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

24 sample cards from the Gastroenterology and Hepatology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Which criteria identify a paracetamol-poisoned patient who needs transfer for liver transplantation (King's College Criteria)?

   Arterial pH < 7.3 after resuscitation; OR all three of: prothrombin time > 100 s (INR > 6.5), creatinine > 300 µmol/L, and grade III/IV hepatic encephalopathy. These predict poor outcome without transplantation.

2. Define acute liver failure and list its cardinal features.

   Acute liver failure is the rapid development of hepatic dysfunction (coagulopathy, INR ≥ 1.5) with hepatic encephalopathy in a patient without pre-existing chronic liver disease. Cardinal features: jaundice, coagulopathy, encephalopathy, and often cerebral oedema and multi-organ failure.

3. What are the components and significance of the Child-Pugh score in cirrhosis?

   It grades cirrhosis severity using 5 variables: bilirubin, albumin, INR (prothrombin time), ascites, and encephalopathy. Classes A, B and C reflect increasing severity and predict surgical risk and mortality.

4. What does the MELD score predict, and which variables does it use?

   The MELD (Model for End-stage Liver Disease) score predicts 3-month mortality and prioritises liver transplant allocation. It uses serum bilirubin, creatinine, INR, and (in MELD-Na) serum sodium.

5. How is hepatic encephalopathy managed, and what precipitants should be sought?

   First-line: lactulose (reduces ammonia absorption, aim for 2-3 soft stools/day), with rifaximin added for recurrence. Precipitants to identify/treat: GI bleeding, infection (including SBP), constipation, dehydration, electrolyte disturbance, sedatives, and high protein load.

6. What is spontaneous bacterial peritonitis, how is it diagnosed, and how treated?

   Infection of ascitic fluid without an obvious surgical source. Diagnosis: ascitic neutrophil (PMN) count > 250 cells/mm³. Treatment: IV broad-spectrum antibiotics (e.g. cefotaxime) plus IV albumin to reduce hepatorenal syndrome. Prophylaxis with a quinolone follows.

7. Contrast the serology of acute hepatitis B, chronic hepatitis B, and immunity from vaccination.

   Acute HBV: HBsAg positive, IgM anti-HBc positive. Chronic HBV: HBsAg positive > 6 months, IgG anti-HBc positive. Vaccination immunity: anti-HBs positive ALONE (anti-HBc negative). Natural past infection: anti-HBs and anti-HBc both positive.

8. What does the presence of hepatitis B 'e' antigen (HBeAg) indicate?

   HBeAg positivity indicates active viral replication and high infectivity. Seroconversion to anti-HBe with loss of HBeAg suggests reduced replication, although 'precore mutant' HBV can have high viral load despite being HBeAg-negative.

9. How is chronic hepatitis C diagnosed and treated, and what is the cure target?

   Diagnosis: anti-HCV antibody screening, confirmed by HCV RNA (PCR) for active infection; genotype guides therapy. Treatment is with direct-acting antivirals (DAAs) for 8-12 weeks. Cure = sustained virological response (SVR): undetectable HCV RNA 12 weeks after treatment.

10. Compare primary biliary cholangitis and primary sclerosing cholangitis (autoantibodies, sex, associations).

    PBC: anti-mitochondrial antibody (AMA) positive, predominantly middle-aged women, intrahepatic small bile duct destruction, associated with other autoimmune disease; treat with ursodeoxycholic acid. PSC: p-ANCA may be positive (AMA negative), more common in men, intra- and extra-hepatic 'beaded' strictures on MRCP, strongly associated with ulcerative colitis and cholangiocarcinoma.

11. What are the diagnostic hallmarks of autoimmune hepatitis?

    Raised transaminases (hepatitic picture), raised IgG, and positive autoantibodies: ANA and anti-smooth muscle antibody (type 1), or anti-LKM-1 (type 2). Liver biopsy shows interface hepatitis. It responds to corticosteroids and azathioprine.

12. What are the key features and diagnostic findings of hereditary haemochromatosis?

    An autosomal recessive HFE (C282Y) gene disorder causing iron overload. Features: fatigue, arthralgia, bronze skin, diabetes ('bronze diabetes'), cardiomyopathy, hypogonadism, cirrhosis. Findings: raised ferritin and transferrin saturation (> 45%); treat with venesection.

13. How is Wilson's disease diagnosed and treated?

    A defect in copper excretion (ATP7B gene). Findings: low serum caeruloplasmin, raised urinary copper, Kayser-Fleischer rings, neuropsychiatric and hepatic disease, typically in young patients. Treatment: copper chelation with penicillamine (or trientine) and zinc.

14. What enzyme deficiency causes alpha-1 antitrypsin deficiency liver and lung disease, and what is the inheritance?

    Deficiency of the protease inhibitor alpha-1 antitrypsin (PiZZ phenotype most severe). Misfolded protein accumulates in hepatocytes causing cirrhosis, while lack of the enzyme in lungs leads to early panacinar (basal) emphysema. It is autosomal codominant inheritance.

15. State the modified Glasgow (Imrie) criteria mnemonic for severity in acute pancreatitis.

    PANCREAS: PaO2 < 8 kPa; Age > 55; Neutrophils (WCC > 15); Calcium < 2 mmol/L; Renal (urea > 16 mmol/L); Enzymes (LDH > 600, AST > 200); Albumin < 32 g/L; Sugar (glucose > 10 mmol/L). A score ≥ 3 within 48 h indicates severe pancreatitis.

16. What are the two most common causes of acute pancreatitis, and how is it diagnosed?

    Gallstones and alcohol (the 'GET SMASHED' mnemonic lists others). Diagnosis requires 2 of 3: characteristic epigastric pain radiating to the back; serum amylase or lipase > 3 times the upper limit of normal; and characteristic imaging (CT/US). Lipase is more specific and stays elevated longer.

17. What is the cornerstone of management of acute pancreatitis?

    Aggressive IV fluid resuscitation, analgesia, oxygen, and enteral nutrition as tolerated. There is no role for routine prophylactic antibiotics; antibiotics are reserved for confirmed infected necrosis. ERCP is indicated for gallstone pancreatitis with cholangitis/obstruction.

18. What triad characterises chronic pancreatitis, and how is exocrine insufficiency managed?

    The classic triad: abdominal pain, diabetes (endocrine failure), and steatorrhoea (exocrine failure). Pancreatic calcification may be seen on imaging. Exocrine insufficiency is treated with pancreatic enzyme replacement (e.g. Creon) and fat-soluble vitamin supplementation (A, D, E, K).

19. What test assesses pancreatic exocrine function in suspected chronic pancreatitis?

    Faecal elastase-1: a low level indicates pancreatic exocrine insufficiency. It is a simple, non-invasive marker that remains stable during gut transit and is unaffected by enzyme supplementation.

20. Define Charcot's triad and Reynolds' pentad in ascending cholangitis.

    Charcot's triad: right upper quadrant pain, fever (with rigors), and jaundice. Reynolds' pentad adds hypotension (septic shock) and confusion (altered mental status), indicating severe suppurative cholangitis requiring urgent biliary decompression (e.g. ERCP).

21. Distinguish biliary colic, acute cholecystitis, and ascending cholangitis.

    Biliary colic: RUQ pain after fatty meals, no fever, normal inflammatory markers (cystic duct transiently obstructed). Acute cholecystitis: persistent RUQ pain, fever, positive Murphy's sign, raised inflammatory markers (gallbladder inflammation). Cholangitis: pain, fever and jaundice (Charcot's triad) due to infected obstructed common bile duct.

22. What is refeeding syndrome, and which electrolyte abnormality is its hallmark?

    A potentially fatal shift in fluids/electrolytes when feeding is reintroduced after starvation; insulin surge drives intracellular uptake of phosphate, potassium and magnesium. The hallmark is hypophosphataemia. Also seen: hypokalaemia, hypomagnesaemia, and thiamine deficiency.

23. How is refeeding syndrome prevented in a high-risk patient?

    Identify high-risk patients (e.g. BMI < 16, little intake > 10 days, low baseline K/Mg/PO4); start feeding at a low rate (e.g. 10 kcal/kg/day) and increase slowly; supplement electrolytes (phosphate, potassium, magnesium); and give thiamine and B vitamins before and during refeeding.

24. When is parenteral nutrition indicated over enteral nutrition?

    Enteral nutrition ('if the gut works, use it') is always preferred. Parenteral nutrition is reserved for a non-functioning, inaccessible, or perforated GI tract — e.g. prolonged ileus, short bowel syndrome, high-output fistula, or severe malabsorption — where enteral feeding is impossible or unsafe.

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