MRCP Part 1 Gastroenterology: 50 Rapid-Review Facts
- Crack Medicine
- Oct 27
- 5 min read
TL;DR This article gives you MRCP Part 1 gastroenterology: 50 rapid-review facts — a compact, high-yield set of pointers for liver disease, IBD, GI bleeding, malabsorption and more. Use this as a last-minute check or memory scaffold while practising with question banks or mocks.
Why this matters in MRCP Part 1
Gastroenterology and hepatology remain a staple component of MRCP Part 1—the exam tests not just isolated facts but pattern recognition (e.g. enzyme profiles, cholestatic vs hepatocellular injury, IBD versus IBS).According to the Federation of the Royal Colleges, MRCP(UK) Part 1 is designed to assess a broad base of scientific and clinical knowledge in multiple domains. thefederation.uk+1Missing the deeper logic behind common GI patterns often costs candidates marks. These 50 facts will help anchor your recall, reduce guesswork, and reinforce your QBank performance.
We will also include a short clinical mini-case, and a focused study-tip checklist to help you integrate these facts into your revision plan.
5 High-Yield Gastroenterology Subtopics + 5 Tricky “Traps”
Before the 50 facts, it helps to be aware of the five most tested GI/hepatology areas and five common traps that mislead candidates in MRCP Part 1.
Top 5 tested subtopics in GI / hepatology
Liver enzyme interpretation & patterns (hepatocellular vs cholestatic injury)
Viral, autoimmune, and cholestatic liver diseases
Inflammatory bowel disease (Crohn’s, ulcerative colitis)
Peptic ulcer disease, GI bleeding, varices
Malabsorption syndromes and celiac disease
5 Common Traps & Pitfalls
Mistaking an isolated ALP rise as hepatic without checking GGT.
Interpreting mild bilirubin rise as always pathological—even Gilbert’s syndrome can be benign.
Thinking that all Crohn’s disease involves the colon (skip lesions and small bowel-only disease exist).
Assuming that ANA positivity always implies autoimmune hepatitis (there is overlap and false positives).
Focusing on rare causes (e.g. Wilson’s or hemochromatosis) before mastering common ones.
50 Rapid-Review Facts for GI & Hepatology (MRCP Part 1)
Below is a grouped list for easier retention:
Liver Enzyme & Function Patterns (Facts 1–7)
ALT > AST (especially >2:1) → viral or drug-induced hepatocellular injury.
AST > ALT, ratio >2:1 → alcoholic liver disease.
ALP + GGT rise → cholestatic picture; if ALP rises but GGT is normal, suspect bone origin.
Albumin decline is a marker of chronic liver disease, not acute injury.
Prothrombin time (PT) prolongation is an early signal of synthetic failure.
Bilirubin pattern: conjugated (direct) rise implicates biliary obstruction or hepatocellular damage; unconjugated (indirect) often due to hemolysis or Gilbert’s.
In cholestatic injury, conjugated bilirubin and alkaline phosphatase tend to rise together.
Cirrhosis & Portal Hypertension (Facts 8–14)
Leading causes: alcohol, non-alcoholic steatohepatitis, viral hepatitis, autoimmune liver disease.
Complications: variceal bleeding, ascites, hepatic encephalopathy, hepatocellular carcinoma.
Serum-ascites albumin gradient (SAAG) > 1.1 g/dL suggests portal hypertension.
Non-selective beta-blockers (e.g. propranolol, nadolol) reduce first variceal bleed risk.
Refractory ascites or recurrent variceal bleeding may merit TIPSS (transjugular intrahepatic portosystemic shunt).
Spontaneous bacterial peritonitis (SBP) diagnosis: ascitic neutrophil count > 250/mm³.
Hepatic encephalopathy responds to reduction of ammonia via lactulose or rifaximin.
Viral, Autoimmune & Cholestatic Liver Diseases (Facts 15–22)
HBsAg positive > 6 months = chronic HBV infection.
Anti-HBs positive with HBsAg negative implies immunity (past infection or vaccine).
High-titre anti-mitochondrial antibody (AMA) → primary biliary cholangitis (PBC).
Anti–smooth muscle antibody (SMA) often points to autoimmune hepatitis.
Primary sclerosing cholangitis (PSC) is strongly associated with ulcerative colitis.
Secondary causes of cholestasis: drugs (e.g. amoxicillin-clavulanate, chlorpromazine), obstruction, PBC or PSC.
Overlap syndromes exist (e.g. autoimmune hepatitis plus cholestatic features).
In cholestatic disease, ursodeoxycholic acid is often first-line therapy for PBC.
GI Bleeding & Peptic Ulcer Disease (Facts 23–30)
Upper GI bleed: peptic ulcer > varices > Mallory–Weiss tear.
Lower GI bleed: diverticular disease, angiodysplasia, colorectal carcinoma.
For variceal bleed: start octreotide (or terlipressin in UK settings).
Rockall score or Blatchford score help stratify mortality/rebleed risk.
Main causes of peptic ulcer: Helicobacter pylori + NSAIDs.
Duodenal ulcers often relieved by meals; gastric ulcers often worsen after eating.
Standard H. pylori eradication: PPI + amoxicillin + clarithromycin (or alternative regimens based on resistance).
Refractory ulcers should prompt evaluation for Zollinger–Ellison syndrome or malignancy.
Inflammatory Bowel Disease & Malabsorption (Facts 31–38)
Ulcerative colitis: continuous mucosal inflammation, always involves rectum.
Crohn’s disease: skip lesions, transmural inflammation, can affect any GI tract segment.
Cobblestone appearance, fistulae, strictures are hallmark of Crohn’s.
Ulcerative colitis bears increased colorectal cancer risk after 8–10 years.
Maintenance agents: mesalazine, sulfasalazine; in severe disease biologics or immunosuppressants.
Anti-tissue transglutaminase (tTG) IgA is first-choice screen for coeliac disease.
Histology in coeliac: villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes.
Typical nutrient deficiencies: iron, folate, calcium, vitamin D, B12 in malabsorption.
Pancreatic, Biliary & GI Malignancy (Facts 39–47)
Acute pancreatitis: amylase (or lipase) > 3× upper limit of normal.
Common causes: gallstones, alcohol.
CRP > 150 mg/L at 48 h suggests severe pancreatitis.
Chronic pancreatitis presents with steatorrhea, weight loss and secondary diabetes.
CT is the imaging modality of choice to detect complications (necrosis, pseudocysts).
Right-sided colon cancer often presents with occult bleeding and iron-deficiency anemia.
Left-sided cancer more likely to cause bowel obstruction or change in habit.
AFP rise suggests hepatocellular carcinoma (HCC).
PSC + ulcerative colitis raises cholangiocarcinoma risk; periodic imaging surveillance is often considered.
Miscellaneous (Facts 48–50)
Wilson’s disease: low ceruloplasmin, Kayser–Fleischer rings, hepatic + neuro features.
Hemochromatosis: high ferritin, high transferrin saturation; treat with phlebotomy.
Gilbert’s syndrome: isolated unconjugated bilirubin occasionally elevated, often benign; no specific treatment.
Mini-Case / MCQ with Explanation
Case: A 47-year-old man presents with progressive fatigue and pruritus. Liver tests show ALP 320 U/L (normal <120), GGT elevated, bilirubin mildly raised (direct predominant). AMA is strongly positive. Ultrasound shows no ductal stone.
Question: What is the most likely diagnosis, and what first-line therapy is indicated?
Answer & Reasoning: Diagnosis: Primary biliary cholangitis (PBC).Rationale: The cholestatic LFT pattern (ALP + GGT rise), AMA positivity, and middle-aged female predominance (though men can present) are classic features. Therapy: First-line therapy is ursodeoxycholic acid (UDCA) to slow disease progression and improve biochemical markers.
Study-Tip Checklist: How to Memorise & Apply These Facts
Use spaced repetition: review the 50 facts in flashcard format at intervals (e.g. Day 1, 3, 7, 14).
Pair facts with clinical vignettes or QBank stems (so that you see patterns in context).
After each QBank session, map your mistakes to these facts and reinforce the relevant fact immediately.
Maintain a “GI cheat sheet” of enzyme patterns and key associations (e.g. PSC ↔ UC, PBC ↔ AMA).
Before each mock or timed session, skim this list as a high-yield “last pass.”
FAQs
How many GI/hepatology questions are in MRCP Part 1?
Typically, about 10–15% of MRCP Part 1 content is GI/hepatology (liver disease, IBD, pancreatitis, GI bleeding).
Do MRCP Part 1 questions include images of endoscopy or radiology?
No — the exam format for Part 1 is two papers of multiple-choice best-of-five, without images. thefederation.uk
Is it necessary to memorise enzyme normal ranges?
Yes—commonly tested enzymes (AST, ALT, ALP, GGT, bilirubin fractions) and their cutoff multiples (e.g., “>3× normal”) are frequent in stems.
Should I prioritise rare conditions like Wilson’s disease or hemochromatosis?Not in early revision. Master common patterns (e.g. cholestatic vs hepatocellular injury) first; rare conditions help in tie-breaker or challenge Qs.
What resources are reliable for MRCP GI revision?
Use the official MRCP(UK) site for exam specs (thefederation.uk). thefederation.uk+1 Also consider gastro-specific MCQ banks or modules such as GastroTraining’s MCQ collection. gastrotraining.com
Ready to start?
Use this 50-fact set as a brain scaffold while practising MRCP-style QBank sessions. After each QBank block, revisit this list to reinforce weak areas.
If you’d like structured GI MCQ bundles or full mock exams under timed conditions, check out our MRCP QBank and mock test offerings (via Crack Medicine). In your broader MRCP Part 1 journey, explore our core hub on MRCP Part 1 for topic-wise deep dives and integrated plans.
Best of luck — confident pattern recognition beats rote trivia in exam conditions.
Sources
The Federation of the Royal Colleges of Physicians: MRCP(UK) Part 1 details thefederation.uk+1
Royal College of Physicians of Edinburgh — MRCP(UK) Examinations rcpe.ac.uk
PMC article: “Obtaining the MRCP diploma” — insights into exam strategy and structure pmc.ncbi.nlm.nih.gov
Gastro Training — GI / hepatology MCQ & educational resources gastrotraining.com
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