Membership of the Royal College of Physicians (MRCP UK) Gastroenterology and Hepatology Syllabus

Gastroenterology and Hepatology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Gastroenterology and Hepatology in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Upper Gastrointestinal Disorders

   4 topics

   • Gastro-oesophageal reflux and Barrett's oesophagus
   • Peptic ulcer disease and Helicobacter pylori
     • Eradication regimens
   • Upper GI bleeding
     • Glasgow-Blatchford and Rockall scores
     • Variceal versus non-variceal bleeding
   • Dysphagia and oesophageal motility disorders
2. 2

   Lower Gastrointestinal Disorders

   5 topics

   • Inflammatory bowel disease
     • Crohn's disease management
     • Ulcerative colitis and acute severe colitis
     • Biologic and immunomodulator therapy
   • Irritable bowel syndrome and functional disorders
   • Coeliac disease and malabsorption
   • Colorectal cancer and screening
   • Lower GI bleeding and diverticular disease
3. 3

   Liver Disease

   5 topics

   • Acute liver failure and paracetamol toxicity
     • King's College criteria for transplantation
   • Chronic liver disease and cirrhosis
     • Ascites and spontaneous bacterial peritonitis
     • Hepatic encephalopathy and hepatorenal syndrome
   • Viral hepatitis B and C
     • Serological interpretation and antiviral therapy
   • Autoimmune and cholestatic liver disease
     • Primary biliary cholangitis and primary sclerosing cholangitis
   • Metabolic and inherited liver disease
     • Haemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency
4. 4

   Pancreaticobiliary and Nutritional Disorders

   4 topics

   • Acute pancreatitis
     • Severity scoring and complications
   • Chronic pancreatitis and exocrine insufficiency
   • Gallstone disease and cholangitis
   • Nutritional support and refeeding syndrome

Gastroenterology and Hepatology flashcards for Membership of the Royal College of Physicians (MRCP UK)

24 of 55 cards from the Gastroenterology and Hepatology deck — real questions with worked answers.

1. What histological change defines Barrett's oesophagus, and why does it matter clinically?

   Replacement of the normal stratified squamous epithelium of the distal oesophagus by metaplastic columnar epithelium (intestinal metaplasia with goblet cells). It is a premalignant condition predisposing to oesophageal adenocarcinoma (roughly 0.3-0.5% annual progression risk).

2. What is the first-line management of GORD, and which alarm features warrant urgent endoscopy?

   Lifestyle measures plus a proton pump inhibitor (PPI) are first-line. Alarm (ALARMS) features mandating urgent endoscopy include: Anaemia, Loss of weight, Anorexia, Recent onset/progressive symptoms, Melaena/haematemesis, and Swallowing difficulty (dysphagia).

3. How is Barrett's oesophagus with high-grade dysplasia managed?

   Endoscopic therapy is preferred: radiofrequency ablation, often combined with endoscopic mucosal resection of any visible/nodular lesions. This avoids oesophagectomy in most cases. Low-grade dysplasia is also typically treated with ablation; non-dysplastic Barrett's undergoes surveillance endoscopy.

4. Which two factors are the dominant causes of peptic ulcer disease?

   Helicobacter pylori infection and NSAID use. H. pylori is the leading cause of duodenal ulcers; NSAIDs (via COX inhibition reducing protective prostaglandins) are the other major cause, especially for gastric ulcers.

5. What is the standard first-line eradication regimen for Helicobacter pylori in a penicillin-tolerant patient (UK)?

   A 7-day triple therapy: a PPI plus amoxicillin plus either clarithromycin or metronidazole, all twice daily. In penicillin allergy, a PPI plus clarithromycin plus metronidazole is used.

6. Which non-invasive tests confirm H. pylori eradication, and what must be stopped beforehand?

   The urea breath test or stool antigen test. PPIs should be stopped for at least 2 weeks and antibiotics for at least 4 weeks before testing to avoid false negatives. Eradication is confirmed no sooner than 4 weeks after completing therapy.

7. What scoring systems are used in upper GI bleeding before and after endoscopy?

   The Glasgow-Blatchford score is used pre-endoscopy to identify low-risk patients who may avoid admission (score 0 = consider discharge). The Rockall score (full version uses endoscopic findings) estimates rebleeding and mortality risk after endoscopy.

8. What is the role of terlipressin and antibiotics in suspected variceal upper GI bleeding?

   In suspected variceal bleeding, give terlipressin (a vasopressin analogue that reduces portal pressure) and prophylactic broad-spectrum antibiotics (e.g. a quinolone or ceftriaxone) at presentation, before or alongside endoscopy. Both improve survival.

9. What is the endoscopic treatment of choice for oesophageal varices, and what is the next step if it fails?

   Endoscopic variceal band ligation is first-line. If bleeding is uncontrolled, options include balloon tamponade (Sengstaken-Blakemore tube) as a temporising bridge, then a TIPS (transjugular intrahepatic portosystemic shunt) procedure.

10. What is the Forrest classification used for, and which grades carry high rebleeding risk?

    It grades endoscopic appearance of bleeding peptic ulcers to predict rebleeding. High-risk: Forrest Ia (spurting), Ib (oozing), IIa (visible vessel), IIb (adherent clot). Low-risk: IIc (flat pigmented spot) and III (clean base). High-risk lesions require endoscopic haemostasis.

11. Differentiate the typical causes of oropharyngeal versus oesophageal dysphagia.

    Oropharyngeal (transfer) dysphagia: difficulty initiating swallowing, often neuromuscular (stroke, Parkinson's, myasthenia gravis, bulbar palsy). Oesophageal dysphagia: food sticking after swallowing, due to mechanical obstruction (stricture, cancer, web/ring) or motility disorders (achalasia, spasm).

12. What are the classic manometric and radiological findings of achalasia?

    Manometry shows absent oesophageal peristalsis with failure of lower oesophageal sphincter relaxation and often raised LOS pressure. Barium swallow shows a dilated oesophagus tapering to a 'bird's beak' at the gastro-oesophageal junction.

13. Compare the dysphagia patterns of mechanical obstruction versus a motility disorder.

    Mechanical obstruction typically causes progressive dysphagia to solids first, then liquids. A motility disorder (e.g. achalasia, diffuse oesophageal spasm) typically causes dysphagia to solids AND liquids from the outset, often intermittent and non-progressive.

14. Contrast the typical distribution and depth of inflammation in ulcerative colitis versus Crohn's disease.

    Ulcerative colitis: continuous, mucosal/submucosal inflammation starting at the rectum and extending proximally, confined to the colon. Crohn's disease: discontinuous 'skip lesions', transmural inflammation affecting any part of the GI tract (mouth to anus), commonly the terminal ileum.

15. Which histological and imaging features distinguish Crohn's disease from ulcerative colitis?

    Crohn's: non-caseating granulomas, transmural inflammation, cobblestone mucosa, fistulae, strictures, 'rose-thorn' ulcers and string sign on imaging. UC: crypt abscesses, goblet cell depletion, pseudopolyps, continuous mucosal disease without granulomas.

16. What is the management of an acute severe flare of ulcerative colitis, including the Truelove and Witts criteria threshold?

    IV corticosteroids (e.g. hydrocortisone) are first-line for acute severe UC. If no response by day 3 (assessed using stool frequency/CRP, e.g. the Travis criteria), rescue therapy with IV ciclosporin or infliximab, or colectomy, is considered. Acute severe UC = ≥6 bloody stools/day plus systemic upset.

17. What is the first-line therapy to induce and maintain remission in mild-to-moderate ulcerative colitis?

    Aminosalicylates (5-ASA, e.g. mesalazine), topical and/or oral, are first-line to induce and maintain remission in mild-to-moderate UC. Mesalazine is notably less effective in Crohn's disease, where it is not routinely recommended.

18. List the key extra-intestinal manifestations of inflammatory bowel disease that correlate with disease activity versus those that do not.

    Activity-related: erythema nodosum, episcleritis, peripheral (large-joint) arthritis, aphthous ulcers. Independent of activity: pyoderma gangrenosum, anterior uveitis, axial arthritis (sacroiliitis/ankylosing spondylitis), and primary sclerosing cholangitis (strongly linked to UC).

19. What are the Rome IV-based diagnostic features of irritable bowel syndrome?

    Recurrent abdominal pain, on average at least 1 day per week in the last 3 months, associated with two or more of: relation to defecation, change in stool frequency, and change in stool form/appearance. Diagnosis requires exclusion of red-flag/organic features.

20. Which red-flag features in suspected IBS should prompt investigation for organic disease?

    Weight loss, rectal bleeding, anaemia, age over 60 with change in bowel habit, family history of bowel/ovarian cancer, abdominal/rectal masses, and raised inflammatory markers or faecal calprotectin. These mandate further investigation (e.g. colonoscopy).

21. What is the first-line pharmacological management of IBS by predominant symptom?

    Antispasmodics (e.g. mebeverine, hyoscine) for pain/cramps; loperamide for diarrhoea-predominant IBS; soluble fibre (e.g. ispaghula) or laxatives such as macrogols for constipation (avoid lactulose). A low-dose tricyclic antidepressant is second-line for pain.

22. What is the autoantibody and HLA association of coeliac disease, and what test is most sensitive?

    Coeliac disease is associated with HLA-DQ2 and HLA-DQ8. The most sensitive/specific serological test is anti-tissue transglutaminase (anti-tTG) IgA, with total IgA measured to exclude deficiency. Endomysial antibodies (EMA) are a confirmatory test.

23. What must a patient do before coeliac serology and biopsy, and what is the gold-standard diagnostic finding?

    The patient must be consuming gluten (e.g. >1 meal/day) for at least 6 weeks before testing, otherwise results may be falsely negative. The gold standard is duodenal biopsy showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis.

24. Name the classic complications and associated conditions of coeliac disease.

    Complications: iron/folate/B12 deficiency anaemia, osteoporosis, hyposplenism, dermatitis herpetiformis, and enteropathy-associated T-cell lymphoma (EATL) and small bowel adenocarcinoma. Associations: type 1 diabetes, autoimmune thyroid disease, and IgA deficiency.

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