Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Identify gastric and duodenal ulcer disease, address Helicobacter pylori and ulcerogenic medicines, recognise bleeding, perforation and obstruction early, and prove healing where a gastric lesion could conceal malignancy.
The gastroduodenal mucosa normally resists acid through mucus, bicarbonate, epithelial integrity, blood flow and prostaglandin-dependent repair. H. pylori disrupts regulation and generates chronic inflammation; NSAIDs impair cyclo-oxygenase-dependent defence. These factors can coexist, making combined infection and NSAID exposure particularly important. Smoking slows healing, while physiological stress in critical illness and rare gastrinoma syndromes belong to different clinical contexts.
Uncomplicated ulcer may produce burning or gnawing epigastric pain, nausea and nocturnal symptoms, yet some ulcers are silent until they bleed. Dyspepsia is a low-specificity syndrome and should be separated from alarm features and from an acute abdomen. Endoscopy is indicated when cancer referral criteria, bleeding, recurrent vomiting, anaemia, diagnostic uncertainty or treatment failure changes the risk–benefit balance; non-invasive H. pylori testing is appropriate only when endoscopy is not otherwise needed.
Management removes the cause and allows mucosal healing. H. pylori-positive disease receives combination eradication; NSAID-related disease receives acid suppression and medicine modification. A gastric ulcer is followed to documented healing and adequate histology. Failure to heal should trigger a systematic check of adherence, ongoing NSAID use, persistent H. pylori, smoking, malignancy, Crohn's disease, infection in an immunocompromised host and acid hypersecretion rather than indefinite empirical PPI escalation.
Chronic H. pylori gastritis alters acid regulation and mucosal defence, causing most non-NSAID duodenal and many gastric ulcers.
Cyclo-oxygenase inhibition reduces protective prostaglandins, mucus, bicarbonate and mucosal blood flow, with antithrombotics and corticosteroids amplifying bleeding risk.
Smoking, severe physiological illness and uncommon hypersecretory states modify ulcer risk, while gastric ulcers warrant careful consideration of underlying malignancy.
Reduced epithelial protection or excessive acid-pepsin exposure causes focal mucosal necrosis extending beyond the muscularis mucosae.
Ongoing inflammation and digestion penetrate submucosa, exposing vessels and muscular or serosal layers as mucosal defence fails.
Fibrotic repair may narrow the outlet, while uncontrolled depth causes arterial haemorrhage or free perforation into the peritoneum.
Localised upper abdominal discomfort, nausea or nocturnal pain may fit ulcer disease, but examination can be normal and the relationship to eating cannot determine site or histology.
Fatigue, exertional dyspnoea or iron-deficiency anaemia may reflect chronic ulcer bleeding. Search for an upper and lower GI cause as appropriate rather than attributing anaemia to dyspepsia alone.
Haematemesis, coffee-ground vomit, melaena, postural symptoms or shock requires acute upper-GI bleeding assessment. Bright rectal blood can occur with a brisk proximal bleed.
Abrupt severe pain with guarding suggests free perforation; pain radiating to the back or persistent focal pain may reflect posterior penetration. Both require urgent imaging and surgical review.
Early satiety, succussion splash, weight loss and recurrent non-bilious vomiting of stale food suggest pyloric or duodenal narrowing and commonly produce chloride, potassium and volume depletion.
Progressive weight loss, early satiety, persistent vomiting, dysphagia, a mass or unexplained anaemia changes the pathway. A gastric ulcer is a lesion requiring histology and healing confirmation, not a symptom label.
A compatible symptom pattern with no ulcer or other structural explanation supports functional disease; meal timing alone cannot distinguish it.
Weight loss, anaemia, irregular margins or non-healing gastric ulcer requires multiple biopsies and documented reassessment to exclude malignancy.
Right-upper-quadrant attacks, jaundice, back-radiating pain or abnormal pancreatic and biliary imaging suggests a non-peptic source of symptoms.
Arterial erosion causes haematemesis or melaena, shock and rebleeding risk, while chronic oozing produces iron-deficiency anaemia.
Full-thickness penetration releases gastroduodenal contents into the peritoneum, causing abrupt pain, sepsis and urgent source-control need.
Acute oedema or chronic pyloroduodenal scarring retains food, causing vomiting, dehydration, alkalosis and nutritional decline from retained contents.
The traditional meal relationship of gastric and duodenal pain is insufficiently reliable for site diagnosis; investigation and causal assessment matter more.
Finding H. pylori does not make regular ibuprofen irrelevant, and identifying NSAID exposure does not remove the need to seek infection.
Acute whole-blood loss initially removes plasma and cells together, so the first concentration may look deceptively preserved despite shock.
Repeat examination of a gastric ulcer verifies healing and revisits sampling because infiltrative cancer can initially mimic benign inflammation.
PPI withdrawal before gastrin assessment can provoke dangerous acid rebound in genuine hypersecretion, so this is not a casual primary-care test.
Diagnosing ulcer site from whether food relieves or worsens the pain.
Failing to ask about over-the-counter NSAIDs and combination cold or analgesic products.
Assuming a gastric ulcer is benign because its edges look smooth at the first endoscopy.
Stopping secondary-prevention aspirin without weighing cardiovascular harm or involving the responsible team.
Using a negative H. pylori test obtained during PPI treatment as definitive exclusion.
Ordering fasting gastrin while continuing a PPI and interpreting the predictable elevation as gastrinoma.
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Endoscopy shows a 15 mm gastric ulcer. Biopsies show inflammation without cancer, H. pylori is treated and symptoms resolve. Which follow-up is most appropriate?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Use a named formulary product and review long-term need. Check interactions, renal and hepatic context, magnesium and B12 risk when prolonged, enteric infection risk and rebound symptoms; PPI use can invalidate H. pylori testing.
Reconcile the full combination, pregnancy, allergy, QT and CYP interactions, renal and liver function and previous macrolide, nitroimidazole or fluoroquinolone use. Persistent symptoms alone do not justify repeated antibiotics.