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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Two main causes: H. pylori infection (~60% DU, ~40% GU) and NSAID use — always identify and address the cause
- Duodenal ulcer: epigastric pain relieved by eating; Gastric ulcer: pain worsened by eating
- Test for H. pylori (urea breath test or stool antigen) and eradicate if positive with triple therapy
- Gastric ulcers require repeat OGD at 6–8 weeks to confirm healing and exclude malignancy (duodenal ulcers do not)
- Complications: haemorrhage (most common), perforation (rigid abdomen, pneumoperitoneum), gastric outlet obstruction
Overview
Peptic ulcer disease describes mucosal breaks in the stomach (gastric ulcer, GU) or duodenum (duodenal ulcer, DU) that extend through the muscularis mucosae. The two principal aetiologies are H. pylori infection and NSAID use. H. pylori is a Gram-negative spiral bacterium that colonises gastric epithelium and causes chronic active gastritis, predisposing to ulceration. NSAIDs inhibit cyclooxygenase-1, reducing prostaglandin-mediated mucosal protection. Other causes include Zollinger-Ellison syndrome (gastrinoma), stress ulcers in critically ill patients, and rarely Crohn's disease.
Epidemiology
Peptic ulcer disease has a lifetime prevalence of approximately 5–10% in the UK. Duodenal ulcers are 2–3 times more common than gastric ulcers. H. pylori prevalence in the UK is approximately 30–40% overall (higher in older age groups and lower socioeconomic groups). NSAID-related ulcers are increasingly common in an ageing population on long-term anti-inflammatory medication. The incidence of PUD has declined with widespread H. pylori eradication and PPI co-prescription with NSAIDs.
Clinical Features
Symptoms
Epigastric pain (burning or gnawing)
Duodenal ulcer: pain relieved by eating, worse 2–3 hours after meals and at night (hunger pain)
Gastric ulcer: pain worsened by eating
Nausea and vomiting
Bloating and early satiety
Haematemesis or melaena (bleeding ulcer)
Sudden severe epigastric pain (suggests perforation)
Unexplained weight loss (raises concern for gastric malignancy)
Signs
Epigastric tenderness
Signs of anaemia (pallor, tachycardia) if chronic blood loss
Rigid "board-like" abdomen with absent bowel sounds (perforated ulcer)
Succussion splash (gastric outlet obstruction)
Haemodynamic instability (significant haemorrhage)
Investigations
First-line
H. pylori testingUrea breath test (13C-UBT) or stool antigen test. Stop PPI ≥2 weeks and antibiotics ≥4 weeks before testing
FBCIron deficiency anaemia from chronic blood loss
U&Es and coagulationIf bleeding — assess for uraemia (which impairs platelet function)
Second-line
Upper GI endoscopy (OGD)Gold standard for diagnosis. Biopsy gastric ulcers to exclude malignancy. CLO test (rapid urease test) for H. pylori on biopsy
Erect chest X-rayIf perforation suspected — pneumoperitoneum (free air under diaphragm) in ~75% of cases
Specialist
Fasting serum gastrinIf recurrent/refractory ulcers despite H. pylori eradication and NSAID cessation — screen for Zollinger-Ellison syndrome (gastrinoma)
CT abdomenIf perforation suspected and CXR non-diagnostic; also for staging if malignancy found
1
H. pylori-positive ulcer
- Triple therapy: PPI (full dose BD) + amoxicillin 1 g BD + clarithromycin 500 mg BD (or metronidazole 400 mg BD) for 7 days
- Confirm eradication ≥4 weeks post-treatment with UBT or stool antigen
- Continue PPI for 4–8 weeks for ulcer healing (8 weeks for gastric ulcer)
2
NSAID-related ulcer
- Stop NSAID if possible
- Full-dose PPI for 8 weeks
- If NSAID must continue: co-prescribe PPI long-term; consider switching to COX-2 selective inhibitor + PPI
- If H. pylori co-exists, eradicate before restarting NSAID
3
Follow-up
- Gastric ulcers: MUST have repeat OGD at 6–8 weeks with rebiopsy to confirm healing and exclude malignancy
- Duodenal ulcers: repeat OGD not routinely required unless complicated or symptomatic
- Refractory ulcers: consider adherence, ongoing NSAID use, Zollinger-Ellison syndrome, or Crohn's disease
4
Complications management
- Haemorrhage: resuscitate, urgent OGD with endoscopic haemostasis (adrenaline injection, thermal coagulation, clips)
- Perforation: emergency laparotomy/laparoscopy with omental patch repair (Graham patch)
- Gastric outlet obstruction: endoscopic balloon dilatation or surgical gastrojejunostomy
Complications
- Haemorrhage: Most common complication — presents with haematemesis, melaena, or both. Posterior DU may erode into gastroduodenal artery
- Perforation: Anterior DU most commonly perforates. Presents with sudden severe epigastric pain, peritonism, pneumoperitoneum on erect CXR
- Gastric outlet obstruction: Chronic scarring/oedema at pylorus or duodenum. Presents with projectile vomiting, weight loss, succussion splash
- Malignant transformation: Gastric ulcers carry ~1–2% malignancy risk — hence mandatory rebiopsy. DU almost never malignant
UKMLA Exam Tips
- 1DU pain: relieved by eating (food buffers acid). GU pain: worsened by eating (food stimulates acid secretion onto ulcer)
- 2Gastric ulcers = always biopsy and re-scope at 6–8 weeks (malignancy risk). Duodenal ulcers do NOT require rebiopsy
- 3Posterior DU → gastroduodenal artery erosion → massive haemorrhage. Anterior DU → perforation
- 4Zollinger-Ellison: suspect if multiple/recurrent ulcers, unusual locations (jejunum), diarrhoea, or refractory to PPI. Fasting gastrin >1000 pg/mL diagnostic
- 5Stop PPI ≥2 weeks before H. pylori breath test or stool antigen — PPIs suppress H. pylori and cause false negatives
- 6NSAID + H. pylori = additive ulcer risk — eradicate H. pylori before starting long-term NSAID therapy
practicetest your knowledge on peptic ulcer diseaseApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — gastroenterology and beyond.
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