{"id":36926,"date":"2026-06-03T20:08:31","date_gmt":"2026-06-03T14:38:31","guid":{"rendered":"https:\/\/atsixty.com\/?p=36926"},"modified":"2026-06-03T20:09:26","modified_gmt":"2026-06-03T14:39:26","slug":"git-series-oncology-vascular-surgery","status":"publish","type":"post","link":"https:\/\/atsixty.com\/index.php\/cms\/git-series-oncology-vascular-surgery\/","title":{"rendered":"GIT Series &#8211; Oncology, Vascular &amp; Surgery"},"content":{"rendered":"\n\n\n<link href=\"https:\/\/fonts.googleapis.com\/css2?family=Playfair+Display:ital,wght@0,400;0,600;0,700;1,400;1,600&#038;family=Source+Serif+4:ital,wght@0,300;0,400;0,600;1,400&#038;display=swap\" rel=\"stylesheet\">\n<style>\n\/* ============================================================\n   Morning Rounds \u00b7 GIT Quiz 07 \u00b7 Oncology, Vascular & Surgery\n   Namespace: #git07\n   Palette: deep teal-green (GIT series standard)\n   Template: git06 \u2014 plain diff label, exp + Extra Points\n   10 questions \/ MAX 40\n   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.mr-stem{font-size:0.9rem}\n  #git07 .mr-opt-text{font-size:0.86rem}\n}\n<\/style>\n\n<div id=\"git07\">\n\n  <div class=\"mr-header\">\n    <div class=\"mr-eyebrow\">Morning Rounds &middot; GIT Series<\/div>\n    <div class=\"mr-title\">\n      Completing the Series<br><em>Oncology, Vascular &amp; Surgery<\/em>\n    <\/div>\n    <div class=\"mr-subtitle\">Ten high-yield clinical cases &middot; +4 \/ &minus;1 scoring &middot; NEET-PG and UPSC CMS<\/div>\n    <div class=\"mr-chips\">\n      <span class=\"mr-chip\">10 Cases<\/span>\n      <span class=\"mr-chip\">+4 \/ &minus;1 scoring<\/span>\n      <span class=\"mr-chip\">Options reshuffled<\/span>\n    <\/div>\n  <\/div>\n\n  <div class=\"mr-sentinel\" id=\"git07-sentinel\"><\/div>\n\n  <div class=\"mr-progress\" id=\"git07-progress\">\n    <div class=\"mr-prog-inner\">\n      <div class=\"mr-pips\" id=\"git07-pips\"><\/div>\n    <\/div>\n  <\/div>\n\n  <div class=\"mr-body\">\n    <div id=\"git07-cases\"><\/div>\n    <div class=\"mr-submit-wrap\">\n      <button class=\"mr-btn\" id=\"git07-submit\">Submit for Debrief<\/button>\n    <\/div>\n    <div class=\"mr-score\" id=\"git07-score\">\n      <div class=\"mr-score-in\">\n        <div class=\"mr-score-ey\">Round Complete<\/div>\n        <div class=\"mr-ring\" id=\"git07-ring\">\n          <div class=\"mr-ring-in\">\n            <span class=\"mr-ring-pct\" id=\"git07-pct\">0%<\/span>\n            <span class=\"mr-ring-sub\">net<\/span>\n          <\/div>\n        <\/div>\n        <div class=\"mr-score-title\">Your Debrief<\/div>\n        <div class=\"mr-score-net\" id=\"git07-net\"><\/div>\n        <div class=\"mr-verdict\" id=\"git07-verdict\"><\/div>\n        <div class=\"mr-bands\">\n          <span class=\"mr-band mr-band-c\" id=\"git07-ct-c\"><\/span>\n          <span class=\"mr-band mr-band-w\" id=\"git07-ct-w\"><\/span>\n          <span class=\"mr-band mr-band-s\" id=\"git07-ct-s\"><\/span>\n        <\/div>\n        <button class=\"mr-retry\" id=\"git07-retry\">&#8635; New Round<\/button>\n      <\/div>\n    <\/div>\n  <\/div>\n<\/div>\n\n<script>\n\/* ============================================================\n   Morning Rounds \u00b7 GIT Quiz 07 \u00b7 Oncology, Vascular & Surgery\n   Namespace : git07\n   TOTAL     : 10 questions  |  MAX : 40  |  +4 \/ \u22121\n   Shuffle   : Fisher-Yates on options each build()\n   Correct   : matched by answer TEXT\n   Debrief   : q.exp = main text; q.extra = Extra Points para\n   ============================================================ *\/\n(function () {\n  'use strict';\n\n  var NS    = 'git07';\n  var TOTAL = 10;\n  var MAX   = 40;\n  var LTRS  = ['A','B','C','D'];\n\n  \/* ================================================================\n     QUESTION BANK \u2014 Oncology, Vascular & Surgery\n\n     Q1  HCC \u2014 AFP, SURVEILLANCE, BCLC (Medium)\n     Q2  HCC \u2014 FIBROLAMELLAR, TREATMENT OPTIONS (Hard)\n     Q3  HAEMORRHOIDS \u2014 DEGREES & TREATMENT (Easy)\n     Q4  ANAL FISSURE \u2014 SITE, SPASM, TREATMENT (Easy)\n     Q5  FISTULA-IN-ANO \u2014 GOODSALL'S RULE, PARKS (Medium)\n     Q6  ANORECTAL ABSCESS \u2014 SPACES & MANAGEMENT (Medium)\n     Q7  CARCINOID TUMOUR \u2014 5-HIAA, HEART, LIVER METS (Medium)\n     Q8  ACUTE MESENTERIC ISCHAEMIA \u2014 PAIN, AF, X-RAY (Hard)\n     Q9  UPPER GI BLEED \u2014 ROCKALL, FORREST (Medium)\n     Q10 LOWER GI BLEED \u2014 CAUSES BY AGE, DIVERTICULAR (Medium)\n     ================================================================ *\/\n\n  var QS = [\n\n    \/* ---- Q1 : HCC \u2014 Surveillance & BCLC ---- *\/\n    {\n      id:   1,\n      diff: 'Medium',\n      tag:  'Oncology &mdash; Hepatocellular Carcinoma',\n      stem: 'A <strong>58-year-old man<\/strong> with <strong>hepatitis B-related cirrhosis<\/strong> undergoes 6-monthly surveillance ultrasound. A <strong>2.4 cm arterially enhancing nodule<\/strong> with washout on portal venous phase is detected in the right lobe. His AFP is 320 ng\/mL. He has no ascites, no encephalopathy, and his bilirubin is normal (Child-Pugh A). Which statement correctly describes the diagnostic significance of the imaging pattern, his BCLC stage, and the preferred treatment?',\n      correct: 'Arterial enhancement with portal venous washout on dynamic CT\/MRI is diagnostic of HCC without biopsy (LI-RADS 5 \/ EASL criteria); BCLC stage A (single tumour, Child-Pugh A, PS 0); surgical resection or radiofrequency ablation are potentially curative options',\n      opts: [\n        'Arterial enhancement with portal venous washout on dynamic CT\/MRI is diagnostic of HCC without biopsy (LI-RADS 5 \/ EASL criteria); BCLC stage A (single tumour, Child-Pugh A, PS 0); surgical resection or radiofrequency ablation are potentially curative options',\n        'AFP >200 ng\/mL alone is diagnostic of HCC and imaging is not required for confirmation; BCLC stage B indicates multinodular disease requiring TACE as first-line treatment',\n        'Biopsy is always mandatory before any treatment for a liver nodule in cirrhosis; BCLC stage C indicates portal invasion and sorafenib is the only option regardless of liver function',\n        'Arterial enhancement without washout is sufficient for HCC diagnosis; BCLC stage 0 (very early) applies to all single nodules in Child-Pugh A; liver transplantation is the only curative option for any HCC regardless of size'\n      ],\n      exp: '<strong>HCC diagnosis<\/strong> in a cirrhotic liver can be made <em>non-invasively<\/em> by dynamic CT or MRI when a nodule &gt;1 cm shows the characteristic vascular pattern: <strong>arterial hyperenhancement<\/strong> (hypervascular tumour supplied by arterial neovascularisation) followed by <strong>washout<\/strong> in the portal venous or delayed phase. This pattern \u2014 called <em>LI-RADS 5<\/em> (liver imaging reporting) or meeting EASL\/AASLD criteria \u2014 is diagnostic without biopsy. <strong>AFP<\/strong> is a useful marker (elevated in ~60\u201370% of HCC) but is neither sensitive nor specific enough to diagnose alone; AFP &gt;400 ng\/mL with a compatible mass is strongly suggestive. <strong>BCLC staging (Barcelona Clinic Liver Cancer):<\/strong><br>Stage 0 (Very early): single &lt;2 cm, Child-Pugh A \u2014 resection or ablation.<br>Stage A (Early): single or up to 3 nodules &lt;3 cm, Child-Pugh A\/B, PS 0 \u2014 <strong>resection, ablation, or transplantation<\/strong>.<br>Stage B (Intermediate): multinodular, no vascular invasion \u2014 TACE.<br>Stage C (Advanced): vascular invasion or extrahepatic spread \u2014 sorafenib\/lenvatinib.<br>Stage D (Terminal): Child-Pugh C \u2014 best supportive care.',\n      extra: '<strong>Surveillance protocol:<\/strong> 6-monthly ultrasound \u00b1 AFP in all cirrhotic patients, regardless of aetiology. Non-cirrhotic HBV carriers with family history of HCC or high viral load also qualify. Surveillance detects HCC at an earlier, potentially curable stage \u2014 this is the entire rationale. <strong>Milan criteria<\/strong> for liver transplantation in HCC: single nodule \u22645 cm, or up to 3 nodules each \u22643 cm, no vascular invasion, no extrahepatic spread. Within Milan criteria, transplantation cures both HCC and the underlying cirrhosis \u2014 5-year survival ~70%. <strong>CMS relevance:<\/strong> A district physician\\'s role is to identify risk (cirrhosis, HBV, HCV, NAFLD, aflatoxin exposure) and ensure the patient is enrolled in a surveillance programme \u2014 referral for curative treatment is time-sensitive.'\n    },\n\n    \/* ---- Q2 : HCC \u2014 Fibrolamellar & Treatment ---- *\/\n    {\n      id:   2,\n      diff: 'Hard',\n      tag:  'Oncology &mdash; HCC Variants &amp; Treatment',\n      stem: 'A <strong>24-year-old woman<\/strong> with <strong>no liver disease, no viral hepatitis, and no alcohol use<\/strong> presents with a <strong>large hepatic mass and upper abdominal pain<\/strong>. AFP is normal. Biopsy shows large polygonal tumour cells separated by dense lamellar fibrous bands. A <strong>62-year-old man<\/strong> with <strong>Child-Pugh B cirrhosis and portal vein tumour thrombus<\/strong> is found to have multinodular HCC. For the first patient, the diagnosis and preferred treatment; and for the second patient, the systemic therapy of choice and its mechanism:',\n      correct: 'Fibrolamellar HCC: young patient, no cirrhosis, normal AFP, lamellar fibrosis on biopsy; surgical resection offers the best prognosis. Second patient: sorafenib (multikinase inhibitor \u2014 blocks RAF\/VEGFR\/PDGFR); first approved systemic agent for advanced HCC; lenvatinib is an alternative first-line option',\n      opts: [\n        'Fibrolamellar HCC: young patient, no cirrhosis, normal AFP, lamellar fibrosis on biopsy; surgical resection offers the best prognosis. Second patient: sorafenib (multikinase inhibitor \u2014 blocks RAF\/VEGFR\/PDGFR); first approved systemic agent for advanced HCC; lenvatinib is an alternative first-line option',\n        'Hepatoblastoma: most common liver tumour in young adults, AFP always elevated, treated with cisplatin-based chemotherapy. Second patient: TACE is the treatment of choice for portal vein thrombosis as it is minimally invasive and preserves liver function',\n        'Cholangiocarcinoma: presents with normal AFP and no cirrhosis in young patients; treated with gemcitabine + cisplatin. Second patient: regorafenib is the first-line systemic agent for advanced HCC with portal vein invasion',\n        'Fibrolamellar HCC: elevated AFP distinguishes it from conventional HCC; liver transplantation is always required regardless of resectability. Second patient: immunotherapy with nivolumab is the only approved first-line option for BCLC stage C'\n      ],\n      exp: '<strong>Fibrolamellar HCC (FL-HCC)<\/strong> is a distinct variant of hepatocellular carcinoma with unique characteristics: affects <em>young adults<\/em> (teens\u201330s) with <em>no underlying liver disease<\/em>, <em>normal AFP<\/em>, and characteristic histology \u2014 large eosinophilic polygonal tumour cells with prominent nucleoli embedded in <em>dense lamellar fibrous bands<\/em>. It is caused by a DNAJB1-PRKACA fusion gene. Prognosis is better than conventional HCC when resectable. <strong>Surgical resection<\/strong> is the treatment of choice; recurrence is common but repeat resection is feasible. <strong>Sorafenib<\/strong> \u2014 the first systemic therapy approved for advanced HCC (BCLC stage C: portal vein invasion, extrahepatic spread, or ECOG PS 1\u20132 with Child-Pugh A\/B). Mechanism: multikinase inhibitor blocking RAF kinase, VEGFR-2\/3, and PDGFR-\u03b2, thereby inhibiting tumour proliferation and angiogenesis. Modest survival benefit (~3 months median OS improvement). <strong>Lenvatinib<\/strong> is non-inferior to sorafenib and now an alternative first-line option. <strong>TACE is contraindicated<\/strong> in main portal vein tumour thrombus \u2014 it risks hepatic infarction.',\n      extra: '<strong>Systemic therapy landscape for HCC<\/strong> has evolved rapidly: Atezolizumab + bevacizumab (IMbrave150 trial) has now become the preferred first-line systemic therapy in Child-Pugh A patients with BCLC stage C, superseding sorafenib as the top choice in guidelines that have caught up. However, sorafenib remains the most examined agent in current NEET-PG and CMS syllabi. <strong>TACE (Transarterial chemoembolisation)<\/strong>: for BCLC stage B (intermediate, multinodular, no vascular invasion, preserved liver function) \u2014 injects chemotherapy (doxorubicin\/cisplatin) + embolic agent into the hepatic artery feeding the tumour, exploiting the fact that HCC is almost entirely arterially supplied while normal liver parenchyma gets dual supply. Reduces tumour size and delays progression.'\n    },\n\n    \/* ---- Q3 : Haemorrhoids ---- *\/\n    {\n      id:   3,\n      diff: 'Easy',\n      tag:  'Anorectal &mdash; Haemorrhoids',\n      stem: 'A <strong>38-year-old man<\/strong> presents with <strong>bright red blood per rectum<\/strong> on the toilet paper after defaecation, with no pain. He mentions a soft lump that protrudes during straining and <strong>reduces spontaneously<\/strong>. A second patient, a <strong>45-year-old woman<\/strong>, has a painful, irreducible perianal lump that appeared after straining at stool. Examination shows a tense, oedematous, purplish mass at 3 o\\'clock position that cannot be pushed back. Which degree of haemorrhoid does the first patient have, what is the second patient\\'s condition, and what is the definitive surgical treatment for grade III\u2013IV haemorrhoids?',\n      correct: 'First patient: Grade II haemorrhoid (prolapses on straining, reduces spontaneously); Second patient: thrombosed external haemorrhoid (external plexus, acutely thrombosed, irreducible, painful); haemorrhoidectomy (Milligan-Morgan open or Ferguson closed technique) is the definitive surgical treatment for Grade III\u2013IV',\n      opts: [\n        'First patient: Grade II haemorrhoid (prolapses on straining, reduces spontaneously); Second patient: thrombosed external haemorrhoid (external plexus, acutely thrombosed, irreducible, painful); haemorrhoidectomy (Milligan-Morgan open or Ferguson closed technique) is the definitive surgical treatment for Grade III\u2013IV',\n        'First patient: Grade III haemorrhoid (requires manual reduction after prolapse); Second patient: strangulated internal haemorrhoid requiring emergency haemorrhoidectomy within 6 hours; rubber band ligation is the definitive treatment for all grades',\n        'First patient: Grade I haemorrhoid (no prolapse, bleeding only); Second patient: perianal haematoma from ruptured external haemorrhoid; injection sclerotherapy is the definitive surgical treatment for Grade III\u2013IV haemorrhoids',\n        'First patient: Grade IV haemorrhoid (permanently prolapsed and irreducible); Second patient: acute anal fissure causing thrombosis; MIPH (procedure for prolapse and haemorrhoids \/ stapled haemorrhoidopexy) is the only surgical option for thrombosed haemorrhoids'\n      ],\n      exp: '<strong>Haemorrhoid grading (internal haemorrhoids):<\/strong><br>Grade I: bleeding only, no prolapse \u2014 visible on proctoscopy.<br>Grade II: prolapse on straining, <em>reduces spontaneously<\/em> \u2014 this patient.<br>Grade III: prolapse on straining, requires <em>manual reduction<\/em>.<br>Grade IV: permanently prolapsed, <em>irreducible<\/em>.<br><br><strong>Internal vs external haemorrhoids:<\/strong> Internal haemorrhoids arise from the internal haemorrhoidal plexus above the dentate line \u2014 covered by insensate mucosa, therefore <em>painless<\/em>. External haemorrhoids arise below the dentate line \u2014 covered by sensitive anoderm, therefore <em>painful<\/em> when thrombosed. <strong>Thrombosed external haemorrhoid:<\/strong> sudden onset of severe perianal pain, tense bluish-purple lump at the anal verge \u2014 acutely thrombosed venous plexus. Treatment: if within 72 hours of onset \u2192 excision under local anaesthesia (not simple incision \u2014 excision of the entire thrombus); after 72 hours \u2192 conservative (sitz baths, analgesia, stool softeners). <strong>Treatment by grade:<\/strong> I\u2013II: dietary fibre + rubber band ligation; III: RBL or haemorrhoidectomy; IV: haemorrhoidectomy.',\n      extra: '<strong>Haemorrhoids occur at 3, 7, and 11 o\\'clock positions<\/strong> (with patient in lithotomy position) \u2014 corresponding to the three main terminal branches of the superior rectal artery. The 3 o\\'clock position in this patient is consistent with a primary haemorrhoid site. <strong>Rubber band ligation (RBL)<\/strong>: the most widely used office procedure for Grade II\u2013III haemorrhoids \u2014 a rubber band placed at the base of the haemorrhoid above the dentate line causes ischaemic necrosis and sloughing. Done above the dentate line (insensate mucosa) \u2014 no local anaesthesia required. <strong>Injection sclerotherapy<\/strong> (5% phenol in almond oil): Grade I\u2013II; produces submucosal fibrosis. <strong>MIPH\/Stapled haemorrhoidopexy (Longo procedure)<\/strong>: staples the prolapsed mucosa back to its anatomical position; faster recovery, less pain, but higher recurrence rate than conventional haemorrhoidectomy.'\n    },\n\n    \/* ---- Q4 : Anal Fissure ---- *\/\n    {\n      id:   4,\n      diff: 'Easy',\n      tag:  'Anorectal &mdash; Anal Fissure',\n      stem: 'A <strong>32-year-old woman<\/strong> presents with <strong>severe tearing pain during and after defaecation<\/strong>, lasting up to an hour, associated with small amounts of bright red blood on the toilet paper. She has been constipated since her recent delivery. Examination reveals a <strong>linear crack in the posterior midline<\/strong> of the anal canal with a skin tag (sentinel pile) at its base. Digital rectal examination is too painful to complete. Which statement correctly identifies the most common site, the mechanism perpetuating chronicity, and the first-line medical treatment?',\n      correct: 'Posterior midline is the most common site (~90%) due to relative ischaemia from poor vascular supply; internal anal sphincter (IAS) hypertonia perpetuates chronicity by reducing mucosal blood flow and preventing healing; topical glyceryl trinitrate (GTN) 0.2% is first-line \u2014 it relaxes the IAS by releasing nitric oxide',\n      opts: [\n        'Posterior midline is the most common site (~90%) due to relative ischaemia from poor vascular supply; internal anal sphincter (IAS) hypertonia perpetuates chronicity by reducing mucosal blood flow and preventing healing; topical glyceryl trinitrate (GTN) 0.2% is first-line \u2014 it relaxes the IAS by releasing nitric oxide',\n        'Anterior midline is the most common site due to the direction of defaecatory force; external anal sphincter spasm perpetuates chronicity; topical diltiazem is the gold standard first-line treatment as it has fewer side effects than GTN',\n        'Lateral position (3 or 9 o\\'clock) is the most common site; infection by Staphylococcus aureus perpetuates chronicity; oral metronidazole is first-line medical treatment to eradicate the infective component',\n        'Posterior midline is most common; the fissure perpetuates itself through external sphincter hypertonia increasing faecal impaction; lateral internal sphincterotomy is always required as first-line treatment without trying medical management first'\n      ],\n      exp: '<strong>Anal fissure<\/strong> is a longitudinal tear in the anoderm (squamous epithelium) of the anal canal, extending from the dentate line to the anal verge. <strong>Site:<\/strong> <em>posterior midline in ~90%<\/em> of cases. The posterior commissure has the poorest vascular supply (terminal branches of the inferior rectal artery) and bears the greatest mechanical stress during defaecation \u2014 hence its vulnerability. Anterior midline fissures occur in ~10% (more common in women, especially post-partum). <strong>Fissures not in the midline<\/strong> should raise suspicion for Crohn\\'s disease, TB, syphilis, HIV, or malignancy. <strong>Chronicity mechanism:<\/strong> acute fissure \u2192 pain \u2192 reflex <em>internal anal sphincter (IAS) hypertonia<\/em> \u2192 reduced anodermal blood flow \u2192 impaired healing \u2192 chronic fissure (with sentinel pile and hypertrophied anal papilla \u2014 the triad of chronic fissure). <strong>First-line treatment:<\/strong> Topical <strong>GTN (glyceryl trinitrate) 0.2%<\/strong> bd \u2014 releases NO \u2192 relaxes IAS \u2192 improves mucosal blood flow \u2192 promotes healing. Side effect: headache (common, limits compliance).',\n      extra: '<strong>Treatment ladder:<\/strong> (1) Conservative: dietary fibre, sitz baths, topical anaesthetic \u2014 for acute fissures. (2) Topical GTN 0.2% or <strong>topical diltiazem 2%<\/strong> (calcium channel blocker \u2014 fewer headaches, comparable efficacy) \u2014 first-line for chronic fissure. (3) <strong>Botulinum toxin injection<\/strong> into the IAS: second-line; paralysis of IAS for 3 months allows healing; risk of temporary incontinence. (4) <strong>Lateral internal sphincterotomy (LIS)<\/strong>: surgical gold standard; divides the lower third of the IAS at the 3 o\\'clock position; >95% healing rate; small risk of incontinence (especially for flatus\/liquid stool). LIS is reserved for medically refractory chronic fissures. <strong>Important distinction:<\/strong> the sentinel pile (skin tag at the base of a chronic fissure) is often mistaken for a haemorrhoid \u2014 it is not; it is scar tissue and resolves with treatment of the fissure.'\n    },\n\n    \/* ---- Q5 : Fistula-in-Ano ---- *\/\n    {\n      id:   5,\n      diff: 'Medium',\n      tag:  'Anorectal &mdash; Fistula-in-Ano',\n      stem: 'A <strong>40-year-old man<\/strong> presents with a <strong>persistent discharging sinus in the left perianal region<\/strong> at 4 o\\'clock (posterior to the transverse anal line). He had an anorectal abscess drained six months ago. On examination, an external opening is visible 3 cm from the anal verge. Proctoscopy confirms an internal opening in the posterior midline at the dentate line. The rule predicting the internal opening\\'s location, the most common type of fistula in this case, and the surgical principle that guides treatment are:',\n      correct: 'Goodsall\\'s rule: external openings posterior to the transverse anal line track curvilinearly to the posterior midline; intersphincteric fistula (Parks type I \u2014 most common overall); the sphincter mechanism must be preserved to prevent incontinence \u2014 laid-open fistulotomy for simple low fistulae, seton for high\/complex fistulae',\n      opts: [\n        'Goodsall\\'s rule: external openings posterior to the transverse anal line track curvilinearly to the posterior midline; intersphincteric fistula (Parks type I \u2014 most common overall); the sphincter mechanism must be preserved to prevent incontinence \u2014 laid-open fistulotomy for simple low fistulae, seton for high\/complex fistulae',\n        'Goodsall\\'s rule: all external openings regardless of position track in a straight radial line to the nearest point of the dentate line; transsphincteric fistula is the most common type; complete division of all sphincter muscles is required to achieve cure',\n        'Salmon\\'s law: external openings anterior to the transverse line track to the posterior midline; suprasphincteric fistula is the most common type requiring MRI for diagnosis; antibiotic therapy alone cures most fistulae without surgery',\n        'Goodsall\\'s rule: external openings anterior to the transverse anal line track curvilinearly; extrasphincteric fistula is the most common type; colostomy is the primary treatment for all anorectal fistulae to divert faecal stream'\n      ],\n      exp: '<strong>Goodsall\\'s rule<\/strong> predicts the location of the internal opening of a fistula-in-ano based on the position of the external opening relative to a transverse line drawn through the centre of the anus:<br>\u2022 External opening <em>anterior<\/em> to the transverse line \u2192 tracks in a <em>straight radial line<\/em> to the nearest point on the dentate line.<br>\u2022 External opening <em>posterior<\/em> to the transverse line \u2192 tracks in a <em>curved line<\/em> to the <strong>posterior midline<\/strong> of the dentate line.<br>Exception: anterior external openings &gt;3 cm from the anal verge may also curve to the posterior midline (horseshoe fistula). <strong>Parks classification:<\/strong><br>Type I \u2014 <strong>Intersphincteric<\/strong> (most common, ~45%): tracks between internal and external sphincters.<br>Type II \u2014 <strong>Transsphincteric<\/strong> (~30%): crosses both sphincters.<br>Type III \u2014 Suprasphincteric: passes above the puborectalis.<br>Type IV \u2014 Extrasphincteric: outside all sphincters, often from pelvic pathology. <strong>Treatment principle:<\/strong> cure the fistula without causing faecal incontinence. Laying open (fistulotomy) is curative for low fistulae that cross minimal sphincter. High fistulae crossing significant sphincter require a <strong>seton<\/strong> (thread passed through fistula tract) \u2014 cutting or draining seton.',\n      extra: '<strong>Aetiology of fistula-in-ano:<\/strong> ~90% arise from cryptoglandular infection \u2014 an anal gland at the dentate line becomes infected, forms an anorectal abscess, and then a fistula tract. <strong>Secondary causes<\/strong> to always consider: Crohn\\'s disease (complex, multiple, non-healing fistulae \u2014 treat with infliximab\/adalimumab before surgery), tuberculosis, actinomycosis, malignancy, radiation, trauma. <strong>MRI pelvis<\/strong> is the gold standard for delineating complex fistula anatomy (suprasphincteric, horseshoe, recurrent) \u2014 essential before surgery to avoid inadvertent sphincter damage. <strong>Horseshoe fistula:<\/strong> a complex fistula that extends from the posterior midline across both ischioanal fossae \u2014 requires counter drainage of both limbs.'\n    },\n\n    \/* ---- Q6 : Anorectal Abscess ---- *\/\n    {\n      id:   6,\n      diff: 'Medium',\n      tag:  'Anorectal &mdash; Anorectal Abscess',\n      stem: 'A <strong>35-year-old man<\/strong> presents with <strong>severe throbbing perianal pain, fever, and a tender fluctuant swelling<\/strong> at the right side of the anus. He is diabetic and immunosuppressed. A second patient presents with <strong>deep-seated rectal pain and fever without any visible perianal swelling<\/strong>. Digital rectal examination in the second patient reveals a <strong>tender boggy mass palpable above the anorectal ring on the right side<\/strong>. Identify the type of abscess in each patient, the most important principle in management, and which patient is at higher risk of necrotising infection?',\n      correct: 'First: perianal abscess (most common, superficial, visible at anal verge); Second: ischiorectal (ischioanal) abscess (deep, no visible swelling, felt above anorectal ring on DRE); incision and drainage without waiting for frank fluctuation is the rule \u2014 antibiotics alone do not cure anorectal abscess; the diabetic immunosuppressed patient is at higher risk of Fournier\\'s gangrene',\n      opts: [\n        'First: perianal abscess (most common, superficial, visible at anal verge); Second: ischiorectal (ischioanal) abscess (deep, no visible swelling, felt above anorectal ring on DRE); incision and drainage without waiting for frank fluctuation is the rule \u2014 antibiotics alone do not cure anorectal abscess; the diabetic immunosuppressed patient is at higher risk of Fournier\\'s gangrene',\n        'First: ischiorectal abscess (always presents with visible swelling); Second: supralevator abscess (palpable above the anorectal ring only on transabdominal examination); antibiotics alone are sufficient for all anorectal abscesses in immunocompetent patients',\n        'First: intersphincteric abscess (causes visible swelling at the anal verge without fever); Second: perianal abscess (DRE is the only way to detect perianal abscesses); waiting for frank fluctuation before drainage reduces post-operative fistula rate',\n        'First: supralevator abscess (located above the levator ani, always visible); Second: intersphincteric abscess (causes deep rectal pain without external signs); Fournier\\'s gangrene only occurs in patients with perianal Crohn\\'s disease'\n      ],\n      exp: '<strong>Anorectal abscess spaces and types:<\/strong><br>\u2022 <strong>Perianal<\/strong> (most common, ~60%): immediately adjacent to anal verge; visible, tender, fluctuant swelling; easily diagnosed clinically.<br>\u2022 <strong>Ischiorectal (ischioanal)<\/strong>: in the ischioanal fossa lateral to the external sphincter; presents with deep-seated pain, fever, and induration; swelling may not be visible but is palpable as a brawny, tender mass lateral to the rectum on DRE or bimanual examination. Can be bilateral (horseshoe abscess).<br>\u2022 <strong>Intersphincteric<\/strong>: between the internal and external sphincters; severe anorectal pain without visible swelling; diagnosed by DRE (tender swelling above the dentate line).<br>\u2022 <strong>Supralevator<\/strong>: above the levator ani; rare; presents with pelvic pain, fever, no external signs; requires CT\/MRI for diagnosis.<br><strong>Management principle:<\/strong> <em>Incision and drainage is mandatory<\/em> \u2014 anorectal abscesses do not resolve with antibiotics alone (poor penetration into the cavity). Do not wait for fluctuation; cellulitis stage is also an indication for drainage in this region. Antibiotics are adjuncts in immunosuppressed or diabetic patients or if there is systemic sepsis.',\n      extra: '<strong>Fournier\\'s gangrene<\/strong>: necrotising fasciitis of the perineum and scrotum\/labia \u2014 a rapidly progressive, life-threatening polymicrobial infection (aerobic-anaerobic synergy) involving the fascial planes of the perineum. Risk factors: diabetes mellitus, immunosuppression, obesity, malignancy. Hallmarks: disproportionate pain, rapid tissue necrosis, crepitus (gas in tissues), systemic sepsis. <strong>Treatment: emergency wide surgical debridement<\/strong> (often repeated), broad-spectrum antibiotics (carbapenem + metronidazole), and hyperbaric oxygen as adjunct where available. Mortality: 20\u201340% even with aggressive treatment. A diabetic patient presenting with perianal pain and systemic sepsis must be examined for early Fournier\\'s \u2014 delay in recognition is the key preventable cause of death. This is a high-yield CMS emergency scenario.'\n    },\n\n    \/* ---- Q7 : Carcinoid Tumour ---- *\/\n    {\n      id:   7,\n      diff: 'Medium',\n      tag:  'Oncology &mdash; Carcinoid Tumour',\n      stem: 'A <strong>52-year-old man<\/strong> presents with a <strong>5-year history of episodic facial flushing, watery diarrhoea, and wheezing<\/strong>. On examination he has a <strong>fixed tricuspid regurgitation murmur<\/strong>. CT abdomen shows a <strong>1.8 cm ileal mass with liver metastases<\/strong>. His 24-hour urinary 5-HIAA is markedly elevated. Which statement correctly explains why carcinoid syndrome only manifests with liver metastases, identifies the specific cardiac finding and its pathological mechanism, and names the first-line medical treatment for symptomatic control?',\n      correct: 'Carcinoid syndrome occurs only when liver metastases are present because serotonin from gut carcinoids is normally inactivated by hepatic first-pass metabolism; right-sided valvular disease (tricuspid regurgitation and pulmonary stenosis) results from serotonin-induced fibrous plaques on the right heart valves \u2014 left heart is protected by pulmonary metabolism; octreotide (somatostatin analogue) is first-line for symptom control',\n      opts: [\n        'Carcinoid syndrome occurs only when liver metastases are present because serotonin from gut carcinoids is normally inactivated by hepatic first-pass metabolism; right-sided valvular disease (tricuspid regurgitation and pulmonary stenosis) results from serotonin-induced fibrous plaques on the right heart valves \u2014 left heart is protected by pulmonary metabolism; octreotide (somatostatin analogue) is first-line for symptom control',\n        'Carcinoid syndrome occurs regardless of liver metastases as serotonin bypasses the liver via the lymphatics; left-sided valvular disease (mitral stenosis and aortic regurgitation) is the classic cardiac finding as serotonin acts preferentially on left heart valves; cyproheptadine is the first-line treatment',\n        'Carcinoid syndrome requires both liver and lung metastases simultaneously; the cardiac finding is biventricular failure from serotonin cardiomyopathy affecting all four chambers equally; interferon-alpha is first-line for all carcinoid tumours',\n        'Carcinoid syndrome occurs only with bronchial carcinoids which directly release serotonin into the systemic circulation without first-pass metabolism; urinary 5-HIAA is only elevated in pancreatic carcinoids, not midgut carcinoids'\n      ],\n      exp: '<strong>Carcinoid tumours<\/strong> are well-differentiated neuroendocrine tumours (NETs) secreting serotonin (5-HT) and other vasoactive substances. Arise most commonly in the <em>midgut<\/em> (ileum, appendix). <strong>Why liver mets are needed for carcinoid syndrome:<\/strong> serotonin secreted by gut carcinoids drains via the portal system to the liver, where it is almost completely inactivated by MAO and aldehyde dehydrogenase (first-pass metabolism). When <em>liver metastases<\/em> are present, tumour cells secrete directly into hepatic veins \u2192 systemic circulation \u2192 carcinoid syndrome. Exception: bronchial\/ovarian carcinoids drain directly into systemic circulation and cause syndrome without liver mets. <strong>Carcinoid syndrome features:<\/strong> episodic flushing (bradykinin, histamine), watery diarrhoea (5-HT), bronchospasm (wheezing), and <strong>carcinoid heart disease<\/strong> (Hedinger syndrome). <strong>Cardiac lesion:<\/strong> fibrous endocardial plaques on the <em>right heart valves<\/em> \u2014 tricuspid regurgitation + pulmonary stenosis. Left valves are protected because serotonin is inactivated by pulmonary endothelium before reaching the left heart. <strong>Diagnosis:<\/strong> 24-hr urinary 5-HIAA (5-hydroxyindoleacetic acid) \u2014 serotonin metabolite; elevated in midgut carcinoids.',\n      extra: '<strong>Treatment:<\/strong> <strong>Octreotide<\/strong> (long-acting somatostatin analogue \u2014 LAR formulation monthly): first-line for symptomatic control; inhibits hormone secretion; also has antiproliferative effect (PROMID trial). <strong>Lanreotide<\/strong> is an alternative somatostatin analogue. <strong>Surgical resection<\/strong> when feasible \u2014 even debulking hepatic metastases reduces hormonal burden and improves symptoms. <strong>PRRT (Peptide receptor radionuclide therapy)<\/strong> with Lu-177 DOTATATE: for somatostatin receptor-positive progressive midgut NETs \u2014 NETTER-1 trial. <strong>Carcinoid crisis:<\/strong> life-threatening surge of vasoactive substances during anaesthesia, biopsy, or chemotherapy \u2192 severe flushing, bronchospasm, haemodynamic instability. Prevented and treated with IV octreotide. <strong>Appendiceal carcinoid:<\/strong> most common site; if &lt;2 cm \u2192 appendicectomy curative; if &gt;2 cm \u2192 right hemicolectomy (risk of lymph node spread). This size threshold is a reliable one-liner for both CMS and NEET-PG.'\n    },\n\n    \/* ---- Q8 : Acute Mesenteric Ischaemia ---- *\/\n    {\n      id:   8,\n      diff: 'Hard',\n      tag:  'Vascular &mdash; Acute Mesenteric Ischaemia',\n      stem: 'A <strong>72-year-old man<\/strong> with known <strong>atrial fibrillation on irregular warfarin use<\/strong> presents with <strong>sudden-onset severe periumbilical pain<\/strong> that is out of proportion to the abdominal findings \u2014 the abdomen is soft with mild generalised tenderness. His INR today is 1.2. Over the next four hours despite analgesia the pain persists and he develops bloody diarrhoea. Plain X-ray abdomen shows <strong>thumb-printing<\/strong> in the transverse colon region. His lactate is 4.8 mmol\/L. Which mechanism explains his presentation, what does the X-ray finding indicate, and what is the time-critical intervention?',\n      correct: 'Acute mesenteric ischaemia from superior mesenteric artery embolism (cardiac source from AF); thumbprinting on plain X-ray indicates submucosal oedema and haemorrhage from bowel wall ischaemia; CT angiography confirms the diagnosis and emergency surgical embolectomy or catheter-directed thrombolysis is the time-critical intervention',\n      opts: [\n        'Acute mesenteric ischaemia from superior mesenteric artery embolism (cardiac source from AF); thumbprinting on plain X-ray indicates submucosal oedema and haemorrhage from bowel wall ischaemia; CT angiography confirms the diagnosis and emergency surgical embolectomy or catheter-directed thrombolysis is the time-critical intervention',\n        'Acute mesenteric ischaemia from inferior mesenteric artery thrombosis; thumbprinting indicates gas in the bowel wall (pneumatosis intestinalis) confirming transmural infarction; conservative management with IV antibiotics is appropriate as surgery carries prohibitive risk in the elderly',\n        'Ischaemic colitis from low-flow state; thumbprinting indicates free air under the diaphragm confirming bowel perforation; immediate laparotomy for peritonitis is the only appropriate management',\n        'Acute pancreatitis causing mesenteric venous thrombosis; thumbprinting indicates pancreatic calcification on the plain X-ray; ERCP is the emergency intervention to decompress the pancreatic duct and restore mesenteric flow'\n      ],\n      exp: '<strong>Acute mesenteric ischaemia (AMI)<\/strong> \u2014 a surgical emergency with mortality exceeding 60\u201380% if diagnosis is delayed beyond 12\u201324 hours. <strong>Causes:<\/strong><br>\u2022 <em>SMA embolism<\/em> (~50%): cardiac emboli (AF, recent MI, valvular disease) \u2014 sudden onset, often mid-jejunum sparing (collateral at SMA origin). Most common cause.<br>\u2022 <em>SMA thrombosis<\/em> (~25%): atherosclerosis, usually preceded by chronic mesenteric angina (postprandial pain, food fear, weight loss).<br>\u2022 <em>Non-occlusive mesenteric ischaemia (NOMI)<\/em> (~20%): low cardiac output states (shock, CCF, vasopressors).<br>\u2022 <em>Mesenteric venous thrombosis<\/em> (~5%): hypercoagulable states.<br><strong>Classic presentation:<\/strong> <em>pain out of proportion to physical findings<\/em> \u2014 severe abdominal pain with a deceptively benign abdomen (no peritonism initially). This disparity is pathognomonic. As ischaemia progresses \u2192 bowel infarction \u2192 peritonitis, bloody diarrhoea, lactic acidosis, septic shock. <strong>Thumbprinting:<\/strong> thickened mucosal folds due to submucosal oedema and haemorrhage \u2014 indicates ischaemia but not yet full-thickness infarction. <strong>Pneumatosis intestinalis<\/strong> (gas in bowel wall) = transmural infarction \u2014 very poor prognosis.',\n      extra: '<strong>Investigation:<\/strong> <strong>CT angiography<\/strong> (mesenteric CT angiogram) is the gold standard \u2014 shows the occlusion site, bowel wall enhancement, pneumatosis, portal venous gas. Plain X-ray may be normal early; thumbprinting, pneumatosis, and portal gas are late signs. <strong>Treatment:<\/strong> Resuscitation \u2192 CT angiogram \u2192 emergency surgery (embolectomy + bowel resection of non-viable bowel) or catheter-directed thrombolysis\/mechanical thrombectomy in selected patients without peritonism. A second-look laparotomy at 24\u201348 hours is standard to assess bowel viability. <strong>Chronic mesenteric ischaemia:<\/strong> postprandial abdominal pain (intestinal angina) + weight loss + food fear in an elderly atherosclerotic patient \u2014 bruit may be audible. Investigated by CT angiography; treated by mesenteric artery stenting or bypass. <strong>CMS relevance:<\/strong> the classic clinical exam question \u2014 elderly patient with AF + sudden severe abdominal pain + soft abdomen = mesenteric ischaemia until proven otherwise. Do not be reassured by the absence of peritonism.'\n    },\n\n    \/* ---- Q9 : Upper GI Bleed ---- *\/\n    {\n      id:   9,\n      diff: 'Medium',\n      tag:  'GI Bleeding &mdash; Upper GI Haemorrhage',\n      stem: 'A <strong>65-year-old man<\/strong> with a history of <strong>NSAID use<\/strong> presents with <strong>haematemesis and melaena<\/strong>. On admission his pulse is 112\/min and BP 96\/60 mmHg. He has no previous history of GI bleed and no liver disease. After resuscitation, urgent upper GI endoscopy reveals a <strong>duodenal ulcer with a visible non-bleeding vessel<\/strong> in its base. Which score quantifies his rebleed and mortality risk before endoscopy, what Forrest classification applies to his endoscopic finding, and what is the endoscopic treatment of choice?',\n      correct: 'Rockall score quantifies risk before and after endoscopy \u2014 pre-endoscopy score based on age, shock, and comorbidity; Forrest IIa (visible non-bleeding vessel \u2014 high risk of rebleed ~50%); dual endoscopic therapy (injection of adrenaline + thermal coagulation or haemoclip) is the treatment of choice',\n      opts: [\n        'Rockall score quantifies risk before and after endoscopy \u2014 pre-endoscopy score based on age, shock, and comorbidity; Forrest IIa (visible non-bleeding vessel \u2014 high risk of rebleed ~50%); dual endoscopic therapy (injection of adrenaline + thermal coagulation or haemoclip) is the treatment of choice',\n        'Glasgow-Blatchford score is used post-endoscopy to quantify rebleed risk; Forrest Ib (oozing without visible vessel) applies to a visible vessel in the ulcer base; injection of adrenaline alone is sufficient endoscopic treatment for all high-risk lesions',\n        'Ranson score quantifies UGIB severity; Forrest IIb (adherent clot) describes a visible non-bleeding vessel; argon plasma coagulation alone is contraindicated for duodenal ulcer bleeding and surgery is the first-line intervention',\n        'MELD score predicts UGIB mortality in all patients; Forrest Ia (spurting arterial bleed) describes a non-bleeding visible vessel; PPI therapy alone without endoscopic treatment is sufficient for Forrest II lesions'\n      ],\n      exp: '<strong>Upper GI bleed (UGIB)<\/strong> \u2014 causes: peptic ulcer disease (~50%, most common), oesophageal varices (~20%), Mallory-Weiss tear (~10%), oesophagitis, Dieulafoy lesion, gastric cancer. <strong>Rockall score<\/strong>: stratifies risk of rebleed and mortality. Pre-endoscopy variables: age (&lt;60\/60\u201379\/\u226580), shock (none\/tachycardia\/hypotension), comorbidity (none\/CCF, IHD\/renal failure, liver failure, malignancy). Post-endoscopy adds: diagnosis and stigmata of haemorrhage. Score &lt;3 = low risk; \u22658 = very high risk. <strong>Glasgow-Blatchford score<\/strong>: pre-endoscopy score that predicts need for intervention (transfusion, endoscopy, surgery) \u2014 uses BUN, Hb, BP, pulse, melaena, syncope, liver disease, cardiac failure. Score 0 = safe for outpatient management. <strong>Forrest classification:<\/strong><br>Ia: spurting arterial bleed (~90% rebleed)<br>Ib: oozing (~55%)<br>IIa: <strong>visible non-bleeding vessel (~50%)<\/strong> \u2014 this patient<br>IIb: adherent clot (~30%)<br>IIc: flat pigmented spot (~10%)<br>III: clean base (&lt;5%)<br>Forrest I and IIa require endoscopic intervention. <strong>Dual therapy<\/strong> (adrenaline injection + thermal\/mechanical haemostasis) is superior to monotherapy.',\n      extra: '<strong>Medical management:<\/strong> IV PPI (omeprazole\/pantoprazole) infusion reduces rebleed rate in high-risk ulcers \u2014 start before endoscopy. Erythromycin 250 mg IV 30 minutes before endoscopy: prokinetic that clears the stomach of blood clots, improving visualisation. <strong>Variceal vs non-variceal bleed:<\/strong> if varices suspected (known cirrhosis, stigmata of CLD) \u2192 terlipressin + prophylactic antibiotics before endoscopy; endoscopic band ligation for oesophageal varices. <strong>Second-look endoscopy<\/strong>: routine second-look is not recommended; reserved for patients with ongoing signs of haemorrhage or inadequate first endoscopy. <strong>Interventional radiology (TIPSS or embolisation)<\/strong>: for refractory bleeding after two endoscopic attempts. <strong>Surgery<\/strong>: last resort \u2014 underrunning the bleeding vessel + vagotomy. With modern endoscopy and IR, surgery for UGIB is now rare.'\n    },\n\n    \/* ---- Q10 : Lower GI Bleed ---- *\/\n    {\n      id:   10,\n      diff: 'Medium',\n      tag:  'GI Bleeding &mdash; Lower GI Haemorrhage',\n      stem: 'A <strong>72-year-old woman<\/strong> presents with <strong>painless, large-volume bright red rectal bleeding<\/strong> that stops spontaneously. She has no anal pain, no change in bowel habit, and no weight loss. Colonoscopy performed after bowel prep shows <strong>multiple diverticula throughout the colon<\/strong> but no active bleeding source is identified. A second patient \u2014 a <strong>28-year-old man<\/strong> \u2014 presents with <strong>small amounts of bright red blood mixed with mucus and diarrhoea<\/strong> with lower abdominal cramps for six weeks. Which is the most likely diagnosis in each patient, what does the age distribution of lower GI bleeding causes indicate, and what is the most important investigation to exclude malignancy in the first patient?',\n      correct: 'First: diverticular bleeding (most common cause of major LGIB in >60 years \u2014 painless, large volume, usually right-sided diverticula despite left predominance); Second: inflammatory bowel disease (blood mixed with mucus + diarrhoea in young adult); colonoscopy with biopsy is the most important investigation to exclude colorectal carcinoma in the first patient',\n      opts: [\n        'First: diverticular bleeding (most common cause of major LGIB in >60 years \u2014 painless, large volume, usually right-sided diverticula despite left predominance); Second: inflammatory bowel disease (blood mixed with mucus + diarrhoea in young adult); colonoscopy with biopsy is the most important investigation to exclude colorectal carcinoma in the first patient',\n        'First: angiodysplasia (most common cause of LGIB in all age groups; treated with colonoscopic argon plasma coagulation); Second: colorectal carcinoma presenting atypically in a young patient; barium enema is the gold standard investigation to exclude malignancy',\n        'First: colorectal carcinoma (painless rectal bleeding is always malignant in patients over 60); Second: infective colitis; CT colonography is the investigation of choice and colonoscopy is contraindicated in active diverticular disease',\n        'First: ischaemic colitis (large-volume bleeding in elderly with diverticula); Second: haemorrhoids (blood mixed with mucus and diarrhoea in young adults is pathognomonic of haemorrhoidal bleeding); flexible sigmoidoscopy is sufficient to exclude malignancy in the sigmoid colon'\n      ],\n      exp: '<strong>Lower GI bleeding (LGIB)<\/strong> \u2014 causes vary significantly with age:<br><strong>Young (&lt;40):<\/strong> IBD (most common), infective colitis, haemorrhoids, anal fissure, Meckel\\'s diverticulum (in children\/young adults \u2014 ectopic gastric mucosa \u2192 ulceration \u2192 bleeding), colorectal polyps.<br><strong>Middle-aged (40\u201360):<\/strong> IBD, colorectal polyps, carcinoma, haemorrhoids, diverticular disease beginning.<br><strong>Elderly (&gt;60):<\/strong> <strong>Diverticular bleeding<\/strong> (most common cause of major LGIB), <strong>angiodysplasia<\/strong> (second most common, right colon, arteriovenous malformations), colorectal carcinoma, ischaemic colitis.<br><strong>Diverticular bleeding:<\/strong> painless (no inflammation), large volume, bright red or maroon, stops spontaneously in ~80%. Paradoxically, bleeding diverticula are more commonly in the <em>right colon<\/em> (thinner wall, wider neck) despite left-sided predominance of diverticula overall. <strong>Angiodysplasia:<\/strong> submucosal vascular ectasia; right colon; associated with aortic stenosis (Heyde syndrome) and von Willebrand disease. Treated with argon plasma coagulation (APC) at colonoscopy. <strong>Second patient:<\/strong> IBD \u2014 blood mixed with mucus + diarrhoea + cramps in a young adult = UC or Crohn\\'s colitis until proven otherwise.',\n      extra: '<strong>Investigation strategy for LGIB:<\/strong> After resuscitation, <strong>colonoscopy<\/strong> (after bowel prep) is the first-line investigation \u2014 diagnostic and therapeutic (adrenaline injection, APC, haemoclip for diverticular\/angiodysplastic bleeding). If colonoscopy negative and bleeding continues: <strong>CT angiography<\/strong> (detects bleeding rate &gt;0.5 mL\/min) \u2192 interventional radiology embolisation. <strong>Radionuclide scan<\/strong> (Tc-99m RBC scan): detects bleeding as slow as 0.1 mL\/min \u2014 useful to localise before angiography. <strong>Colonoscopy to exclude malignancy<\/strong> is mandatory in any patient over 45\u201350 with rectal bleeding, even if a benign cause (diverticula, haemorrhoids) is identified \u2014 haemorrhoids and carcinoma coexist. <strong>Meckel\\'s diverticulum:<\/strong> the rule of 2s \u2014 2% of population, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic tissue (gastric most common, pancreatic), presents within first 2 years of life most often. Diagnosed by Meckel\\'s scan (Tc-99m pertechnetate \u2014 taken up by ectopic gastric mucosa).'\n    }\n\n  ];\n  \/* ================================================================\n     END OF CONTENT \u2014 engine logic below, do not edit\n     ================================================================ *\/\n\n  var answers  = {};\n  var answered = 0;\n  var shuffled = {};\n  var done     = false;\n\n  function byId(id) { return document.getElementById(id); }\n  function gid(sfx) { return byId(NS + '-' + sfx); }\n\n  function shuffleArr(arr) {\n    var a = arr.slice(), i, j, t;\n    for (i = a.length - 1; i > 0; i--) {\n      j = Math.floor(Math.random() * (i + 1));\n      t = a[i]; a[i] = a[j]; a[j] = t;\n    }\n    return a;\n  }\n\n  function countVal(val) {\n    var k, n = 0;\n    for (k in answers) {\n      if (answers.hasOwnProperty(k) && answers[k] === val) n++;\n    }\n    return n;\n  }\n\n  function buildPips() {\n    var cont = gid('pips'), i, q, wl, wp, line, pip;\n    if (!cont) return;\n    cont.innerHTML = '';\n    for (i = 0; i < QS.length; i++) {\n      q = QS[i];\n      if (i > 0) {\n        wl = document.createElement('div'); wl.className = 'mr-pip-wrap';\n        line = document.createElement('div'); line.className = 'mr-pip-line';\n        line.id = NS + '-pl' + q.id;\n        wl.appendChild(line); cont.appendChild(wl);\n      }\n      wp  = document.createElement('div'); wp.className = 'mr-pip-wrap';\n      pip = document.createElement('div'); pip.className = 'mr-pip';\n      pip.id = NS + '-pip' + q.id;\n      pip.textContent = String(q.id);\n      wp.appendChild(pip); cont.appendChild(wp);\n    }\n  }\n\n  function build() {\n    var cont, i, q, opts, card, top, nd, meta, tagRow, tg, dl,\n        st, rule, od, ed, lb, tx, ep, epl, ept, j, oe, ls, ts;\n    cont = gid('cases');\n    if (!cont) return;\n    cont.innerHTML = '';\n    answers = {}; answered = 0; shuffled = {}; done = false;\n    if (gid('score')) gid('score').style.display = 'none';\n    buildPips();\n    for (i = 0; i < QS.length; i++) {\n      q    = QS[i];\n      opts = shuffleArr(q.opts);\n      shuffled[q.id] = opts;\n\n      card = document.createElement('div'); card.className = 'mr-case';\n      top  = document.createElement('div'); top.className  = 'mr-case-top';\n      nd   = document.createElement('div'); nd.className   = 'mr-num';\n      nd.textContent = q.id < 10 ? 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