{"id":36821,"date":"2026-05-13T04:33:40","date_gmt":"2026-05-12T23:03:40","guid":{"rendered":"https:\/\/atsixty.com\/?p=36821"},"modified":"2026-05-13T04:34:17","modified_gmt":"2026-05-12T23:04:17","slug":"cms-2019-p1-part-b","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/2026\/05\/13\/cms-2019-p1-part-b\/","title":{"rendered":"CMS 2019 P1 Part-B"},"content":{"rendered":"\n\n\n<!DOCTYPE html>\n<html lang=\"en\">\n<head>\n<meta charset=\"UTF-8\">\n<meta name=\"viewport\" content=\"width=device-width, initial-scale=1.0\">\n<title>CMS 2019 Paper I \u2013 Part B (Q41\u2013Q80)<\/title>\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:wght@600;700&#038;family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&#038;display=swap\" rel=\"stylesheet\">\n<style>\n#cms19p1b*,#cms19p1b *::before,#cms19p1b 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.2s}\n#cms19p1b .rb:hover{background:var(--teal);color:var(--wh)}\n@media(max-width:480px){#cms19p1b .hd h1{font-size:1.15rem}#cms19p1b .qt{font-size:.88rem}#cms19p1b .ox{font-size:.84rem}}\n<\/style>\n<\/head>\n<body>\n<div id=\"cms19p1b\">\n<div class=\"sn\" id=\"cms19p1b-sn\"><\/div>\n<div class=\"sb\" id=\"cms19p1b-sb\">\n  <div class=\"sr\">\n    <div class=\"ti\" id=\"cms19p1b-ti\">\u23f1&nbsp;<strong id=\"cms19p1b-td\">40:00<\/strong><\/div>\n    <div class=\"si\">\u2705&nbsp;<strong id=\"cms19p1b-sc\">0<\/strong><\/div>\n    <div class=\"si\">\u274c&nbsp;<strong id=\"cms19p1b-sw\">0<\/strong><\/div>\n    <div class=\"si\">\u23f3&nbsp;<strong id=\"cms19p1b-sr\">40<\/strong>&nbsp;left<\/div>\n    <div class=\"ss\"><\/div>\n    <div class=\"si\">Net&nbsp;<strong id=\"cms19p1b-sn\">0<\/strong>&nbsp;\/&nbsp;<strong id=\"cms19p1b-sm\">160<\/strong><\/div>\n  <\/div>\n  <div class=\"sp\"><div class=\"sf\" id=\"cms19p1b-sf\"><\/div><\/div>\n<\/div>\n<div class=\"gr\" id=\"cms19p1b-gr\">\n  <div class=\"gb\"><h3>Time's Up!<\/h3><p>Submitting in<\/p><div class=\"gc\" id=\"cms19p1b-gc\">10<\/div><button class=\"gn\" id=\"cms19p1b-gn\">Submit Now<\/button><\/div>\n<\/div>\n<div class=\"hd\">\n  <h1>Combined Medical Services Examination 2019<br>Paper I &nbsp;\u00b7&nbsp; Part B<\/h1>\n  <p>Gastroenterology \u00b7 Nephrology \u00b7 Neurology \u00b7 Haematology \u00b7 Endocrinology \u00b7 Infectious Diseases \u00b7 Rheumatology<\/p>\n  <div class=\"mt\">\n    <span class=\"bd\">Questions 41 \u2013 80<\/span>\n    <span class=\"bd\">Options reshuffled<\/span>\n    <button class=\"tb\" id=\"cms19p1b-tb\">\u23f1 Start Timed Mode<\/button>\n  <\/div>\n<\/div>\n<div class=\"bd2\">\n  <div id=\"cms19p1b-qs\"><\/div>\n  <div class=\"sw\"><button class=\"bt\" id=\"cms19p1b-sub\">Submit Answers<\/button><\/div>\n  <div class=\"sc\" id=\"cms19p1b-sc-box\">\n    <div class=\"rg\" id=\"cms19p1b-rg\"><div class=\"ri\"><span class=\"rp\" id=\"cms19p1b-rp\">0%<\/span><span class=\"rs\">score<\/span><\/div><\/div>\n    <h2>Your Result<\/h2>\n    <div class=\"nl\" id=\"cms19p1b-nl\"><\/div>\n    <div class=\"vd\" id=\"cms19p1b-vd\"><\/div>\n    <div class=\"bs\"><span class=\"bn bc\" id=\"cms19p1b-bc\"><\/span><span class=\"bn bw\" id=\"cms19p1b-bw\"><\/span><span class=\"bn bk\" id=\"cms19p1b-bk\"><\/span><\/div>\n    <button class=\"rb\" id=\"cms19p1b-rb\">\u21ba Retry Quiz<\/button>\n  <\/div>\n<\/div>\n<\/div>\n<script>\n(function(){\n'use strict';\nvar NS='cms19p1b',TOTAL=40,MAX=160,TSECS=2400,GSECS=10;\nvar QS=[\n{id:41,stem:'Long term use of proton pump inhibitor in elderly puts the patient at risk of which of the following?\\n1. Community acquired pneumonia\\n2. Clostridium difficile associated disease\\n3. Urinary tract infection\\nSelect the correct answer:',correct:'1 and 2',options:['1 only','2 only','1 and 2','2 and 3'],exp:'Long-term PPI risks in elderly: Community-acquired pneumonia \u2714 \u2014 gastric acid suppression allows bacterial overgrowth in the stomach; micro-aspiration of gastric contents (colonised by gram-negative organisms) \u2192 pneumonia. Also: PPIs reduce mucociliary clearance via unclear mechanisms. C. difficile associated disease \u2714 \u2014 gastric acid is a major defence against C. diff spores; PPIs allow survival and germination of spores reaching the colon; strongly associated with CDI risk. Other PPI risks: hypomagnesaemia, vitamin B12 deficiency, osteoporosis\/fractures, iron malabsorption, SIBO, rebound acid hypersecretion. UTI: NOT a recognised association with PPI use. Answer: 1 and 2.'},\n{id:42,stem:'Regardless of the infectious agent, the most characteristic symptom of infectious esophagitis is:',correct:'Odynophagia',options:['Dysphagia','Chest pain','Odynophagia','Haematemesis'],exp:'INFECTIOUS OESOPHAGITIS (Candida, CMV, HSV, HIV): The MOST CHARACTERISTIC symptom is ODYNOPHAGIA \u2014 painful swallowing. Pain on swallowing (odynophagia) is the cardinal symptom that distinguishes infectious oesophagitis from other oesophageal disorders. This is true regardless of the causative organism (Candida = most common in immunocompromised; CMV\/HSV also cause painful ulcers). Dysphagia (difficulty swallowing) is present but less specific. Chest pain: can occur but is not the most characteristic. Haematemesis: uncommon. Odynophagia is the hallmark of infectious oesophagitis and prompts upper GI endoscopy in immunocompromised patients. Answer: Odynophagia.'},\n{id:43,stem:'The parameters used in modified Child-Pugh classification for staging cirrhosis are:',correct:'Serum albumin, Serum bilirubin, prothrombin time, ascites, hepatic encephalopathy',options:['Serum bilirubin, serum albumin only','Serum albumin, serum bilirubin, prothrombin time only','Serum albumin, serum bilirubin, prothrombin time, ascites only','Serum albumin, Serum bilirubin, prothrombin time, ascites, hepatic encephalopathy'],exp:'Modified Child-Pugh Score \u2014 5 parameters (each scored 1\u20133, total 5\u201315): (1) Serum Bilirubin. (2) Serum Albumin. (3) Prothrombin Time (or INR). (4) Ascites (absent\/mild\/moderate-severe). (5) Hepatic Encephalopathy (absent\/Grade I-II\/Grade III-IV). Classification: Class A (5\u20136) = well-compensated; Class B (7\u20139) = significant compromise; Class C (10\u201315) = decompensated (poorest prognosis). All five parameters are required for the modified Child-Pugh score. Answer: All five \u2014 serum albumin, bilirubin, PT, ascites, hepatic encephalopathy.'},\n{id:44,stem:'All of the following are consistent with a diagnosis of Irritable Bowel Syndrome EXCEPT:',correct:'Weight loss',options:['Recurrent lower abdominal pain','Altered bowel habits','Symptoms during periods of stress','Weight loss'],exp:'IBS (Irritable Bowel Syndrome) \u2014 a functional disorder (Rome IV criteria): Recurrent abdominal pain \u2714 (\u22651 day\/week, last 3 months, related to defecation\/stool form\/frequency). Altered bowel habits \u2714 (diarrhoea-predominant IBS-D, constipation-predominant IBS-C, mixed IBS-M). Stress exacerbation \u2714 \u2014 a characteristic feature; symptoms often worse with psychological stress (strong gut-brain axis connection). WEIGHT LOSS: a RED FLAG symptom \u2014 NOT a feature of IBS. Unexplained weight loss in a patient with GI symptoms suggests organic disease (malignancy, IBD, malabsorption, chronic infection). IBS does NOT cause weight loss. Other red flags: rectal bleeding, anaemia, nocturnal symptoms, family history of colon cancer\/IBD, onset >50 years. Answer: Weight loss \u2014 EXCEPT.'},\n{id:45,stem:'A 26-year old HIV infected male presents with odynophagia. Upper GI endoscopy demonstrates serpiginous ulcers in a normal surrounding mucosa in distal esophagus. The most likely diagnosis is:',correct:'Cytomegalovirus esophagitis',options:['Gastro esophageal reflux disease','Cytomegalovirus esophagitis','Candida esophagitis','Herpetic esophagitis'],exp:'Oesophageal ulcers in HIV \u2014 endoscopic pattern distinguishes: CMV OESOPHAGITIS \u2714 \u2014 LARGE, SERPIGINOUS (snake-like\/linear), SHALLOW ULCERS in the DISTAL oesophagus with NORMAL SURROUNDING MUCOSA. This is the classic endoscopic description of CMV oesophagitis. CMV infects stromal cells\/endothelium \u2192 large ulcers. HSV oesophagitis: multiple small, PUNCHED-OUT vesicular\/ulcerative lesions, often mid-oesophagus; herpetic vesicles with surrounding erythema. Candida oesophagitis: WHITE PLAQUES\/pseudomembranes adherent to the mucosa \u2014 not ulcers with normal surrounding mucosa. GERD: not in the context of HIV with discrete ulcers. SERPIGINOUS large ulcers + normal surrounding mucosa = CMV. Answer: CMV esophagitis.'},\n{id:46,stem:'Cytomegalovirus esophagitis is particularly common in which group of patients?',correct:'Organ transplant recipients',options:['Diabetes mellitus','Chronic liver disease','Alcoholics','Organ transplant recipients'],exp:'CMV OESOPHAGITIS \u2014 risk groups: CMV is an OPPORTUNISTIC infection occurring in IMMUNOCOMPROMISED patients: ORGAN TRANSPLANT RECIPIENTS \u2714 \u2014 highest risk group; post-transplant immunosuppression (calcineurin inhibitors, mycophenolate, steroids) \u2192 CMV reactivation from latency; CMV is the most common serious infection in transplant recipients (solid organ and HSCT). HIV\/AIDS patients (CD4 <100\/mm\u00b3) \u2014 CMV retinitis, colitis, oesophagitis. Also: haematological malignancy, chemotherapy. CMV is latent in >90% of adults; reactivates under immunosuppression. DM, chronic liver disease, alcoholism cause some immune compromise but are NOT the high-risk groups for CMV oesophagitis. Answer: Organ transplant recipients.'},\n{id:47,stem:'Which of the following is the most important complication in a patient with coeliac disease, previously doing well on a gluten-free diet and now not responding to gluten restriction?',correct:'Intestinal lymphoma',options:['Intestinal infection','Intestinal lymphoma','Resistant coeliac disease','Type II Diabetes mellitus'],exp:'Coeliac disease \u2014 long-term complication when GFD fails: When a coeliac patient was PREVIOUSLY well-controlled on a gluten-free diet and RELAPSES \/ stops responding to GFD: The most important complication to exclude is INTESTINAL LYMPHOMA \u2714 \u2014 specifically ENTEROPATHY-ASSOCIATED T-CELL LYMPHOMA (EATL), a rare but aggressive complication of coeliac disease. Features: worsening abdominal symptoms, weight loss, failure of GFD, intestinal ulcers. Diagnosis: small bowel imaging + biopsy + immunohistochemistry. Prognosis: poor. Other complications of coeliac disease: refractory coeliac disease (Type I or II \u2014 RCD), small bowel adenocarcinoma, oropharyngeal carcinoma. The MOST IMPORTANT (life-threatening) to consider when GFD fails = intestinal lymphoma (EATL). Answer: Intestinal lymphoma.'},\n{id:48,stem:'Which of the following are potential side effects of Anti-TNF therapies?\\n1. Infusion reactions\\n2. Melanoma\\n3. T-cell lymphoma\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1 and 3 only','2 and 3 only','1 and 2 only','1, 2 and 3'],exp:'Anti-TNF therapy side effects (infliximab, adalimumab, etanercept, certolizumab, golimumab): Infusion reactions \u2714 \u2014 acute (fever, chills, urticaria, hypotension during IV infusion \u2014 infliximab IV) and delayed reactions; injection site reactions (SC forms). Melanoma \u2714 \u2014 increased risk of skin malignancies including melanoma with anti-TNF therapy (TNF has anti-tumour surveillance role; blocking it reduces immune surveillance). T-cell lymphoma \u2714 \u2014 specifically Hepatosplenic T-cell lymphoma (HSTCL) reported with combination anti-TNF + thiopurine (azathioprine\/6-MP); also other lymphomas. Other risks: reactivation of TB (screen before starting), serious bacterial infections, demyelination, heart failure exacerbation, lupus-like reactions. All three are recognised side effects. Answer: 1, 2 and 3.'},\n{id:49,stem:'Presence of gastrinoma tumour should be suspected in which of the following conditions?\\n1. Ulcers in unusual location\\n2. Ulcers in the presence of H. pylori\\n3. Ulcers with frank complication like perforation\\nSelect the correct answer:',correct:'1 and 3 only',options:['1, 2 and 3','2 and 3 only','1 and 3 only','1 and 2 only'],exp:'GASTRINOMA (Zollinger-Ellison syndrome) \u2014 when to suspect: Ulcers in UNUSUAL LOCATION \u2714 \u2014 beyond the first part of the duodenum (jejunum), multiple ulcers; normal peptic ulcers are in the duodenal bulb\/stomach. Ulcers with FRANK COMPLICATIONS \u2714 \u2014 perforation, haemorrhage, obstruction; refractory ulcers despite adequate PPI therapy. Hypersecretion of gastrin \u2192 massive acid \u2192 severe\/recurrent disease. Multiple endocrine neoplasia type 1 (MEN1), diarrhoea from acid hypersecretion, failure of standard therapy. ULCERS IN THE PRESENCE OF H. pylori: H. pylori is the MOST COMMON cause of peptic ulcers \u2014 finding H. pylori explains the ulcer; this does NOT suggest gastrinoma. In ZES, H. pylori is often absent (acid hypersecretion kills H. pylori). Statement 2 is NOT a reason to suspect gastrinoma. Answer: 1 and 3 only.'},\n{id:50,stem:'Coeliac disease is associated with which of the following medical conditions?\\n1. Dermatitis herpetiformis\\n2. Diabetes mellitus type II\\n3. Turner syndrome\\n4. IgA deficiency\\nSelect the correct answer:',correct:'1, 3 and 4',options:['1, 2 and 3','2, 3 and 4','1, 3 and 4','1, 2 and 4'],exp:'Coeliac disease associations: Dermatitis herpetiformis \u2714 \u2014 cutaneous manifestation of coeliac disease (gluten-sensitive skin blistering; IgA deposits in papillary dermis; responds to GFD + dapsone). Turner syndrome \u2714 \u2014 increased prevalence of coeliac disease in Turner syndrome (especially 45,X0; autoimmune conditions more common). IgA deficiency \u2714 \u2014 strongly associated; IgA deficiency causes false-negative anti-tTG IgA tests (must test IgA levels); also IgA nephropathy. TYPE 1 DIABETES MELLITUS (not Type 2) is associated with coeliac disease (both autoimmune; shared HLA-DQ2\/DQ8 haplotypes). TYPE II DM has no specific association with coeliac disease \u2014 this is NOT a recognised association. Down syndrome (not Turner) is another association. Answer: 1, 3 and 4.'},\n{id:51,stem:'Which of the following features are characteristics of Whipple disease?\\n1. Migratory small joint arthropathy\\n2. Diarrhoea with steatorrhoea\\n3. Weight loss with Arthralgia\\n4. Ophthalmic and CNS symptoms\\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:'Whipple\\'s disease (Tropheryma whipplei) features: Migratory arthropathy \u2714 \u2014 often affects LARGE joints (not small); migratory, seronegative; may precede GI symptoms by years. Diarrhoea with steatorrhoea \u2714 \u2014 malabsorption; foamy macrophages in SI biopsy (PAS-positive). Weight loss \u2714 \u2014 from malabsorption + systemic disease. Ophthalmic and CNS symptoms \u2714 \u2014 oculomasticatory myorhythmia (pathognomonic \u2014 pendular convergent nystagmus + synchronous masticatory muscle contractions), encephalopathy, dementia, supranuclear ophthalmoplegia. The arthropathy in Whipple\\'s characteristically affects LARGE joints (not small joints typically). Statement 3 says \"weight loss with arthralgia\" \u2014 weight loss is correct but calling it \"small joint\" (statement 1) is debatable. Per UPSC convention: 1, 2 and 4 are the characteristic features. Answer: 1, 2 and 4.'},\n{id:52,stem:'Which of the following are suggestive of protein losing enteropathy?\\n1. Steatorrhoea and diarrhoea\\n2. Peripheral oedema\\n3. Marked reduction of serum albumin with normal serum globulin\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'Protein-losing enteropathy (PLE) \u2014 excessive protein loss through the GI tract: Steatorrhoea and diarrhoea \u2714 \u2014 often the presenting GI symptoms; malabsorption syndrome with fat loss. Peripheral oedema \u2714 \u2014 hypoalbuminaemia from protein loss \u2192 reduced oncotic pressure \u2192 oedema (legs, face, ascites). Marked reduction of serum albumin with NORMAL serum globulin \u2714 \u2014 KEY distinguishing feature of PLE: albumin is predominantly lost (largest protein, longest half-life \u2014 most affected by gut loss), while immunoglobulins (globulins) are also lost but compensated or less dramatically reduced. In liver disease, BOTH albumin and globulins are abnormal (globulins often elevated). Normal globulin with low albumin = protein loss, not reduced synthesis. All three features are characteristic. Answer: 1, 2 and 3.'},\n{id:53,stem:'Which of the following statements regarding Ankylosing spondylitis (AS) are true?\\n1. AS occurs in about 10% of IBD patients\\n2. The AS activity is related to bowel activity in IBD patients\\n3. The AS activity does remit with glucocorticoids or colectomy in IBD patients\\nSelect the correct answer:',correct:'1 only',options:['2 and 3','1 and 3','3 only','1 only'],exp:'AS and IBD relationship: (1) AS in IBD patients \u2714 TRUE \u2014 AS occurs in ~5\u201310% of IBD patients (Crohn\\'s more than UC); IBD-associated spondyloarthropathy is well-recognised. (2) AS activity related to bowel activity: PARTIALLY TRUE for PERIPHERAL arthritis in IBD (peripheral arthritis activity DOES correlate with bowel disease activity). However, AXIAL disease (AS\/sacroiliitis) in IBD runs an INDEPENDENT course \u2014 NOT related to bowel disease activity. Statement 2 is FALSE for AS specifically. (3) AS remits with colectomy\/glucocorticoids: AXIAL disease does NOT remit with colectomy or glucocorticoids (unlike peripheral arthritis which improves with bowel disease treatment). Statement 3 is FALSE. Only statement 1 is unambiguously true. Answer: 1 only.'},\n{id:54,stem:'Which of the following are the renal complications of radiological investigations?\\n1. Contrast nephrotoxicity\\n2. Cholesterol atheroembolism\\n3. Nephrogenic sclerosing fibrosis of skin\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'Renal complications of radiological investigations: Contrast-induced nephropathy (CIN) \u2714 \u2014 iodinated contrast \u2192 renal vasoconstriction + direct tubular toxicity \u2192 AKI; risk highest with pre-existing CKD, DM, high osmolar contrast, large volumes. Cholesterol atheroembolism \u2714 \u2014 during angiography\/intervention, disruption of atheromatous plaques \u2192 cholesterol crystal emboli to renal arteries \u2192 \"blue toe syndrome,\" livedo reticularis, AKI (progressive, not immediate); eosinophilia and eosinophiluria. Nephrogenic systemic fibrosis (NSF) \u2714 \u2014 gadolinium-based contrast used in MRI \u2192 in severe CKD patients \u2192 systemic fibrosis affecting skin (formerly called nephrogenic sclerosing fibrosis of skin), muscles, organs; now prevented by avoiding gadolinium in eGFR <30. All three are renal\/systemic complications of radiological contrast agents. Answer: 1, 2 and 3.'},\n{id:55,stem:'A middle aged diabetic male with recurrent chest pain undergoes coronary artery angiogram. The following day, he develops haematuria, proteinuria and renal impairment. Most likely diagnosis:',correct:'Atheroembolism',options:['Renal artery stenosis','Acute renal infarction','Atheroembolism','Haemolytic Uraemic syndrome'],exp:'Clinical scenario: Diabetic + coronary angiography \u2192 next day: haematuria + proteinuria + renal impairment. This is ATHEROEMBOLISM (cholesterol crystal embolism): During catheter manipulation in the aorta\/coronary arteries \u2192 dislodgement of atheromatous plaques \u2192 cholesterol crystal emboli \u2192 renal microvasculature obstruction \u2192 AKI + haematuria + proteinuria. Clinical features: haematuria, proteinuria, AKI appearing 1\u201314 days post-procedure; \"trash foot\" (blue toes, livedo reticularis), eosinophilia, eosinophiluria. CIN (contrast nephropathy) usually presents within 24\u201348 hours with oliguria but no haematuria\/eosinophilia. Renal artery stenosis: chronic problem. HUS: typically post-diarrhoeal illness (E. coli O157:H7), microangiopathic haemolytic anaemia. Answer: Atheroembolism.'},\n{id:56,stem:'Which of the following are contraindications for renal biopsy?\\n1. Normal size kidney\\n2. Uncontrolled hypertension\\n3. Solitary kidney\\n4. Disordered coagulation\\nSelect the correct answer:',correct:'2, 3 and 4',options:['1, 2 and 4','1, 2 and 3','2, 3 and 4','1, 3 and 4'],exp:'Renal biopsy contraindications (absolute\/relative): Uncontrolled hypertension \u2714 \u2014 markedly elevated BP increases risk of severe post-biopsy haemorrhage; must control BP <140\/90 before biopsy. Solitary kidney \u2714 \u2014 loss of the single kidney post-biopsy would require dialysis; absolute contraindication unless very strong indication. Disordered coagulation \u2714 \u2014 bleeding diathesis \u2192 haemorrhage post-biopsy; correct coagulopathy before proceeding. NORMAL SIZED KIDNEY: is an INDICATION for biopsy (not a contraindication) \u2014 CKD with normal-sized kidneys warrants biopsy to find a treatable cause. Small kidneys (<9 cm) = contraindication (end-stage fibrosis; biopsy unhelpful and technically difficult). Normal-sized kidney does NOT contraindicate biopsy. Answer: 2, 3 and 4.'},\n{id:57,stem:'The most specific test that establishes the diagnosis of Myasthenia gravis is:',correct:'Anti-acetylcholine receptor antibody',options:['Anti-acetylcholine receptor antibody','Repetitive nerve stimulation test','Edrophonium test','MRI brain'],exp:'Myasthenia gravis diagnosis: Anti-AChR antibody (anti-acetylcholine receptor antibody) \u2714 \u2014 MOST SPECIFIC test. Present in ~85% of generalised MG and ~50% of ocular MG. If anti-AChR negative \u2192 test anti-MuSK antibody (muscle-specific kinase \u2014 in seronegative MG). Edrophonium (Tensilon) test: pharmacological test (AChE inhibitor \u2192 brief improvement) \u2014 positive in MG but NOT specific (false positives in other conditions; also dangerous). Repetitive nerve stimulation (RNS): shows decremental response (>10% decrement at 3 Hz stimulation) \u2014 sensitive but not specific. MRI brain: no role in MG diagnosis (MG is a NMJ disease). The anti-AChR antibody is PATHOGNOMONIC (when positive) = most specific. Answer: Anti-acetylcholine receptor antibody.'},\n{id:58,stem:'The commonest cause for new-onset seizures in patients older than 65 years is:',correct:'Cerebrovascular disease',options:['Trauma','Cerebrovascular disease','Tumors','Degenerative disease'],exp:'New-onset seizures in elderly (>65 years): The most common cause is CEREBROVASCULAR DISEASE (stroke) \u2714 \u2014 accounting for ~30\u201340% of new-onset seizures in elderly. Ischaemic stroke leaves an epileptogenic focus (cortical irritation, glial scar). Post-stroke epilepsy is a major form of late-onset seizures. Other causes in elderly: Metabolic (hypo\/hyperglycaemia, hyponatraemia), Brain tumours (primary and metastatic), Alcohol withdrawal, Drugs, Dementia (Alzheimer\\'s \u2014 late seizures), Head trauma, CNS infection. Trauma: not the most common. Tumours: 10\u201315%. Degenerative diseases: less common. Cerebrovascular disease = most common cause of new-onset seizures >65 years. Answer: Cerebrovascular disease.'},\n{id:59,stem:'Ipsilateral 3rd cranial nerve palsy with contralateral cerebellar signs is seen in:',correct:'Claude syndrome',options:['Weber syndrome','Wallenberg syndrome','Parinaud syndrome','Claude syndrome'],exp:'Brainstem syndromes: WEBER SYNDROME (midbrain \u2014 ventral): Ipsilateral CN III palsy + Contralateral hemiplegia (corticospinal tract). CLAUDE SYNDROME (midbrain \u2014 dorsal\/tegmentum): Ipsilateral CN III palsy + Contralateral CEREBELLAR SIGNS (ataxia, tremor \u2014 red nucleus\/superior cerebellar peduncle involvement). BENEDIKT SYNDROME: Ipsilateral CN III + contralateral tremor\/ataxia (red nucleus) + contralateral hemiplegia. WALLENBERG SYNDROME (lateral medulla): Ipsilateral face pain\/numbness, Horner\\'s, ataxia + contralateral body pain\/temperature loss. PARINAUD SYNDROME (dorsal midbrain): upgaze palsy, convergence-retraction nystagmus, light-near dissociation \u2014 NOT CN III palsy + cerebellar. CN III palsy + contralateral cerebellar signs = CLAUDE SYNDROME. Answer: Claude syndrome.'},\n{id:60,stem:'Incongruous contralateral homonymous hemianopia is due to lesion at:',correct:'Optic tract',options:['Optic nerve','Optic chiasma','Optic tract','Optic radiation'],exp:'Visual field defects by lesion location: OPTIC NERVE: monocular blindness (ipsilateral eye). OPTIC CHIASMA: bitemporal hemianopia (nasal fibres cross; lateral fibres uncrossed \u2014 lesion destroys crossed fibres from both nasal retinae \u2192 loss of both temporal fields). OPTIC TRACT: INCONGRUOUS contralateral homonymous hemianopia \u2014 fibres from both eyes present but not yet \"sorted\" retinotopically; the representation is incomplete \u2192 INCONGRUOUS (asymmetric) hemianopia. OPTIC RADIATION \/ VISUAL CORTEX: CONGRUOUS (symmetric) contralateral homonymous hemianopia \u2014 complete retinotopic mapping; defects are mirror-image identical in both eyes. Key rule: more anterior the lesion \u2192 more incongruous; more posterior \u2192 more congruous. Optic tract = incongruous contralateral homonymous hemianopia. Answer: Optic tract.'},\n{id:61,stem:'Macrocytosis is seen in all of the following conditions EXCEPT:',correct:'Post splenectomy',options:['Liver disease','Post splenectomy','Hypothyroidism','Myelodysplastic syndrome'],exp:'Macrocytosis (MCV >100 fL) causes: Liver disease \u2714 \u2014 accumulation of lipids in RBC membrane \u2192 target cells and macrocytes; also associated with alcoholism. Hypothyroidism \u2714 \u2014 reduced metabolic rate affects erythropoiesis; often mild macrocytosis. Myelodysplastic syndrome \u2714 \u2014 dysplastic erythropoiesis \u2192 macrocytosis (often with hypersegmented neutrophils, cytopenias). B12\/folate deficiency, alcohol, drugs (hydroxyurea, methotrexate), reticulocytosis, pregnancy. POST SPLENECTOMY: causes HOWELL-JOLLY BODIES (nuclear remnants \u2014 normally removed by spleen), target cells, and thrombocytosis \u2014 but NOT macrocytosis. The spleen normally removes old\/abnormal RBCs; its loss causes morphological changes but not increased MCV. Answer: Post splenectomy \u2014 EXCEPT.'},\n{id:62,stem:'All of the following cause microcytic hypochromic anaemia EXCEPT:',correct:'Haemolytic uraemic syndrome',options:['Thalassaemia','Anaemia of chronic disease','Sideroblastic anaemia','Haemolytic uraemic syndrome'],exp:'Microcytic hypochromic anaemia (MCV <80 fL, MCH <27 pg) causes: Thalassaemia \u2714 (alpha\/beta \u2014 reduced globin chain synthesis \u2192 small pale RBCs). Anaemia of chronic disease \u2714 (usually normocytic-normochromic, but can be microcytic in ~25\u201330% \u2014 sequestration of iron in macrophages via hepcidin). Sideroblastic anaemia \u2714 (defective haem synthesis \u2192 iron accumulates in mitochondria \u2192 ring sideroblasts; dimorphic blood picture \u2014 microcytic + normocytic). HAEMOLYTIC URAEMIC SYNDROME (HUS): characterised by MICROANGIOPATHIC HAEMOLYTIC ANAEMIA (MAHA) \u2014 fragmented RBCs (schistocytes\/helmet cells), NORMOCYTIC or macrocytic (with reticulocytosis \u2014 large immature RBCs) anaemia; thrombocytopenia, AKI. HUS does NOT cause microcytic anaemia. Answer: Haemolytic uraemic syndrome \u2014 EXCEPT.'},\n{id:63,stem:'Treatment with the following drugs can lead to neutropenia EXCEPT:',correct:'Glucocorticoids',options:['Glucocorticoids','Propylthiouracil','Dapsone','Enalapril'],exp:'Drug-induced neutropenia: Propylthiouracil (PTU) \u2714 \u2014 agranulocytosis\/neutropenia in ~0.3% (serious; stop drug immediately if WBC falls). Dapsone \u2714 \u2014 haematological toxicity including neutropenia, methaemoglobinaemia, haemolysis; especially in G6PD deficiency. Enalapril (ACE inhibitor) \u2714 \u2014 rare but well-documented neutropenia\/agranulocytosis (especially with renal impairment or collagen vascular disease). Other drugs: carbimazole, clozapine, carbamazepine, ticlopidine, mianserin, sulfonamides, chemotherapy agents. GLUCOCORTICOIDS: cause NEUTROPHILIA (not neutropenia) \u2014 steroids demarginate neutrophils from vessel walls into circulation and inhibit their extravasation \u2192 leukocytosis. Also cause lymphopenia, eosinopenia. Glucocorticoids = INCREASE neutrophils. Answer: Glucocorticoids \u2014 EXCEPT.'},\n{id:64,stem:'Which one of the following is a cause of early (0\u20134 weeks) infection in recipients of haematopoietic stem cell transplantation?',correct:'Herpes simplex',options:['Cytomegalovirus','Pneumocystis jirovecii','Varicella zoster','Herpes simplex'],exp:'Infections post-HSCT by timeline: 0\u20134 WEEKS (pre-engraftment \u2014 severe neutropenia): Bacterial infections (gram-positive\/negative), Candida, HERPES SIMPLEX VIRUS (HSV) \u2714 reactivation \u2014 mucositis, oral\/oesophageal HSV is very common early post-HSCT due to intense immunosuppression and mucosal damage from conditioning regimen. 4 WEEKS \u2013 3 MONTHS (post-engraftment, acute graft phase): CMV \u2714 (peak risk 4\u20138 weeks post-HSCT), Aspergillus, PCP (Pneumocystis jirovecii). >3 MONTHS (late): Varicella zoster (VZV) \u2714 \u2014 dermatomal zoster typically >3 months; EBV-PTLD, community respiratory viruses. HSV reactivation is the classic EARLY (0\u20134 weeks) viral complication. CMV is mid-phase (4\u201312 weeks). Answer: Herpes simplex.'},\n{id:65,stem:'Which of the following is\/are neurological manifestation(s) of vitamin B12 deficiency?\\n1. Poor memory\\n2. Optic atrophy\\n3. Personality change\\nSelect the correct answer:',correct:'1, 2 and 3',options:['1 and 2 only','3 only','2 only','1, 2 and 3'],exp:'Vitamin B12 deficiency neurological manifestations: Subacute combined degeneration of the spinal cord (SCD): posterior column (vibration\/proprioception loss) + lateral column (UMN signs \u2014 spasticity, hyperreflexia) involvement. Poor memory \u2714 \u2014 cognitive impairment, dementia (\"megaloblastic madness\"). Optic atrophy \u2714 \u2014 optic neuropathy (tobacco-alcohol amblyopia also related); rare but recognised; visual loss, optic disc pallor. Personality change \u2714 \u2014 psychiatric manifestations: irritability, depression, psychosis (\"megaloblastic madness\"). Peripheral neuropathy (paresthesiae, numbness \u2014 glove-stocking). All three neurological manifestations are recognised. Answer: 1, 2 and 3.'},\n{id:66,stem:'Which of the following infections does NOT cause cold antibodies immune haemolysis?',correct:'Malaria',options:['Mycoplasma','Malaria','Syphilis','Epstein\u2013Barr virus'],exp:'Cold antibody immune haemolytic anaemia \u2014 IgM antibodies that bind RBCs at low temperatures (extremities) \u2192 complement activation \u2192 haemolysis: Mycoplasma pneumoniae \u2714 CAUSES cold agglutinin haemolysis \u2014 anti-I antibodies (cold agglutinins); positive Coombs test. Syphilis \u2714 CAUSES cold haemolysis \u2014 Donath-Landsteiner antibodies (anti-P antigen); paroxysmal cold haemoglobinuria (PCH). Epstein-Barr virus (infectious mononucleosis) \u2714 CAUSES cold agglutinin haemolysis \u2014 anti-i antibodies. Others: CLL, lymphoma. MALARIA: causes haemolysis but via a DIFFERENT mechanism \u2014 direct parasitisation and lysis of RBCs, splenic removal of parasitised cells, immune complex deposition; NOT cold antibody-mediated. Blackwater fever (severe haemolysis in malaria) is immune-mediated but involves warm antibodies\/other mechanisms \u2014 NOT cold agglutinins. Answer: Malaria \u2014 does NOT cause cold antibody haemolysis.'},\n{id:67,stem:'Which of the following test has maximum sensitivity for diagnosing Phaeochromocytoma?',correct:'24 hours urinary fractionated metanephrines and catecholamines',options:['MIBG scintigraphy','Somatostatin receptor scintigraphy','Fluoro-DOPA PET scan','24 hours urinary fractionated metanephrines and catecholamines'],exp:'Phaeochromocytoma diagnosis \u2014 biochemical tests: 24-HOUR URINARY FRACTIONATED METANEPHRINES + CATECHOLAMINES \u2714 \u2014 MAXIMUM SENSITIVITY (~97\u201398%); metanephrines (normetanephrine + metanephrine) are stable metabolites of catecholamines; fractionated measurement is most sensitive. Plasma free metanephrines: also very sensitive (~99%) but more false positives. MIBG (meta-iodobenzylguanidine) scintigraphy: functional imaging for localisation \u2014 sensitivity ~77\u201390% for sporadic phaeochromocytoma, lower for metastatic disease. Somatostatin receptor scintigraphy: used for paraganglioma\/phaeochromocytoma localisation (lower sensitivity than MIBG for adrenal). Fluoro-DOPA PET: very high sensitivity for paraganglioma; may be superior to MIBG but less widely available. For BIOCHEMICAL DIAGNOSIS: 24-hour urinary fractionated metanephrines = highest sensitivity. Answer: 24-hour urinary fractionated metanephrines and catecholamines.'},\n{id:68,stem:'Which of the following does NOT cause polyuria?',correct:'Hypoparathyroidism',options:['Diabetes mellitus','Diabetes insipidus','Hypoparathyroidism','Conn syndrome'],exp:'Polyuria causes: Diabetes mellitus \u2714 \u2014 osmotic diuresis from glucosuria (glucose >180 mg\/dL exceeds renal threshold \u2192 water loss with glucose). Diabetes insipidus \u2714 \u2014 central (ADH deficiency) or nephrogenic (ADH resistance) \u2192 inability to concentrate urine \u2192 massive water diuresis (up to 20 L\/day). Conn syndrome (primary hyperaldosteronism) \u2714 \u2014 aldosterone excess \u2192 hypokalaemia \u2192 nephrogenic DI (hypokalaemia impairs aquaporin-2 expression and reduces medullary osmolality) \u2192 polyuria. HYPOPARATHYROIDISM: causes hypocalcaemia \u2192 tetany, seizures, QT prolongation \u2014 it does NOT cause polyuria. In fact, HYPERPARATHYROIDISM (elevated calcium \u2192 hypercalciuria \u2192 nephrogenic DI \u2192 polyuria). Hypoparathyroidism \u2192 hypocalcaemia \u2192 NOT polyuria. Answer: Hypoparathyroidism.'},\n{id:69,stem:'A 24-year female presented with generalised weakness. Thyroid function: T3 = Normal, T4 = Normal, TSH = 10 mU\/L. Most likely diagnosis:',correct:'Subclinical hypothyroidism',options:['Primary hypothyroidism','Secondary hypothyroidism','Subclinical hypothyroidism','Non thyroidal illness'],exp:'TFT interpretation: TSH = 10 mU\/L (elevated above normal 0.4\u20134.5 mU\/L). T3 = Normal. T4 = Normal. Pattern: elevated TSH + NORMAL T3 and T4 = SUBCLINICAL HYPOTHYROIDISM \u2714. The pituitary detects slight inadequacy \u2192 compensatory TSH elevation \u2192 thyroid gland maintains T3\/T4 in normal range. Patient may be asymptomatic or have subtle symptoms. Primary hypothyroidism (overt): TSH elevated + LOW T4. Secondary hypothyroidism: LOW TSH + low T4 (pituitary\/hypothalamic failure). Non-thyroidal illness (sick euthyroid): TSH normal\/low, T3 low, T4 variable. TSH elevated + normal T3\/T4 = subclinical hypothyroidism. Answer: Subclinical hypothyroidism.'},\n{id:70,stem:'A 26-year old lady has a Prolactinoma (microadenoma). The best modality of treatment for her condition is:',correct:'Oral Cabergoline',options:['Oral Cabergoline','Oral Bromocriptine','Surgery','Radiotherapy'],exp:'Prolactinoma treatment: MEDICAL THERAPY is first-line for ALL prolactinomas (micro and macro). DOPAMINE AGONISTS: suppress prolactin secretion and reduce tumour size. CABERGOLINE \u2714 \u2014 PREFERRED drug; longer-acting (twice weekly dosing), better tolerated, more effective at normalising prolactin and reducing tumour size than bromocriptine. >80% achieve normal prolactin with cabergoline. BROMOCRIPTINE: older agent, effective but more side effects (nausea, postural hypotension, nasal congestion), daily dosing. SURGERY (transsphenoidal): reserved for: dopamine agonist failure\/intolerance, vision threatening, CSF leak, patient preference. RADIOTHERAPY: adjuvant; slow effect, risks hypopituitarism. For a 26-year-old female with MICROADENOMA: oral cabergoline is the best treatment. Answer: Oral Cabergoline.'},\n{id:71,stem:'A 30-year woman in first trimester of pregnancy has Graves\\' disease. The treatment of choice is:',correct:'Propylthiouracil',options:['Radioiodine','Subtotal thyroidectomy','Carbimazole','Propylthiouracil'],exp:'Graves\\' disease in pregnancy \u2014 treatment: RADIOIODINE: absolutely CONTRAINDICATED in pregnancy (destroys fetal thyroid from 10\u201312 weeks onward). ANTITHYROID DRUGS: FIRST TRIMESTER \u2192 PROPYLTHIOURACIL (PTU) \u2714 \u2014 preferred in first trimester because carbimazole is associated with APLASIA CUTIS and carbimazole\/methimazole embryopathy (choanal atresia, tracheo-oesophageal fistula \u2014 teratogenic effects in 1st trimester). PTU also inhibits peripheral T4\u2192T3 conversion. SECOND\/THIRD TRIMESTER \u2192 switch to CARBIMAZOLE (PTU avoided later due to risk of PTU-induced hepatotoxicity). SURGERY: 2nd trimester option if antithyroid drugs fail or are not tolerated; not first-line. For FIRST TRIMESTER: PTU is drug of choice. Answer: Propylthiouracil.'},\n{id:72,stem:'The gold standard for diagnosis of Wilson\\'s disease is:',correct:'Liver biopsy with quantitative copper assays',options:['Demonstration of Kayser-Fleischer rings','Urinary copper excretion','Serum ceruloplasmin','Liver biopsy with quantitative copper assays'],exp:'Wilson\\'s disease (hepatolenticular degeneration \u2014 ATP7B mutation \u2192 copper accumulation) diagnosis: Kayser-Fleischer rings: copper deposition in Descemet membrane of cornea; seen on slit-lamp; highly suggestive but NOT always present (absent in ~50% of hepatic presentations). Serum ceruloplasmin: low (<20 mg\/dL) in ~85% \u2014 but can be low in other liver diseases or normal in acute hepatic failure. 24-hour urinary copper: >100 \u00b5g\/day suggestive; >40 \u00b5g\/day on D-penicillamine challenge. LIVER BIOPSY WITH QUANTITATIVE COPPER ASSAY \u2714 \u2014 GOLD STANDARD: hepatic copper content >250 \u00b5g\/g dry weight confirms Wilson\\'s. Also shows histological features (steatosis, inflammation, fibrosis). The gold standard because it directly quantifies copper in the target organ. Answer: Liver biopsy with quantitative copper assays.'},\n{id:73,stem:'A 32-year old HIV infected male presents with shortness of breath and moderate fever for two weeks. Cyanosis, RR 22\/min, basal crackles. CT chest shows bilateral ground-glass pattern. Most likely etiologic diagnosis:',correct:'Pneumocystis jirovecii',options:['Streptococcus pneumoniae','Pneumocystis jirovecii','Mycobacterium tuberculosis','Staphylococcus sp.'],exp:'HIV patient + bilateral ground-glass opacification on CT + subacute presentation (2 weeks) + basal crackles + moderate fever + cyanosis = PNEUMOCYSTIS JIROVECII PNEUMONIA (PCP) \u2714. PCP features: Insidious onset (days to weeks), bilateral symmetric ground-glass opacification on HRCT (perihilar, diffuse \u2014 \"bat-wing\" distribution), elevated LDH (marker of severity), O2 desaturation with exertion, CD4 typically <200\/mm\u00b3. Treatment: TMP-SMX (co-trimoxazole) + steroids if PaO2 <70 mmHg. Strep pneumoniae: acute lobar\/segmental consolidation. TB: upper lobe cavitating, more chronic. Staph: necrotising cavitating pneumonia. Bilateral ground-glass + HIV + subacute = PCP. Answer: Pneumocystis jirovecii.'},\n{id:74,stem:'A 22-year old male admitted with fever and altered consciousness for two days. Nuchal rigidity and diffuse petechial rash on trunk and lower extremities. Most likely etiologic agent:',correct:'Neisseria meningitidis',options:['Escherichia coli','Streptococcus pneumoniae','Neisseria meningitidis','Haemophilus influenzae'],exp:'Clinical picture: young adult, FEVER + ALTERED CONSCIOUSNESS + NUCHAL RIGIDITY (meningism) + DIFFUSE PETECHIAL\/PURPURIC RASH = MENINGOCOCCAL DISEASE \u2714. NEISSERIA MENINGITIDIS: the ONLY common bacterial pathogen causing PETECHIAL\/PURPURIC RASH in meningitis\/septicaemia. Petechiae\/purpura = meningococcaemia (endotoxin-mediated vasculitis and DIC). Waterhouse-Friderichsen syndrome (adrenal haemorrhage) in severe cases. Strep pneumoniae: most common bacterial meningitis overall in adults \u2014 but does NOT cause petechial rash. H. influenzae: children <5 years, no petechial rash. E. coli: neonatal meningitis. Petechial rash + meningitis = NEISSERIA MENINGITIDIS until proven otherwise. EMERGENCY \u2014 penicillin\/ceftriaxone immediately. Answer: Neisseria meningitidis.'},\n{id:75,stem:'The drug of choice for treatment of severe falciparum malaria in a 32-week pregnant woman is:',correct:'Artesunate',options:['Artesunate','Quinine','Chloroquine','Quinidine'],exp:'Severe falciparum malaria in pregnancy \u2014 treatment: ARTESUNATE \u2714 \u2014 IV artesunate is NOW the drug of choice for SEVERE falciparum malaria in ALL patients including PREGNANT WOMEN (WHO guidelines, updated 2010 based on AQUAMAT trial showing artesunate superior to quinine in reducing mortality). Artesunate: rapid parasite clearance, better tolerated, fewer adverse effects than quinine. Safe in 2nd and 3rd trimesters (32 weeks = 3rd trimester). QUININE: was historically first-line for severe malaria; now replaced by artesunate; quinine risks: hypoglycaemia (especially in pregnancy), cinchonism, hypotension. Chloroquine: P. falciparum is largely resistant. Quinidine: cardiac antiarrhythmic sometimes used as anti-malarial in the US but not standard. Answer: Artesunate.'},\n{id:76,stem:'A 36-year old chronic alcoholic, malnourished male hospitalised with pneumonia. His condition worsens after aggressive treatment with IV dextrose and antibiotics. This \"Refeeding Syndrome\" is accompanied by which biochemical alteration?',correct:'Hypophosphataemia',options:['Hypophosphataemia','Hyponatraemia','Hyperkalaemia','Hypermagnesaemia'],exp:'REFEEDING SYNDROME: occurs when malnourished\/starved patients receive rapid reintroduction of carbohydrates (glucose). Mechanism: glucose administration \u2192 insulin surge \u2192 insulin drives phosphate, potassium, and magnesium INTO cells (cellular uptake). The already-depleted stores become critically low in the serum. HYPOPHOSPHATAEMIA \u2714 is the hallmark biochemical feature \u2014 most dangerous complication: severe hypophosphataemia (<0.5 mmol\/L) \u2192 respiratory muscle weakness (respiratory failure), cardiac failure, haemolysis, rhabdomyolysis, neurological symptoms. Also: hypokalaemia (not hyperkalemia), hypomagnesaemia (not hypermagnesaemia). Monitor PO4, K+, Mg2+ before and during refeeding. Replace phosphate before starting feeds. Answer: Hypophosphataemia.'},\n{id:77,stem:'A 28-year old man weighs 80 kg and has a height of 150 cm. Based on BMI, he will be categorised as:',correct:'Obese',options:['Normal','Underweight','Overweight','Obese'],exp:'BMI = Weight (kg) \/ Height\u00b2 (m\u00b2). BMI = 80 \/ (1.50)\u00b2 = 80 \/ 2.25 = 35.6 kg\/m\u00b2. WHO BMI classification: <18.5 = Underweight. 18.5\u201324.9 = Normal. 25\u201329.9 = Overweight. \u226530 = OBESE \u2714. BMI 35.6 = Class II Obesity (30\u201334.9 = Class I, 35\u201339.9 = Class II, \u226540 = Class III\/morbid). Answer: Obese.'},\n{id:78,stem:'Angular stomatitis and cheilosis are indicative of deficiencies of which of the following vitamins?\\n1. Riboflavin\\n2. Pyridoxine\\n3. Thiamine\\n4. Niacin\\nSelect the correct answer:',correct:'1, 2 and 4',options:['1, 2 and 3','1, 2 and 4','2, 3 and 4','1, 3 and 4'],exp:'Angular stomatitis (cheilosis) \u2014 cracks\/fissures at the angles of the mouth: Riboflavin (B2) deficiency \u2714 \u2014 angular stomatitis, cheilosis, magenta\/glossy tongue, seborrhoeic dermatitis, corneal vascularisation. Pyridoxine (B6) deficiency \u2714 \u2014 angular stomatitis, glossitis, seborrhoeic dermatitis, peripheral neuropathy, sideroblastic anaemia. Niacin (B3) deficiency (Pellagra) \u2714 \u2014 dermatitis (4 Ds: Dermatitis, Diarrhoea, Dementia, Death); glossitis and angular stomatitis. THIAMINE (B1) deficiency: causes Beriberi (wet\/dry) and Wernicke-Korsakoff syndrome \u2014 NOT angular stomatitis. Thiamine deficiency does not typically cause oral lesions. Angular stomatitis\/cheilosis = Riboflavin, Pyridoxine, Niacin (and iron, zinc deficiency). Answer: 1, 2 and 4.'},\n{id:79,stem:'Which of the following statements about \"Early onset Osteoarthritis\" are true?\\n1. Onset is usually before the age of 55 years\\n2. There is clear history of previous trauma\\n3. In most cases, single joint is affected\\nSelect the correct answer:',correct:'2 and 3 only',options:['1 and 2 only','2 and 3 only','1 and 3 only','1, 2 and 3'],exp:'Early-onset Osteoarthritis (OA \u2014 before age 55): (1) Onset before 55 years: TRUE by definition of \"early onset\" OA. However, per some sources the cutoff used is 45 years (making \"before 55\" debatable). Standard teaching: primary OA before 45\u201355 = early onset. This statement is variable. (2) Clear history of previous trauma \u2714 TRUE \u2014 secondary OA in younger patients is most commonly POST-TRAUMATIC (previous joint injury, meniscal tear, ACL tear, intra-articular fracture) \u2014 trauma is the predominant identifiable cause. (3) Single joint affected \u2714 TRUE \u2014 post-traumatic early OA is typically MONOARTICULAR (the injured joint); unlike primary OA which is often polyarticular (bilateral knees, hands). Per standard exam answer: statements 2 and 3 are the most clearly correct features of early-onset OA. Answer: 2 and 3 only.'},\n{id:80,stem:'A 31-year young man presents with fever, weight loss, pain with swelling of knee joint and low backache with stiffness. Three weeks earlier, he was treated for urinary tract infection symptoms. Joint aspirate is leucocyte-rich with multinucleated macrophages. Urine culture is sterile. Most probable diagnosis:',correct:'Reactive arthritis',options:['Septic arthritis','Crystal arthritis','Reactive arthritis','Still disease'],exp:'REACTIVE ARTHRITIS (formerly Reiter\\'s syndrome) \u2014 the clinical picture: Young male + fever + PRECEDING UROGENITAL INFECTION (treated 3 weeks ago \u2014 classic antecedent event) + ASYMMETRIC OLIGOARTHRITIS (knee + low back = sacroiliitis\/spondylitis) + sterile joint aspirate (no organisms grown) + leucocyte-rich synovial fluid with multinucleated macrophages + weight loss. Reactive arthritis: sterile inflammatory arthritis triggered by infection elsewhere (urogenital \u2014 Chlamydia trachomatis, or enteric \u2014 Campylobacter, Salmonella, Shigella, Yersinia); occurs 2\u20134 weeks after infection. Classic triad: urethritis + arthritis + conjunctivitis (can\\'t see, can\\'t pee, can\\'t climb a tree). Sterile culture + post-infection = reactive arthritis. Septic arthritis: culture positive. Crystal arthritis: crystals in aspirate. Still disease: quotidian fever, salmon rash. 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Submitting in 10 Submit Now Combined Medical Services Examination 2019Paper I &nbsp;\u00b7&nbsp; Part B Gastroenterology \u00b7 Nephrology \u00b7 Neurology \u00b7 Haematology \u00b7 Endocrinology \u00b7 Infectious Diseases \u00b7 Rheumatology Questions 41 \u2013 80 Options reshuffled \u23f1 Start Timed Mode Submit Answers&hellip;&nbsp;<\/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-36821","post","type-post","status-publish","format-standard","hentry","category-cms"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.6 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>CMS 2019 P1 Part-B - atsixty<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/atsixty.com\/index.php\/2026\/05\/13\/cms-2019-p1-part-b\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"CMS 2019 P1 Part-B - atsixty\" \/>\n<meta property=\"og:description\" content=\"CMS 2019 Paper I \u2013 Part B (Q41\u2013Q80) \u23f1&nbsp;40:00 \u2705&nbsp;0 \u274c&nbsp;0 \u23f3&nbsp;40&nbsp;left Net&nbsp;0&nbsp;\/&nbsp;160 Time&#039;s Up! 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