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Common symptoms: heartburn, dysphagia, dyspepsia, nausea and vomiting, abdominal pain, diarrhoea, constipation, weight loss, bleeding. Alarm features: age over 55 with new dyspepsia, progressive dysphagia, persistent vomiting, unexplained weight loss, iron deficiency anaemia, gastrointestinal bleeding, palpable mass, family history of upper gastrointestinal cancer. These require early endoscopy. Functional disorders (functional dyspepsia, irritable bowel syndrome, diagnosed by Rome IV criteria) are common after organic disease is excluded.

Mechanisms: transient lower oesophageal sphincter relaxations, hiatus hernia, reduced clearance, delayed gastric emptying, obesity. Typical symptoms: heartburn and regurgitation; extra-oesophageal: chronic cough, laryngitis, asthma, dental erosion. Diagnosis: clinical response to a trial of proton pump inhibitors; endoscopy for alarm features or refractory symptoms; pH-impedance monitoring if diagnosis is uncertain. Treatment: lifestyle (weight loss, avoid late meals, raise the head of the bed), proton pump inhibitors for 4-8 weeks then step down, antireflux surgery (fundoplication) or endoscopic therapy for refractory disease. Barrett oesophagus is surveilled endoscopically.

H. pylori: Gram-negative spiral bacterium colonising the gastric mucosa; produces urease. Associated with gastritis, peptic ulcer, gastric adenocarcinoma and MALT lymphoma. Diagnosis: urea breath test or stool antigen (stop PPI two weeks before), endoscopic biopsy with histology, culture. Eradication: PPI plus two or three antibiotics (clarithromycin, amoxicillin, metronidazole) or bismuth quadruple therapy for 10-14 days, confirm eradication. Peptic ulcer: epigastric pain relieved or worsened by food, bleeding, perforation; gastric ulcers are biopsied to exclude cancer; NSAID ulcers are treated by stopping the drug and PPIs. Zollinger-Ellison syndrome: gastrinoma with severe multiple ulcers.

1. List the alarm features of dyspepsia. 2. What is first-line therapy for GERD? 3. How is H. pylori diagnosed non-invasively? 4. Which drug combinations are used for eradication?

1. Age over 55 with new symptoms, dysphagia, persistent vomiting, weight loss, anaemia, bleeding, mass, family history of gastric or oesophageal cancer. 2. Lifestyle measures and a proton pump inhibitor. 3. Urea breath test or stool antigen test. 4. PPI with two antibiotics (clarithromycin, amoxicillin, metronidazole) or bismuth quadruple therapy.

Causes: pancreatic insufficiency (chronic pancreatitis: steatorrhoea), bile salt deficiency (cholestasis), mucosal disease (coeliac disease, Crohn disease, giardiasis, tropical sprue), lactose intolerance, small intestinal bacterial overgrowth and short bowel. Features: chronic diarrhoea, steatorrhoea, weight loss, anaemia, deficiency of fat-soluble vitamins, oedema, bone disease. Tests: faecal elastase, stool fat, breath tests, small bowel biopsy.

Genetics: HLA-DQ2 or DQ8. Mechanism: gliadin peptides deamidated by tissue transglutaminase activate T cells, causing villous atrophy. Presentation: diarrhoea, weight loss, bloating, iron deficiency, osteoporosis, dermatitis herpetiformis, or asymptomatic. Diagnosis: IgA anti-tissue transglutaminase (and total IgA) on a gluten-containing diet, confirmed by duodenal biopsy showing villous atrophy, crypt hyperplasia and intraepithelial lymphocytes (serology alone may suffice in children with very high titres). Treatment: lifelong gluten-free diet. Complications: refractory disease, enteropathy-associated T-cell lymphoma, small bowel adenocarcinoma.

Ulcerative colitis: continuous mucosal inflammation from the rectum; bloody diarrhoea, urgency, tenesmus; risk of toxic megacolon and colorectal cancer (surveillance colonoscopy after 8 years). Crohn disease: transmural skip lesions, terminal ileum, abdominal pain, diarrhoea, weight loss, fistulae, strictures, perianal disease; smoking worsens it. Diagnosis: ileocolonoscopy with biopsies, faecal calprotectin, CRP, MR enterography. Extraintestinal manifestations: arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis. Treatment: 5-aminosalicylates (UC), corticosteroids for flares, thiopurines or methotrexate, biologics (anti-TNF, vedolizumab, ustekinumab), JAK inhibitors, and surgery (colectomy for refractory UC; resection for Crohn complications).

1. Which serological test screens for coeliac disease? 2. List causes of steatorrhoea. 3. Compare the distribution of Crohn disease and ulcerative colitis. 4. What is the role of faecal calprotectin?

1. IgA anti-tissue transglutaminase antibodies (with total IgA). 2. Pancreatic insufficiency, cholestasis, small bowel mucosal disease, bacterial overgrowth, short bowel. 3. Crohn: patchy, transmural, anywhere from mouth to anus. UC: continuous from the rectum, mucosal only. 4. It indicates intestinal inflammation and helps distinguish IBD from irritable bowel syndrome.

Causes: viral hepatitis B and C, alcohol, MASLD (metabolic dysfunction-associated steatotic liver disease), autoimmune hepatitis, haemochromatosis, Wilson disease, biliary diseases. Cirrhosis: nodules and fibrosis; complications: ascites (treated with sodium restriction, spironolactone, paracentesis with albumin), variceal bleeding (beta-blockers, band ligation), spontaneous bacterial peritonitis, hepatic encephalopathy (lactulose, rifaximin), hepatorenal syndrome, hepatocellular carcinoma (surveillance by ultrasound every 6 months). Staging: Child-Pugh and MELD scores; liver transplantation for decompensated disease.

Steatosis in more than 5 percent of hepatocytes with at least one cardiometabolic risk factor (obesity, type 2 diabetes, dyslipidaemia, hypertension) and no other cause. Spectrum: simple steatosis, steatohepatitis (MASH), fibrosis, cirrhosis and hepatocellular carcinoma (also without cirrhosis). Non-invasive fibrosis assessment: FIB-4 score, elastography. Treatment: weight loss of 7-10 percent, Mediterranean diet, exercise, control of diabetes and lipids; resmetirom for MASH with fibrosis; cardiovascular risk is the main cause of death.

Biliary: gallstones (biliary colic, cholecystitis, choledocholithiasis, cholangitis: Charcot triad), primary biliary cholangitis (antimitochondrial antibodies; ursodeoxycholic acid) and primary sclerosing cholangitis (associated with IBD; cholangiocarcinoma risk). Acute pancreatitis: gallstones and alcohol; severe epigastric pain radiating to the back; lipase at least three times normal; supportive care with fluids and early enteral feeding; ERCP for cholangitis or persistent obstruction; complications necrosis, infection, pseudocyst. Chronic pancreatitis: pain, exocrine and endocrine insufficiency.

Upper: peptic ulcer, varices, oesophagitis, Mallory-Weiss tear, malignancy (haematemesis, melaena). Lower: diverticular disease, angiodysplasia, colitis, haemorrhoids, colorectal cancer (haematochezia). Management: airway and haemodynamic resuscitation, transfusion with a restrictive threshold (haemoglobin about 7 g/dL), risk scores (Glasgow-Blatchford), early endoscopy within 24 hours; PPI after endoscopic therapy; for variceal bleeding, vasoactive drugs (terlipressin or octreotide), antibiotics and band ligation; TIPS for failure.

1. Name complications of cirrhosis and their treatments. 2. How is MASLD fibrosis assessed non-invasively? 3. What are the diagnostic criteria of acute pancreatitis? 4. Describe the initial management of upper GI bleeding.

1. Ascites (diuretics, paracentesis), varices (beta-blockers, banding), encephalopathy (lactulose), SBP (antibiotics), HCC (surveillance). 2. FIB-4 score and elastography. 3. Typical pain plus lipase or amylase at least three times normal and/or characteristic imaging. 4. Resuscitation, restrictive transfusion, PPI, endoscopy within 24 hours; vasoactive drugs, antibiotics and band ligation for varices.