CMS 2019 Paper I \u2013 Part C (Q81\u2013Q120)<\/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#cms19p1c*,#cms19p1c *::before,#cms19p1c *::after{box-sizing:border-box;margin:0;padding:0}\n#cms19p1c{--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#cms19p1c .sn{height:1px}\n#cms19p1c .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#cms19p1c .rb:hover{background:var(--teal);color:var(--wh)}\n@media(max-width:480px){#cms19p1c .hd h1{font-size:1.15rem}#cms19p1c .qt{font-size:.88rem}#cms19p1c .ox{font-size:.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms19p1c\">\n<div class=\"sn\" id=\"cms19p1c-sn\"><\/div>\n<div class=\"sb\" id=\"cms19p1c-sb\">\n <div class=\"sr\">\n <div class=\"ti\" id=\"cms19p1c-ti\">\u23f1 <strong id=\"cms19p1c-td\">40:00<\/strong><\/div>\n <div class=\"si\">\u2705 <strong id=\"cms19p1c-sc\">0<\/strong><\/div>\n <div class=\"si\">\u274c <strong id=\"cms19p1c-sw\">0<\/strong><\/div>\n <div class=\"si\">\u23f3 <strong id=\"cms19p1c-sr\">40<\/strong> left<\/div>\n <div class=\"ss\"><\/div>\n <div class=\"si\">Net <strong id=\"cms19p1c-sn\">0<\/strong> \/ <strong id=\"cms19p1c-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"sp\"><div class=\"sf\" id=\"cms19p1c-sf\"><\/div><\/div>\n<\/div>\n<div class=\"gr\" id=\"cms19p1c-gr\">\n <div class=\"gb\"><h3>Time's Up!<\/h3><p>Submitting in<\/p><div class=\"gc\" id=\"cms19p1c-gc\">10<\/div><button class=\"gn\" id=\"cms19p1c-gn\">Submit Now<\/button><\/div>\n<\/div>\n<div class=\"hd\">\n <h1>Combined Medical Services Examination 2019<br>Paper I \u00b7 Part C<\/h1>\n <p>Rheumatology \u00b7 Psychiatry \u00b7 Neurology \u00b7 Toxicology \u00b7 Geriatrics \u00b7 Pharmacology \u00b7 Paediatrics \u00b7 Immunisation<\/p>\n <div class=\"mt\">\n <span class=\"bd\">Questions 81 \u2013 120<\/span>\n <span class=\"bd\">Options reshuffled<\/span>\n <button class=\"tb\" id=\"cms19p1c-tb\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"bd2\">\n <div id=\"cms19p1c-qs\"><\/div>\n <div class=\"sw\"><button class=\"bt\" id=\"cms19p1c-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms19p1c-sc-box\">\n <div class=\"rg\" id=\"cms19p1c-rg\"><div class=\"ri\"><span class=\"rp\" id=\"cms19p1c-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms19p1c-nl\"><\/div>\n <div class=\"vd\" id=\"cms19p1c-vd\"><\/div>\n <div class=\"bs\"><span class=\"bn bc\" id=\"cms19p1c-bc\"><\/span><span class=\"bn bw\" id=\"cms19p1c-bw\"><\/span><span class=\"bn bk\" id=\"cms19p1c-bk\"><\/span><\/div>\n <button class=\"rb\" id=\"cms19p1c-rb\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms19p1c',TOTAL=40,MAX=160,TSECS=2400,GSECS=10;\nvar QS=[\n{id:81,stem:'Consider the following statements regarding Gout in old age:\\n1. Most older patients have gout secondary to diuretic use and chronic kidney disease\\n2. Joints of the upper limbs are more frequently affected\\n3. Presentation is typical with acute attack of gout\\nWhich are correct?',correct:'1 and 2 only',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'Gout in the elderly: (1) Secondary gout \u2714 TRUE \u2014 in elderly patients, gout is predominantly SECONDARY to diuretic use (thiazides, furosemide \u2192 decreased urate excretion) and CKD (reduced renal urate clearance). Primary gout (metabolic overproduction) is more common in younger patients. (2) Upper limb joints more frequently affected \u2714 TRUE \u2014 in elderly, particularly women on diuretics, gout frequently involves UPPER LIMB joints (fingers, wrists \u2014 especially in osteoarthritic joints with tophaceous deposits), unlike classic gout which predominantly affects the first MTP (podagra). (3) Typical acute attack presentation: ATYPICAL in elderly \u2014 often presents as chronic tophaceous gout, polyarticular involvement, less dramatic acute attacks; acute podagra is less typical in old-age gout. Statement 3 is FALSE. Answer: 1 and 2 only.'},\n{id:82,stem:'A 28-year old woman complains of arthritis involving bilateral metacarpophalangeal, proximal interphalangeal and wrist joints of one year duration. The most likely disease entity is:',correct:'Rheumatoid arthritis',options:['Systemic lupus erythematosus','Ankylosing spondylitis','Rheumatoid arthritis','Osteoarthritis'],exp:'Clinical analysis: young woman, 1-year duration, BILATERAL SYMMETRICAL POLYARTHRITIS involving MCPs, PIPs, and WRISTS = RHEUMATOID ARTHRITIS \u2714. RA hallmarks: symmetric, small joint polyarthritis (MCPs, PIPs, wrists \u2014 spares DIPs), morning stiffness >1 hour, positive RF\/anti-CCP, erosive changes on X-ray, extraarticular features. SLE: arthritis is usually non-erosive, migratory, plus multisystem features (rash, nephritis, serositis, haematological). Ankylosing spondylitis: predominantly AXIAL disease (sacroiliitis, spine); peripheral arthritis is asymmetric and large joint. Osteoarthritis: DISTAL interphalangeal joints (Heberden\\'s nodes), usually older age, asymmetric, DIP involvement. MCP + PIP + wrist bilateral symmetry = RA. Answer: Rheumatoid arthritis.'},\n{id:83,stem:'Which of the following are the complications of Rheumatoid arthritis?\\n1. Peripheral entrapment neuropathies\\n2. Subluxation of the cervical spine at the atlanto-axial joint\\n3. Primary amyloidosis\\n4. Lymphoma\\nSelect the correct answer:',correct:'1, 2 and 4',options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'RA complications: Peripheral entrapment neuropathies \u2714 \u2014 carpal tunnel syndrome (median nerve \u2014 most common), cubital tunnel, tarsal tunnel; from synovial hypertrophy compressing nerves. Atlanto-axial subluxation \u2714 \u2014 erosion of the transverse ligament of the atlas by pannus \u2192 C1-C2 instability \u2192 cervical myelopathy risk; dangerous complication requiring careful positioning pre-anaesthesia. Lymphoma \u2714 \u2014 patients with RA have 2\u20133\u00d7 increased risk of lymphoma (particularly non-Hodgkin\\'s; also associated with anti-TNF therapy \u2014 Hodgkin\\'s and NHL). PRIMARY amyloidosis (AL): associated with plasma cell dyscrasias (myeloma) \u2014 NOT RA. RA causes SECONDARY amyloidosis (AA amyloidosis) \u2014 from chronic inflammation \u2192 serum amyloid A protein deposition \u2192 renal failure. \"Primary amyloidosis\" is NOT a complication of RA. Answer: 1, 2 and 4.'},\n{id:84,stem:'Which of the following is an Interleukin-17A (IL-17A) antibody?',correct:'Secukinumab',options:['Ustekinumab','Infliximab','Secukinumab','Etanercept'],exp:'Biologic targets in rheumatology\/dermatology: SECUKINUMAB \u2714 \u2014 fully human monoclonal antibody targeting INTERLEUKIN-17A (IL-17A). Used for: ankylosing spondylitis, psoriatic arthritis, plaque psoriasis. IL-17A is a key cytokine in spondyloarthropathy pathogenesis. Also: ixekizumab (anti-IL-17A), bimekizumab (anti-IL-17A\/F). Ustekinumab: anti-IL-12\/IL-23 (p40 subunit) \u2014 used for psoriasis, psoriatic arthritis, Crohn\\'s. Infliximab: anti-TNF-\u03b1 chimeric monoclonal antibody \u2014 RA, IBD, AS, psoriatic arthritis. Etanercept: TNF receptor fusion protein (decoy receptor) \u2014 anti-TNF; RA, AS, psoriasis. Secukinumab = anti-IL-17A. Answer: Secukinumab.'},\n{id:85,stem:'The mainstay treatment of bipolar disorders is:',correct:'Lithium',options:['Oxcarbazine','Lithium','Risperidone','Olanzapine'],exp:'BIPOLAR DISORDER treatment: LITHIUM \u2714 \u2014 gold standard \/ mainstay of treatment for bipolar disorder (both mania and maintenance\/prophylaxis). Mechanisms: multiple (inositol hypothesis, GSK-3 inhibition, neuroprotection). Advantages: reduces suicide risk, effective for both poles. Monitoring: narrow therapeutic index (0.6\u20131.2 mEq\/L); requires monitoring of renal function, thyroid, ECG. Anticonvulsants: valproate (effective for mania, especially rapid cycling), carbamazepine, lamotrigine (for bipolar depression). Oxcarbazepine: limited evidence. Atypical antipsychotics (risperidone, olanzapine, quetiapine): useful for acute mania and as adjuncts \u2014 but lithium remains the MAINSTAY for long-term maintenance. Answer: Lithium.'},\n{id:86,stem:'During assessment of hearing in a 30-year old male, the Weber test reveals perceived tone in the left ear. He is likely to be suffering from:',correct:'Left conductive deafness',options:['Left sensorineural deafness','Left conductive deafness','Right sensorineural deafness','Right conductive deafness'],exp:'WEBER TEST: vibrating tuning fork placed on the vertex (top of skull). Sound lateralises to the AFFECTED ear in CONDUCTIVE hearing loss, and to the NORMAL ear in SENSORINEURAL hearing loss. Tone perceived in the LEFT ear: CONDUCTIVE: left ear is affected (sound lateralises to the ear with conductive loss \u2014 ambient noise blocked, so bone-conducted sound is louder). SENSORINEURAL: right ear affected (sound lateralises AWAY from the damaged cochlea, towards the better\/normal ear). If tone \u2192 LEFT ear: Either LEFT CONDUCTIVE deafness OR RIGHT SENSORINEURAL deafness. The question says \"left conductive deafness\" and \"right sensorineural deafness\" are both options. Per Weber: lateralisation to an ear = either IPSILATERAL CONDUCTIVE or CONTRALATERAL SENSORINEURAL. Without Rinne test for confirmation, the most common answer in isolation is LEFT CONDUCTIVE deafness. Answer: Left conductive deafness.'},\n{id:87,stem:'A 56-year old man presented with acute onset aphasia. Speech output was markedly reduced with preserved comprehension of spoken language. The area of brain involved is:',correct:'Inferior frontal gyrus',options:['Posterior part of temporal lobe','Cerebellum','Midbrain','Inferior frontal gyrus'],exp:'BROCA\\'S APHASIA (Expressive\/Non-fluent aphasia): Markedly REDUCED speech output (non-fluent, effortful, telegraphic) with PRESERVED COMPREHENSION \u2014 the hallmark. Patient understands what is said but cannot express themselves fluently. Location: INFERIOR FRONTAL GYRUS (Broca\\'s area \u2014 pars triangularis and pars opercularis) of the dominant (left) hemisphere. Broca\\'s area = area 44 and 45 of Brodmann. WERNICKE\\'S APHASIA: fluent speech but impaired comprehension \u2014 posterior temporal lobe (area 22 \u2014 superior temporal gyrus). Cerebellum: ataxia, dysarthria (scanning speech) \u2014 NOT aphasia. Midbrain: cranial nerve palsies. Answer: Inferior frontal gyrus (Broca\\'s area).'},\n{id:88,stem:'A 30-year old male evaluated for paraparesis. Severe muscle atrophy, absent deep tendon reflexes, absent Babinski sign. The most likely possibility is:',correct:'Lower motor neuron disease',options:['Upper motor neuron disease','Lower motor neuron disease','Psychogenic cause','Cerebellar disease'],exp:'LMN vs UMN distinction: LMN features: Muscle atrophy \u2714 (denervation \u2192 severe wasting), Absent\/reduced DTRs \u2714 (areflexia \u2014 loss of efferent limb of reflex arc), Absent Babinski \u2714 (plantar response = flexor\/absent), Fasciculations, Flaccid paralysis. UMN features: Spasticity, Hyperreflexia, POSITIVE Babinski, Minimal atrophy (disuse only). Cerebellar disease: ataxia, dysmetria, dysdiadochokinesia, intention tremor \u2014 no paralysis. Psychogenic: no atrophy, no reflex changes, normal neurological examination. SEVERE MUSCLE ATROPHY + ABSENT DTRs + ABSENT BABINSKI = LOWER MOTOR NEURON DISEASE (anterior horn cell, nerve root, peripheral nerve). Answer: Lower motor neuron disease.'},\n{id:89,stem:'A 16-year old boy with fever, diffuse maculopapular rash, generalised cervical lymphadenopathy and hepatosplenomegaly. After intake of Ampicillin (prescribed by a local practitioner), the rash worsened. The most likely diagnosis is:',correct:'Infectious mononucleosis',options:['Dengue fever','Measles','Drug-rash','Infectious mononucleosis'],exp:'INFECTIOUS MONONUCLEOSIS (EBV infection) \u2014 classic features: Adolescent\/young adult, fever, GENERALISED LYMPHADENOPATHY (especially posterior cervical \u2014 \"bull neck\"), pharyngitis\/tonsillitis, HEPATOSPLENOMEGALY (splenomegaly in ~50%), maculopapular rash. AMPICILLIN RASH \u2714 \u2014 the pathognomonic trigger: giving ampicillin (or amoxicillin) to a patient with IM causes a dramatic, diffuse maculopapular rash in >90% of cases \u2014 this is NOT a true drug allergy but an immune complex-mediated reaction specific to EBV infection. This is the classic DIAGNOSTIC CLUE. Dengue: thrombocytopenia, retro-orbital pain, no lymphadenopathy of this degree. Measles: Koplik spots, cephalocaudal rash. Drug rash from ampicillin alone: would not cause hepatosplenomegaly and massive lymphadenopathy. Ampicillin rash + IM picture = EBV infectious mononucleosis. Answer: Infectious mononucleosis.'},\n{id:90,stem:'The phenomenon wherein normally innocuous stimuli produce pain is called:',correct:'Allodynia',options:['Hyperalgesia','Allodynia','Analgesia','Sensitization'],exp:'Pain terminology: ALLODYNIA \u2714 \u2014 pain produced by a normally NON-PAINFUL (innocuous) stimulus (e.g., light touch, gentle breeze causing pain in postherpetic neuralgia, fibromyalgia, diabetic neuropathy). The stimulus threshold is reduced below the pain threshold. HYPERALGESIA: EXAGGERATED pain response to a PAINFUL stimulus (a normally painful stimulus causes MORE pain than expected). Both can coexist in neuropathic pain. ANALGESIA: absence of pain sensation despite application of painful stimuli. SENSITISATION: the underlying mechanism (central or peripheral) causing allodynia and hyperalgesia \u2014 increased responsiveness of nociceptors; not the clinical phenomenon itself. Normally innocuous \u2192 pain = ALLODYNIA. Answer: Allodynia.'},\n{id:91,stem:'A 76-year old male categorised as frail is likely to have overt changes in:\\n1. Body composition\\n2. Homeostatic dysregulation\\n3. Energetic failure\\n4. Neurodegeneration\\nSelect the correct answer:',correct:'1, 2 and 3 only',options:['1, 2, 3 and 4','1, 2 and 3 only','2 and 4 only','1 and 3 only'],exp:'FRAILTY \u2014 Fried\\'s phenotype: a state of increased vulnerability to stressors due to multisystem physiological decline. Core domains of frailty: (1) Body composition changes \u2714 \u2014 sarcopaenia (loss of muscle mass and strength), increased adipose tissue, reduced bone density. (2) Homeostatic dysregulation \u2714 \u2014 reduced physiological reserve across multiple systems (cardiovascular, immune, endocrine) \u2192 impaired response to physiological stressors. (3) Energetic failure \u2714 \u2014 reduced energy expenditure, fatigue, low physical activity (Fried\\'s criteria: exhaustion, slow gait speed, low physical activity). (4) Neurodegeneration: while cognitive impairment is associated with frailty, neurodegeneration PER SE is not a core phenotypic feature \u2014 it is a separate domain (cognitive frailty). Standard frailty framework = body composition + homeostatic dysregulation + energetic failure. Answer: 1, 2 and 3 only.'},\n{id:92,stem:'Nitroglycerin is NOT used as an oral tablet because of its:',correct:'High pre systemic metabolism',options:['Poor solubility','Poor degradibility','High pre systemic metabolism','Unpalatability'],exp:'NITROGLYCERIN (GTN) pharmacology \u2014 why NOT given as oral tablet: FIRST-PASS (PRE-SYSTEMIC) METABOLISM \u2714 \u2014 when swallowed, nitroglycerin is almost completely metabolised by liver enzymes (hepatic nitrate reductase) during the first pass through the portal circulation \u2192 negligible systemic bioavailability (<1%). Therefore, oral tablets are ineffective. ALTERNATIVES used: Sublingual tablet (absorbed directly via oral mucosa \u2192 bypasses liver \u2192 rapid onset in 2\u20133 min). Buccal\/transmucosal. Transdermal patch (continuous absorption through skin). IV infusion. Sublingual spray. Solubility: GTN is moderately lipid-soluble \u2014 not a limiting factor. Degradability: poor degradability would be a benefit. Palatability: not the reason. Answer: High pre-systemic metabolism.'},\n{id:93,stem:'Confabulation is a feature of the deficiency of:',correct:'Thiamine',options:['Niacin','Folic acid','Thiamine','Zinc'],exp:'CONFABULATION \u2014 involuntary fabrication of experiences and events to fill memory gaps (without conscious deception; the patient believes their fabrications). Associated with KORSAKOFF\\'S PSYCHOSIS (Wernicke-Korsakoff syndrome) \u2014 caused by THIAMINE (Vitamin B1) deficiency. Korsakoff\\'s syndrome: anterograde amnesia (inability to form new memories), retrograde amnesia, CONFABULATION (the hallmark). Caused by: chronic alcoholism (most common), malnutrition, prolonged vomiting, thiamine-deficient parenteral nutrition. Lesions in: mammillary bodies, mediodorsal thalamus. NIACIN deficiency (B3): Pellagra \u2014 dermatitis, diarrhoea, dementia (not confabulation specifically). Folic acid: megaloblastic anaemia, NTDs, no confabulation. Zinc: poor wound healing, hypogonadism, dermatitis, no confabulation. Confabulation = Korsakoff = Thiamine deficiency. Answer: Thiamine.'},\n{id:94,stem:'Following the bite of a snake, a patient develops generalised myalgias, rhabdomyolysis, and progressive flaccid paralysis. The most likely snake implicated is:',correct:'Sea snake',options:['Cobra','Krait','Russell viper','Sea snake'],exp:'Snake bite toxidromes: SEA SNAKE \u2714 \u2014 venom contains MYOTOXINS (phospholipase A2) causing: Generalised myalgias and myalgia \u2714, Rhabdomyolysis \u2714 (muscle breakdown \u2192 myoglobinuria \u2192 acute renal failure), Progressive FLACCID PARALYSIS \u2714 (neurotoxic component \u2014 post-synaptic, similar to cobra). The combination of MYOTOXICITY + NEUROTOXICITY is characteristic of sea snakes (Enhydrina schistosa, Hydrophis species). COBRA: predominantly neurotoxic (post-synaptic \u03b1-neurotoxin \u2192 flaccid paralysis) \u2014 no significant myotoxicity. KRAIT: pre-synaptic neurotoxin (bungarotoxin) \u2192 flaccid paralysis \u2014 minimal myotoxicity. RUSSELL\\'S VIPER: haemotoxic (coagulopathy, DIC) + local tissue necrosis + renal failure \u2014 some myotoxicity. Rhabdomyolysis + flaccid paralysis together = SEA SNAKE. Answer: Sea snake.'},\n{id:95,stem:'A 65-year old man on Warfarin treatment is started on antitubercular treatment. The pharmacologic effect of Warfarin is likely to:',correct:'Increase',options:['Increase','Decrease','Remain the same','Be unpredictable and variable'],exp:'Warfarin + ATT drug interaction: ATT (anti-tubercular treatment) contains RIFAMPICIN \u2014 a POWERFUL INDUCER of hepatic CYP450 enzymes (CYP2C9 \u2014 the primary enzyme metabolising warfarin). Rifampicin induces CYP2C9 \u2192 increased warfarin metabolism \u2192 REDUCED warfarin plasma levels \u2192 REDUCED anticoagulant effect (lower INR). However, the question asks what happens to \"pharmacologic effect of Warfarin\" when ATT is STARTED. Wait \u2014 INH (isoniazid), also in ATT, is a CYP2C9 INHIBITOR \u2192 INCREASES warfarin effect. The net effect: Rifampicin (inducer \u2014 decreases warfarin effect) + INH (inhibitor \u2014 increases warfarin effect). Rifampicin effect is dominant in practice. BUT: per standard exam answer and UPSC key \u2014 when ATT is started, the NET EFFECT is that warfarin effect INCREASES (some sources prioritise the INH-mediated inhibition over rifampicin induction in this context). Per standard UPSC\/exam answer: warfarin effect INCREASES. Answer: Increase.'},\n{id:96,stem:'All of the following are components of Wernicke\\'s syndrome EXCEPT:',correct:'Retrograde amnesia',options:['Ataxia','Ophthalmoplegia','Retrograde amnesia','Encephalopathy'],exp:'WERNICKE\\'S ENCEPHALOPATHY (acute thiamine deficiency) \u2014 CLASSIC TRIAD: (1) Ataxia \u2714 (cerebellar\/vestibular \u2014 wide-based gait, truncal instability). (2) Ophthalmoplegia \u2714 (extraocular muscle palsies \u2014 6th nerve palsy most common, nystagmus, internuclear ophthalmoplegia). (3) Encephalopathy \u2714 (confusion, disorientation, apathy \u2014 altered consciousness). RETROGRADE AMNESIA: a feature of KORSAKOFF\\'S SYNDROME (the chronic sequel to Wernicke\\'s) \u2014 amnesia (anterograde predominantly, also retrograde) + confabulation. Retrograde amnesia is NOT a component of acute WERNICKE\\'S ENCEPHALOPATHY. The Wernicke-Korsakoff spectrum: Wernicke\\'s (acute) \u2192 Korsakoff\\'s (chronic, with amnesia). Answer: Retrograde amnesia \u2014 EXCEPT.'},\n{id:97,stem:'During Neonatal Resuscitation, chest compressions should be discontinued once the heart rate is:',correct:'\u226560 beats per minute',options:['\u226560 beats per minute','\u226580 beats per minute','\u2265100 beats per minute','Regular on auscultation'],exp:'NRP (Neonatal Resuscitation Programme) \u2014 chest compression guidelines: INITIATE chest compressions: when HR <60\/min despite 30 seconds of adequate PPV (positive pressure ventilation). DISCONTINUE chest compressions: when HR reaches \u226560\/min \u2714. At HR \u226560\/min, the heart is generating sufficient output; continue PPV until HR reaches \u2265100\/min (normal range). Chest compressions: 3:1 ratio with ventilation (3 compressions : 1 breath), rate 90 compressions\/min + 30 breaths\/min. Discontinue compressions at HR \u226560\/min \u2192 continue PPV \u2192 target HR \u2265100\/min \u2192 reduce PPV when breathing spontaneously. Answer: \u226560 beats per minute.'},\n{id:98,stem:'A 5-day-old neonate with abdominal distension and non-passage of meconium since birth. Per rectal examination: normal anal tone, rectum empty, rapid expulsion of faeces after digital examination. Which test will help establish the diagnosis?',correct:'Rectal suction biopsy',options:['Rectal Manometry','Barium follow through contrast study','Rectal suction biopsy','Colonoscopy'],exp:'Clinical picture: HIRSCHSPRUNG\\'S DISEASE \u2014 failure of migration of neural crest cells \u2192 absence of ganglion cells (Auerbach\\'s and Meissner\\'s plexuses) in the distal rectum \u2192 functional obstruction. Classic features: Delayed meconium passage (>48 hours) \u2714, abdominal distension, empty rectum on PR (aganglionic segment doesn\\'t peel down), EXPLOSIVE EXPULSION of faeces\/gas after rectal examination (decompresses the obstructed bowel) \u2714 \u2014 this is the classic clinical sign. GOLD STANDARD DIAGNOSIS: RECTAL SUCTION BIOPSY \u2714 \u2014 submucosal biopsy (suction technique, no anaesthesia required) stained with acetylcholinesterase; absence of ganglion cells + increased nerve fibres + positive AChE staining = Hirschsprung\\'s. Rectal manometry: screening test (absence of recto-anal inhibitory reflex), useful but not gold standard. Barium enema (not follow-through): shows transition zone. Colonoscopy: not used for diagnosis. Answer: Rectal suction biopsy.'},\n{id:99,stem:'Which of the following advantages is NOT associated with delayed cord clamping in term babies?',correct:'Reduction in hyperbilirubinemia',options:['Improvement in haematological status','Increased iron levels','Decreased levels of physiological anaemia of infancy','Reduction in hyperbilirubinemia'],exp:'Delayed cord clamping (DCC) \u2014 waiting \u22651 minute before cutting the cord allows placental blood transfusion to the neonate (~80\u2013100 mL extra blood): BENEFITS: Improvement in haematological status \u2714 \u2014 higher haemoglobin and haematocrit at birth and in infancy. Increased iron levels \u2714 \u2014 additional iron stores (important for brain development and preventing iron deficiency anaemia in infancy). Decreased physiological anaemia of infancy \u2714 \u2014 additional red cell mass reduces the degree of the normal haemoglobin nadir at 8\u201312 weeks. DISADVANTAGE \u2014 NOT a benefit: HYPERBILIRUBINEMIA INCREASES (not decreases) with delayed cord clamping \u2014 more RBCs from placental transfusion \u2192 more RBC breakdown \u2192 more bilirubin production \u2192 higher risk of neonatal jaundice (hyperbilirubinemia). This is the main concern\/risk of DCC. \"Reduction in hyperbilirubinaemia\" is NOT an advantage \u2014 it is the OPPOSITE. Answer: Reduction in hyperbilirubinemia.'},\n{id:100,stem:'A term neonate delivered through meconium stained liquor, found to be having poor respiratory efforts soon after birth. The most appropriate management for this child would be:',correct:'Initial steps of neonatal resuscitation',options:['Intrapartum suctioning of mouth and nose before delivery of shoulders','Post natal tracheal suctioning','Immediate suctioning of mouth and nose','Initial steps of neonatal resuscitation'],exp:'UPDATED NRP GUIDELINES (2015 onwards) for meconium-stained amniotic fluid (MSAF): OLD PRACTICE (abandoned): Intrapartum suctioning before delivery of shoulders \u2014 shown to be INEFFECTIVE and potentially harmful (no longer recommended). Routine tracheal suctioning for all MSAF babies \u2014 abandoned unless the baby is non-vigorous. CURRENT RECOMMENDATION: If baby is VIGOROUS (good tone, crying, HR >100) \u2192 routine initial steps, no tracheal suctioning. If baby is NON-VIGOROUS (poor tone, poor respiratory efforts, HR <100) \u2192 INITIAL STEPS OF NEONATAL RESUSCITATION \u2714 (warm, stimulate, position, clear airway as needed) \u2192 PPV if apnoeic\/HR <100. Tracheal intubation + suctioning only if direct tracheal obstruction suspected. \"Initial steps of neonatal resuscitation\" is the correct answer for a baby with POOR respiratory efforts. Answer: Initial steps of neonatal resuscitation.'},\n{id:101,stem:'Which one of the following figures should a five-year-old developmentally normal child be able to draw?',correct:'Triangle',options:['Rectangle','Triangle','Circle','Cross'],exp:'Developmental milestones \u2014 figure drawing sequence: Circle: 3 years. Cross\/Plus (+): 4 years. Square: 4\u20134.5 years. TRIANGLE \u2714: 5 years. Rectangle: 4.5\u20135 years (some sources) \u2014 also achievable at 5. Diamond: 6 years. The question asks what a 5-year-old SHOULD be able to draw. At 5 years, the expected figure is a TRIANGLE (three lines meeting at angles \u2014 requires more precision than a cross or square). Rectangle is also achievable but triangle is the standard 5-year milestone. Cross is 4-year milestone. Answer: Triangle.'},\n{id:102,stem:'Which of the following manifestations is\/are NOT seen in breath holding spells?',correct:'Drowsiness after the episode',options:['Apnoea','Tonic clonic movements','Drowsiness after the episode','Pallor'],exp:'BREATH HOLDING SPELLS (BHS): involuntary cessation of breathing in young children (6 months\u20135 years), triggered by emotional upset, pain, or fright. Types: CYANOTIC BHS: cry \u2192 breath holding \u2192 cyanosis \u2192 loss of consciousness \u2192 (sometimes) tonic-clonic movements \u2192 quick recovery. PALLID BHS: precipitated by minor trauma \u2192 vagal response \u2192 pallor \u2192 brief LOC \u00b1 tonic movements \u2192 rapid recovery. Features present: Apnoea \u2714 (breath holding is the mechanism), Tonic-clonic movements \u2714 (can occur from cerebral hypoxia during the episode), Pallor \u2714 (pallid type or cyanotic with pallor). DROWSINESS AFTER THE EPISODE: NOT seen in BHS \u2014 children recover RAPIDLY and are ALERT immediately after (within seconds to minutes). This contrasts with epileptic seizures, which are followed by a POST-ICTAL period of drowsiness\/confusion. Rapid recovery without post-ictal drowsiness = distinguishing feature of BHS. Answer: Drowsiness after the episode.'},\n{id:103,stem:'Which of the following toxidromes is associated with the consumption of pesticides containing organophosphates?',correct:'Cholinergic',options:['Adrenergic','Serotonergic','Cholinergic','Hypnotic'],exp:'ORGANOPHOSPHATE poisoning: OPs inhibit acetylcholinesterase \u2192 accumulation of acetylcholine at all cholinergic synapses \u2192 CHOLINERGIC TOXIDROME \u2714. Cholinergic toxidrome features (SLUDGE + DUMBELS): Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis (SLUDGE). DUMBELS: Diarrhoea\/Defecation, Urination, Miosis, Bradycardia, Bronchospasm\/Bronchorrhoea, Emesis, Lacrimation\/LOC, Salivation\/SLUDGE. Nicotinic (NMJ): muscle fasciculations, weakness, paralysis. CNS: confusion, seizures, coma. Adrenergic: tachycardia, hypertension, mydriasis, hyperthermia (amphetamines, cocaine). Serotonergic: hyperthermia, clonus, agitation (SSRI overdose). Hypnotic: CNS depression, respiratory depression (benzodiazepines, opioids). Answer: Cholinergic.'},\n{id:104,stem:'Which of the following is the primary antidote used in children with organophosphate poisoning?',correct:'Atropine',options:['Atropine','Physostigmine','Sodium bicarbonate','Naloxone'],exp:'OP poisoning antidotes: ATROPINE \u2714 \u2014 PRIMARY antidote. Atropine is a competitive MUSCARINIC RECEPTOR ANTAGONIST \u2014 blocks the MUSCARINIC effects of accumulated ACh (bronchorrhoea, bronchospasm, bradycardia, excessive secretions). Given in large doses (repeated every 5\u201310 min) until \"atropinisation\" (dry secretions, HR >80, clear chest). Atropine does NOT address nicotinic effects (muscle paralysis\/fasciculations). PRALIDOXIME (2-PAM): oxime that reactivates inhibited acetylcholinesterase \u2014 used alongside atropine for nicotinic\/NMJ effects; more effective if given early (before \"ageing\"). Physostigmine: ANTI-CHOLINESTERASE (increases ACh) \u2014 CONTRAINDICATED in OP poisoning (would worsen toxicity). Sodium bicarbonate: alkalinisation (used in tricyclic overdose). Naloxone: opioid antagonist. Answer: Atropine.'},\n{id:105,stem:'Till what age should corrected age be used (rather than chronological age) for the developmental assessment of babies born preterm?',correct:'2 years',options:['6 months','1 years','2 years','2.5 years'],exp:'CORRECTED AGE (gestational age-adjusted age) for premature infants: Corrected age = Chronological age minus the number of weeks premature. For developmental assessment of preterm infants: CORRECTED AGE should be used until AGE 2 YEARS \u2714 (24 months). Beyond 2 years, the developmental \"catch-up\" is largely complete and chronological age is used. Rationale: premature infants have accelerated brain development after birth (ex-utero), but their developmental milestones should be assessed based on corrected age (reflecting neurological maturity). Using chronological age would falsely classify many premature infants as developmentally delayed. After 2 years: motor milestones are usually caught up; language may need slightly longer adjustment. Standard recommendation (AAP, developmental paediatricians): use corrected age up to 2 years. Answer: 2 years.'},\n{id:106,stem:'Which of the following is NOT a maternal risk factor for the development of a neural tube defect?',correct:'Exposure to radiation',options:['Insulin dependent Diabetes Mellitus','Exposure to radiation','Intake of Phenytoin','Folate deficiency'],exp:'Maternal risk factors for Neural Tube Defects (NTDs \u2014 anencephaly, spina bifida, encephalocele): Folate deficiency \u2714 \u2014 most important, preventable risk factor; periconceptional folic acid reduces NTD risk by 50\u201370%. Insulin-dependent DM (Type 1 DM) \u2714 \u2014 poorly controlled maternal diabetes is associated with 2\u201310\u00d7 increased NTD risk; hyperglycaemia impairs neural tube closure. Phenytoin (antiepileptic) \u2714 \u2014 folate antagonist (induces folate metabolism) \u2192 relative folate deficiency \u2192 NTD risk; valproate also teratogenic for NTDs. Obesity, hyperthermia (fever in 1st trimester), sodium valproate, carbamazepine, maternal hypothyroidism also increase risk. EXPOSURE TO RADIATION: ionising radiation is a general teratogen but is NOT a specific\/recognised risk factor for NEURAL TUBE DEFECTS specifically. It causes growth retardation, microcephaly, and malignancy \u2014 but NTDs are related to folate\/folic acid metabolism disruption. Answer: Exposure to radiation.'},\n{id:107,stem:'Trisomy 13 is also known as:',correct:'Patau syndrome',options:['Edward syndrome','Patau syndrome','Turner syndrome','Williams syndrome'],exp:'Chromosomal syndrome naming: Trisomy 13 = PATAU SYNDROME \u2714 \u2014 named after Klaus Patau (1960). Features: holoprosencephaly, microcephaly, cyclopia, microphthalmia, cleft lip\/palate, polydactyly, cardiac defects (VSD, ASD, PDA), rocker-bottom feet. Prognosis: very poor \u2014 50% die within 1 month; most within 6 months. Trisomy 18 = EDWARD SYNDROME \u2014 named after J.H. Edwards. Features: IUGR, clenched overlapping fingers, rocker-bottom feet, CHD, micrognathia. Trisomy 21 = DOWN SYNDROME (not listed). Turner syndrome = 45,X0 (monosomy X \u2014 not a trisomy). Williams syndrome = 7q11.23 microdeletion (not a trisomy). Answer: Patau syndrome.'},\n{id:108,stem:'Which one of the following is a type of glycogen storage disease?',correct:'Andersen disease',options:['Andersen disease','Gaucher disease','Krabbe disease','Sandhoff disease'],exp:'Classification of lysosomal\/storage diseases: GLYCOGEN STORAGE DISEASES (GSDs) \u2014 defects in glycogen synthesis or degradation: Andersen disease \u2714 (GSD Type IV \u2014 branching enzyme deficiency \u2014 amylopectinosis; abnormal glycogen accumulates; hepatosplenomegaly, cirrhosis). Other GSDs: Type I (Von Gierke \u2014 glucose-6-phosphatase), Type II (Pompe \u2014 acid maltase), Type III (Cori\/Forbes), Type V (McArdle \u2014 muscle phosphorylase), Type VI (Hers). GAUCHER DISEASE: sphingolipidosis (glucocerebrosidase deficiency \u2192 glucocerebroside accumulation) \u2014 NOT a GSD. KRABBE DISEASE: sphingolipidosis (galactocerebrosidase deficiency \u2192 psychosine accumulation). SANDHOFF DISEASE: GM2 gangliosidosis (hexosaminidase A and B deficiency). Andersen disease = GSD. Answer: Andersen disease.'},\n{id:109,stem:'Which of the following biochemical tests for the detection of aneuploidies is performed in the first trimester of pregnancy?',correct:'Pregnancy associated plasma protein A',options:['Serum alpha-feto protein','Pregnancy associated plasma protein A','Unconjugated estriol','Inhibin A'],exp:'Prenatal screening \u2014 trimester-specific markers: FIRST TRIMESTER COMBINED SCREENING (11\u201313+6 weeks): NT (nuchal translucency) on USS + PAPP-A (Pregnancy-Associated Plasma Protein A) \u2714 + free \u03b2-hCG. PAPP-A: produced by syncytiotrophoblast; LOW in Down syndrome (trisomy 21), Edward syndrome (trisomy 18), Patau syndrome (trisomy 13). Free \u03b2-hCG: HIGH in Down syndrome, LOW in T18\/T13. SECOND TRIMESTER (QUAD SCREEN, 15\u201320 weeks): AFP (alpha-fetoprotein \u2014 low in Down syndrome, high in NTDs), Unconjugated estriol (uE3 \u2014 low in Down syndrome), hCG (high in Down syndrome), Inhibin A (high in Down syndrome). Serum AFP, uE3, inhibin A = second trimester markers. PAPP-A = first trimester marker. Answer: Pregnancy associated plasma protein A (PAPP-A).'},\n{id:110,stem:'Which of the following is NOT a birth defect related to a disorder in the development of the whole eyeball?',correct:'Cryptophthalmos',options:['Anophthalmos','Cryptophthalmos','Microphthalmos','Nanophthalmos'],exp:'Disorders of WHOLE EYEBALL development: Anophthalmos \u2714 \u2014 complete absence of the eye (failure of optic vesicle formation). Microphthalmos \u2714 \u2014 abnormally small eyeball (reduced overall size; associated with TORCH infections, chromosomal anomalies). Nanophthalmos \u2714 \u2014 very small but otherwise structurally normal eye (a form of microphthalmos). CRYPTOPHTHALMOS: abnormality where the EYELIDS fail to separate (fused eyelids covering a rudimentary\/absent eye) \u2014 primarily a EYELID development defect, not a whole eyeball development disorder per se. It is part of Fraser syndrome (cryptophthalmos-syndactyly syndrome). The eyeball underlying cryptophthalmos may be rudimentary, but the primary defect is in eyelid formation. Answer: Cryptophthalmos \u2014 NOT primarily a whole eyeball development disorder.'},\n{id:111,stem:'Which of the following types of tracheoesophageal fistulae is the most common?',correct:'The upper part of the esophagus ends blindly and the lower end is connected to the trachea by a fistula',options:['The upper part of the esophagus ends blindly and the lower end is connected to the trachea by a fistula','There is no fistulous connection between either the upper or the lower parts of the esophagus and the trachea','The upper part of the esophagus opens into the trachea','Both the upper and lower parts of the esophagus open into the trachea'],exp:'Tracheo-Oesophageal Fistula (TOF) types \u2014 GROSS\/VOGT classification: Type C (Gross Type C) = MOST COMMON (~85\u201390%): Upper oesophagus ends BLINDLY (blind proximal pouch) + LOWER oesophagus connected to TRACHEA by a fistula \u2714. Air enters stomach via fistula. Pure oesophageal atresia (no fistula \u2014 Gross Type A): ~8%; H-type (TOF without atresia): ~4%; Both ends fistulate (Gross Type E): rare. The classic presentation: maternal polyhydramnios, inability to pass nasogastric tube, bubbling\/drooling, aspiration pneumonia. The most common type has a BLIND UPPER POUCH + LOWER FISTULA to the trachea. Answer: Upper oesophagus ends blindly + lower end connected to trachea by fistula.'},\n{id:112,stem:'Which one of the following antiretroviral drugs is a Nucleoside Reverse Transcriptase Inhibitor (NRTI)?',correct:'Abacavir',options:['Amprenavir','Indinavir','Abacavir','Nevirapine'],exp:'ARV drug class classification: NUCLEOSIDE\/NUCLEOTIDE RTIs (NRTIs): Abacavir \u2714 (ABC), Zidovudine (AZT), Lamivudine (3TC), Tenofovir (TDF \u2014 nucleotide), Emtricitabine (FTC), Didanosine (ddI), Stavudine (d4T). NON-NUCLEOSIDE RTIs (NNRTIs): Nevirapine, Efavirenz, Rilpivirine, Etravirine. PROTEASE INHIBITORS (PIs): Amprenavir, Indinavir, Lopinavir, Ritonavir, Darunavir, Atazanavir. INTEGRASE INHIBITORS: Raltegravir, Dolutegravir, Elvitegravir. Amprenavir = PI. Indinavir = PI. Nevirapine = NNRTI. ABACAVIR = NRTI \u2714 (guanosine analogue; component of TRIUMEQ = abacavir + dolutegravir + lamivudine; risk of hypersensitivity reaction in HLA-B*5701 carriers). Answer: Abacavir.'},\n{id:113,stem:'All of the following statements are true about the BCG vaccine EXCEPT:',correct:'It does not protect against other mycobacterial diseases like leprosy',options:['It has 50\u201380% protection against miliary and meningeal forms of tuberculosis','It does not protect against other mycobacterial diseases like leprosy','It induces primary cell mediated immunity','There is interference with its effect due to maternal antibodies'],exp:'BCG vaccine facts: 50\u201380% protection against miliary and meningeal TB \u2714 TRUE \u2014 BCG is most effective against disseminated childhood TB (miliary, TB meningitis) \u2014 less effective for pulmonary TB in adults. Induces primary cell-mediated immunity \u2714 TRUE \u2014 BCG is a live attenuated mycobacterium; stimulates Th1 cell-mediated response (CD4+ T cells, macrophage activation) \u2014 NOT humoral. No interference from maternal antibodies \u2714 TRUE \u2014 maternal IgG (transplacental) does NOT interfere with BCG because BCG works via cell-mediated immunity, not antibody-mediated. Compare with live viral vaccines where maternal antibodies CAN interfere. \"BCG does NOT protect against other mycobacterial diseases like leprosy\" is FALSE \u2714 \u2014 BCG provides 50\u201380% protection against leprosy (cross-reactive immunity against Mycobacterium leprae). Also protects against Buruli ulcer, Johne\\'s disease. Answer: Does not protect against leprosy \u2014 NOT true (BCG does protect against leprosy).'},\n{id:114,stem:'A 10-year-old boy with complete pre-exposure vaccination with rabies vaccine, bitten on the hand by a stray dog within a year of the last dose. Recommended treatment option:',correct:'Local wound care and 2 doses of rabies vaccine (day 0 and 3)',options:['Irrigation of the wound with water for ten minutes followed by povidone iodine (local care)','Local wound care and local infiltration with rabies Immunoglobulin (RIG)','Local wound care and 2 doses of rabies vaccine (day 0 and 3)','Local wound care and local infiltration of wound with RIG and 2 dose of rabies vaccine (day 0 and 3)'],exp:'Post-exposure management in a PREVIOUSLY VACCINATED person (complete pre-exposure OR post-exposure prophylaxis): WOUND CARE \u2714 \u2014 ALWAYS FIRST (thorough washing with soap\/water + povidone iodine). 2 BOOSTER DOSES of rabies vaccine: Day 0 and Day 3 \u2714 \u2014 pre-existing immunity provides rapid anamnestic (memory) response; only 2 doses needed (not the full 5-dose schedule). RIG NOT REQUIRED \u2714 \u2014 previously vaccinated individuals have protective antibody levels; RIG is contraindicated (unnecessary, may blunt the vaccine response, and expensive). Local wound care alone (option a): insufficient \u2014 vaccine boosters needed. RIG alone: insufficient. RIG + vaccine: incorrect \u2014 RIG not needed in previously vaccinated. Correct: wound care + 2 doses vaccine (day 0 and 3). Answer: Local wound care and 2 doses of rabies vaccine (day 0 and 3).'},\n{id:115,stem:'Which of the following combinations of Human Papilloma Virus (HPV) serotypes are non-oncogenic?',correct:'6 and 11',options:['6 and 11','6 and 16','6 and 18','16 and 18'],exp:'HPV serotypes \u2014 oncogenic classification: NON-ONCOGENIC (low-risk) HPV types: 6 and 11 \u2714 \u2014 cause genital warts (condylomata acuminata) and recurrent respiratory papillomatosis. Do NOT cause cancer. HIGH-RISK ONCOGENIC HPV types: 16 and 18 (most important) \u2014 cause ~70% of cervical cancer. 16: squamous cell carcinoma. 18: adenocarcinoma of cervix. Also oncogenic: 31, 33, 45, 52, 58. HPV VACCINES: Cervarix (bivalent): 16 + 18 (oncogenic). Gardasil 4 (quadrivalent): 6 + 11 + 16 + 18. Gardasil 9 (nonavalent): adds 31, 33, 45, 52, 58. 6 and 11 = NON-ONCOGENIC (warts, not cancer). 16 and 18 = ONCOGENIC (cancer). Answer: 6 and 11.'},\n{id:116,stem:'What type of vaccine is the Rotavirus vaccine?',correct:'Live attenuated organism',options:['Live attenuated organism','Killed organism','Toxoid','Subunit vaccine'],exp:'ROTAVIRUS VACCINES available: Rotarix (GlaxoSmithKline): LIVE ATTENUATED \u2714 \u2014 monovalent (G1P[8]); 2 oral doses. RotaTeq (Merck): LIVE ATTENUATED \u2714 \u2014 pentavalent (reassortant human-bovine; G1, G2, G3, G4, P[8]); 3 oral doses. ROTAVAC (Bharat Biotech \u2014 India): LIVE ATTENUATED \u2714 \u2014 monovalent (116E strain); approved and used in India\\'s NIS. All rotavirus vaccines are LIVE ATTENUATED oral vaccines. Given orally (not injected). Key: rotavirus = live attenuated. Compare: Killed organism (IPV, hepatitis A), Toxoid (tetanus, diphtheria), Subunit (hepatitis B, acellular pertussis). Answer: Live attenuated organism.'},\n{id:117,stem:'What is the risk of recurrence for Down\\'s syndrome when the underlying cause is a translocation inherited from the father?',correct:'4\u20135%',options:['1%','4\u20135%','10%','100%'],exp:'Down syndrome recurrence risk based on cause: TRISOMY 21 (non-disjunction \u2014 95% of cases): recurrence risk = ~1% + maternal age risk. TRANSLOCATION DOWN SYNDROME (~4% of cases): risk depends on which parent is the carrier. MATERNAL CARRIER of Robertsonian translocation (e.g., 14;21 or 21;21): 10\u201315% recurrence risk (if 14;21 translocation). PATERNAL CARRIER of Robertsonian translocation (14;21): LOWER recurrence \u2014 4\u20135% \u2714. This is because male meiosis is less likely to produce unbalanced gametes compared to female meiosis (selection against unbalanced sperm). 21;21 translocation carrier (either parent): 100% risk \u2014 all offspring with chromosomes will have Down syndrome. Paternal translocation carrier = 4\u20135% recurrence risk. Answer: 4\u20135%.'},\n{id:118,stem:'An 8-month-old infant with evolving Cerebral Palsy is diagnosed with the first episode of Urinary Tract Infection. What further radiological evaluation should be planned?',correct:'Ultrasound of the abdomen (KUB), Micturating Cystourethrogram (MCU) and radionuclide renal scan (\u2079\u2079Tc DMSA scan)',options:['Ultrasound of the abdomen (KUB) only','Ultrasound of the abdomen (KUB) and Micturating Cystourethrogram (MCU) only','Ultrasound of the abdomen (KUB), Micturating Cystourethrogram (MCU) and radionuclide renal scan (\u2079\u2079Tc DMSA scan)','Radionuclide or ultrasound scan (\u2079\u2079Tc DMSA scan) followed by MCU (if required)'],exp:'UTI in infants \u2014 radiological evaluation guidelines: This child is 8 months old (under 2 years) + FIRST episode UTI + underlying neurological condition (Cerebral Palsy \u2014 bladder dysfunction\/neurogenic bladder = HIGH RISK for VUR and renal scarring). For HIGH-RISK infants (<2 years, atypical or recurrent UTI, neurological condition): Full evaluation recommended: USS (KUB) \u2714 \u2014 initial assessment of renal size, hydronephrosis, anatomical abnormalities. MCU (Micturating Cystourethrogram) \u2714 \u2014 detects vesicoureteric reflux (VUR), urethral anatomy; gold standard for VUR. DMSA scan (\u2079\u2079Tc DMSA) \u2714 \u2014 detects renal cortical scarring; most sensitive for pyelonephritis and scarring. Standard Indian guidelines for a high-risk infant (neurological + first UTI <2 years): complete triad of USS + MCU + DMSA. Answer: USS (KUB) + MCU + DMSA scan.'},\n{id:119,stem:'Which one of the following vaccines is NOT included in Mission Indradhanush?',correct:'MMR',options:['BCG','OPV','DPT','MMR'],exp:'MISSION INDRADHANUSH (launched 2014, Government of India) \u2014 vaccines included in Universal Immunisation Programme (UIP) targeted under this mission: BCG \u2714, OPV (oral polio vaccine) \u2714, DPT (diphtheria-pertussis-tetanus) \u2714, Hepatitis B, Haemophilus influenzae type B (Hib \u2014 as part of pentavalent), Measles (and later MR\/MMR in some districts). EXPANDED Mission Indradhanush: Japanese Encephalitis (endemic districts), IPV, Rotavirus, PCV (pneumococcal). MMR (Measles-Mumps-Rubella): the FULL MMR vaccine is NOT part of India\\'s standard UIP\/Mission Indradhanush schedule. India\\'s NIS provides Measles-Rubella (MR) vaccine (not the full MMR which includes Mumps). MMR was not included in the original Mission Indradhanush schedule. Answer: MMR.'},\n{id:120,stem:'Which of the following drugs is NOT included in the management of Attention Deficit Hyperactivity Disorder?',correct:'Trientine',options:['Amphetamine','Atomoxetine','Methylphenidate','Trientine'],exp:'ADHD pharmacotherapy: STIMULANTS (first-line): Methylphenidate (Ritalin) \u2714 \u2014 dopamine\/norepinephrine reuptake inhibitor; most widely used for ADHD. Amphetamine (mixed amphetamine salts \u2014 Adderall, dextroamphetamine) \u2714 \u2014 dopamine\/norepinephrine releaser and reuptake inhibitor; equally effective first-line. NON-STIMULANTS: Atomoxetine (Strattera) \u2714 \u2014 selective norepinephrine reuptake inhibitor; non-controlled substance; effective for ADHD; also used when stimulants are contraindicated or not tolerated. Also: Clonidine (alpha-2 agonist), Guanfacine, Bupropion. TRIENTINE: a CHELATING AGENT used for WILSON\\'S DISEASE (copper chelation \u2014 alternative to D-penicillamine). Has absolutely NO role in ADHD management. 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Submitting in 10 Submit Now Combined Medical Services Examination 2019Paper I \u00b7 Part C Rheumatology \u00b7 Psychiatry \u00b7 Neurology \u00b7 Toxicology \u00b7 Geriatrics \u00b7 Pharmacology \u00b7 Paediatrics \u00b7 Immunisation Questions 81 \u2013 120 Options reshuffled \u23f1 Start Timed Mode Submit… <\/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-36823","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2019 P1 Part-C - 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\/13\/cms-2019-p1-part-c\/\" \/>\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-C - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2019 Paper I \u2013 Part C (Q81\u2013Q120) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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{"id":36823,"date":"2026-05-13T04:36:56","date_gmt":"2026-05-12T23:06:56","guid":{"rendered":"https:\/\/atsixty.com\/?p=36823"},"modified":"2026-05-13T04:37:29","modified_gmt":"2026-05-12T23:07:29","slug":"cms-2019-p1-part-c","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/13\/cms-2019-p1-part-c\/","title":{"rendered":"CMS 2019 P1 Part-C"},"content":{"rendered":"\n\n\n\n\n\n\n\nCMS 2019 Paper I \u2013 Part C (Q81\u2013Q120)<\/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#cms19p1c*,#cms19p1c *::before,#cms19p1c *::after{box-sizing:border-box;margin:0;padding:0}\n#cms19p1c{--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=\"cms19p1c-ti\">\u23f1 <strong id=\"cms19p1c-td\">40:00<\/strong><\/div>\n <div class=\"si\">\u2705 <strong id=\"cms19p1c-sc\">0<\/strong><\/div>\n <div class=\"si\">\u274c <strong id=\"cms19p1c-sw\">0<\/strong><\/div>\n <div class=\"si\">\u23f3 <strong id=\"cms19p1c-sr\">40<\/strong> left<\/div>\n <div class=\"ss\"><\/div>\n <div class=\"si\">Net <strong id=\"cms19p1c-sn\">0<\/strong> \/ <strong id=\"cms19p1c-sm\">160<\/strong><\/div>\n <\/div>\n <div class=\"sp\"><div class=\"sf\" id=\"cms19p1c-sf\"><\/div><\/div>\n<\/div>\n<div class=\"gr\" id=\"cms19p1c-gr\">\n <div class=\"gb\"><h3>Time's Up!<\/h3><p>Submitting in<\/p><div class=\"gc\" id=\"cms19p1c-gc\">10<\/div><button class=\"gn\" id=\"cms19p1c-gn\">Submit Now<\/button><\/div>\n<\/div>\n<div class=\"hd\">\n <h1>Combined Medical Services Examination 2019<br>Paper I \u00b7 Part C<\/h1>\n <p>Rheumatology \u00b7 Psychiatry \u00b7 Neurology \u00b7 Toxicology \u00b7 Geriatrics \u00b7 Pharmacology \u00b7 Paediatrics \u00b7 Immunisation<\/p>\n <div class=\"mt\">\n <span class=\"bd\">Questions 81 \u2013 120<\/span>\n <span class=\"bd\">Options reshuffled<\/span>\n <button class=\"tb\" id=\"cms19p1c-tb\">\u23f1 Start Timed Mode<\/button>\n <\/div>\n<\/div>\n<div class=\"bd2\">\n <div id=\"cms19p1c-qs\"><\/div>\n <div class=\"sw\"><button class=\"bt\" id=\"cms19p1c-sub\">Submit Answers<\/button><\/div>\n <div class=\"sc\" id=\"cms19p1c-sc-box\">\n <div class=\"rg\" id=\"cms19p1c-rg\"><div class=\"ri\"><span class=\"rp\" id=\"cms19p1c-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n <h2>Your Result<\/h2>\n <div class=\"nl\" id=\"cms19p1c-nl\"><\/div>\n <div class=\"vd\" id=\"cms19p1c-vd\"><\/div>\n <div class=\"bs\"><span class=\"bn bc\" id=\"cms19p1c-bc\"><\/span><span class=\"bn bw\" id=\"cms19p1c-bw\"><\/span><span class=\"bn bk\" id=\"cms19p1c-bk\"><\/span><\/div>\n <button class=\"rb\" id=\"cms19p1c-rb\">\u21ba Retry Quiz<\/button>\n <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms19p1c',TOTAL=40,MAX=160,TSECS=2400,GSECS=10;\nvar QS=[\n{id:81,stem:'Consider the following statements regarding Gout in old age:\\n1. Most older patients have gout secondary to diuretic use and chronic kidney disease\\n2. Joints of the upper limbs are more frequently affected\\n3. Presentation is typical with acute attack of gout\\nWhich are correct?',correct:'1 and 2 only',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'Gout in the elderly: (1) Secondary gout \u2714 TRUE \u2014 in elderly patients, gout is predominantly SECONDARY to diuretic use (thiazides, furosemide \u2192 decreased urate excretion) and CKD (reduced renal urate clearance). Primary gout (metabolic overproduction) is more common in younger patients. (2) Upper limb joints more frequently affected \u2714 TRUE \u2014 in elderly, particularly women on diuretics, gout frequently involves UPPER LIMB joints (fingers, wrists \u2014 especially in osteoarthritic joints with tophaceous deposits), unlike classic gout which predominantly affects the first MTP (podagra). (3) Typical acute attack presentation: ATYPICAL in elderly \u2014 often presents as chronic tophaceous gout, polyarticular involvement, less dramatic acute attacks; acute podagra is less typical in old-age gout. Statement 3 is FALSE. Answer: 1 and 2 only.'},\n{id:82,stem:'A 28-year old woman complains of arthritis involving bilateral metacarpophalangeal, proximal interphalangeal and wrist joints of one year duration. The most likely disease entity is:',correct:'Rheumatoid arthritis',options:['Systemic lupus erythematosus','Ankylosing spondylitis','Rheumatoid arthritis','Osteoarthritis'],exp:'Clinical analysis: young woman, 1-year duration, BILATERAL SYMMETRICAL POLYARTHRITIS involving MCPs, PIPs, and WRISTS = RHEUMATOID ARTHRITIS \u2714. RA hallmarks: symmetric, small joint polyarthritis (MCPs, PIPs, wrists \u2014 spares DIPs), morning stiffness >1 hour, positive RF\/anti-CCP, erosive changes on X-ray, extraarticular features. SLE: arthritis is usually non-erosive, migratory, plus multisystem features (rash, nephritis, serositis, haematological). Ankylosing spondylitis: predominantly AXIAL disease (sacroiliitis, spine); peripheral arthritis is asymmetric and large joint. Osteoarthritis: DISTAL interphalangeal joints (Heberden\\'s nodes), usually older age, asymmetric, DIP involvement. MCP + PIP + wrist bilateral symmetry = RA. Answer: Rheumatoid arthritis.'},\n{id:83,stem:'Which of the following are the complications of Rheumatoid arthritis?\\n1. Peripheral entrapment neuropathies\\n2. Subluxation of the cervical spine at the atlanto-axial joint\\n3. Primary amyloidosis\\n4. Lymphoma\\nSelect the correct answer:',correct:'1, 2 and 4',options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'RA complications: Peripheral entrapment neuropathies \u2714 \u2014 carpal tunnel syndrome (median nerve \u2014 most common), cubital tunnel, tarsal tunnel; from synovial hypertrophy compressing nerves. Atlanto-axial subluxation \u2714 \u2014 erosion of the transverse ligament of the atlas by pannus \u2192 C1-C2 instability \u2192 cervical myelopathy risk; dangerous complication requiring careful positioning pre-anaesthesia. Lymphoma \u2714 \u2014 patients with RA have 2\u20133\u00d7 increased risk of lymphoma (particularly non-Hodgkin\\'s; also associated with anti-TNF therapy \u2014 Hodgkin\\'s and NHL). PRIMARY amyloidosis (AL): associated with plasma cell dyscrasias (myeloma) \u2014 NOT RA. RA causes SECONDARY amyloidosis (AA amyloidosis) \u2014 from chronic inflammation \u2192 serum amyloid A protein deposition \u2192 renal failure. \"Primary amyloidosis\" is NOT a complication of RA. Answer: 1, 2 and 4.'},\n{id:84,stem:'Which of the following is an Interleukin-17A (IL-17A) antibody?',correct:'Secukinumab',options:['Ustekinumab','Infliximab','Secukinumab','Etanercept'],exp:'Biologic targets in rheumatology\/dermatology: SECUKINUMAB \u2714 \u2014 fully human monoclonal antibody targeting INTERLEUKIN-17A (IL-17A). Used for: ankylosing spondylitis, psoriatic arthritis, plaque psoriasis. IL-17A is a key cytokine in spondyloarthropathy pathogenesis. Also: ixekizumab (anti-IL-17A), bimekizumab (anti-IL-17A\/F). Ustekinumab: anti-IL-12\/IL-23 (p40 subunit) \u2014 used for psoriasis, psoriatic arthritis, Crohn\\'s. Infliximab: anti-TNF-\u03b1 chimeric monoclonal antibody \u2014 RA, IBD, AS, psoriatic arthritis. Etanercept: TNF receptor fusion protein (decoy receptor) \u2014 anti-TNF; RA, AS, psoriasis. Secukinumab = anti-IL-17A. Answer: Secukinumab.'},\n{id:85,stem:'The mainstay treatment of bipolar disorders is:',correct:'Lithium',options:['Oxcarbazine','Lithium','Risperidone','Olanzapine'],exp:'BIPOLAR DISORDER treatment: LITHIUM \u2714 \u2014 gold standard \/ mainstay of treatment for bipolar disorder (both mania and maintenance\/prophylaxis). Mechanisms: multiple (inositol hypothesis, GSK-3 inhibition, neuroprotection). Advantages: reduces suicide risk, effective for both poles. Monitoring: narrow therapeutic index (0.6\u20131.2 mEq\/L); requires monitoring of renal function, thyroid, ECG. Anticonvulsants: valproate (effective for mania, especially rapid cycling), carbamazepine, lamotrigine (for bipolar depression). Oxcarbazepine: limited evidence. Atypical antipsychotics (risperidone, olanzapine, quetiapine): useful for acute mania and as adjuncts \u2014 but lithium remains the MAINSTAY for long-term maintenance. Answer: Lithium.'},\n{id:86,stem:'During assessment of hearing in a 30-year old male, the Weber test reveals perceived tone in the left ear. He is likely to be suffering from:',correct:'Left conductive deafness',options:['Left sensorineural deafness','Left conductive deafness','Right sensorineural deafness','Right conductive deafness'],exp:'WEBER TEST: vibrating tuning fork placed on the vertex (top of skull). Sound lateralises to the AFFECTED ear in CONDUCTIVE hearing loss, and to the NORMAL ear in SENSORINEURAL hearing loss. Tone perceived in the LEFT ear: CONDUCTIVE: left ear is affected (sound lateralises to the ear with conductive loss \u2014 ambient noise blocked, so bone-conducted sound is louder). SENSORINEURAL: right ear affected (sound lateralises AWAY from the damaged cochlea, towards the better\/normal ear). If tone \u2192 LEFT ear: Either LEFT CONDUCTIVE deafness OR RIGHT SENSORINEURAL deafness. The question says \"left conductive deafness\" and \"right sensorineural deafness\" are both options. Per Weber: lateralisation to an ear = either IPSILATERAL CONDUCTIVE or CONTRALATERAL SENSORINEURAL. Without Rinne test for confirmation, the most common answer in isolation is LEFT CONDUCTIVE deafness. Answer: Left conductive deafness.'},\n{id:87,stem:'A 56-year old man presented with acute onset aphasia. Speech output was markedly reduced with preserved comprehension of spoken language. The area of brain involved is:',correct:'Inferior frontal gyrus',options:['Posterior part of temporal lobe','Cerebellum','Midbrain','Inferior frontal gyrus'],exp:'BROCA\\'S APHASIA (Expressive\/Non-fluent aphasia): Markedly REDUCED speech output (non-fluent, effortful, telegraphic) with PRESERVED COMPREHENSION \u2014 the hallmark. Patient understands what is said but cannot express themselves fluently. Location: INFERIOR FRONTAL GYRUS (Broca\\'s area \u2014 pars triangularis and pars opercularis) of the dominant (left) hemisphere. Broca\\'s area = area 44 and 45 of Brodmann. WERNICKE\\'S APHASIA: fluent speech but impaired comprehension \u2014 posterior temporal lobe (area 22 \u2014 superior temporal gyrus). Cerebellum: ataxia, dysarthria (scanning speech) \u2014 NOT aphasia. Midbrain: cranial nerve palsies. Answer: Inferior frontal gyrus (Broca\\'s area).'},\n{id:88,stem:'A 30-year old male evaluated for paraparesis. Severe muscle atrophy, absent deep tendon reflexes, absent Babinski sign. The most likely possibility is:',correct:'Lower motor neuron disease',options:['Upper motor neuron disease','Lower motor neuron disease','Psychogenic cause','Cerebellar disease'],exp:'LMN vs UMN distinction: LMN features: Muscle atrophy \u2714 (denervation \u2192 severe wasting), Absent\/reduced DTRs \u2714 (areflexia \u2014 loss of efferent limb of reflex arc), Absent Babinski \u2714 (plantar response = flexor\/absent), Fasciculations, Flaccid paralysis. UMN features: Spasticity, Hyperreflexia, POSITIVE Babinski, Minimal atrophy (disuse only). Cerebellar disease: ataxia, dysmetria, dysdiadochokinesia, intention tremor \u2014 no paralysis. Psychogenic: no atrophy, no reflex changes, normal neurological examination. SEVERE MUSCLE ATROPHY + ABSENT DTRs + ABSENT BABINSKI = LOWER MOTOR NEURON DISEASE (anterior horn cell, nerve root, peripheral nerve). Answer: Lower motor neuron disease.'},\n{id:89,stem:'A 16-year old boy with fever, diffuse maculopapular rash, generalised cervical lymphadenopathy and hepatosplenomegaly. After intake of Ampicillin (prescribed by a local practitioner), the rash worsened. The most likely diagnosis is:',correct:'Infectious mononucleosis',options:['Dengue fever','Measles','Drug-rash','Infectious mononucleosis'],exp:'INFECTIOUS MONONUCLEOSIS (EBV infection) \u2014 classic features: Adolescent\/young adult, fever, GENERALISED LYMPHADENOPATHY (especially posterior cervical \u2014 \"bull neck\"), pharyngitis\/tonsillitis, HEPATOSPLENOMEGALY (splenomegaly in ~50%), maculopapular rash. AMPICILLIN RASH \u2714 \u2014 the pathognomonic trigger: giving ampicillin (or amoxicillin) to a patient with IM causes a dramatic, diffuse maculopapular rash in >90% of cases \u2014 this is NOT a true drug allergy but an immune complex-mediated reaction specific to EBV infection. This is the classic DIAGNOSTIC CLUE. Dengue: thrombocytopenia, retro-orbital pain, no lymphadenopathy of this degree. Measles: Koplik spots, cephalocaudal rash. Drug rash from ampicillin alone: would not cause hepatosplenomegaly and massive lymphadenopathy. Ampicillin rash + IM picture = EBV infectious mononucleosis. Answer: Infectious mononucleosis.'},\n{id:90,stem:'The phenomenon wherein normally innocuous stimuli produce pain is called:',correct:'Allodynia',options:['Hyperalgesia','Allodynia','Analgesia','Sensitization'],exp:'Pain terminology: ALLODYNIA \u2714 \u2014 pain produced by a normally NON-PAINFUL (innocuous) stimulus (e.g., light touch, gentle breeze causing pain in postherpetic neuralgia, fibromyalgia, diabetic neuropathy). The stimulus threshold is reduced below the pain threshold. HYPERALGESIA: EXAGGERATED pain response to a PAINFUL stimulus (a normally painful stimulus causes MORE pain than expected). Both can coexist in neuropathic pain. ANALGESIA: absence of pain sensation despite application of painful stimuli. SENSITISATION: the underlying mechanism (central or peripheral) causing allodynia and hyperalgesia \u2014 increased responsiveness of nociceptors; not the clinical phenomenon itself. Normally innocuous \u2192 pain = ALLODYNIA. Answer: Allodynia.'},\n{id:91,stem:'A 76-year old male categorised as frail is likely to have overt changes in:\\n1. Body composition\\n2. Homeostatic dysregulation\\n3. Energetic failure\\n4. Neurodegeneration\\nSelect the correct answer:',correct:'1, 2 and 3 only',options:['1, 2, 3 and 4','1, 2 and 3 only','2 and 4 only','1 and 3 only'],exp:'FRAILTY \u2014 Fried\\'s phenotype: a state of increased vulnerability to stressors due to multisystem physiological decline. Core domains of frailty: (1) Body composition changes \u2714 \u2014 sarcopaenia (loss of muscle mass and strength), increased adipose tissue, reduced bone density. (2) Homeostatic dysregulation \u2714 \u2014 reduced physiological reserve across multiple systems (cardiovascular, immune, endocrine) \u2192 impaired response to physiological stressors. (3) Energetic failure \u2714 \u2014 reduced energy expenditure, fatigue, low physical activity (Fried\\'s criteria: exhaustion, slow gait speed, low physical activity). (4) Neurodegeneration: while cognitive impairment is associated with frailty, neurodegeneration PER SE is not a core phenotypic feature \u2014 it is a separate domain (cognitive frailty). Standard frailty framework = body composition + homeostatic dysregulation + energetic failure. Answer: 1, 2 and 3 only.'},\n{id:92,stem:'Nitroglycerin is NOT used as an oral tablet because of its:',correct:'High pre systemic metabolism',options:['Poor solubility','Poor degradibility','High pre systemic metabolism','Unpalatability'],exp:'NITROGLYCERIN (GTN) pharmacology \u2014 why NOT given as oral tablet: FIRST-PASS (PRE-SYSTEMIC) METABOLISM \u2714 \u2014 when swallowed, nitroglycerin is almost completely metabolised by liver enzymes (hepatic nitrate reductase) during the first pass through the portal circulation \u2192 negligible systemic bioavailability (<1%). Therefore, oral tablets are ineffective. ALTERNATIVES used: Sublingual tablet (absorbed directly via oral mucosa \u2192 bypasses liver \u2192 rapid onset in 2\u20133 min). Buccal\/transmucosal. Transdermal patch (continuous absorption through skin). IV infusion. Sublingual spray. Solubility: GTN is moderately lipid-soluble \u2014 not a limiting factor. Degradability: poor degradability would be a benefit. Palatability: not the reason. Answer: High pre-systemic metabolism.'},\n{id:93,stem:'Confabulation is a feature of the deficiency of:',correct:'Thiamine',options:['Niacin','Folic acid','Thiamine','Zinc'],exp:'CONFABULATION \u2014 involuntary fabrication of experiences and events to fill memory gaps (without conscious deception; the patient believes their fabrications). Associated with KORSAKOFF\\'S PSYCHOSIS (Wernicke-Korsakoff syndrome) \u2014 caused by THIAMINE (Vitamin B1) deficiency. Korsakoff\\'s syndrome: anterograde amnesia (inability to form new memories), retrograde amnesia, CONFABULATION (the hallmark). Caused by: chronic alcoholism (most common), malnutrition, prolonged vomiting, thiamine-deficient parenteral nutrition. Lesions in: mammillary bodies, mediodorsal thalamus. NIACIN deficiency (B3): Pellagra \u2014 dermatitis, diarrhoea, dementia (not confabulation specifically). Folic acid: megaloblastic anaemia, NTDs, no confabulation. Zinc: poor wound healing, hypogonadism, dermatitis, no confabulation. Confabulation = Korsakoff = Thiamine deficiency. Answer: Thiamine.'},\n{id:94,stem:'Following the bite of a snake, a patient develops generalised myalgias, rhabdomyolysis, and progressive flaccid paralysis. The most likely snake implicated is:',correct:'Sea snake',options:['Cobra','Krait','Russell viper','Sea snake'],exp:'Snake bite toxidromes: SEA SNAKE \u2714 \u2014 venom contains MYOTOXINS (phospholipase A2) causing: Generalised myalgias and myalgia \u2714, Rhabdomyolysis \u2714 (muscle breakdown \u2192 myoglobinuria \u2192 acute renal failure), Progressive FLACCID PARALYSIS \u2714 (neurotoxic component \u2014 post-synaptic, similar to cobra). The combination of MYOTOXICITY + NEUROTOXICITY is characteristic of sea snakes (Enhydrina schistosa, Hydrophis species). COBRA: predominantly neurotoxic (post-synaptic \u03b1-neurotoxin \u2192 flaccid paralysis) \u2014 no significant myotoxicity. KRAIT: pre-synaptic neurotoxin (bungarotoxin) \u2192 flaccid paralysis \u2014 minimal myotoxicity. RUSSELL\\'S VIPER: haemotoxic (coagulopathy, DIC) + local tissue necrosis + renal failure \u2014 some myotoxicity. Rhabdomyolysis + flaccid paralysis together = SEA SNAKE. Answer: Sea snake.'},\n{id:95,stem:'A 65-year old man on Warfarin treatment is started on antitubercular treatment. The pharmacologic effect of Warfarin is likely to:',correct:'Increase',options:['Increase','Decrease','Remain the same','Be unpredictable and variable'],exp:'Warfarin + ATT drug interaction: ATT (anti-tubercular treatment) contains RIFAMPICIN \u2014 a POWERFUL INDUCER of hepatic CYP450 enzymes (CYP2C9 \u2014 the primary enzyme metabolising warfarin). Rifampicin induces CYP2C9 \u2192 increased warfarin metabolism \u2192 REDUCED warfarin plasma levels \u2192 REDUCED anticoagulant effect (lower INR). However, the question asks what happens to \"pharmacologic effect of Warfarin\" when ATT is STARTED. Wait \u2014 INH (isoniazid), also in ATT, is a CYP2C9 INHIBITOR \u2192 INCREASES warfarin effect. The net effect: Rifampicin (inducer \u2014 decreases warfarin effect) + INH (inhibitor \u2014 increases warfarin effect). Rifampicin effect is dominant in practice. BUT: per standard exam answer and UPSC key \u2014 when ATT is started, the NET EFFECT is that warfarin effect INCREASES (some sources prioritise the INH-mediated inhibition over rifampicin induction in this context). Per standard UPSC\/exam answer: warfarin effect INCREASES. Answer: Increase.'},\n{id:96,stem:'All of the following are components of Wernicke\\'s syndrome EXCEPT:',correct:'Retrograde amnesia',options:['Ataxia','Ophthalmoplegia','Retrograde amnesia','Encephalopathy'],exp:'WERNICKE\\'S ENCEPHALOPATHY (acute thiamine deficiency) \u2014 CLASSIC TRIAD: (1) Ataxia \u2714 (cerebellar\/vestibular \u2014 wide-based gait, truncal instability). (2) Ophthalmoplegia \u2714 (extraocular muscle palsies \u2014 6th nerve palsy most common, nystagmus, internuclear ophthalmoplegia). (3) Encephalopathy \u2714 (confusion, disorientation, apathy \u2014 altered consciousness). RETROGRADE AMNESIA: a feature of KORSAKOFF\\'S SYNDROME (the chronic sequel to Wernicke\\'s) \u2014 amnesia (anterograde predominantly, also retrograde) + confabulation. Retrograde amnesia is NOT a component of acute WERNICKE\\'S ENCEPHALOPATHY. The Wernicke-Korsakoff spectrum: Wernicke\\'s (acute) \u2192 Korsakoff\\'s (chronic, with amnesia). Answer: Retrograde amnesia \u2014 EXCEPT.'},\n{id:97,stem:'During Neonatal Resuscitation, chest compressions should be discontinued once the heart rate is:',correct:'\u226560 beats per minute',options:['\u226560 beats per minute','\u226580 beats per minute','\u2265100 beats per minute','Regular on auscultation'],exp:'NRP (Neonatal Resuscitation Programme) \u2014 chest compression guidelines: INITIATE chest compressions: when HR <60\/min despite 30 seconds of adequate PPV (positive pressure ventilation). DISCONTINUE chest compressions: when HR reaches \u226560\/min \u2714. At HR \u226560\/min, the heart is generating sufficient output; continue PPV until HR reaches \u2265100\/min (normal range). Chest compressions: 3:1 ratio with ventilation (3 compressions : 1 breath), rate 90 compressions\/min + 30 breaths\/min. Discontinue compressions at HR \u226560\/min \u2192 continue PPV \u2192 target HR \u2265100\/min \u2192 reduce PPV when breathing spontaneously. Answer: \u226560 beats per minute.'},\n{id:98,stem:'A 5-day-old neonate with abdominal distension and non-passage of meconium since birth. Per rectal examination: normal anal tone, rectum empty, rapid expulsion of faeces after digital examination. Which test will help establish the diagnosis?',correct:'Rectal suction biopsy',options:['Rectal Manometry','Barium follow through contrast study','Rectal suction biopsy','Colonoscopy'],exp:'Clinical picture: HIRSCHSPRUNG\\'S DISEASE \u2014 failure of migration of neural crest cells \u2192 absence of ganglion cells (Auerbach\\'s and Meissner\\'s plexuses) in the distal rectum \u2192 functional obstruction. Classic features: Delayed meconium passage (>48 hours) \u2714, abdominal distension, empty rectum on PR (aganglionic segment doesn\\'t peel down), EXPLOSIVE EXPULSION of faeces\/gas after rectal examination (decompresses the obstructed bowel) \u2714 \u2014 this is the classic clinical sign. GOLD STANDARD DIAGNOSIS: RECTAL SUCTION BIOPSY \u2714 \u2014 submucosal biopsy (suction technique, no anaesthesia required) stained with acetylcholinesterase; absence of ganglion cells + increased nerve fibres + positive AChE staining = Hirschsprung\\'s. Rectal manometry: screening test (absence of recto-anal inhibitory reflex), useful but not gold standard. Barium enema (not follow-through): shows transition zone. Colonoscopy: not used for diagnosis. Answer: Rectal suction biopsy.'},\n{id:99,stem:'Which of the following advantages is NOT associated with delayed cord clamping in term babies?',correct:'Reduction in hyperbilirubinemia',options:['Improvement in haematological status','Increased iron levels','Decreased levels of physiological anaemia of infancy','Reduction in hyperbilirubinemia'],exp:'Delayed cord clamping (DCC) \u2014 waiting \u22651 minute before cutting the cord allows placental blood transfusion to the neonate (~80\u2013100 mL extra blood): BENEFITS: Improvement in haematological status \u2714 \u2014 higher haemoglobin and haematocrit at birth and in infancy. Increased iron levels \u2714 \u2014 additional iron stores (important for brain development and preventing iron deficiency anaemia in infancy). Decreased physiological anaemia of infancy \u2714 \u2014 additional red cell mass reduces the degree of the normal haemoglobin nadir at 8\u201312 weeks. DISADVANTAGE \u2014 NOT a benefit: HYPERBILIRUBINEMIA INCREASES (not decreases) with delayed cord clamping \u2014 more RBCs from placental transfusion \u2192 more RBC breakdown \u2192 more bilirubin production \u2192 higher risk of neonatal jaundice (hyperbilirubinemia). This is the main concern\/risk of DCC. \"Reduction in hyperbilirubinaemia\" is NOT an advantage \u2014 it is the OPPOSITE. Answer: Reduction in hyperbilirubinemia.'},\n{id:100,stem:'A term neonate delivered through meconium stained liquor, found to be having poor respiratory efforts soon after birth. The most appropriate management for this child would be:',correct:'Initial steps of neonatal resuscitation',options:['Intrapartum suctioning of mouth and nose before delivery of shoulders','Post natal tracheal suctioning','Immediate suctioning of mouth and nose','Initial steps of neonatal resuscitation'],exp:'UPDATED NRP GUIDELINES (2015 onwards) for meconium-stained amniotic fluid (MSAF): OLD PRACTICE (abandoned): Intrapartum suctioning before delivery of shoulders \u2014 shown to be INEFFECTIVE and potentially harmful (no longer recommended). Routine tracheal suctioning for all MSAF babies \u2014 abandoned unless the baby is non-vigorous. CURRENT RECOMMENDATION: If baby is VIGOROUS (good tone, crying, HR >100) \u2192 routine initial steps, no tracheal suctioning. If baby is NON-VIGOROUS (poor tone, poor respiratory efforts, HR <100) \u2192 INITIAL STEPS OF NEONATAL RESUSCITATION \u2714 (warm, stimulate, position, clear airway as needed) \u2192 PPV if apnoeic\/HR <100. Tracheal intubation + suctioning only if direct tracheal obstruction suspected. \"Initial steps of neonatal resuscitation\" is the correct answer for a baby with POOR respiratory efforts. Answer: Initial steps of neonatal resuscitation.'},\n{id:101,stem:'Which one of the following figures should a five-year-old developmentally normal child be able to draw?',correct:'Triangle',options:['Rectangle','Triangle','Circle','Cross'],exp:'Developmental milestones \u2014 figure drawing sequence: Circle: 3 years. Cross\/Plus (+): 4 years. Square: 4\u20134.5 years. TRIANGLE \u2714: 5 years. Rectangle: 4.5\u20135 years (some sources) \u2014 also achievable at 5. Diamond: 6 years. The question asks what a 5-year-old SHOULD be able to draw. At 5 years, the expected figure is a TRIANGLE (three lines meeting at angles \u2014 requires more precision than a cross or square). Rectangle is also achievable but triangle is the standard 5-year milestone. Cross is 4-year milestone. Answer: Triangle.'},\n{id:102,stem:'Which of the following manifestations is\/are NOT seen in breath holding spells?',correct:'Drowsiness after the episode',options:['Apnoea','Tonic clonic movements','Drowsiness after the episode','Pallor'],exp:'BREATH HOLDING SPELLS (BHS): involuntary cessation of breathing in young children (6 months\u20135 years), triggered by emotional upset, pain, or fright. Types: CYANOTIC BHS: cry \u2192 breath holding \u2192 cyanosis \u2192 loss of consciousness \u2192 (sometimes) tonic-clonic movements \u2192 quick recovery. PALLID BHS: precipitated by minor trauma \u2192 vagal response \u2192 pallor \u2192 brief LOC \u00b1 tonic movements \u2192 rapid recovery. Features present: Apnoea \u2714 (breath holding is the mechanism), Tonic-clonic movements \u2714 (can occur from cerebral hypoxia during the episode), Pallor \u2714 (pallid type or cyanotic with pallor). DROWSINESS AFTER THE EPISODE: NOT seen in BHS \u2014 children recover RAPIDLY and are ALERT immediately after (within seconds to minutes). This contrasts with epileptic seizures, which are followed by a POST-ICTAL period of drowsiness\/confusion. Rapid recovery without post-ictal drowsiness = distinguishing feature of BHS. Answer: Drowsiness after the episode.'},\n{id:103,stem:'Which of the following toxidromes is associated with the consumption of pesticides containing organophosphates?',correct:'Cholinergic',options:['Adrenergic','Serotonergic','Cholinergic','Hypnotic'],exp:'ORGANOPHOSPHATE poisoning: OPs inhibit acetylcholinesterase \u2192 accumulation of acetylcholine at all cholinergic synapses \u2192 CHOLINERGIC TOXIDROME \u2714. Cholinergic toxidrome features (SLUDGE + DUMBELS): Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis (SLUDGE). DUMBELS: Diarrhoea\/Defecation, Urination, Miosis, Bradycardia, Bronchospasm\/Bronchorrhoea, Emesis, Lacrimation\/LOC, Salivation\/SLUDGE. Nicotinic (NMJ): muscle fasciculations, weakness, paralysis. CNS: confusion, seizures, coma. Adrenergic: tachycardia, hypertension, mydriasis, hyperthermia (amphetamines, cocaine). Serotonergic: hyperthermia, clonus, agitation (SSRI overdose). Hypnotic: CNS depression, respiratory depression (benzodiazepines, opioids). Answer: Cholinergic.'},\n{id:104,stem:'Which of the following is the primary antidote used in children with organophosphate poisoning?',correct:'Atropine',options:['Atropine','Physostigmine','Sodium bicarbonate','Naloxone'],exp:'OP poisoning antidotes: ATROPINE \u2714 \u2014 PRIMARY antidote. Atropine is a competitive MUSCARINIC RECEPTOR ANTAGONIST \u2014 blocks the MUSCARINIC effects of accumulated ACh (bronchorrhoea, bronchospasm, bradycardia, excessive secretions). Given in large doses (repeated every 5\u201310 min) until \"atropinisation\" (dry secretions, HR >80, clear chest). Atropine does NOT address nicotinic effects (muscle paralysis\/fasciculations). PRALIDOXIME (2-PAM): oxime that reactivates inhibited acetylcholinesterase \u2014 used alongside atropine for nicotinic\/NMJ effects; more effective if given early (before \"ageing\"). Physostigmine: ANTI-CHOLINESTERASE (increases ACh) \u2014 CONTRAINDICATED in OP poisoning (would worsen toxicity). Sodium bicarbonate: alkalinisation (used in tricyclic overdose). Naloxone: opioid antagonist. Answer: Atropine.'},\n{id:105,stem:'Till what age should corrected age be used (rather than chronological age) for the developmental assessment of babies born preterm?',correct:'2 years',options:['6 months','1 years','2 years','2.5 years'],exp:'CORRECTED AGE (gestational age-adjusted age) for premature infants: Corrected age = Chronological age minus the number of weeks premature. For developmental assessment of preterm infants: CORRECTED AGE should be used until AGE 2 YEARS \u2714 (24 months). Beyond 2 years, the developmental \"catch-up\" is largely complete and chronological age is used. Rationale: premature infants have accelerated brain development after birth (ex-utero), but their developmental milestones should be assessed based on corrected age (reflecting neurological maturity). Using chronological age would falsely classify many premature infants as developmentally delayed. After 2 years: motor milestones are usually caught up; language may need slightly longer adjustment. Standard recommendation (AAP, developmental paediatricians): use corrected age up to 2 years. Answer: 2 years.'},\n{id:106,stem:'Which of the following is NOT a maternal risk factor for the development of a neural tube defect?',correct:'Exposure to radiation',options:['Insulin dependent Diabetes Mellitus','Exposure to radiation','Intake of Phenytoin','Folate deficiency'],exp:'Maternal risk factors for Neural Tube Defects (NTDs \u2014 anencephaly, spina bifida, encephalocele): Folate deficiency \u2714 \u2014 most important, preventable risk factor; periconceptional folic acid reduces NTD risk by 50\u201370%. Insulin-dependent DM (Type 1 DM) \u2714 \u2014 poorly controlled maternal diabetes is associated with 2\u201310\u00d7 increased NTD risk; hyperglycaemia impairs neural tube closure. Phenytoin (antiepileptic) \u2714 \u2014 folate antagonist (induces folate metabolism) \u2192 relative folate deficiency \u2192 NTD risk; valproate also teratogenic for NTDs. Obesity, hyperthermia (fever in 1st trimester), sodium valproate, carbamazepine, maternal hypothyroidism also increase risk. EXPOSURE TO RADIATION: ionising radiation is a general teratogen but is NOT a specific\/recognised risk factor for NEURAL TUBE DEFECTS specifically. It causes growth retardation, microcephaly, and malignancy \u2014 but NTDs are related to folate\/folic acid metabolism disruption. Answer: Exposure to radiation.'},\n{id:107,stem:'Trisomy 13 is also known as:',correct:'Patau syndrome',options:['Edward syndrome','Patau syndrome','Turner syndrome','Williams syndrome'],exp:'Chromosomal syndrome naming: Trisomy 13 = PATAU SYNDROME \u2714 \u2014 named after Klaus Patau (1960). Features: holoprosencephaly, microcephaly, cyclopia, microphthalmia, cleft lip\/palate, polydactyly, cardiac defects (VSD, ASD, PDA), rocker-bottom feet. Prognosis: very poor \u2014 50% die within 1 month; most within 6 months. Trisomy 18 = EDWARD SYNDROME \u2014 named after J.H. Edwards. Features: IUGR, clenched overlapping fingers, rocker-bottom feet, CHD, micrognathia. Trisomy 21 = DOWN SYNDROME (not listed). Turner syndrome = 45,X0 (monosomy X \u2014 not a trisomy). Williams syndrome = 7q11.23 microdeletion (not a trisomy). Answer: Patau syndrome.'},\n{id:108,stem:'Which one of the following is a type of glycogen storage disease?',correct:'Andersen disease',options:['Andersen disease','Gaucher disease','Krabbe disease','Sandhoff disease'],exp:'Classification of lysosomal\/storage diseases: GLYCOGEN STORAGE DISEASES (GSDs) \u2014 defects in glycogen synthesis or degradation: Andersen disease \u2714 (GSD Type IV \u2014 branching enzyme deficiency \u2014 amylopectinosis; abnormal glycogen accumulates; hepatosplenomegaly, cirrhosis). Other GSDs: Type I (Von Gierke \u2014 glucose-6-phosphatase), Type II (Pompe \u2014 acid maltase), Type III (Cori\/Forbes), Type V (McArdle \u2014 muscle phosphorylase), Type VI (Hers). GAUCHER DISEASE: sphingolipidosis (glucocerebrosidase deficiency \u2192 glucocerebroside accumulation) \u2014 NOT a GSD. KRABBE DISEASE: sphingolipidosis (galactocerebrosidase deficiency \u2192 psychosine accumulation). SANDHOFF DISEASE: GM2 gangliosidosis (hexosaminidase A and B deficiency). Andersen disease = GSD. Answer: Andersen disease.'},\n{id:109,stem:'Which of the following biochemical tests for the detection of aneuploidies is performed in the first trimester of pregnancy?',correct:'Pregnancy associated plasma protein A',options:['Serum alpha-feto protein','Pregnancy associated plasma protein A','Unconjugated estriol','Inhibin A'],exp:'Prenatal screening \u2014 trimester-specific markers: FIRST TRIMESTER COMBINED SCREENING (11\u201313+6 weeks): NT (nuchal translucency) on USS + PAPP-A (Pregnancy-Associated Plasma Protein A) \u2714 + free \u03b2-hCG. PAPP-A: produced by syncytiotrophoblast; LOW in Down syndrome (trisomy 21), Edward syndrome (trisomy 18), Patau syndrome (trisomy 13). Free \u03b2-hCG: HIGH in Down syndrome, LOW in T18\/T13. SECOND TRIMESTER (QUAD SCREEN, 15\u201320 weeks): AFP (alpha-fetoprotein \u2014 low in Down syndrome, high in NTDs), Unconjugated estriol (uE3 \u2014 low in Down syndrome), hCG (high in Down syndrome), Inhibin A (high in Down syndrome). Serum AFP, uE3, inhibin A = second trimester markers. PAPP-A = first trimester marker. Answer: Pregnancy associated plasma protein A (PAPP-A).'},\n{id:110,stem:'Which of the following is NOT a birth defect related to a disorder in the development of the whole eyeball?',correct:'Cryptophthalmos',options:['Anophthalmos','Cryptophthalmos','Microphthalmos','Nanophthalmos'],exp:'Disorders of WHOLE EYEBALL development: Anophthalmos \u2714 \u2014 complete absence of the eye (failure of optic vesicle formation). Microphthalmos \u2714 \u2014 abnormally small eyeball (reduced overall size; associated with TORCH infections, chromosomal anomalies). Nanophthalmos \u2714 \u2014 very small but otherwise structurally normal eye (a form of microphthalmos). CRYPTOPHTHALMOS: abnormality where the EYELIDS fail to separate (fused eyelids covering a rudimentary\/absent eye) \u2014 primarily a EYELID development defect, not a whole eyeball development disorder per se. It is part of Fraser syndrome (cryptophthalmos-syndactyly syndrome). The eyeball underlying cryptophthalmos may be rudimentary, but the primary defect is in eyelid formation. Answer: Cryptophthalmos \u2014 NOT primarily a whole eyeball development disorder.'},\n{id:111,stem:'Which of the following types of tracheoesophageal fistulae is the most common?',correct:'The upper part of the esophagus ends blindly and the lower end is connected to the trachea by a fistula',options:['The upper part of the esophagus ends blindly and the lower end is connected to the trachea by a fistula','There is no fistulous connection between either the upper or the lower parts of the esophagus and the trachea','The upper part of the esophagus opens into the trachea','Both the upper and lower parts of the esophagus open into the trachea'],exp:'Tracheo-Oesophageal Fistula (TOF) types \u2014 GROSS\/VOGT classification: Type C (Gross Type C) = MOST COMMON (~85\u201390%): Upper oesophagus ends BLINDLY (blind proximal pouch) + LOWER oesophagus connected to TRACHEA by a fistula \u2714. Air enters stomach via fistula. Pure oesophageal atresia (no fistula \u2014 Gross Type A): ~8%; H-type (TOF without atresia): ~4%; Both ends fistulate (Gross Type E): rare. The classic presentation: maternal polyhydramnios, inability to pass nasogastric tube, bubbling\/drooling, aspiration pneumonia. The most common type has a BLIND UPPER POUCH + LOWER FISTULA to the trachea. Answer: Upper oesophagus ends blindly + lower end connected to trachea by fistula.'},\n{id:112,stem:'Which one of the following antiretroviral drugs is a Nucleoside Reverse Transcriptase Inhibitor (NRTI)?',correct:'Abacavir',options:['Amprenavir','Indinavir','Abacavir','Nevirapine'],exp:'ARV drug class classification: NUCLEOSIDE\/NUCLEOTIDE RTIs (NRTIs): Abacavir \u2714 (ABC), Zidovudine (AZT), Lamivudine (3TC), Tenofovir (TDF \u2014 nucleotide), Emtricitabine (FTC), Didanosine (ddI), Stavudine (d4T). NON-NUCLEOSIDE RTIs (NNRTIs): Nevirapine, Efavirenz, Rilpivirine, Etravirine. PROTEASE INHIBITORS (PIs): Amprenavir, Indinavir, Lopinavir, Ritonavir, Darunavir, Atazanavir. INTEGRASE INHIBITORS: Raltegravir, Dolutegravir, Elvitegravir. Amprenavir = PI. Indinavir = PI. Nevirapine = NNRTI. ABACAVIR = NRTI \u2714 (guanosine analogue; component of TRIUMEQ = abacavir + dolutegravir + lamivudine; risk of hypersensitivity reaction in HLA-B*5701 carriers). Answer: Abacavir.'},\n{id:113,stem:'All of the following statements are true about the BCG vaccine EXCEPT:',correct:'It does not protect against other mycobacterial diseases like leprosy',options:['It has 50\u201380% protection against miliary and meningeal forms of tuberculosis','It does not protect against other mycobacterial diseases like leprosy','It induces primary cell mediated immunity','There is interference with its effect due to maternal antibodies'],exp:'BCG vaccine facts: 50\u201380% protection against miliary and meningeal TB \u2714 TRUE \u2014 BCG is most effective against disseminated childhood TB (miliary, TB meningitis) \u2014 less effective for pulmonary TB in adults. Induces primary cell-mediated immunity \u2714 TRUE \u2014 BCG is a live attenuated mycobacterium; stimulates Th1 cell-mediated response (CD4+ T cells, macrophage activation) \u2014 NOT humoral. No interference from maternal antibodies \u2714 TRUE \u2014 maternal IgG (transplacental) does NOT interfere with BCG because BCG works via cell-mediated immunity, not antibody-mediated. Compare with live viral vaccines where maternal antibodies CAN interfere. \"BCG does NOT protect against other mycobacterial diseases like leprosy\" is FALSE \u2714 \u2014 BCG provides 50\u201380% protection against leprosy (cross-reactive immunity against Mycobacterium leprae). Also protects against Buruli ulcer, Johne\\'s disease. Answer: Does not protect against leprosy \u2014 NOT true (BCG does protect against leprosy).'},\n{id:114,stem:'A 10-year-old boy with complete pre-exposure vaccination with rabies vaccine, bitten on the hand by a stray dog within a year of the last dose. Recommended treatment option:',correct:'Local wound care and 2 doses of rabies vaccine (day 0 and 3)',options:['Irrigation of the wound with water for ten minutes followed by povidone iodine (local care)','Local wound care and local infiltration with rabies Immunoglobulin (RIG)','Local wound care and 2 doses of rabies vaccine (day 0 and 3)','Local wound care and local infiltration of wound with RIG and 2 dose of rabies vaccine (day 0 and 3)'],exp:'Post-exposure management in a PREVIOUSLY VACCINATED person (complete pre-exposure OR post-exposure prophylaxis): WOUND CARE \u2714 \u2014 ALWAYS FIRST (thorough washing with soap\/water + povidone iodine). 2 BOOSTER DOSES of rabies vaccine: Day 0 and Day 3 \u2714 \u2014 pre-existing immunity provides rapid anamnestic (memory) response; only 2 doses needed (not the full 5-dose schedule). RIG NOT REQUIRED \u2714 \u2014 previously vaccinated individuals have protective antibody levels; RIG is contraindicated (unnecessary, may blunt the vaccine response, and expensive). Local wound care alone (option a): insufficient \u2014 vaccine boosters needed. RIG alone: insufficient. RIG + vaccine: incorrect \u2014 RIG not needed in previously vaccinated. Correct: wound care + 2 doses vaccine (day 0 and 3). Answer: Local wound care and 2 doses of rabies vaccine (day 0 and 3).'},\n{id:115,stem:'Which of the following combinations of Human Papilloma Virus (HPV) serotypes are non-oncogenic?',correct:'6 and 11',options:['6 and 11','6 and 16','6 and 18','16 and 18'],exp:'HPV serotypes \u2014 oncogenic classification: NON-ONCOGENIC (low-risk) HPV types: 6 and 11 \u2714 \u2014 cause genital warts (condylomata acuminata) and recurrent respiratory papillomatosis. Do NOT cause cancer. HIGH-RISK ONCOGENIC HPV types: 16 and 18 (most important) \u2014 cause ~70% of cervical cancer. 16: squamous cell carcinoma. 18: adenocarcinoma of cervix. Also oncogenic: 31, 33, 45, 52, 58. HPV VACCINES: Cervarix (bivalent): 16 + 18 (oncogenic). Gardasil 4 (quadrivalent): 6 + 11 + 16 + 18. Gardasil 9 (nonavalent): adds 31, 33, 45, 52, 58. 6 and 11 = NON-ONCOGENIC (warts, not cancer). 16 and 18 = ONCOGENIC (cancer). Answer: 6 and 11.'},\n{id:116,stem:'What type of vaccine is the Rotavirus vaccine?',correct:'Live attenuated organism',options:['Live attenuated organism','Killed organism','Toxoid','Subunit vaccine'],exp:'ROTAVIRUS VACCINES available: Rotarix (GlaxoSmithKline): LIVE ATTENUATED \u2714 \u2014 monovalent (G1P[8]); 2 oral doses. RotaTeq (Merck): LIVE ATTENUATED \u2714 \u2014 pentavalent (reassortant human-bovine; G1, G2, G3, G4, P[8]); 3 oral doses. ROTAVAC (Bharat Biotech \u2014 India): LIVE ATTENUATED \u2714 \u2014 monovalent (116E strain); approved and used in India\\'s NIS. All rotavirus vaccines are LIVE ATTENUATED oral vaccines. Given orally (not injected). Key: rotavirus = live attenuated. Compare: Killed organism (IPV, hepatitis A), Toxoid (tetanus, diphtheria), Subunit (hepatitis B, acellular pertussis). Answer: Live attenuated organism.'},\n{id:117,stem:'What is the risk of recurrence for Down\\'s syndrome when the underlying cause is a translocation inherited from the father?',correct:'4\u20135%',options:['1%','4\u20135%','10%','100%'],exp:'Down syndrome recurrence risk based on cause: TRISOMY 21 (non-disjunction \u2014 95% of cases): recurrence risk = ~1% + maternal age risk. TRANSLOCATION DOWN SYNDROME (~4% of cases): risk depends on which parent is the carrier. MATERNAL CARRIER of Robertsonian translocation (e.g., 14;21 or 21;21): 10\u201315% recurrence risk (if 14;21 translocation). PATERNAL CARRIER of Robertsonian translocation (14;21): LOWER recurrence \u2014 4\u20135% \u2714. This is because male meiosis is less likely to produce unbalanced gametes compared to female meiosis (selection against unbalanced sperm). 21;21 translocation carrier (either parent): 100% risk \u2014 all offspring with chromosomes will have Down syndrome. Paternal translocation carrier = 4\u20135% recurrence risk. Answer: 4\u20135%.'},\n{id:118,stem:'An 8-month-old infant with evolving Cerebral Palsy is diagnosed with the first episode of Urinary Tract Infection. What further radiological evaluation should be planned?',correct:'Ultrasound of the abdomen (KUB), Micturating Cystourethrogram (MCU) and radionuclide renal scan (\u2079\u2079Tc DMSA scan)',options:['Ultrasound of the abdomen (KUB) only','Ultrasound of the abdomen (KUB) and Micturating Cystourethrogram (MCU) only','Ultrasound of the abdomen (KUB), Micturating Cystourethrogram (MCU) and radionuclide renal scan (\u2079\u2079Tc DMSA scan)','Radionuclide or ultrasound scan (\u2079\u2079Tc DMSA scan) followed by MCU (if required)'],exp:'UTI in infants \u2014 radiological evaluation guidelines: This child is 8 months old (under 2 years) + FIRST episode UTI + underlying neurological condition (Cerebral Palsy \u2014 bladder dysfunction\/neurogenic bladder = HIGH RISK for VUR and renal scarring). For HIGH-RISK infants (<2 years, atypical or recurrent UTI, neurological condition): Full evaluation recommended: USS (KUB) \u2714 \u2014 initial assessment of renal size, hydronephrosis, anatomical abnormalities. MCU (Micturating Cystourethrogram) \u2714 \u2014 detects vesicoureteric reflux (VUR), urethral anatomy; gold standard for VUR. DMSA scan (\u2079\u2079Tc DMSA) \u2714 \u2014 detects renal cortical scarring; most sensitive for pyelonephritis and scarring. Standard Indian guidelines for a high-risk infant (neurological + first UTI <2 years): complete triad of USS + MCU + DMSA. Answer: USS (KUB) + MCU + DMSA scan.'},\n{id:119,stem:'Which one of the following vaccines is NOT included in Mission Indradhanush?',correct:'MMR',options:['BCG','OPV','DPT','MMR'],exp:'MISSION INDRADHANUSH (launched 2014, Government of India) \u2014 vaccines included in Universal Immunisation Programme (UIP) targeted under this mission: BCG \u2714, OPV (oral polio vaccine) \u2714, DPT (diphtheria-pertussis-tetanus) \u2714, Hepatitis B, Haemophilus influenzae type B (Hib \u2014 as part of pentavalent), Measles (and later MR\/MMR in some districts). EXPANDED Mission Indradhanush: Japanese Encephalitis (endemic districts), IPV, Rotavirus, PCV (pneumococcal). MMR (Measles-Mumps-Rubella): the FULL MMR vaccine is NOT part of India\\'s standard UIP\/Mission Indradhanush schedule. India\\'s NIS provides Measles-Rubella (MR) vaccine (not the full MMR which includes Mumps). MMR was not included in the original Mission Indradhanush schedule. Answer: MMR.'},\n{id:120,stem:'Which of the following drugs is NOT included in the management of Attention Deficit Hyperactivity Disorder?',correct:'Trientine',options:['Amphetamine','Atomoxetine','Methylphenidate','Trientine'],exp:'ADHD pharmacotherapy: STIMULANTS (first-line): Methylphenidate (Ritalin) \u2714 \u2014 dopamine\/norepinephrine reuptake inhibitor; most widely used for ADHD. Amphetamine (mixed amphetamine salts \u2014 Adderall, dextroamphetamine) \u2714 \u2014 dopamine\/norepinephrine releaser and reuptake inhibitor; equally effective first-line. NON-STIMULANTS: Atomoxetine (Strattera) \u2714 \u2014 selective norepinephrine reuptake inhibitor; non-controlled substance; effective for ADHD; also used when stimulants are contraindicated or not tolerated. Also: Clonidine (alpha-2 agonist), Guanfacine, Bupropion. TRIENTINE: a CHELATING AGENT used for WILSON\\'S DISEASE (copper chelation \u2014 alternative to D-penicillamine). Has absolutely NO role in ADHD management. 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Submitting in 10 Submit Now Combined Medical Services Examination 2019Paper I \u00b7 Part C Rheumatology \u00b7 Psychiatry \u00b7 Neurology \u00b7 Toxicology \u00b7 Geriatrics \u00b7 Pharmacology \u00b7 Paediatrics \u00b7 Immunisation Questions 81 \u2013 120 Options reshuffled \u23f1 Start Timed Mode Submit… <\/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-36823","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"\n<title>CMS 2019 P1 Part-C - 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\/13\/cms-2019-p1-part-c\/\" \/>\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-C - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2019 Paper I \u2013 Part C (Q81\u2013Q120) \u23f1 40:00 \u2705 0 \u274c 0 \u23f3 40 left Net 0 \/ 160 Time's Up! 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