{"id":36770,"date":"2026-05-06T22:17:05","date_gmt":"2026-05-06T16:47:05","guid":{"rendered":"https:\/\/atsixty.com\/?p=36770"},"modified":"2026-05-06T22:17:28","modified_gmt":"2026-05-06T16:47:28","slug":"cms-2017-p1-part-b","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/06\/cms-2017-p1-part-b\/","title":{"rendered":"CMS 2017 P1 Part-B"},"content":{"rendered":"\n\n\n\n\n\n\n\nCMS 2017 Paper I \u2013 Part B (Q41\u2013Q80)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&display=swap\" rel=\"stylesheet\">\n<style>\n\/* \u2500\u2500 Namespace: cms17p1b \u2500\u2500 *\/\n#cms17p1b *,#cms17p1b *::before,#cms17p1b *::after{box-sizing:border-box;margin:0;padding:0}\n#cms17p1b{\n --ter:#C0603A;--ter-light:#e8825f;--ter-pale:#fdf1ec;\n --teal:#2A7A6F;--teal-light:#3da394;--teal-pale:#eaf4f3;\n --ink:#1a1a1a;--ink-mid:#444;--ink-soft:#777;\n --line:#e0d8d4;--bg:#fdfaf8;--white:#ffffff;\n --correct:#1e6f46;--correct-bg:#eaf7ef;--correct-border:#43a047;\n --wrong:#b83232;--wrong-bg:#fdf0f0;--wrong-border:#e53935;\n --radius:10px;\n font-family:'Source Serif 4',Georgia,serif;\n font-size:16px;color:var(--ink);background:var(--bg);\n line-height:1.7;padding:0 0 48px;\n}\n#cms17p1b .cq-sentinel{height:1px}\n#cms17p1b .cq-statusbar{position:fixed;top:0;left:0;right:0;z-index:99999;background:var(--white);border-bottom:2px solid var(--line);border-left:4px solid var(--ter);box-shadow:0 2px 12px rgba(0,0,0,0.11);opacity:0;pointer-events:none;transform:translateY(-110%);transition:opacity 0.22s ease,transform 0.22s ease;}\n#cms17p1b .cq-statusbar.visible{opacity:1;pointer-events:auto;transform:translateY(0)}\n#cms17p1b .cq-sb-stats{display:flex;align-items:center;padding:0.38rem 0.7rem;font-size:0.73rem;color:var(--ink-soft);}\n#cms17p1b .cq-sb-item{display:flex;align-items:center;gap:0.18rem;padding:0.1rem 0.5rem;border-right:1px 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.cq-band-c{background:var(--correct-bg);color:var(--correct)}\n#cms17p1b .cq-band-w{background:var(--wrong-bg);color:var(--wrong)}\n#cms17p1b .cq-band-s{background:var(--teal-pale);color:var(--teal)}\n#cms17p1b .cq-retry-btn{margin-top:22px;background:transparent;border:2px solid var(--teal);color:var(--teal);border-radius:8px;padding:10px 28px;font-family:'Playfair Display',serif;font-size:0.95rem;font-weight:700;cursor:pointer;transition:background 0.2s,color 0.2s;}\n#cms17p1b .cq-retry-btn:hover{background:var(--teal);color:var(--white)}\n@media(max-width:480px){\n #cms17p1b .cq-header h1{font-size:1.15rem}\n #cms17p1b .cq-qtext{font-size:0.88rem}\n #cms17p1b .cq-opt-text{font-size:0.84rem}\n}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms17p1b\">\n <div class=\"cq-sentinel\" id=\"cms17p1b-sentinel\"><\/div>\n <div class=\"cq-statusbar\" id=\"cms17p1b-statusbar\">\n <div class=\"cq-sb-stats\">\n <div class=\"cq-timer-item\" id=\"cms17p1b-timer-item\">\u23f1 <strong id=\"cms17p1b-timer-display\">40:00<\/strong><\/div>\n <div class=\"cq-sb-item\">\u2705 <strong id=\"cms17p1b-sc\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u274c <strong id=\"cms17p1b-sw\">0<\/strong><\/div>\n <div class=\"cq-sb-item\">\u23f3 <strong id=\"cms17p1b-sr\">40<\/strong> left<\/div>\n <div class=\"cq-sb-sep\"><\/div>\n <div class=\"cq-sb-item\">Net <strong id=\"cms17p1b-sn\">0<\/strong> \/ <strong id=\"cms17p1b-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"cq-sb-progress\"><div class=\"cq-sb-fill\" id=\"cms17p1b-fill\"><\/div><\/div>\n <\/div>\n <div class=\"cq-grace\" id=\"cms17p1b-grace\">\n <div class=\"cq-grace-box\">\n <h3>Time's Up!<\/h3>\n <p>Submitting in<\/p>\n <div class=\"cq-grace-count\" id=\"cms17p1b-grace-count\">10<\/div>\n <button class=\"cq-grace-btn\" id=\"cms17p1b-grace-now\">Submit Now<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-header\">\n <h1>Combined Medical Services Examination 2017<br>Paper I \u00b7 Part B<\/h1>\n <p>General Medicine \u00b7 Paediatrics<\/p>\n <div class=\"cq-meta\">\n <span class=\"cq-badge\">Questions 41 \u2013 80<\/span>\n <span class=\"cq-badge\">Options reshuffled<\/span>\n <button class=\"cq-timer-btn\" id=\"cms17p1b-timer-btn\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n <\/div>\n <div class=\"cq-body\">\n <div id=\"cms17p1b-questions\"><\/div>\n <div class=\"cq-submit-wrap\">\n <button class=\"cq-btn\" id=\"cms17p1b-submit\">Submit Answers<\/button>\n <\/div>\n <div class=\"cq-score\" id=\"cms17p1b-score\">\n <div class=\"cq-score-ring\" id=\"cms17p1b-ring\">\n <div class=\"cq-ring-inner\">\n <span class=\"cq-ring-pct\" id=\"cms17p1b-ring-pct\">0%<\/span>\n <span class=\"cq-ring-sub\">score<\/span>\n <\/div>\n <\/div>\n <h2>Your Result<\/h2>\n <div class=\"cq-net-line\" id=\"cms17p1b-net-line\"><\/div>\n <div class=\"cq-verdict\" id=\"cms17p1b-verdict\"><\/div>\n <div class=\"cq-score-bands\">\n <span class=\"cq-band cq-band-c\" id=\"cms17p1b-ct-c\"><\/span>\n <span class=\"cq-band cq-band-w\" id=\"cms17p1b-ct-w\"><\/span>\n <span class=\"cq-band cq-band-s\" id=\"cms17p1b-ct-s\"><\/span>\n <\/div>\n <button class=\"cq-retry-btn\" id=\"cms17p1b-retry\">\u21ba Retry Quiz<\/button>\n <\/div>\n <\/div>\n<\/div>\n<script>\n(function(){\n 'use strict';\n const NS='cms17p1b', TOTAL=40, MAX=TOTAL*4;\n const TIMER_SECS=40*60, GRACE_SECS=10;\n\n const QUESTIONS=[\n {\n id:41,\n stem:'\"TIPS\" procedure in the treatment of cirrhosis of the liver stands for:',\n correct:'Transjugular intrahepatic portosystemic shunt',\n options:['Transvenous intrahepatic portal shunt','Transvenous intraabdominal portal shunt','Transjugular intrahepatic portosystemic shunt','Transjugular intrahepatic peritoneal shunt'],\n exp:'TIPS (Transjugular Intrahepatic Portosystemic Shunt) is an interventional radiology procedure in which a stent is placed between the portal vein and hepatic vein through the liver parenchyma, accessed via the transjugular route. It creates a low-resistance shunt that decompresses the portal system. Indications: refractory variceal bleeding, refractory ascites, hepatic hydrothorax. Limitation: worsens hepatic encephalopathy by shunting portal blood (rich in ammonia) away from the liver. Each word in the acronym is specific: Transjugular (access), Intrahepatic (route through liver), Portosystemic (connects portal to systemic venous system) Shunt.'\n },\n {\n id:42,\n stem:'The drug of choice in the treatment of oesophageal candidiasis is:',\n correct:'Fluconazole',\n options:['Fluconazole','Nystatin oral suspension','IV amphotericin','Griseofulvin'],\n exp:'Oesophageal candidiasis is the most common cause of infectious oesophagitis, especially in HIV\/AIDS patients (CD4 <100). Treatment of choice is oral FLUCONAZOLE (triazole antifungal) 200 mg loading dose then 100 mg daily for 14\u201321 days. Nystatin is effective for oropharyngeal candidiasis only \u2014 it is not absorbed systemically and cannot treat oesophageal disease adequately. IV amphotericin is reserved for refractory or systemic\/invasive candidiasis. Griseofulvin is used for dermatophyte fungal infections, not Candida. Fluconazole oral is the standard of care.'\n },\n {\n id:43,\n stem:'Which of the following statements is NOT true regarding neuroleptic malignant syndrome?',\n correct:'There is stimulation of central dopamine receptors in the hypothalamus',\n options:['Caused by haloperidol','Characterized by muscle rigidity and hyperthermia','There is stimulation of central dopamine receptors in the hypothalamus','Treated by IV dantrolene'],\n exp:'Neuroleptic Malignant Syndrome (NMS): caused by antipsychotics (haloperidol is the classic culprit), characterised by hyperthermia, lead-pipe muscle rigidity, altered consciousness, and autonomic instability (diaphoresis, tachycardia). Treated with: discontinuation of the offending drug, IV dantrolene (reduces muscle rigidity\/heat production), bromocriptine (dopamine agonist), and supportive care. The pathophysiology involves BLOCKADE (not stimulation) of central dopamine receptors in the hypothalamus and striatum \u2014 this is what causes hyperthermia (loss of thermoregulation) and rigidity. Statement (c) is NOT true.'\n },\n {\n id:44,\n stem:'Type IV renal tubular acidosis may be caused by all of the following EXCEPT:',\n correct:'Penicillin',\n options:['Low molecular weight heparin','NSAIDs','Penicillin','Trimethoprim'],\n exp:'Type IV RTA is caused by hypoaldosteronism (true or effective) \u2014 characterised by hyperkalaemia and hyperchloraemic metabolic acidosis. Drugs causing Type IV RTA by reducing aldosterone levels or action: low molecular weight heparin (suppresses aldosterone synthesis), NSAIDs (reduce renin \u2192 reduce aldosterone), ACE inhibitors\/ARBs, spironolactone, and trimethoprim (blocks collecting duct ENaC sodium channels, mimicking aldosterone deficiency \u2192 hyperkalaemia). Penicillin causes non-anion gap acidosis via Type I or II RTA mechanisms (distal tubular toxicity) but is NOT a recognised cause of Type IV RTA. Penicillin is the exception.'\n },\n {\n id:45,\n stem:'Treatment options available for management of renal artery stenosis is\/are:',\n correct:'All of these',\n options:['Medical treatment for hypertension by antihypertensive drugs','Angioplasty with or without stenting','Renal artery bypass surgery','All of these'],\n exp:'Renal artery stenosis (RAS \u2014 atherosclerotic or fibromuscular dysplasia) can be managed by: (1) Medical therapy \u2014 ACE inhibitors\/ARBs (caution in bilateral RAS), calcium channel blockers, statins, antiplatelet drugs \u2014 used in stable patients with mild functional impairment. (2) Percutaneous transluminal renal angioplasty (PTRA) \u00b1 stenting \u2014 first choice for revascularisation, especially for fibromuscular dysplasia. (3) Surgical renal artery bypass \u2014 for complex anatomy, failed angioplasty, or combined aortic surgery. All three approaches are established management options, making \"all of these\" the correct answer.'\n },\n {\n id:46,\n stem:'A reversible cause of dementia is:',\n correct:'Subdural haematoma',\n options:['Alzheimer disease','Huntington chorea','Parkinson disease','Subdural haematoma'],\n exp:'Reversible (\"treatable\") causes of dementia \u2014 the \"DEMENTIA\" mnemonic: Drugs, Emotional (depression \u2014 pseudodementia), Metabolic (hypothyroidism, B12 deficiency, Wilson\\'s), Ears\/Eyes (sensory deprivation), Normal pressure hydrocephalus, Trauma (subdural haematoma), Infections (neurosyphilis, HIV), Alcohol\/Arterial. Subdural haematoma causes cognitive decline, confusion, and gait disturbance by compressing brain tissue \u2014 surgical evacuation reverses the dementia. Alzheimer\\'s, Huntington\\'s, and Parkinson\\'s are all neurodegenerative dementias with irreversible progressive neuronal loss. Subdural haematoma is the classic surgically reversible cause of dementia.'\n },\n {\n id:47,\n stem:'In Wallenberg syndrome, where is the site of lesion?',\n correct:'Lateral medulla',\n options:['Lateral medulla','Medial medulla','Pontomedullary junction','Dorsal midbrain'],\n exp:'Wallenberg syndrome (lateral medullary syndrome) = infarction of the LATERAL MEDULLA, most commonly from posterior inferior cerebellar artery (PICA) occlusion or vertebral artery occlusion. Features: ipsilateral \u2014 facial pain\/temperature loss (V), Horner\\'s syndrome, cerebellar ataxia (limb), dysphagia\/dysarthria (IX, X), palatal palsy; contralateral \u2014 body pain\/temperature loss (spinothalamic). Medial medullary syndrome (Dejerine syndrome) = contralateral hemiplegia, contralateral loss of vibration\/proprioception, ipsilateral tongue weakness. Lateral medulla = Wallenberg.'\n },\n {\n id:48,\n stem:'The following are features of polycythaemia vera EXCEPT:',\n correct:'Elevated plasma erythropoietin levels',\n options:['Elevated red cell mass','Normal arterial oxygen saturation','Splenomegaly','Elevated plasma erythropoietin levels'],\n exp:'Polycythaemia vera (PCV) is a JAK2 mutation-driven myeloproliferative neoplasm with autonomous RBC overproduction. Features: elevated red cell mass (primary), normal arterial O\u2082 saturation (distinguishes from secondary polycythaemia), splenomegaly (extramedullary haematopoiesis), hyperviscosity, thrombosis, plethora, and aquagenic pruritus. Erythropoietin is SUPPRESSED\/LOW in PCV \u2014 because the autonomous overproduction of RBCs suppresses the normal feedback EPO stimulus (negative feedback). Elevated EPO would indicate SECONDARY polycythaemia (hypoxia, renal tumour). Elevated plasma EPO is the feature that does NOT fit PCV.'\n },\n {\n id:49,\n stem:'Which of the following conditions is associated with cigarette smoking?',\n correct:'Desquamative interstitial pneumonia',\n options:['Non-specific interstitial pneumonia','Acute interstitial pneumonia','Cryptogenic organising pneumonia','Desquamative interstitial pneumonia'],\n exp:'Smoking-related interstitial lung diseases: Desquamative Interstitial Pneumonia (DIP) \u2014 strongly associated with heavy smoking (>90% are smokers); macrophage accumulation in alveolar spaces. Respiratory Bronchiolitis-ILD (RB-ILD) \u2014 also smoking-related. Pulmonary Langerhans cell histiocytosis \u2014 almost exclusively in smokers. Non-specific interstitial pneumonia (NSIP) is associated with connective tissue diseases and drug reactions, not smoking. Acute interstitial pneumonia (Hamman-Rich) is idiopathic acute lung injury. Cryptogenic organising pneumonia follows infections\/drugs. DIP is the smoking-associated ILD among the options.'\n },\n {\n id:50,\n stem:'Which of the following is NOT true of Wilson disease?',\n correct:'Serum ceruloplasmin is increased',\n options:['There is hepatolenticular degeneration','Autosomal recessive transmission','Serum ceruloplasmin is increased','Urinary copper is increased'],\n exp:'Wilson\\'s disease (hepatolenticular degeneration, ATP7B mutation): (1) Hepatolenticular degeneration \u2014 liver + basal ganglia (lenticular nuclei) \u2014 TRUE. (2) Autosomal recessive \u2014 TRUE. (4) Urinary copper elevated (>100 \u00b5g\/24h) because copper cannot be incorporated into ceruloplasmin and excreted into bile \u2014 TRUE. Serum ceruloplasmin is characteristically DECREASED (<20 mg\/dL) in ~85% of cases \u2014 because ceruloplasmin requires copper incorporation for stability, and without ATP7B function, apo-ceruloplasmin is rapidly degraded. Increased ceruloplasmin is NOT true \u2014 it is the exception.'\n },\n {\n id:51,\n stem:'A 55-year-old patient on anti-TB treatment with Rifampicin, Isoniazid, Pyrazinamide and Ethambutol complains of pain in large and small joints. Which one of the following investigations will you order?',\n correct:'Serum uric acid',\n options:['Serum creatinine','Serum amylase','SGOT\/SGPT','Serum uric acid'],\n exp:'Pyrazinamide (PZA) is the anti-TB drug responsible for arthralgia and joint pain. PZA is metabolised to pyrazinoic acid, which competitively inhibits tubular secretion of uric acid by the renal tubules \u2192 hyperuricaemia \u2192 gouty arthritis (affecting both large and small joints). The investigation of choice is SERUM URIC ACID \u2014 a level >7 mg\/dL confirms hyperuricaemia. Management: allopurinol, NSAIDs, colchicine, hydration. Liver enzymes (SGOT\/SGPT) would be checked if hepatitis is suspected. Serum creatinine is for nephrotoxicity (aminoglycosides). Serum amylase is for pancreatitis.'\n },\n {\n id:52,\n stem:'The following diseases can cause bullous lesions in the skin EXCEPT:',\n correct:'Pityriasis rosea',\n options:['Pemphigus','Impetigo','Toxic epidermal necrolysis','Pityriasis rosea'],\n exp:'Bullous (blistering) skin conditions: Pemphigus vulgaris \u2014 intraepidermal acantholytic bullae; Nikolsky sign positive. Bullous impetigo \u2014 superficial vesiculopustules from S. aureus exfoliatin toxin. Toxic epidermal necrolysis (TEN) \u2014 massive full-thickness epidermal detachment causing large bullae (>30% BSA) \u2014 life-threatening drug reaction. Pityriasis rosea is a self-limiting viral eruption (HHV-7 suspected) characterised by a herald patch followed by a salmon-coloured \"Christmas tree\" papulosquamous rash on the trunk \u2014 it is NOT a bullous disease. Pityriasis rosea causes scaling plaques, NOT bullae.'\n },\n {\n id:53,\n stem:'Which of the following disorders is autosomal recessive?',\n correct:'Cystic fibrosis',\n options:['Cystic fibrosis','Nail-patella syndrome','Myotonic dystrophy','Huntington disease'],\n exp:'Inheritance patterns: Cystic fibrosis (CFTR mutation, chromosome 7) = AUTOSOMAL RECESSIVE \u2014 the most common lethal autosomal recessive disorder in Caucasians. Nail-patella syndrome (LMX1B mutation) = autosomal dominant. Myotonic dystrophy (DMPK trinucleotide repeat expansion) = autosomal dominant (with anticipation). Huntington disease (HTT CAG repeat expansion) = autosomal dominant (with anticipation). Cystic fibrosis is the only autosomal recessive condition in this list.'\n },\n {\n id:54,\n stem:'Which one of the following is the most appropriate treatment for overdose aspirin ingestion?',\n correct:'Sodium bicarbonate',\n options:['Acetazolamide','Sodium bicarbonate','Allopurinol','N-acetyl-cysteine'],\n exp:'Salicylate (aspirin) poisoning treatment: IV sodium bicarbonate is the cornerstone \u2014 it alkalinises blood and urine (target urine pH 7.5\u20138.5). In alkaline urine, salicylate (a weak acid) is ionised \u2192 trapped in renal tubular lumen \u2192 cannot be reabsorbed \u2192 enhanced urinary excretion. This \"ion trapping\" dramatically increases salicylate clearance. Acetazolamide is contraindicated \u2014 it alkalinises urine but acidifies blood, worsening salicylate CNS penetration. N-acetylcysteine is for paracetamol (acetaminophen) overdose. Allopurinol has no role. Haemodialysis is for severe cases (level >700 mg\/L).'\n },\n {\n id:55,\n stem:'Killer T cells responsible for defence against intracellular pathogens are expressed by which of the following CD phenotypes?',\n correct:'CD 8',\n options:['CD 2','CD 5','CD 8','CD 10'],\n exp:'Cytotoxic T lymphocytes (CTLs, \"killer T cells\") express CD8 as their co-receptor \u2014 they recognise antigen presented on MHC Class I molecules (expressed on ALL nucleated cells). CD8+ CTLs kill virus-infected cells, tumour cells, and intracellular bacteria by perforin\/granzyme-mediated apoptosis and FasL-Fas interaction. CD4+ T cells (helper T cells) recognise MHC Class II and co-ordinate immune responses. CD2 is a pan-T cell marker (adhesion). CD5 is on T cells and B1 B cells. CD10 (CALLA) is on B cell precursors and germinal centre cells. CD8 = cytotoxic T cells = defence against intracellular pathogens.'\n },\n {\n id:56,\n stem:'Intravenous immunoglobulin therapy is approved in the following conditions EXCEPT:',\n correct:'Severe rheumatoid arthritis',\n options:['Kawasaki disease','Severe rheumatoid arthritis','Guillain-Barr\u00e9 syndrome','Dermatomyositis'],\n exp:'Approved indications for IVIg: Kawasaki disease (prevents coronary aneurysms \u2014 single dose 2 g\/kg), Guillain-Barr\u00e9 syndrome (accelerates recovery), dermatomyositis\/polymyositis (refractory cases), ITP, primary immunodeficiency, myasthenia gravis crisis, CIDP, and haemolytic disease of the newborn. Severe rheumatoid arthritis is NOT an approved indication for IVIg \u2014 RA is managed with DMARDs (methotrexate, sulfasalazine), biologics (anti-TNF, anti-IL-6, rituximab), and steroids. IVIg has no established role in RA management. Rheumatoid arthritis is the exception.'\n },\n {\n id:57,\n stem:'Which of the following does NOT cause small vessel vasculitis?',\n correct:'Kawasaki disease',\n options:['Churg-Strauss Syndrome','Henoch-Sch\u00f6nlein purpura','Kawasaki disease','Granulomatosis with polyangiitis'],\n exp:'Chapel Hill Consensus Conference classification: Small vessel vasculitis \u2014 affects arterioles, capillaries, venules: Churg-Strauss (eosinophilic granulomatosis with polyangiitis), Henoch-Sch\u00f6nlein purpura (IgA vasculitis), Granulomatosis with polyangiitis (Wegener\\'s), microscopic polyangiitis, cryoglobulinaemic vasculitis. Kawasaki disease is a MEDIUM vessel vasculitis (affects medium-sized arteries \u2014 coronary, renal, hepatic arteries) along with polyarteritis nodosa. The coronary artery aneurysm in Kawasaki disease results from medium vessel involvement. Kawasaki does NOT cause small vessel vasculitis.'\n },\n {\n id:58,\n stem:'Most common cells in the peripheral blood smear of chronic myeloid leukaemia are:',\n correct:'Neutrophils',\n options:['Myeloblasts','Promyelocytes','Metamyelocytes','Neutrophils'],\n exp:'CML (BCR-ABL, Philadelphia chromosome t(9;22)) is characterised by massive granulocytic proliferation. The peripheral blood smear shows the full \"myeloid series shift\" \u2014 cells at all stages of maturation \u2014 but the PREDOMINANT cell is the mature NEUTROPHIL (segmented neutrophil). The differential in CML typically shows: neutrophils ~40\u201350%, bands ~15\u201320%, metamyelocytes ~10%, myelocytes ~10%, promyelocytes ~5%, blasts <2% in chronic phase. Basophilia and eosinophilia are also characteristic. Blast predominance (>20%) indicates blast crisis (transformation to acute leukaemia). Neutrophils are the most common cells in the CML smear.'\n },\n {\n id:59,\n stem:'Consider the following statements about infective endocarditis:\\n1. Modified Duke criteria are used for clinical diagnosis\\n2. Echocardiographic findings form one of the major Duke criteria\\n3. Presence of one major and two minor criteria is considered diagnostic of endocarditis\\n4. Presence of glomerulonephritis is a minor Duke criterion\\n\\nWhich of the statements given above are correct?',\n correct:'1, 2 and 4 only',\n options:['1, 2 and 3 only','1, 2 and 4 only','3 and 4 only','1, 2, 3 and 4'],\n exp:'Modified Duke Criteria (MDC): DEFINITE IE = 2 major, OR 1 major + 3 minor, OR 5 minor criteria. POSSIBLE IE = 1 major + 1 minor, or 3 minor. (1) MDC is the standard clinical diagnostic framework \u2014 CORRECT. (2) Echocardiographic evidence (vegetation, abscess, new valvular regurgitation) IS a major criterion \u2014 CORRECT. (3) 1 major + 2 minor = POSSIBLE, not definite IE \u2014 statement 3 is WRONG. (4) Glomerulonephritis (immune complex deposition) IS a minor criterion (under \"vascular\/immunological phenomena\") \u2014 CORRECT. Statements 1, 2, and 4 are correct.'\n },\n {\n id:60,\n stem:'A 16-year-old had an acute episode of dyspnoea, wheezing and coughing during early morning hours. The episode resolved spontaneously. What is the likely diagnosis?',\n correct:'Asthma',\n options:['Pulmonary oedema','Asthma','Panic attack','Pneumonia'],\n exp:'Acute reversible dyspnoea with wheezing and cough in a teenager, occurring in the early morning hours (circadian dip in cortisol and peak in histamine\/bronchoconstriction), and resolving spontaneously \u2014 this is classic bronchial asthma. Nocturnal\/early morning symptoms are characteristic of asthma due to circadian variation in airway tone. Spontaneous resolution (bronchodilation as cortisol rises) further supports asthma. Pulmonary oedema would not be expected in a 16-year-old without cardiac disease. Pneumonia does not resolve spontaneously within hours. Panic attack does not cause objective wheezing.'\n },\n {\n id:61,\n stem:'An elderly patient had a cerebrovascular accident diagnosed as ischaemic in nature. Which of the following is a contraindication for thrombolysis?\\n1. Onset of symptoms to time of drug administration is \u22644.5 hours\\n2. Gastrointestinal bleeding in the preceding 21 days\\n\\nSelect the correct answer:',\n correct:'2 only',\n options:['1 only','2 only','Both 1 and 2','Neither 1 nor 2'],\n exp:'IV alteplase (rt-PA) thrombolysis for acute ischaemic stroke: the therapeutic window is \u22644.5 hours from symptom onset \u2014 this is an INDICATION (eligibility criterion), NOT a contraindication. Statement 1 is therefore WRONG as a contraindication. GI bleeding within the preceding 21 days IS an absolute contraindication for thrombolysis \u2014 active or recent haemorrhage significantly increases the risk of life-threatening bleeding after rt-PA. Other contraindications: BP >185\/110, recent surgery\/trauma, platelet count <100,000, anticoagulant use, prior intracranial haemorrhage. Only statement 2 is a contraindication.'\n },\n {\n id:62,\n stem:'Consider the following insulin preparations:\\n1. Aspart\\n2. Glulisine\\n3. Detemir\\n4. Regular\\n\\nWhich of the above are considered short-acting insulin?',\n correct:'1, 2 and 4 only',\n options:['1 and 2 only','3 and 4 only','1, 2 and 4 only','1, 2, 3 and 4'],\n exp:'Insulin classification: Rapid-acting analogues: Aspart (1), Lispro, Glulisine (2) \u2014 onset 10\u201315 min, peak 1\u20132 hr, duration 3\u20135 hr. Short-acting: Regular\/soluble insulin (4) \u2014 onset 30\u201360 min, peak 2\u20134 hr, duration 6\u20138 hr. Intermediate-acting: NPH\/Isophane. Long-acting basal: Glargine, Detemir (3), Degludec \u2014 onset 1\u20134 hr, minimal peak, duration 12\u201324+ hr. The question groups rapid-acting and regular as \"short-acting\" (as opposed to basal). Detemir (3) is long-acting basal insulin. Aspart, Glulisine, and Regular (1, 2, 4) are all short\/rapid-acting. Answer: 1, 2 and 4.'\n },\n {\n id:63,\n stem:'A middle-aged male, known smoker, presented with recurrent sinusitis, haemoptysis, haematuria, arthralgia and palpable purpura. What is the most likely diagnosis?',\n correct:'Wegener granulomatosis',\n options:['Wegener granulomatosis','Goodpasture syndrome','Polyarteritis nodosa','Systemic lupus erythematosus'],\n exp:'Granulomatosis with polyangiitis (GPA, formerly Wegener\\'s): classic triad of upper respiratory tract (recurrent sinusitis, otitis, saddle nose), lower respiratory tract (haemoptysis, pulmonary nodules\/cavities), and renal involvement (haematuria, glomerulonephritis). Arthralgia and palpable purpura from small vessel vasculitis. Associated with c-ANCA (PR3-ANCA) in >90% of cases. Smoking is a risk factor. Goodpasture syndrome lacks sinusitis and purpura. PAN spares small vessels and kidneys glomerularly. SLE would show ANA\/anti-dsDNA. The upper + lower airway + renal + vasculitic skin triad = GPA.'\n },\n {\n id:64,\n stem:'A patient presents with diarrhoea, steatorrhoea and weight loss. Which of the following diseases is LEAST possible?',\n correct:'Menetrier disease',\n options:['Whipple disease','Tropical sprue','Coeliac disease','Menetrier disease'],\n exp:'Malabsorption syndrome (diarrhoea + steatorrhoea + weight loss) causes: Whipple disease (Tropheryma whipplei infection of intestinal macrophages \u2014 classic malabsorption in middle-aged men), tropical sprue (malabsorption + megaloblastic anaemia in tropical regions), and coeliac disease (gluten-sensitive enteropathy \u2014 villous atrophy, malabsorption). Menetrier disease (giant hypertrophic gastropathy) is a protein-LOSING GASTROPATHY \u2014 patients lose protein into the stomach lumen (hypoalbuminaemia, oedema) and have epigastric pain, but do NOT primarily present with steatorrhoea\/fat malabsorption. Menetrier disease is LEAST possible as the cause.'\n },\n {\n id:65,\n stem:'Consider the following statements regarding post-streptococcal glomerulonephritis (PSGN):\\n1. Immunosuppressive therapy is effective\\n2. PSGN develops one to three weeks after streptococcal pharyngitis\\n3. PSGN develops two to six weeks after impetigo\\n4. The classic presentation is acute nephritis\\n\\nWhich of the statements given above are correct?',\n correct:'2, 3 and 4 only',\n options:['1, 2 and 3 only','2, 3 and 4 only','1 and 4 only','1, 2, 3 and 4'],\n exp:'PSGN: (1) Immunosuppressive therapy is NOT effective \u2014 PSGN is self-limiting; treatment is supportive (antihypertensives, diuretics, salt restriction). Steroids\/immunosuppressants do not alter outcome \u2014 statement 1 is WRONG. (2) Latent period of 1\u20133 weeks after Group A strep PHARYNGITIS \u2014 CORRECT (shorter latent period). (3) Latent period of 2\u20136 weeks after impetigo (skin infection) \u2014 CORRECT (longer latent period due to different streptococcal strains and skin vs mucosal immunity). (4) Acute nephritis syndrome (haematuria, oedema, hypertension, oliguria, proteinuria) is the classic presentation \u2014 CORRECT. Statements 2, 3, and 4 are correct.'\n },\n {\n id:66,\n stem:'A patient with a long-term implantable cardioverter defibrillator device developed neck and facial swelling, hoarseness of voice, nasal congestion, dysphagia and haemoptysis. The facial swelling increased in the supine position. This patient most likely developed:',\n correct:'Superior vena cava obstruction',\n options:['Cardiac tamponade','Intracardiac thrombosis','Superior vena cava obstruction','Pulmonary thromboembolism'],\n exp:'Superior Vena Cava (SVC) syndrome: obstruction of SVC venous return to the right atrium causes: facial\/neck\/arm oedema (especially worse on lying down \u2014 increased venous pressure without gravity assistance), dilated neck\/chest veins, hoarseness (recurrent laryngeal nerve), nasal congestion, dysphagia (oesophageal compression), and haemoptysis (venous hypertension). In this case, the ICD lead\/device causes SVC thrombosis or fibrous stricture \u2014 an important device complication. Tamponade causes Beck\\'s triad (\u2193BP, \u2191JVP, muffled heart sounds). PE causes pleuritic pain and dyspnoea without facial oedema. SVC syndrome fits precisely.'\n },\n {\n id:67,\n stem:'A patient with AIDS developed ophthalmoplegia, ataxia and global confusion. He is likely to have the deficiency of:',\n correct:'Thiamine',\n options:['Biotin','Niacin','Pyridoxine','Thiamine'],\n exp:'Wernicke\\'s encephalopathy (Wernicke-Korsakoff syndrome) is caused by THIAMINE (Vitamin B1) deficiency. Classic triad: ophthalmoplegia (CN VI palsy \u2014 horizontal nystagmus, lateral rectus palsy), cerebellar ataxia, and global confusion\/altered consciousness. In AIDS, thiamine deficiency occurs due to poor nutrition, malabsorption, and increased metabolic demands. Thiamine is required for pyruvate dehydrogenase and \u03b1-ketoglutarate dehydrogenase (Krebs cycle) \u2014 deficiency causes neuronal energy failure preferentially in the mammillary bodies, thalamus, and periaqueductal grey. Treatment: immediate high-dose IV thiamine.'\n },\n {\n id:68,\n stem:'An elderly male presents with persistent productive cough with large-volume purulent sputum production. He has had several episodes in the past. He also has digital clubbing. He is a case of:',\n correct:'Bronchiectasis',\n options:['Empyema','Bronchiectasis','Bronchopneumonia','Necrotising pneumonia'],\n exp:'Bronchiectasis is the diagnosis \u2014 defined by abnormal, permanent dilatation of bronchi with destruction of bronchial walls. Classic features: chronic productive cough with LARGE volumes of purulent sputum (300\u2013500 mL\/day in severe cases), \"three-layer sputum\" (frothy top, mucopurulent middle, dense sediment), recurrent respiratory infections, haemoptysis, and DIGITAL CLUBBING (chronic hypoxia + chronic infection). Empyema is a pleural collection. Bronchopneumonia is acute. Necrotising pneumonia is acute with tissue destruction. The chronicity, large sputum volume, recurrent episodes, and clubbing = bronchiectasis.'\n },\n {\n id:69,\n stem:'A chemical factory worker has acute onset dyspnoea with fever, chills and malaise following a few hours of exposure to a new chemical. These symptoms resolve in four to five days after removal from exposure. He is likely to have:',\n correct:'Hypersensitivity pneumonitis',\n options:['Hypersensitivity pneumonitis','Atypical pneumonia','Cryptogenic organising pneumonia','Non-specific interstitial pneumonia'],\n exp:'Hypersensitivity pneumonitis (HP, extrinsic allergic alveolitis): an immunological lung disease caused by repeated inhalation of organic dusts\/chemicals. Acute HP: onset 4\u20138 hours after exposure with flu-like symptoms \u2014 fever, chills, malaise, dyspnoea, dry cough. RESOLVES within days of antigen removal (this reversibility on removal is the clinical clue). Subacute and chronic forms develop with continued exposure. Atypical pneumonia has longer course and doesn\\'t resolve within days on exposure removal. COP and NSIP are chronic conditions. The acute onset + resolution on removal + occupational antigen exposure = acute hypersensitivity pneumonitis.'\n },\n {\n id:70,\n stem:'A 25-year-old man presents with nausea, vomiting and diarrhoea with crampy abdominal pain. He gives history of consumption of rice preparation in his last meal. What is the likely organism?',\n correct:'Bacillus cereus',\n options:['Clostridium perfringens','Bacillus cereus','Staphylococcus aureus','Campylobacter jejuni'],\n exp:'Bacillus cereus food poisoning has two distinct syndromes: (1) Emetic form \u2014 associated with RICE and starchy foods, incubation 1\u20136 hours, predominantly vomiting (heat-stable cereulide toxin preformed in food). (2) Diarrhoeal form \u2014 incubation 8\u201316 hours, watery diarrhoea. Rice is the classic vehicle because B. cereus spores survive cooking, germinate on cooling, and produce toxin in stored rice. \"Fried rice syndrome\" is the classic example. Staphylococcal food poisoning also causes rapid-onset vomiting but with dairy\/meat, not rice. Clostridium perfringens causes diarrhoea after meat. Campylobacter has a longer incubation. Rice + vomiting\/diarrhoea = Bacillus cereus.'\n },\n {\n id:71,\n stem:'A five-year-old child was diagnosed with nephrotic syndrome 18 months back. Successfully treated initially. Following the initial episode, the child has had 3 relapses, each successfully treated. What is the diagnosis?',\n correct:'Nephrotic syndrome, frequent relapses',\n options:['Nephrotic syndrome, infrequent relapses','Nephrotic syndrome, frequent relapses','Nephrotic syndrome, steroid dependent','Nephrotic syndrome, steroid resistant'],\n exp:'ISKDC definitions for childhood nephrotic syndrome relapse patterns: Infrequent relapses = <2 relapses in 6 months or <4 per year. Frequent relapses = \u22652 relapses in 6 months or \u22654 relapses in any 12-month period. Steroid-dependent = two consecutive relapses DURING steroid tapering or within 14 days of stopping steroids. Steroid-resistant = no remission after 4 weeks of full-dose prednisolone. This child had 3 relapses over 18 months (initial + 3 = potentially meeting \u22654 in 12 months criterion, or \u22652 in 6 months) and each RESPONDED to prednisolone. Not steroid-dependent (no relapse on tapering stated) and not resistant. FREQUENT RELAPSES is the diagnosis.'\n },\n {\n id:72,\n stem:'A 7-year-old girl presents with non-specific abdominal pain, mild distension, and poor growth. Weight 14 kg, height 95 cm, Hb 7.5 g\/dL (microcytic hypochromic), not responding to iron therapy. Which will be the first investigation to diagnose the condition?',\n correct:'Tissue transglutaminase antibodies',\n options:['Bone marrow aspiration','Tissue transglutaminase antibodies','Lower GI contrast examination','Colonoscopy\/sigmoidoscopy'],\n exp:'The clinical picture \u2014 short stature (height 95 cm at 7 years \u2014 well below 3rd percentile), poor weight gain, abdominal distension, iron-deficiency anaemia refractory to iron supplementation \u2014 in a child is the classic presentation of coeliac disease (gluten-sensitive enteropathy). Iron deficiency not responding to iron therapy strongly suggests malabsorption of iron, pointing to proximal small bowel disease. The FIRST investigation is serology: anti-tissue transglutaminase IgA antibodies (anti-tTG IgA) \u2014 highly sensitive (>95%) and specific screening test. Duodenal biopsy confirms. Bone marrow is not indicated without haematological indication. Colonoscopy examines the wrong segment.'\n },\n {\n id:73,\n stem:'A seven-year-old boy weighing 20 kg presented with upper GI bleeding (haematemesis) for 18 hours. PR 86\/min, RR 16\/min, BP 100\/70 mmHg; spleen palpable 5 cm below costal margin. Liver function tests are normal. What is the next best step in management?',\n correct:'Fluid resuscitation with crystalloids',\n options:['Fluid resuscitation with crystalloids','Intravenous vasopressin','Intravenous propranolol','Transdermal nitroglycerine'],\n exp:'This child has upper GI bleeding with splenomegaly and normal LFTs \u2014 suggesting extrahepatic portal hypertension (EHPH, portal vein thrombosis), the most common cause of portal hypertension in children without liver disease. The vitals show compensated haemodynamic state (BP 100\/70, HR 86). FIRST step: FLUID RESUSCITATION with crystalloids (normal saline or Ringer\\'s lactate) to stabilise haemodynamics before any pharmacological or endoscopic intervention. IV vasopressin\/terlipressin and somatostatin\/octreotide reduce portal pressure and are used after initial resuscitation. Propranolol is for prophylaxis, not acute bleeding. Nitroglycerine has no primary role here.'\n },\n {\n id:74,\n stem:'A seven-year-old girl presents in the emergency room with hypertension, lethargy, headache, seizures and visual disturbances. Fundus examination reveals haemorrhages and exudates. Which treatment regimen is most appropriate?',\n correct:'Intravenous labetalol infusion',\n options:['Sublingual nifedipine','Intravenous labetalol infusion','Intravenous minoxidil','Furosemide'],\n exp:'This child has hypertensive emergency with end-organ damage (hypertensive encephalopathy \u2014 seizures, altered consciousness, visual disturbances, retinal haemorrhages\/exudates). Treatment requires controlled, gradual BP reduction (max 25% in first hour, then gradual over 24\u201348 hours) using continuous IV antihypertensives. IV LABETALOL infusion (combined alpha+beta blocker) is the recommended first-line agent for hypertensive emergencies in children \u2014 allows precise titration. Sublingual nifedipine is CONTRAINDICATED \u2014 causes precipitous uncontrolled BP drop leading to stroke\/MI. IV minoxidil is not a standard agent. Furosemide alone is insufficient for hypertensive emergency.'\n },\n {\n id:75,\n stem:'On routine newborn screening at day 3 of life, the baby was found to have TSH level 40 mU\/L. What should be the next step?',\n correct:'Repeat thyroid profile within one week',\n options:['Repeat thyroid profile within one week','Start child on thyroxine immediately','Repeat thyroid profile after four weeks','Repeat thyroid profile\/start thyroxine if clinical features present, otherwise wait and watch'],\n exp:'Neonatal TSH screening: At birth, TSH physiologically surges to 60\u201380 mU\/L then falls to adult levels by day 3\u20135. A TSH of 40 mU\/L at day 3 is borderline \u2014 above the screening cut-off (usually 10\u201320 mU\/L) but in the zone where confirmation is needed before starting lifelong therapy. The recommended next step: REPEAT THYROID PROFILE (TSH + free T4) within one week to confirm persistent elevation and exclude physiological surge or sampling variation. If confirmed elevated (TSH >10 + low free T4), initiate levothyroxine immediately. Starting treatment without confirmation risks unnecessary lifelong treatment. Waiting 4 weeks would delay treatment if truly hypothyroid.'\n },\n {\n id:76,\n stem:'A five-year-old child was diagnosed with dengue fever after fever for seven days associated with rash, anorexia, myalgia and petechial haemorrhages. Which investigation is most appropriate for making the diagnosis?',\n correct:'Detection of IgM antibodies for dengue',\n options:['Detection of NS1 antigen','Platelet count','IgG capture ELISA','Detection of IgM antibodies for dengue'],\n exp:'Dengue diagnostic timeline: Days 1\u20135: NS1 antigen is detectable (best test in the first 5 days of fever). Days 5\u20137 onwards: IgM antibodies appear. By day 7 of fever, NS1 antigen levels fall while IgM antibodies (ELISA) are now reliably detectable. At day 7 of illness, IgM detection by MAC-ELISA is the most appropriate diagnostic test. IgG appears later (secondary infections). Platelet count is a severity marker, not a diagnostic test. IgG capture ELISA is used to distinguish primary vs secondary infections. For day 7 fever = IgM antibodies.'\n },\n {\n id:77,\n stem:'An eight-year-old boy diagnosed with P. vivax malaria was treated with appropriate chloroquine dosage. Fever subsided but recurred after 3 weeks. Peripheral smear was again positive for P. vivax. This child should now be treated as a case with:',\n correct:'Relapse',\n options:['Relapse','Recrudescence','Either relapse\/recrudescence','Fresh infection'],\n exp:'P. vivax has dormant liver stage parasites called HYPNOZOITES. After primary infection and treatment with chloroquine (which clears blood-stage parasites but NOT hypnozoites), hypnozoites can reactivate weeks to months later causing TRUE RELAPSE of the disease. This is distinct from RECRUDESCENCE (persistence of blood-stage parasites due to inadequate treatment \u2014 specific to P. falciparum which has no hypnozoites). Recurrence at 3 weeks in P. vivax after adequate chloroquine = RELAPSE from hypnozoites. Treatment requires PRIMAQUINE (the only drug killing hypnozoites) in addition to chloroquine, after checking G6PD status.'\n },\n {\n id:78,\n stem:'A two-day-old neonate presents with cyanosis, single second heart sound, and pansystolic murmur on the left sternal border. ECG reveals left axis deviation, right atrial overload and left ventricular hypertrophy. What is the most likely diagnosis?',\n correct:'Tricuspid atresia',\n options:['Tetralogy of Fallot','Tricuspid atresia','Transposition of great arteries','Total anomalous pulmonary venous connection'],\n exp:'Tricuspid atresia: absence of the tricuspid valve \u2192 no blood flow from RA to RV \u2192 RV is hypoplastic. Blood must flow through ASD (right to left) and VSD to reach pulmonary circulation. ECG hallmarks: LEFT AXIS DEVIATION (unusual for a neonate \u2014 points strongly to TA as RV is absent\/hypoplastic), RIGHT ATRIAL ENLARGEMENT (RA receives all systemic venous return), and LEFT VENTRICULAR HYPERTROPHY (LV does all the work). Pansystolic murmur = VSD. Single S2 = hypoplastic pulmonary valve. LAD + RAE + LVH in a cyanotic neonate = tricuspid atresia.'\n },\n {\n id:79,\n stem:'A three-year-old girl cannot stand or walk. She achieved head control at one year of age. Examination reveals generalised hypotonia, brisk knee jerks and ankle clonus. What is the likely diagnosis?',\n correct:'Cerebral palsy',\n options:['Cerebral palsy','Spinal muscular atrophy','Congenital hypothyroidism','Congenital myotonic dystrophy'],\n exp:'The combination of delayed motor milestones (head control at 1 year \u2014 severely delayed, normally 3 months), generalised hypotonia (common in CP, especially in early stages), but with BRISK REFLEXES and ANKLE CLONUS (upper motor neuron signs \u2014 indicates corticospinal tract damage) points to CEREBRAL PALSY \u2014 a non-progressive disorder of movement\/posture from perinatal brain injury. SMA would show absent\/depressed reflexes (lower motor neuron). Congenital hypothyroidism causes hypotonia with depressed reflexes. Myotonic dystrophy shows hypotonia with depressed reflexes. BRISK reflexes + clonus + hypotonia = UMN lesion = cerebral palsy.'\n },\n {\n id:80,\n stem:'A child presents with sensations of itching, burning and a probable foreign body beneath the eyelids. Examination reveals photophobia, large oval follicles within the conjunctiva and preauricular adenopathy. The most likely diagnosis is:',\n correct:'Trachomatous conjunctivitis',\n options:['Epidemic keratoconjunctivitis','Vernal conjunctivitis','Trachomatous conjunctivitis','Phlyctenular conjunctivitis'],\n exp:'Trachoma (Chlamydia trachomatis, serovars A\u2013C): the leading infectious cause of blindness worldwide. Features: foreign body sensation, photophobia, large FOLLICLES on the upper tarsal conjunctiva (Herbert\\'s pits on corneal limbus in chronic cases), PREAURICULAR LYMPHADENOPATHY (a key distinguishing feature from vernal conjunctivitis), and progressive corneal scarring (pannus formation). Vernal conjunctivitis has giant cobblestone papillae on upper tarsus without preauricular nodes. Epidemic keratoconjunctivitis (adenovirus) has smaller follicles and is more acute. Phlyctenular conjunctivitis shows white nodules. 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Submitting in 10 Submit Now Combined Medical Services Examination 2017Paper I \u00b7 Part B General Medicine \u00b7 Paediatrics Questions 41 \u2013 80 Options reshuffled \u23f1 Start Timed Mode Submit Answers 0% score Your Result \u21ba Retry Quiz<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[18],"tags":[],"class_list":["post-36770","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.5 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>CMS 2017 P1 Part-B - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/05\/06\/cms-2017-p1-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2017 P1 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2017 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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