal lymphoedema). Coarctation of Aorta \u2714 (cardiovascular defect \u2014 bicuspid aortic valve + coarctation in ~30\u201350%). Lymphoedema (hands and feet). Shield chest, widely spaced nipples. Primary amenorrhoea (gonadal dysgenesis). Low hairline, ears. Cubitus valgus: INCREASED carrying angle of the elbow (valgus = angled OUTWARD\/laterally) \u2014 NOT narrow. The INCREASED carrying angle (cubitus valgus) is a feature of Turner syndrome; a NARROW carrying angle is NOT. Answer: Narrow carrying angle \u2014 EXCEPT.'},\n{id:25,stem:'Pretibial myxedema is a clinical feature of:',correct:'Graves disease',options:['Hypothyroidism','Graves disease','Cushing disease','Conn syndrome'],exp:'PRETIBIAL MYXOEDEMA (localised\/thyroid dermopathy): non-pitting, indurated, skin thickening over the anterior tibia (shin) and dorsum of feet. Cause: glycosaminoglycan (hyaluronic acid) deposition in the dermis due to TSH receptor antibody (TRAb) stimulation of dermal fibroblasts. Associated EXCLUSIVELY with GRAVES\\' DISEASE (autoimmune hyperthyroidism) \u2014 seen in ~5% of Graves patients, almost always with exophthalmos. NOT a feature of primary hypothyroidism (which causes generalised myxoedema). NOT from Cushing or Conn disease. Paradoxically, pretibial myxoedema can persist even after treatment of hyperthyroidism. Answer: Graves disease.'},\n{id:26,stem:'Match the List I with List II:\\nA. Conn syndrome \u2014 1. Anosmia\\nB. Turner syndrome \u2014 2. Tetany\\nC. Kallman syndrome \u2014 3. Lymphoedema\\nD. Cushing syndrome \u2014 4. Avascular necrosis of hip',correct:'A-2 B-3 C-1 D-4',options:['A-4 B-1 C-3 D-2','A-2 B-3 C-1 D-4','A-2 B-1 C-3 D-4','A-4 B-3 C-1 D-2'],exp:'Matching: A. Conn syndrome (primary hyperaldosteronism) \u2192 2. Tetany \u2014 hypokalaemia causes metabolic alkalosis \u2192 reduced ionised calcium \u2192 tetany (Trousseau\/Chvostek signs). B. Turner syndrome (45,X0) \u2192 3. Lymphoedema \u2014 fetal lymphoedema causes webbed neck, puffy hands\/feet at birth; persistent lower limb lymphoedema. C. Kallmann syndrome (hypogonadotrophic hypogonadism + anosmia) \u2192 1. Anosmia \u2014 failure of GnRH neurons to migrate from olfactory bulb to hypothalamus during development \u2192 absent olfactory bulbs \u2192 anosmia + hypogonadism. D. Cushing syndrome \u2192 4. Avascular necrosis of hip \u2014 chronic glucocorticoid excess (endogenous or exogenous) causes osteonecrosis\/avascular necrosis of femoral head. Answer: A-2 B-3 C-1 D-4.'},\n{id:27,stem:'Which of the following is NOT a part of Koch\\'s postulates?',correct:'The organism may not be reisolated from the incubated diseased host',options:['The same organism must be present in every case of the disease','The organism must be isolated from the diseased host and grown in culture','The isolate must cause the disease when incubated','The organism may not be reisolated from the incubated diseased host'],exp:'Koch\\'s Postulates (4 criteria for establishing causation): (1) The microorganism must be found in all cases of the disease. (2) It must be isolated from the diseased host and grown in pure culture. (3) The cultured organism must cause disease when introduced into a healthy susceptible host. (4) The organism must be RE-ISOLATED from the experimentally diseased host and shown to be identical to the original. \"The organism may NOT be reisolated\" is the OPPOSITE of Koch\\'s 4th postulate \u2014 reisolation IS required. This statement contradicts Koch\\'s postulate #4. Answer: The organism may not be reisolated \u2014 NOT part of Koch\\'s postulates.'},\n{id:28,stem:'All of the following cause dementia EXCEPT:',correct:'Vitamin D toxicity',options:['Huntington\\'s disease','Alzheimer\\'s disease','Vitamin D toxicity','Thiamine deficiency'],exp:'Causes of dementia: Alzheimer\\'s disease \u2714 (most common; amyloid plaques + neurofibrillary tangles). Huntington\\'s disease \u2714 (subcortical dementia; chorea + personality change + dementia; CAG repeat expansion in HTT gene). Thiamine (B1) deficiency \u2714 \u2014 Wernicke-Korsakoff syndrome: Wernicke\\'s (acute \u2014 ophthalmoplegia, ataxia, encephalopathy) \u2192 Korsakoff\\'s (chronic \u2014 anterograde amnesia, confabulation = a form of dementia). Also: Vascular dementia, Lewy body dementia, FTD, B12 deficiency, hypothyroidism, HIV, prion disease, NPH. VITAMIN D TOXICITY (hypervitaminosis D): causes hypercalcaemia \u2192 renal stones, nephrocalcinosis, polyuria, weakness, nausea \u2014 but NOT dementia. Vitamin D toxicity does not cause cognitive impairment or dementia. Answer: Vitamin D toxicity \u2014 EXCEPT.'},\n{id:29,stem:'The therapeutic level of Digoxin in blood is:',correct:'1\u20132 ng\/ml',options:['1\u20132 ng\/ml','4\u20136 ng\/ml','6\u20138 ng\/ml','8\u201310 ng\/ml'],exp:'DIGOXIN therapeutic range: 0.5\u20132.0 ng\/mL (or 0.8\u20132.0 ng\/mL for heart failure; some sources say 0.5\u20130.9 ng\/mL is optimal for HF based on DIG trial). The standard quoted therapeutic range is 1\u20132 ng\/mL. Toxicity occurs above 2\u20132.5 ng\/mL. Digoxin toxicity signs: nausea, vomiting, visual disturbances (yellow-green halos \u2014 xanthopsia), bradycardia, heart block, ventricular arrhythmias. Narrow therapeutic index \u2014 monitoring serum levels is essential. Answer: 1\u20132 ng\/mL.'},\n{id:30,stem:'A 40-year old woman presents with sudden onset palpitations. An ECG done reveals narrow-QRS complex tachycardia. The most likely diagnosis is:',correct:'AV reentry tachycardia',options:['Ventricular tachycardia','Pre-excited tachycardia','Paroxysmal supraventricular tachycardia with aberrancy','AV reentry tachycardia'],exp:'NARROW QRS complex tachycardia (QRS <120 ms) = SUPRAVENTRICULAR ORIGIN (above the His bundle; normal ventricular conduction). Causes: AVNRT (AV nodal reentrant tachycardia \u2014 most common SVT), AVRT (AV reentrant tachycardia \u2014 via accessory pathway orthodromic \u2014 next most common), Atrial tachycardia, Atrial flutter with block, Sinus tachycardia. Ventricular tachycardia: WIDE QRS complex (>120 ms) \u2014 not narrow. Pre-excited tachycardia (WPW antidromic): WIDE QRS \u2014 not narrow. PSVT with aberrancy: WIDE QRS \u2014 not narrow. For this 40-year-old woman with NARROW QRS tachycardia \u2192 AVRT (AV reentry tachycardia via accessory pathway \u2014 orthodromic) or AVNRT. Among the options, AVRT is the specific correct answer. Answer: AV reentry tachycardia.'},\n{id:31,stem:'Which of the following statements are true about management of acute pulmonary oedema?\\n1. Put the patient in relaxed, supine position\\n2. Give high flow, high concentration oxygen\\n3. Administer Furosemide intravenously\\n4. No role of Nitrates\\nSelect the correct answer:',correct:'2 and 3',options:['1 and 2','2 and 3','3 and 4','1 and 4'],exp:'Acute pulmonary oedema (APO) management: POSITION: SIT the patient upright (HIGH FOWLER\\'S position, legs dangling) \u2014 NOT supine. Upright position reduces venous return to the heart (preload reduction) and relieves orthopnoea. Statement 1 (supine) is FALSE. HIGH FLOW OXYGEN \u2714 \u2014 100% O2 via non-rebreather mask; target SpO2 >94%; if refractory \u2192 NIV (CPAP\/BiPAP). Statement 2 TRUE. IV FUROSEMIDE \u2714 \u2014 loop diuretic; reduces preload (initial venodilatory effect within minutes, then diuresis); cornerstone of APO management. Statement 3 TRUE. NITRATES: HAVE A ROLE \u2014 sublingual\/IV nitroglycerine reduces preload (and afterload at high doses); highly effective in APO, especially hypertensive APO. Statement 4 is FALSE. Correct statements: 2 and 3. Answer: 2 and 3.'},\n{id:32,stem:'Which of the following does NOT cause prolongation of QT interval?',correct:'Hyperkalaemia',options:['Hypomagnesaemia','Hyperkalaemia','Erythromycin','Amiodarone'],exp:'QT prolongation causes: Electrolytes: Hypokalaemia \u2714, Hypomagnesaemia \u2714, Hypocalcaemia \u2714. Drugs: Amiodarone \u2714 (class III anti-arrhythmic), Erythromycin \u2714 (and other macrolides), Fluoroquinolones, Antifungals (azoles), Antipsychotics, Methadone, Sotalol, Haloperidol. Congenital: Long QT syndrome (Romano-Ward, Jervell-Lange-Nielsen). Hypothyroidism, myocarditis. HYPERKALAEMIA: does NOT prolong QT. Hyperkalaemia causes: peaked T waves \u2192 prolonged PR \u2192 wide QRS \u2192 sine wave pattern \u2192 VF\/asystole. QT interval may actually be SHORTENED in hyperkalaemia (accelerated repolarisation). Answer: Hyperkalaemia \u2014 does NOT prolong QT.'},\n{id:33,stem:'A 21-year young man presents with high grade fever, fleeting inflammation of knee and ankle joints, occasional palpitations, no history of antecedent sore throat, splenomegaly, and ECG showing prolonged PR interval. What is the most likely diagnosis in India?',correct:'Enteric fever',options:['Still disease','Enteric fever','Rheumatic fever','Reiter\\'s syndrome'],exp:'Clinical analysis: Young male, HIGH GRADE fever, FLEETING POLYARTHRITIS (knees, ankles), palpitations, PR prolongation on ECG, SPLENOMEGALY. Critical clue: NO antecedent SORE THROAT. This distinguishes from RHEUMATIC FEVER (which requires preceding Group A strep pharyngitis \u2014 Jones criteria). ENTERIC FEVER (Typhoid) in India: fever (step-ladder pattern, but can be high grade), relative bradycardia, splenomegaly (very common), PR prolongation (myocarditis \u2014 toxic carditis occurs in ~10% of typhoid), polyarthritis (reactive\/toxic arthritis \u2014 fleeting), rash (rose spots \u2014 uncommon in India). No streptococcal history. All features fit ENTERIC FEVER. Rheumatic fever requires documented preceding streptococcal pharyngitis. Still disease: JIA pattern in young adults. Reiter\\'s: urethritis + arthritis + conjunctivitis. Answer: Enteric fever.'},\n{id:34,stem:'A 50-year gentleman with Type-2 DM for 5 years presents with sudden onset dyspnoea at rest, orthopnoea, and prostration. Pulse is rapid, very weak. BP 100\/70 mmHg. Diffuse crepitations at lung bases. Most likely diagnosis:',correct:'Left heart failure',options:['Mitral stenosis with bacterial endocarditis','Right heart failure','Left heart failure','Constrictive pericarditis'],exp:'Clinical picture: Type 2 DM (high risk of coronary artery disease \u2192 ischaemic cardiomyopathy), sudden onset dyspnoea, ORTHOPNOEA (lying flat worsens breathlessness \u2014 pulmonary oedema in the supine position), diffuse BILATERAL BASAL CREPITATIONS (pulmonary oedema \u2014 fluid in alveoli), low BP + weak rapid pulse (cardiogenic shock\/decompensated heart failure). Orthopnoea + bilateral basal crepitations = LEFT HEART FAILURE (elevated left atrial pressure \u2192 pulmonary venous hypertension \u2192 pulmonary oedema). Right heart failure: peripheral oedema, raised JVP, hepatomegaly \u2014 no bilateral lung crepitations. Constrictive pericarditis: raised JVP, Kussmaul sign, no lung oedema. Answer: Left heart failure.'},\n{id:35,stem:'The \\'Y\\' descent in JVP waveform represents:',correct:'Atrial emptying',options:['Atrial relaxation','Atrial systole','Atrial emptying','Apical displacement of tricuspid valve'],exp:'JVP waveform components: a wave = Atrial systole (atrial contraction). c wave = tricuspid valve closure + carotid artery pulsation (small). x descent = Atrial RELAXATION (after atrial systole; systolic descent). v wave = Venous filling (atria fill while tricuspid is closed during ventricular systole). Y DESCENT = ATRIAL EMPTYING \u2714 \u2014 when the tricuspid valve opens at the start of diastole, the right atrium empties into the right ventricle \u2192 JVP falls = Y descent (diastolic descent). Absent\/blunted Y: pericardial tamponade (impaired ventricular filling). Steep\/prominent Y: constrictive pericarditis (rapid ventricular filling), tricuspid regurgitation. Answer: Atrial emptying.'},\n{id:36,stem:'While distinguishing a venous pulsation from the arterial pulsation in neck, which of the following is NOT correct?',correct:'Venous pulse has a single peak in each cardiac cycle',options:['The height of venous pulse varies with respiration','Abdominal pressure causes rise in venous pulse','Venous pulse has a single peak in each cardiac cycle','Venous pulse is not easily palpable'],exp:'Venous vs arterial neck pulsations: Height varies with respiration \u2714 TRUE \u2014 JVP rises on expiration, falls on inspiration (opposite to IVC in abdomen); posture also affects. Abdominal pressure rises venous pulse \u2714 TRUE \u2014 hepatojugular reflux (HJR): compressing the abdomen raises JVP; venous system is continuous. Venous pulse not easily palpable \u2714 TRUE \u2014 JVP is visible (a wave, v wave, x and y descents) but NOT palpable (low pressure); carotid artery IS palpable (high pressure). VENOUS PULSE HAS A SINGLE PEAK: FALSE \u2714 \u2014 JVP has TWO positive waves per cardiac cycle: a wave (atrial systole) and v wave (venous filling). The carotid\/arterial pulse has a single peak per cycle. \"Single peak\" applies to ARTERIAL pulse, not venous. Answer: Venous pulse has a single peak \u2014 NOT correct.'},\n{id:37,stem:'Which of the following does NOT cause pulmonary infiltrates with eosinophilia?',correct:'Cystic fibrosis',options:['Bronchial asthma','Postradiation pneumonitis','Eosinophilic granulomatosis with polyangiitis','Cystic fibrosis'],exp:'Pulmonary infiltrates with eosinophilia (PIE) syndrome: L\u00f6ffler\\'s syndrome (ascaris larvae migration). ABPA (Allergic bronchopulmonary aspergillosis) \u2014 in asthma\/CF patients, though ABPA itself causes PIE, not CF per se. Bronchial asthma \u2714 \u2014 associated with blood and tissue eosinophilia; ABPA complicating asthma causes PIE. Eosinophilic granulomatosis with polyangiitis (EGPA\/Churg-Strauss) \u2714 \u2014 asthma + eosinophilia + vasculitis + PIE. Drug reactions (nitrofurantoin, sulfonamides). Hypereosinophilic syndrome. CYSTIC FIBROSIS: a genetic disease (CFTR mutation) causing thick secretions, bronchiectasis, and recurrent bacterial infections. CF does NOT cause pulmonary eosinophilia (the infiltrates in CF are from mucus plugging and bacterial infection \u2014 neutrophilic, not eosinophilic). ABPA can complicate CF, but CF itself \u2260 PIE. Answer: Cystic fibrosis \u2014 does NOT cause PIE.'},\n{id:38,stem:'Total lung capacity is decreased in which one of the following conditions?',correct:'Pulmonary fibrosis',options:['Asthma','Chronic bronchitis','Pulmonary fibrosis','Emphysema'],exp:'Total Lung Capacity (TLC) changes: TLC INCREASED (air trapping\/hyperinflation): Asthma \u2714 (during attack \u2014 air trapping), Chronic bronchitis \u2714 (obstructive \u2014 TLC normal or slightly elevated), Emphysema \u2714 (significant hyperinflation \u2014 markedly elevated TLC). TLC DECREASED (restrictive pattern): PULMONARY FIBROSIS \u2714 \u2014 the fibrotic, stiff lungs cannot expand fully \u2192 reduced TLC, VC, FRC. All lung volumes are reduced. FEV1\/FVC ratio is NORMAL or INCREASED (restrictive pattern \u2014 both FEV1 and FVC reduced proportionally). Other restrictive causes: pleural effusion, pneumothorax, obesity, neuromuscular disease, chest wall deformity. Answer: Pulmonary fibrosis.'},\n{id:39,stem:'Which one of the following is the minimum spirometry criterion for diagnosis of bronchial asthma?',correct:'Increase in FEV1 \u2265 12% following administration of inhaled bronchodilators',options:['Decrease in FEV1 \u2265 20% after 6 minutes of exercise','Increase in FEV1 \u2265 12% following administration of inhaled bronchodilators','Increase in 500 ml of FEV1 after glucocorticoids inhalation','Less than 20% diurnal variation on more than 3 days a week on PEF diary'],exp:'GINA spirometry criteria for asthma diagnosis (bronchodilator reversibility test \u2014 most standard): Significant bronchodilator response = FEV1 increase of \u226512% AND \u2265200 mL from baseline after inhaled SABA (salbutamol 400 mcg). This is the minimum standard criterion for diagnosing asthma. Exercise challenge: FEV1 fall \u226510% (not 20%) or >15% is significant. PEF diurnal variation: >10\u201320% (if >20% = significant). Glucocorticoid trial: used when diagnosis uncertain. The MINIMUM STANDARD CRITERION in clinical practice = \u226512% FEV1 increase (+ \u2265200 mL absolute) post-bronchodilator. Answer: Increase in FEV1 \u226512% following inhaled bronchodilators.'},\n{id:40,stem:'Modified Blatchford score is used for the risk stratification of:',correct:'Upper gastrointestinal bleeding',options:['Pancreatitis','Sepsis','Upper gastrointestinal bleeding','Cholangitis'],exp:'GLASGOW-BLATCHFORD SCORE (GBS) \/ Modified Blatchford Score: a pre-endoscopy risk stratification tool for ACUTE UPPER GI BLEEDING (UGIB). Parameters: blood urea, haemoglobin, systolic BP, pulse, presence of melaena, syncope, hepatic disease, cardiac failure. Score 0 = very low risk (can manage outpatient); score >0 = needs endoscopy\/intervention. Predicts need for clinical intervention (blood transfusion, endoscopy, surgery). Pancreatitis: Ranson criteria, APACHE II, Balthazar CT severity index. Sepsis: SOFA, qSOFA, APACHE. Cholangitis: Tokyo guidelines. 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Submitting in 10 Submit Now Combined Medical Services Examination 2019Paper I \u00b7 Part A Cardiology \u00b7 Respiratory \u00b7 Neurology \u00b7 Gastroenterology \u00b7 Haematology \u00b7 Endocrinology Questions 1 \u2013 40 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0%score Your Result… <\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36816","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2019 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\/11\/cms-2019-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 2019 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2019 Paper I \u2013 Part A (Q1\u2013Q40) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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{"id":36816,"date":"2026-05-11T21:59:51","date_gmt":"2026-05-11T16:29:51","guid":{"rendered":"https:\/\/atsixty.com\/?p=36816"},"modified":"2026-05-11T22:00:12","modified_gmt":"2026-05-11T16:30:12","slug":"cms-2019-p1-part-a","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/11\/cms-2019-p1-part-a\/","title":{"rendered":"CMS 2019 P1 Part-A"},"content":{"rendered":"\n\n\n\n\n\n\n\nCMS 2019 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#cms19p1a*,#cms19p1a *::before,#cms19p1a *::after{box-sizing:border-box;margin:0;padding:0}\n#cms19p1a{--ter:#C0603A;--tp:#fdf1ec;--teal:#2A7A6F;--tl:#3da394;--tlp:#eaf4f3;--ink:#1a1a1a;--im:#444;--is:#777;--ln:#e0d8d4;--bg:#fdfaf8;--wh:#fff;--cb:#43a047;--cbg:#eaf7ef;--wb:#e53935;--wbg:#fdf0f0;--r:10px;font-family:'Source Serif 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id=\"cms19p1a-ti\">\u23f1 <strong id=\"cms19p1a-td\">40:00<\/strong><\/div>\n <div class=\"si\">\u2705 <strong id=\"cms19p1a-sc\">0<\/strong><\/div>\n <div class=\"si\">\u274c <strong id=\"cms19p1a-sw\">0<\/strong><\/div>\n <div class=\"si\">\u23f3 <strong id=\"cms19p1a-sr\">40<\/strong> left<\/div>\n <div class=\"ss\"><\/div>\n <div class=\"si\">Net <strong id=\"cms19p1a-sn\">0<\/strong> \/ <strong id=\"cms19p1a-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"sp\"><div class=\"sf\" id=\"cms19p1a-sf\"><\/div><\/div>\n<\/div>\n<div class=\"gr\" id=\"cms19p1a-gr\">\n <div class=\"gb\"><h3>Time's Up!<\/h3><p>Submitting in<\/p><div class=\"gc\" id=\"cms19p1a-gc\">10<\/div><button class=\"gn\" id=\"cms19p1a-gn\">Submit Now<\/button><\/div>\n<\/div>\n<div class=\"hd\">\n <h1>Combined Medical Services Examination 2019<br>Paper I \u00b7 Part A<\/h1>\n <p>Cardiology \u00b7 Respiratory \u00b7 Neurology \u00b7 Gastroenterology \u00b7 Haematology \u00b7 Endocrinology<\/p>\n <div class=\"mt\">\n <span class=\"bd\">Questions 1 \u2013 40<\/span>\n <span class=\"bd\">Options reshuffled<\/span>\n <button class=\"tb\" id=\"cms19p1a-tb\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"bd2\">\n <div id=\"cms19p1a-qs\"><\/div>\n <div class=\"sw\"><button class=\"bt\" id=\"cms19p1a-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms19p1a-sc-box\">\n <div class=\"rg\" id=\"cms19p1a-rg\"><div class=\"ri\"><span class=\"rp\" id=\"cms19p1a-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms19p1a-nl\"><\/div>\n <div class=\"vd\" id=\"cms19p1a-vd\"><\/div>\n <div class=\"bs\"><span class=\"bn bc\" id=\"cms19p1a-bc\"><\/span><span class=\"bn bw\" id=\"cms19p1a-bw\"><\/span><span class=\"bn bk\" id=\"cms19p1a-bk\"><\/span><\/div>\n <button class=\"rb\" id=\"cms19p1a-rb\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms19p1a',TOTAL=40,MAX=160,TSECS=2400,GSECS=10;\nvar QS=[\n{id:1,stem:'Austin Flint Murmur occurs in:',correct:'Severe Aortic Regurgitation',options:['Severe Mitral Stenosis','Severe Mitral Regurgitation','Severe Aortic Regurgitation','Severe Aortic Stenosis'],exp:'Austin Flint murmur: a low-pitched, mid-diastolic (or presystolic) rumbling murmur heard at the apex in SEVERE AORTIC REGURGITATION (AR). Mechanism: the regurgitant jet from the aortic valve hits the anterior leaflet of the mitral valve, causing it to partially close \u2192 functional mitral stenosis \u2192 turbulent flow across the mitral valve. It mimics mitral stenosis but has no opening snap, normal S1, and no signs of mitral valve disease. Key distinguishing feature: disappears\/improves with treatment of AR. Austin Flint = AR (not mitral valve disease). Answer: Severe Aortic Regurgitation.'},\n{id:2,stem:'Which amongst the following should be considered in a patient with acute chest pain and ST segment elevation in the precordial leads?\\n1. Acute myocardial infarction\\n2. Acute hyperkalemia\\n3. Pericarditis\\n4. Hypocalcemia\\n5. Oesophagitis\\n6. Pneumothorax\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1, 2 and 3','1, 3 and 4','1, 4 and 5','2, 3 and 6'],exp:'ST elevation in precordial leads \u2014 differential diagnoses: STEMI \u2714 (acute MI \u2014 convex\/tombstone ST elevation, reciprocal changes). Acute hyperkalemia \u2714 \u2014 peaked T waves in early hyperkalaemia, then widening QRS; severe hyperkalemia can cause ST elevation (sine wave). Pericarditis \u2714 \u2014 saddle-shaped diffuse ST elevation, PR depression in most leads. Hypocalcaemia: causes PROLONGED QT interval (not ST elevation). Oesophagitis: can cause chest pain but no ST elevation. Pneumothorax: may cause ECG changes (right heart strain, reduced voltage) but NOT ST elevation in precordial leads typically. Statements 1, 2 and 3 are correct causes of ST elevation. Answer: 1, 2 and 3.'},\n{id:3,stem:'Which amongst the following is the most powerful independent risk factor for atherosclerosis?',correct:'Hypertension',options:['Age','Hypertension','Gender','Physical Activity'],exp:'Atherosclerosis risk factors \u2014 major independent risk factors: Hypertension \u2714, Hyperlipidaemia (elevated LDL), Smoking, Diabetes mellitus, Family history (premature CAD), Age. Among these, HYPERTENSION is consistently identified as the MOST POWERFUL independent risk factor for atherosclerosis and cardiovascular disease in epidemiological studies. It directly damages endothelium (shear stress, turbulent flow), promotes LDL oxidation, smooth muscle proliferation, and plaque formation. While age is a strong risk factor, it is not modifiable and not as powerful as hypertension in direct causal terms. Physical activity is protective. Gender (male sex) is a risk factor but not the most powerful. Answer: Hypertension.'},\n{id:4,stem:'In which of the following SA node dysfunction conditions, permanent pacing may NOT be required?\\n1. Beta blocker drugs\\n2. Narcotic drugs\\n3. Iatrogenic \u2013 Post RT\/Surgery\\n4. Hypothyroidism\\n5. Sick sinus syndrome\\n6. Raised Intracranial tension\\nSelect the correct answer:',correct:'1, 2, 4 and 6',options:['1, 2, 3 and 4','1, 2, 4 and 5','1, 2, 4 and 6','3, 5 and 6'],exp:'Permanent pacing NOT required when SA node dysfunction is REVERSIBLE\/TREATABLE: Beta blocker drugs \u2714 \u2014 drug-induced bradycardia; stop the drug \u2192 normalises. Narcotic drugs \u2714 \u2014 drug-induced; remove\/antagonise the drug. Hypothyroidism \u2714 \u2014 treat with thyroxine \u2192 SA node function normalises. Raised Intracranial tension \u2714 \u2014 Cushing\\'s reflex causes bradycardia; treat the ICP rise. PERMANENT PACING IS REQUIRED FOR: Sick sinus syndrome (intrinsic SA node disease) \u2714 \u2014 permanent structural dysfunction. Post RT\/Surgery iatrogenic damage \u2714 \u2014 irreversible structural damage to SA node. Reversible causes (drugs, metabolic, autonomic) do NOT need permanent pacing \u2014 treat the underlying cause. Irreversible causes (SSS, post-surgical\/RT) require permanent pacing. Answer: 1, 2, 4 and 6.'},\n{id:5,stem:'Kartagener syndrome has the following features EXCEPT:',correct:'Autosomal Dominant',options:['Recurrent Sinusitis','Transposition of Viscera','Autosomal Dominant','Bronchiectasis'],exp:'Kartagener Syndrome (Primary Ciliary Dyskinesia + situs inversus): Features: Bronchiectasis \u2714 (recurrent pulmonary infections from impaired mucociliary clearance), Recurrent Sinusitis \u2714 (same mechanism \u2014 immotile cilia in sinuses), Situs inversus \/ Transposition of viscera \u2714 (dextrocardia + situs inversus \u2014 visceral asymmetry during embryogenesis requires functional cilia; absent ciliary motion causes random lateralisation \u2192 50% get situs inversus), Male infertility (immotile sperm). INHERITANCE: AUTOSOMAL RECESSIVE \u2014 NOT autosomal dominant. Mutations in DNAI1, DNAH5, and other dynein arm genes. \"Autosomal dominant\" is FALSE. Answer: Autosomal Dominant \u2014 the EXCEPT.'},\n{id:6,stem:'Which of the following pulmonary function set is characteristic of COPD?',correct:'FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2191 DLCO Normal',options:['FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2191 DLCO Normal','FEV1\/FVC < 70% ; FEV1 \u2191 ; FVC \u2193 ; TLC \u2193 DLCO \u2193','FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2191 ; TLC \u2191 DLCO \u2191','FEV1\/FVC < 70% ; FEV1 \u2193 ; FVC \u2193 ; TLC \u2193 DLCO \u2193'],exp:'COPD (chronic obstructive) PFTs: FEV1\/FVC <70% \u2714 (obstructive pattern \u2014 hallmark). FEV1 \u2193 (airflow obstruction). FVC: typically decreased (air trapping) but less than FEV1 reduction. TLC \u2191 (hyperinflation \u2014 air trapping, barrel chest). RV \u2191, FRC \u2191 (gas trapping). DLCO: Normal in chronic bronchitis (airways disease); DECREASED in emphysema (alveolar destruction reduces gas exchange surface). The option showing TLC \u2191 and DLCO Normal best represents chronic bronchitis-predominant COPD. Note: in emphysema, DLCO would be reduced. For COPD as a category (predominantly chronic bronchitis\/mild emphysema): FEV1\u2193, FVC\u2193, TLC\u2191, DLCO normal. Answer: FEV1\/FVC <70%; FEV1\u2193; FVC\u2193; TLC\u2191; DLCO Normal.'},\n{id:7,stem:'Which of the following drugs causes dry cough as a side effect?',correct:'Ramipril',options:['Fluconazole','Ramipril','Cefixime','Atenolol'],exp:'DRY COUGH is a well-recognised side effect of ACE INHIBITORS \u2014 RAMIPRIL \u2714 (and all other ACE inhibitors: enalapril, lisinopril, captopril, etc.). Mechanism: ACE inhibitors block the degradation of bradykinin and substance P in the pulmonary vasculature \u2192 accumulation of these kinins \u2192 irritation of airway sensory nerve fibres (C-fibres) \u2192 persistent dry, non-productive cough. Incidence: 5\u201320% of patients (more common in Asian populations \u2014 up to 40%). Management: switch to ARB (angiotensin receptor blocker \u2014 e.g., losartan) which does not inhibit bradykinin degradation. Fluconazole: antifungal \u2014 no cough. Cefixime: cephalosporin \u2014 no cough. Atenolol: beta-blocker \u2014 can cause bronchospasm (wheeze) in asthmatics, not dry cough. Answer: Ramipril.'},\n{id:8,stem:'For Acid Fast Bacilli (AFB) to be detected in sputum by direct microscopy, the bacillary burden in sputum typically is:',correct:'5,000\u201310,000 organisms',options:['500\u20131,000 organisms','5,000\u201310,000 organisms','10,000\u201320,000 organisms','Any number of organisms'],exp:'AFB direct smear microscopy detection threshold: Ziehl-Neelsen or fluorescent (auramine-rhodamine) staining of sputum smears requires a MINIMUM BACILLARY BURDEN of approximately 5,000\u201310,000 organisms per mL of sputum to yield a positive result. Below this threshold, smear is typically negative even when culture is positive. This explains why: Smear-negative\/culture-positive cases exist (paucibacillary disease). Sensitivity of smear microscopy is 40\u201370% (depending on technique). Multiple sputum samples improve yield. Culture detects as few as 10\u2013100 organisms\/mL. The 5,000\u201310,000 organisms\/mL threshold is the standard quoted in standard texts (Park\\'s, Harrison\\'s). Answer: 5,000\u201310,000 organisms.'},\n{id:9,stem:'The pleural fluid is considered as empyema if following is present in it:',correct:'All of these',options:['Fluid glucose < 60 mg\/dl','Lactate Dehydrogenase (LDH) of more than 1000 U\/L','Fluid pH of less than 7.0','All of these'],exp:'EMPYEMA THORACIS \u2014 diagnostic criteria for complex\/frank empyema (Light\\'s criteria for complicated parapneumonic effusion\/empyema): Pleural fluid pH <7.0 \u2714 (frank empyema; <7.2 = complicated requiring drainage). Pleural fluid glucose <60 mg\/dL \u2714 (bacterial consumption of glucose). Pleural fluid LDH >1000 U\/L \u2714 (intense inflammatory activity). Grossly purulent fluid (frank pus) = empyema by definition. All three biochemical criteria together are consistent with empyema and indicate the need for chest tube drainage. Any one criterion alone suggests complicated parapneumonic effusion; multiple criteria together = frank empyema. Answer: All of these.'},\n{id:10,stem:'Airway secretions contain all of the following antimicrobial peptides EXCEPT:',correct:'Histidine',options:['Defensins','Immunoglobulin A (IgA)','Lysozyme','Histidine'],exp:'Airway innate immune antimicrobial defence \u2014 constituents of airway surface liquid (ASL): Defensins \u2714 \u2014 alpha and beta defensins; cationic peptides disrupting microbial membranes; secreted by airway epithelium and neutrophils. Secretory IgA \u2714 \u2014 major immunoglobulin of mucosal secretions; neutralises pathogens; produced by submucosal plasma cells and transported across epithelium as secretory IgA. Lysozyme \u2714 \u2014 enzyme cleaving bacterial peptidoglycan (NAM-NAG bonds); abundant in nasal\/airway secretions; from serous cells of submucosal glands. Also: lactoferrin, surfactant proteins (SP-A, SP-D), SLPI (secretory leukocyte protease inhibitor), cathelicidins. HISTIDINE: an amino acid \u2014 not a recognised antimicrobial peptide or immune effector in airway secretions. Histatin (related to histidine) is found in saliva but not a standard airway antimicrobial. Answer: Histidine.'},\n{id:11,stem:'The respiratory motor neuron associated with origin of respiratory cycle is located in:',correct:'Ventral Medulla oblongata',options:['Pons','Posterior Medulla oblongata','Ventral Medulla oblongata','Mid brain'],exp:'Respiratory rhythm generation \u2014 central pattern generator: The primary rhythm-generating centre for breathing is the PRE-B\u00d6TZINGER COMPLEX located in the VENTRAL MEDULLA OBLONGATA (specifically the ventral respiratory group \u2014 VRG). It contains pacemaker neurons that generate the basic inspiratory rhythm. Ventral respiratory group (VRG): expiratory neurons (B\u00f6tzinger complex) and inspiratory neurons (pre-B\u00f6tzinger) in the ventromedial medulla. Dorsal respiratory group (DRG): in the posterior\/dorsal medulla (nucleus tractus solitarius) \u2014 integrates afferent input from chemoreceptors and lung stretch receptors. Pneumotaxic centre (pons): modulates rhythm from the medulla. Apneustic centre (lower pons): prolongs inspiration. The ORIGIN of the respiratory cycle = VENTRAL MEDULLA. Answer: Ventral Medulla oblongata.'},\n{id:12,stem:'Which of the above constitute significant or clinically important weight loss?\\n1. 4.5 kg over 6-12 months\\n2. 10 kg over 6-12 months\\n3. More than 5% over 6-12 months\\n4. More than 10% over 6-12 months',correct:'2 and 4',options:['1 and 3','1 and 4','2 and 3','2 and 4'],exp:'Clinically significant weight loss definition: SIGNIFICANT (clinically important, warrants investigation) weight loss is defined as: >10 kg over 6\u201312 months \u2714 (absolute weight loss). OR >10% of body weight over 6\u201312 months \u2714 (proportional loss). Some sources use >5% as a threshold for \"meaningful\" but 10% is the more commonly cited threshold for \"significant\" requiring investigation for malignancy, chronic illness, etc. 4.5 kg or 5% may be meaningful in obese individuals but are not the standard thresholds for \"significant\" weight loss in clinical\/UPSC exam context. The classic teaching: significant = >10 kg or >10% over 6\u201312 months. Answer: 2 and 4.'},\n{id:13,stem:'Which of the following Ascitic Fluid analysis is most compatible with a diagnosis of Ascites secondary to portal hypertension?',correct:'SAAG > 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl',options:['SAAG < 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl','SAAG < 1.1 g\/dl ; Ascitic Fluid Protein > 2.5 g\/dl','SAAG > 1.1 g\/dl ; Ascitic Fluid Protein < 2.5 g\/dl','SAAG > 1.1 g\/dl ; Ascitic Fluid Protein > 2.5 g\/dl'],exp:'SAAG (Serum-Ascites Albumin Gradient) = serum albumin \u2013 ascitic fluid albumin. SAAG \u22651.1 g\/dL \u2192 portal hypertension (97% accuracy). SAAG <1.1 g\/dL \u2192 non-portal hypertension (peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome). For LIVER CIRRHOSIS (most common cause of portal hypertension ascites): SAAG >1.1 \u2714 (portal hypertension). Ascitic fluid protein <2.5 g\/dL \u2714 \u2014 cirrhosis causes low-protein ascites (liver makes less albumin; sinusoidal hypertension \u2192 transudative pattern). Contrast: cardiac failure = SAAG >1.1 but protein >2.5 g\/dL (cardiac ascites is high-protein). Cirrhosis = SAAG >1.1 + low protein (<2.5). Answer: SAAG >1.1 g\/dL; Ascitic Fluid Protein <2.5 g\/dL.'},\n{id:14,stem:'All are the causes of Interstitial lung disease EXCEPT:',correct:'Bronchial Asthma',options:['Idiopathic Pulmonary Fibrosis','Granulomatosis with Polyangiitis','Sarcoidosis','Bronchial Asthma'],exp:'Interstitial Lung Diseases (ILD) \u2014 conditions involving the lung interstitium (alveolar walls, peribronchiolar tissue, connective tissue): ILD causes: Idiopathic Pulmonary Fibrosis (IPF) \u2714, Sarcoidosis \u2714, Granulomatosis with Polyangiitis (GPA\/Wegener\\'s) \u2714, Connective tissue diseases (RA, SLE, SSc), Hypersensitivity pneumonitis, Drug-induced (amiodarone, methotrexate, nitrofurantoin), COP, DIP, NSIP, LIP. BRONCHIAL ASTHMA: an obstructive airway disease \u2014 primarily affects the AIRWAYS (bronchi and bronchioles) with reversible airflow obstruction, not the lung interstitium. Asthma is NOT an ILD. Answer: Bronchial Asthma \u2014 EXCEPT.'},\n{id:15,stem:'The rhythmic activity recorded on scalp by EEG in a normal awake adult lying quietly with eyes closed is:',correct:'8 to 13 Hz \u2013 Alpha rhythm',options:['Less than 4Hz \u2013 Delta rhythm','4 to 7 Hz \u2013 Theta rhythm','8 to 13 Hz \u2013 Alpha rhythm','More than 14 Hz \u2013 Beta rhythm'],exp:'EEG frequency bands and states: Delta (<4 Hz): deep sleep (Stage N3\/slow-wave sleep), coma, encephalopathy. Theta (4\u20137 Hz): light sleep, drowsiness, meditation; also seen in some areas normally. ALPHA (8\u201313 Hz) \u2714: NORMAL AWAKE ADULT at rest with EYES CLOSED \u2014 the dominant rhythm over the occipital regions. Disappears (blocks) when eyes open or during mental concentration (alpha block\/alpha attenuation). Beta (>13\u201314 Hz): active thinking, anxious states, eyes open, benzodiazepine administration. Gamma (>30 Hz): sensory processing, cognitive activity. Key fact: the normal waking EEG with eyes closed = ALPHA rhythm (8\u201313 Hz) predominantly in posterior (occipital) leads. Answer: 8\u201313 Hz \u2013 Alpha rhythm.'},\n{id:16,stem:'Transient Monocular blindness may be due to small platelet emboli that occludes:',correct:'Ophthalmic artery',options:['Posterior Cerebellar artery','Posterior Cerebral artery','Ophthalmic artery','Vertebral artery'],exp:'TRANSIENT MONOCULAR BLINDNESS (Amaurosis Fugax): sudden, brief (seconds to minutes), painless loss of vision in ONE eye \u2014 \"like a curtain coming down.\" Mechanism: platelet-fibrin emboli (from carotid artery atherosclerotic plaques, cardiac emboli) travel to the OPHTHALMIC ARTERY (first branch of internal carotid artery) \u2192 occlusion of the central retinal artery or its branches \u2192 transient retinal ischaemia. The ophthalmic artery supplies the retina via the central retinal artery. Clinical importance: a TIA warning sign; requires urgent carotid imaging (US\/CTA) and antiplatelet therapy. Posterior cerebral artery: binocular visual field defects (homonymous hemianopia). Posterior cerebellar, vertebral: brainstem\/cerebellar symptoms. Answer: Ophthalmic artery.'},\n{id:17,stem:'The phenomenon of sparing of macular vision is due to collateral circulation between:',correct:'middle and posterior cerebral artery',options:['middle and posterior cerebral artery','anterior and middle cerebral artery','anterior and posterior cerebral artery','anterior, middle and posterior cerebral artery'],exp:'MACULAR SPARING in occipital lobe lesions: The occipital cortex (primary visual cortex, V1) is supplied by the POSTERIOR CEREBRAL ARTERY (PCA). The occipital pole (representing the macula\/central vision) receives COLLATERAL BLOOD SUPPLY from the MIDDLE CEREBRAL ARTERY (MCA) via anastomoses at the occipital tip. When the PCA is occluded (e.g., in PCA territory stroke): the peripheral visual cortex (representing peripheral vision) is infarcted. The macular cortex (occipital pole) survives due to MCA collaterals \u2192 MACULAR VISION IS SPARED. Result: contralateral homonymous hemianopia with MACULAR SPARING \u2014 the central (foveal\/macular) vision is preserved. Answer: Middle and posterior cerebral artery.'},\n{id:18,stem:'Characteristic features of Horner\\'s Syndrome are:',correct:'partial ptosis, enophthalmos, constricted pupil, decreased sweating',options:['partial ptosis, enophthalmos, constricted pupil, decreased sweating','partial ptosis, exophthalmos, constricted pupil, decreased sweating','partial ptosis, enophthalmos, dilated pupil, decreased sweating','partial ptosis, enophthalmos, constricted pupil, increased sweating'],exp:'HORNER\\'S SYNDROME (oculosympathetic palsy) \u2014 interruption of the sympathetic pathway to the eye (hypothalamus \u2192 ciliospinal centre of Budge \u2192 superior cervical ganglion \u2192 eye): Partial (incomplete) ptosis \u2714 \u2014 loss of sympathetic tone to Muller\\'s muscle (superior tarsal muscle); upper lid drops slightly, lower lid rises (reverse ptosis \u2192 narrowed palpebral fissure). MIOSIS (constricted pupil) \u2714 \u2014 loss of sympathetic dilator pupillae \u2192 parasympathetic sphincter pupillae unopposed. ENOPHTHALMOS \u2714 \u2014 apparent (not true) sinking of the eyeball due to narrowed palpebral fissure; actually pseudo-enophthalmos. ANHIDROSIS (decreased sweating) \u2714 \u2014 on the ipsilateral face (if lesion at or proximal to the superior cervical ganglion). Also: loss of ciliospinal reflex. Answer: Partial ptosis, enophthalmos, constricted pupil, decreased sweating.'},\n{id:19,stem:'All of the following statements are true EXCEPT:',correct:'Spinal cord ends at lower level of 5th lumbar vertebrae',options:['Dorsal column fibres synapse at the cuneate and gracile nuclei','Pain and temperature sensations are carried by lateral spinothalamic tract','Spinal cord ends at lower level of 5th lumbar vertebrae','Dorsal spinocerebellar tract carries fibres from the same side of the body'],exp:'Spinal cord anatomy statements: Dorsal column fibres (posterior columns \u2014 fine touch, proprioception, vibration) synapse at cuneate (upper limb \u2014 from T6 upward, in fasciculus cuneatus) and gracile nuclei (lower limb \u2014 below T6, in fasciculus gracilis) in the medulla \u2714 TRUE. Pain and temperature \u2192 lateral spinothalamic tract \u2714 TRUE (fibres cross within 1\u20132 segments in the anterior commissure then ascend). Dorsal spinocerebellar tract: carries IPSILATERAL proprioceptive information from the same side (uncrossed) to the ipsilateral cerebellum \u2714 TRUE. SPINAL CORD ENDS: at the lower border of L1 or upper border of L2 (conus medullaris) in adults \u2014 NOT at L5. In neonates it ends slightly lower (~L3). \"Lower level of 5th lumbar vertebrae\" is FALSE. Answer: Spinal cord ends at lower level of 5th lumbar \u2014 EXCEPT.'},\n{id:20,stem:'The following conditions usually present with proximal muscle weakness, EXCEPT:',correct:'Myotonia dystrophica',options:['Facio-scapulo-humeral dystrophy','Myotonia dystrophica','Duchenne\\'s muscular dystrophy','Becker muscular dystrophy'],exp:'Proximal muscle weakness (pelvic and shoulder girdle muscles): Duchenne\\'s MD \u2714 PROXIMAL \u2014 hip extensors, quadriceps, shoulder girdle. Becker MD \u2714 PROXIMAL \u2014 same distribution as DMD but milder. Facioscapulohumeral (FSH) dystrophy \u2714 PROXIMAL \u2014 face, shoulder girdle (scapular winging, biceps, triceps); predominantly upper limb proximal + facial. MYOTONIC DYSTROPHY (Myotonia dystrophica\/DM1): DISTAL muscle weakness \u2014 distal limbs (hand intrinsics, foot dorsiflexors, facial and sternocleidomastoid muscles); myotonia (delayed relaxation after contraction). This is the exception \u2014 it presents with DISTAL weakness, unlike most muscular dystrophies which are proximal. Answer: Myotonia dystrophica \u2014 EXCEPT (presents with distal weakness).'},\n{id:21,stem:'Pel-Ebstein fever is seen in:',correct:'Hodgkin\\'s disease',options:['Hodgkin\\'s disease','Malaria','Kalazar','Typhoid fever'],exp:'PEL-EBSTEIN FEVER: a characteristic cyclical fever pattern where periods of high fever (several days to weeks) alternate with afebrile periods of similar duration, then recur. PATHOGNOMONIC of HODGKIN\\'S LYMPHOMA \u2014 seen in ~10\u201335% of patients; associated with cytokine release (IL-1, TNF) from Reed-Sternberg cells and reactive lymphocytes. The cycle repeats every 1\u20132 weeks. Historical note: named after Wilhelm Ebstein and Pieter Pel who described this fever pattern in Hodgkin\\'s disease. Other fever patterns: Malaria \u2014 quotidian (P. falciparum), tertian (P. vivax\/ovale), quartan (P. malariae). Kala-azar \u2014 twice-daily fever spikes. Typhoid \u2014 step-ladder pattern. Answer: Hodgkin\\'s disease.'},\n{id:22,stem:'All of the following are true regarding acute leukaemias, EXCEPT:',correct:'Auer rods suggest acute lymphocytic leukaemia',options:['Promyelocytic leukaemia may present with DIC','Gum hypertrophy is a feature of monocytic leukaemia','Translocation is a common chromosomal abnormality in acute myeloid leukaemia','Auer rods suggest acute lymphocytic leukaemia'],exp:'Acute leukaemia facts: APL (AML-M3) and DIC \u2714 TRUE \u2014 promyelocytic granules contain procoagulant material \u2192 DIC; treated with ATRA. Gum hypertrophy in monocytic (M4\/M5) AML \u2714 TRUE \u2014 monocytic cells infiltrate gingival tissue; characteristic feature. Translocations in AML \u2714 TRUE \u2014 t(15;17) in APL, t(8;21) in M2, inv(16) in M4Eo; translocations are very common. AUER RODS: these are crystallised lysosomal enzymes (myeloperoxidase-positive) appearing as needle-like pink cytoplasmic inclusions. They are found EXCLUSIVELY in MYELOID (AML) blasts \u2014 NEVER in lymphocytic leukaemia (ALL). Auer rods in blasts = AML (NOT ALL). \"Auer rods suggest ALL\" is FALSE. Answer: Auer rods suggest acute lymphocytic leukaemia \u2014 EXCEPT.'},\n{id:23,stem:'All of the following are clinical features of Polycystic Ovarian Syndrome EXCEPT:',correct:'Menorrhagia',options:['Menorrhagia','Hirsutism','Glucose intolerance','Infertility'],exp:'Polycystic Ovarian Syndrome (PCOS) \u2014 clinical features: Hirsutism \u2714 (androgen excess \u2192 male-pattern hair growth \u2014 upper lip, chin, chest, abdomen, thighs). Glucose intolerance \/ Insulin resistance \u2714 \u2014 ~50\u201370% of PCOS; associated with metabolic syndrome, Type 2 DM risk. Infertility \u2714 \u2014 oligo\/anovulation \u2192 difficulty conceiving; most common cause of anovulatory infertility. Acne, obesity (central), acanthosis nigricans. MENSTRUAL PATTERN in PCOS: OLIGOMENORRHOEA (infrequent, scanty periods) or AMENORRHOEA \u2014 NOT menorrhagia. The anovulatory cycles cause prolonged oestrogen exposure WITHOUT progesterone (no corpus luteum) \u2192 endometrial hyperplasia \u2192 irregular\/scanty bleeding or amenorrhoea. Menorrhagia (heavy periods) is NOT typical of PCOS. Answer: Menorrhagia \u2014 EXCEPT.'},\n{id:24,stem:'Clinical features of Turner syndrome include all EXCEPT:',correct:'Narrow carrying angle of Elbow',options:['Webbing of Neck','Narrow carrying angle of Elbow','Coarctation of Aorta','Short stature'],exp:'Turner Syndrome (45,X0) features: Short stature \u2714 (universal \u2014 absent pubertal growth spurt; height 143\u2013147 cm average). Webbing of neck \u2714 (pterygium colli \u2014 redundant neck skin; from fetal lymphoedema). Coarctation of Aorta \u2714 (cardiovascular defect \u2014 bicuspid aortic valve + coarctation in ~30\u201350%). Lymphoedema (hands and feet). Shield chest, widely spaced nipples. Primary amenorrhoea (gonadal dysgenesis). Low hairline, ears. Cubitus valgus: INCREASED carrying angle of the elbow (valgus = angled OUTWARD\/laterally) \u2014 NOT narrow. The INCREASED carrying angle (cubitus valgus) is a feature of Turner syndrome; a NARROW carrying angle is NOT. Answer: Narrow carrying angle \u2014 EXCEPT.'},\n{id:25,stem:'Pretibial myxedema is a clinical feature of:',correct:'Graves disease',options:['Hypothyroidism','Graves disease','Cushing disease','Conn syndrome'],exp:'PRETIBIAL MYXOEDEMA (localised\/thyroid dermopathy): non-pitting, indurated, skin thickening over the anterior tibia (shin) and dorsum of feet. Cause: glycosaminoglycan (hyaluronic acid) deposition in the dermis due to TSH receptor antibody (TRAb) stimulation of dermal fibroblasts. Associated EXCLUSIVELY with GRAVES\\' DISEASE (autoimmune hyperthyroidism) \u2014 seen in ~5% of Graves patients, almost always with exophthalmos. NOT a feature of primary hypothyroidism (which causes generalised myxoedema). NOT from Cushing or Conn disease. Paradoxically, pretibial myxoedema can persist even after treatment of hyperthyroidism. Answer: Graves disease.'},\n{id:26,stem:'Match the List I with List II:\\nA. Conn syndrome \u2014 1. Anosmia\\nB. Turner syndrome \u2014 2. Tetany\\nC. Kallman syndrome \u2014 3. Lymphoedema\\nD. Cushing syndrome \u2014 4. Avascular necrosis of hip',correct:'A-2 B-3 C-1 D-4',options:['A-4 B-1 C-3 D-2','A-2 B-3 C-1 D-4','A-2 B-1 C-3 D-4','A-4 B-3 C-1 D-2'],exp:'Matching: A. Conn syndrome (primary hyperaldosteronism) \u2192 2. Tetany \u2014 hypokalaemia causes metabolic alkalosis \u2192 reduced ionised calcium \u2192 tetany (Trousseau\/Chvostek signs). B. Turner syndrome (45,X0) \u2192 3. Lymphoedema \u2014 fetal lymphoedema causes webbed neck, puffy hands\/feet at birth; persistent lower limb lymphoedema. C. Kallmann syndrome (hypogonadotrophic hypogonadism + anosmia) \u2192 1. Anosmia \u2014 failure of GnRH neurons to migrate from olfactory bulb to hypothalamus during development \u2192 absent olfactory bulbs \u2192 anosmia + hypogonadism. D. Cushing syndrome \u2192 4. Avascular necrosis of hip \u2014 chronic glucocorticoid excess (endogenous or exogenous) causes osteonecrosis\/avascular necrosis of femoral head. Answer: A-2 B-3 C-1 D-4.'},\n{id:27,stem:'Which of the following is NOT a part of Koch\\'s postulates?',correct:'The organism may not be reisolated from the incubated diseased host',options:['The same organism must be present in every case of the disease','The organism must be isolated from the diseased host and grown in culture','The isolate must cause the disease when incubated','The organism may not be reisolated from the incubated diseased host'],exp:'Koch\\'s Postulates (4 criteria for establishing causation): (1) The microorganism must be found in all cases of the disease. (2) It must be isolated from the diseased host and grown in pure culture. (3) The cultured organism must cause disease when introduced into a healthy susceptible host. (4) The organism must be RE-ISOLATED from the experimentally diseased host and shown to be identical to the original. \"The organism may NOT be reisolated\" is the OPPOSITE of Koch\\'s 4th postulate \u2014 reisolation IS required. This statement contradicts Koch\\'s postulate #4. Answer: The organism may not be reisolated \u2014 NOT part of Koch\\'s postulates.'},\n{id:28,stem:'All of the following cause dementia EXCEPT:',correct:'Vitamin D toxicity',options:['Huntington\\'s disease','Alzheimer\\'s disease','Vitamin D toxicity','Thiamine deficiency'],exp:'Causes of dementia: Alzheimer\\'s disease \u2714 (most common; amyloid plaques + neurofibrillary tangles). Huntington\\'s disease \u2714 (subcortical dementia; chorea + personality change + dementia; CAG repeat expansion in HTT gene). Thiamine (B1) deficiency \u2714 \u2014 Wernicke-Korsakoff syndrome: Wernicke\\'s (acute \u2014 ophthalmoplegia, ataxia, encephalopathy) \u2192 Korsakoff\\'s (chronic \u2014 anterograde amnesia, confabulation = a form of dementia). Also: Vascular dementia, Lewy body dementia, FTD, B12 deficiency, hypothyroidism, HIV, prion disease, NPH. VITAMIN D TOXICITY (hypervitaminosis D): causes hypercalcaemia \u2192 renal stones, nephrocalcinosis, polyuria, weakness, nausea \u2014 but NOT dementia. Vitamin D toxicity does not cause cognitive impairment or dementia. Answer: Vitamin D toxicity \u2014 EXCEPT.'},\n{id:29,stem:'The therapeutic level of Digoxin in blood is:',correct:'1\u20132 ng\/ml',options:['1\u20132 ng\/ml','4\u20136 ng\/ml','6\u20138 ng\/ml','8\u201310 ng\/ml'],exp:'DIGOXIN therapeutic range: 0.5\u20132.0 ng\/mL (or 0.8\u20132.0 ng\/mL for heart failure; some sources say 0.5\u20130.9 ng\/mL is optimal for HF based on DIG trial). The standard quoted therapeutic range is 1\u20132 ng\/mL. Toxicity occurs above 2\u20132.5 ng\/mL. Digoxin toxicity signs: nausea, vomiting, visual disturbances (yellow-green halos \u2014 xanthopsia), bradycardia, heart block, ventricular arrhythmias. Narrow therapeutic index \u2014 monitoring serum levels is essential. Answer: 1\u20132 ng\/mL.'},\n{id:30,stem:'A 40-year old woman presents with sudden onset palpitations. An ECG done reveals narrow-QRS complex tachycardia. The most likely diagnosis is:',correct:'AV reentry tachycardia',options:['Ventricular tachycardia','Pre-excited tachycardia','Paroxysmal supraventricular tachycardia with aberrancy','AV reentry tachycardia'],exp:'NARROW QRS complex tachycardia (QRS <120 ms) = SUPRAVENTRICULAR ORIGIN (above the His bundle; normal ventricular conduction). Causes: AVNRT (AV nodal reentrant tachycardia \u2014 most common SVT), AVRT (AV reentrant tachycardia \u2014 via accessory pathway orthodromic \u2014 next most common), Atrial tachycardia, Atrial flutter with block, Sinus tachycardia. Ventricular tachycardia: WIDE QRS complex (>120 ms) \u2014 not narrow. Pre-excited tachycardia (WPW antidromic): WIDE QRS \u2014 not narrow. PSVT with aberrancy: WIDE QRS \u2014 not narrow. For this 40-year-old woman with NARROW QRS tachycardia \u2192 AVRT (AV reentry tachycardia via accessory pathway \u2014 orthodromic) or AVNRT. Among the options, AVRT is the specific correct answer. Answer: AV reentry tachycardia.'},\n{id:31,stem:'Which of the following statements are true about management of acute pulmonary oedema?\\n1. Put the patient in relaxed, supine position\\n2. Give high flow, high concentration oxygen\\n3. Administer Furosemide intravenously\\n4. No role of Nitrates\\nSelect the correct answer:',correct:'2 and 3',options:['1 and 2','2 and 3','3 and 4','1 and 4'],exp:'Acute pulmonary oedema (APO) management: POSITION: SIT the patient upright (HIGH FOWLER\\'S position, legs dangling) \u2014 NOT supine. Upright position reduces venous return to the heart (preload reduction) and relieves orthopnoea. Statement 1 (supine) is FALSE. HIGH FLOW OXYGEN \u2714 \u2014 100% O2 via non-rebreather mask; target SpO2 >94%; if refractory \u2192 NIV (CPAP\/BiPAP). Statement 2 TRUE. IV FUROSEMIDE \u2714 \u2014 loop diuretic; reduces preload (initial venodilatory effect within minutes, then diuresis); cornerstone of APO management. Statement 3 TRUE. NITRATES: HAVE A ROLE \u2014 sublingual\/IV nitroglycerine reduces preload (and afterload at high doses); highly effective in APO, especially hypertensive APO. Statement 4 is FALSE. Correct statements: 2 and 3. Answer: 2 and 3.'},\n{id:32,stem:'Which of the following does NOT cause prolongation of QT interval?',correct:'Hyperkalaemia',options:['Hypomagnesaemia','Hyperkalaemia','Erythromycin','Amiodarone'],exp:'QT prolongation causes: Electrolytes: Hypokalaemia \u2714, Hypomagnesaemia \u2714, Hypocalcaemia \u2714. Drugs: Amiodarone \u2714 (class III anti-arrhythmic), Erythromycin \u2714 (and other macrolides), Fluoroquinolones, Antifungals (azoles), Antipsychotics, Methadone, Sotalol, Haloperidol. Congenital: Long QT syndrome (Romano-Ward, Jervell-Lange-Nielsen). Hypothyroidism, myocarditis. HYPERKALAEMIA: does NOT prolong QT. Hyperkalaemia causes: peaked T waves \u2192 prolonged PR \u2192 wide QRS \u2192 sine wave pattern \u2192 VF\/asystole. QT interval may actually be SHORTENED in hyperkalaemia (accelerated repolarisation). Answer: Hyperkalaemia \u2014 does NOT prolong QT.'},\n{id:33,stem:'A 21-year young man presents with high grade fever, fleeting inflammation of knee and ankle joints, occasional palpitations, no history of antecedent sore throat, splenomegaly, and ECG showing prolonged PR interval. What is the most likely diagnosis in India?',correct:'Enteric fever',options:['Still disease','Enteric fever','Rheumatic fever','Reiter\\'s syndrome'],exp:'Clinical analysis: Young male, HIGH GRADE fever, FLEETING POLYARTHRITIS (knees, ankles), palpitations, PR prolongation on ECG, SPLENOMEGALY. Critical clue: NO antecedent SORE THROAT. This distinguishes from RHEUMATIC FEVER (which requires preceding Group A strep pharyngitis \u2014 Jones criteria). ENTERIC FEVER (Typhoid) in India: fever (step-ladder pattern, but can be high grade), relative bradycardia, splenomegaly (very common), PR prolongation (myocarditis \u2014 toxic carditis occurs in ~10% of typhoid), polyarthritis (reactive\/toxic arthritis \u2014 fleeting), rash (rose spots \u2014 uncommon in India). No streptococcal history. All features fit ENTERIC FEVER. Rheumatic fever requires documented preceding streptococcal pharyngitis. Still disease: JIA pattern in young adults. Reiter\\'s: urethritis + arthritis + conjunctivitis. Answer: Enteric fever.'},\n{id:34,stem:'A 50-year gentleman with Type-2 DM for 5 years presents with sudden onset dyspnoea at rest, orthopnoea, and prostration. Pulse is rapid, very weak. BP 100\/70 mmHg. Diffuse crepitations at lung bases. Most likely diagnosis:',correct:'Left heart failure',options:['Mitral stenosis with bacterial endocarditis','Right heart failure','Left heart failure','Constrictive pericarditis'],exp:'Clinical picture: Type 2 DM (high risk of coronary artery disease \u2192 ischaemic cardiomyopathy), sudden onset dyspnoea, ORTHOPNOEA (lying flat worsens breathlessness \u2014 pulmonary oedema in the supine position), diffuse BILATERAL BASAL CREPITATIONS (pulmonary oedema \u2014 fluid in alveoli), low BP + weak rapid pulse (cardiogenic shock\/decompensated heart failure). Orthopnoea + bilateral basal crepitations = LEFT HEART FAILURE (elevated left atrial pressure \u2192 pulmonary venous hypertension \u2192 pulmonary oedema). Right heart failure: peripheral oedema, raised JVP, hepatomegaly \u2014 no bilateral lung crepitations. Constrictive pericarditis: raised JVP, Kussmaul sign, no lung oedema. Answer: Left heart failure.'},\n{id:35,stem:'The \\'Y\\' descent in JVP waveform represents:',correct:'Atrial emptying',options:['Atrial relaxation','Atrial systole','Atrial emptying','Apical displacement of tricuspid valve'],exp:'JVP waveform components: a wave = Atrial systole (atrial contraction). c wave = tricuspid valve closure + carotid artery pulsation (small). x descent = Atrial RELAXATION (after atrial systole; systolic descent). v wave = Venous filling (atria fill while tricuspid is closed during ventricular systole). Y DESCENT = ATRIAL EMPTYING \u2714 \u2014 when the tricuspid valve opens at the start of diastole, the right atrium empties into the right ventricle \u2192 JVP falls = Y descent (diastolic descent). Absent\/blunted Y: pericardial tamponade (impaired ventricular filling). Steep\/prominent Y: constrictive pericarditis (rapid ventricular filling), tricuspid regurgitation. Answer: Atrial emptying.'},\n{id:36,stem:'While distinguishing a venous pulsation from the arterial pulsation in neck, which of the following is NOT correct?',correct:'Venous pulse has a single peak in each cardiac cycle',options:['The height of venous pulse varies with respiration','Abdominal pressure causes rise in venous pulse','Venous pulse has a single peak in each cardiac cycle','Venous pulse is not easily palpable'],exp:'Venous vs arterial neck pulsations: Height varies with respiration \u2714 TRUE \u2014 JVP rises on expiration, falls on inspiration (opposite to IVC in abdomen); posture also affects. Abdominal pressure rises venous pulse \u2714 TRUE \u2014 hepatojugular reflux (HJR): compressing the abdomen raises JVP; venous system is continuous. Venous pulse not easily palpable \u2714 TRUE \u2014 JVP is visible (a wave, v wave, x and y descents) but NOT palpable (low pressure); carotid artery IS palpable (high pressure). VENOUS PULSE HAS A SINGLE PEAK: FALSE \u2714 \u2014 JVP has TWO positive waves per cardiac cycle: a wave (atrial systole) and v wave (venous filling). The carotid\/arterial pulse has a single peak per cycle. \"Single peak\" applies to ARTERIAL pulse, not venous. Answer: Venous pulse has a single peak \u2014 NOT correct.'},\n{id:37,stem:'Which of the following does NOT cause pulmonary infiltrates with eosinophilia?',correct:'Cystic fibrosis',options:['Bronchial asthma','Postradiation pneumonitis','Eosinophilic granulomatosis with polyangiitis','Cystic fibrosis'],exp:'Pulmonary infiltrates with eosinophilia (PIE) syndrome: L\u00f6ffler\\'s syndrome (ascaris larvae migration). ABPA (Allergic bronchopulmonary aspergillosis) \u2014 in asthma\/CF patients, though ABPA itself causes PIE, not CF per se. Bronchial asthma \u2714 \u2014 associated with blood and tissue eosinophilia; ABPA complicating asthma causes PIE. Eosinophilic granulomatosis with polyangiitis (EGPA\/Churg-Strauss) \u2714 \u2014 asthma + eosinophilia + vasculitis + PIE. Drug reactions (nitrofurantoin, sulfonamides). Hypereosinophilic syndrome. CYSTIC FIBROSIS: a genetic disease (CFTR mutation) causing thick secretions, bronchiectasis, and recurrent bacterial infections. CF does NOT cause pulmonary eosinophilia (the infiltrates in CF are from mucus plugging and bacterial infection \u2014 neutrophilic, not eosinophilic). ABPA can complicate CF, but CF itself \u2260 PIE. Answer: Cystic fibrosis \u2014 does NOT cause PIE.'},\n{id:38,stem:'Total lung capacity is decreased in which one of the following conditions?',correct:'Pulmonary fibrosis',options:['Asthma','Chronic bronchitis','Pulmonary fibrosis','Emphysema'],exp:'Total Lung Capacity (TLC) changes: TLC INCREASED (air trapping\/hyperinflation): Asthma \u2714 (during attack \u2014 air trapping), Chronic bronchitis \u2714 (obstructive \u2014 TLC normal or slightly elevated), Emphysema \u2714 (significant hyperinflation \u2014 markedly elevated TLC). TLC DECREASED (restrictive pattern): PULMONARY FIBROSIS \u2714 \u2014 the fibrotic, stiff lungs cannot expand fully \u2192 reduced TLC, VC, FRC. All lung volumes are reduced. FEV1\/FVC ratio is NORMAL or INCREASED (restrictive pattern \u2014 both FEV1 and FVC reduced proportionally). Other restrictive causes: pleural effusion, pneumothorax, obesity, neuromuscular disease, chest wall deformity. Answer: Pulmonary fibrosis.'},\n{id:39,stem:'Which one of the following is the minimum spirometry criterion for diagnosis of bronchial asthma?',correct:'Increase in FEV1 \u2265 12% following administration of inhaled bronchodilators',options:['Decrease in FEV1 \u2265 20% after 6 minutes of exercise','Increase in FEV1 \u2265 12% following administration of inhaled bronchodilators','Increase in 500 ml of FEV1 after glucocorticoids inhalation','Less than 20% diurnal variation on more than 3 days a week on PEF diary'],exp:'GINA spirometry criteria for asthma diagnosis (bronchodilator reversibility test \u2014 most standard): Significant bronchodilator response = FEV1 increase of \u226512% AND \u2265200 mL from baseline after inhaled SABA (salbutamol 400 mcg). This is the minimum standard criterion for diagnosing asthma. Exercise challenge: FEV1 fall \u226510% (not 20%) or >15% is significant. PEF diurnal variation: >10\u201320% (if >20% = significant). Glucocorticoid trial: used when diagnosis uncertain. The MINIMUM STANDARD CRITERION in clinical practice = \u226512% FEV1 increase (+ \u2265200 mL absolute) post-bronchodilator. Answer: Increase in FEV1 \u226512% following inhaled bronchodilators.'},\n{id:40,stem:'Modified Blatchford score is used for the risk stratification of:',correct:'Upper gastrointestinal bleeding',options:['Pancreatitis','Sepsis','Upper gastrointestinal bleeding','Cholangitis'],exp:'GLASGOW-BLATCHFORD SCORE (GBS) \/ Modified Blatchford Score: a pre-endoscopy risk stratification tool for ACUTE UPPER GI BLEEDING (UGIB). Parameters: blood urea, haemoglobin, systolic BP, pulse, presence of melaena, syncope, hepatic disease, cardiac failure. Score 0 = very low risk (can manage outpatient); score >0 = needs endoscopy\/intervention. Predicts need for clinical intervention (blood transfusion, endoscopy, surgery). Pancreatitis: Ranson criteria, APACHE II, Balthazar CT severity index. Sepsis: SOFA, qSOFA, APACHE. Cholangitis: Tokyo guidelines. 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Submitting in 10 Submit Now Combined Medical Services Examination 2019Paper I \u00b7 Part A Cardiology \u00b7 Respiratory \u00b7 Neurology \u00b7 Gastroenterology \u00b7 Haematology \u00b7 Endocrinology Questions 1 \u2013 40 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0%score Your Result… <\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36816","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2019 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\/11\/cms-2019-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 2019 P1 Part-A - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2019 Paper I \u2013 Part A (Q1\u2013Q40) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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