01OverviewDefinition, clinical context and the essential points that orientate the chapter.
The mucosal barrier balances acid and pepsin against mucus, bicarbonate, epithelial restitution and blood flow. H pylori disrupts this balance through chronic inflammation and altered gastrin signalling. NSAIDs inhibit prostaglandin-dependent mucosal defence and platelet function. Smoking, critical illness and concomitant antithrombotics amplify injury or bleeding but do not remove the need to identify the dominant cause.
Location changes follow-up. A duodenal ulcer is commonly H pylori-related and usually heals after eradication plus acid suppression. A gastric ulcer may be H pylori- or NSAID-related, but an ulcerated cancer can look deceptively smooth. Biopsy the edge and any irregular base, document size and site, and repeat endoscopy six to eight weeks after treatment begins when H pylori-positive, adjusted for lesion size.
Persistent or recurrent ulceration requires a structured explanation: ongoing NSAID or aspirin exposure, failed eradication, non-adherence, smoking, Crohn disease, cytomegalovirus in immunosuppression, gastrinoma or initial malignant sampling error. The correct response is not indefinite empiricism; it is review of histology, medicines, test validity, healing and the need for specialist assessment.
Key points
- Peptic ulcer is a mucosal defect extending through muscularis mucosae; H pylori and NSAIDs are the dominant acquired causes, but malignancy and hypersecretory states remain important exceptions.
- Duodenal ulcer generally carries negligible primary malignant potential, whereas gastric ulcer requires multiple biopsies and endoscopic healing confirmation.
- Test for active H pylori under valid conditions and eradicate when present; treatment without confirmation can leave recurrent bleeding risk.
- Stop an ulcerogenic NSAID where possible and give eight weeks of full-dose PPI or H2-receptor antagonist for an NSAID-associated diagnosed ulcer under NICE guidance.
- A current omeprazole SmPC uses 20 mg orally once daily; most duodenal ulcers heal in two weeks and gastric ulcers in four weeks, with an equal further interval if not fully healed.
- Haemorrhage, perforation, penetration and gastric outlet obstruction are mechanism-specific complications, each requiring more than simply increasing acid suppression.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Helicobacter pylori
Chronic bacterial gastritis alters acid regulation and weakens mucosal defence, producing antral-predominant duodenal-ulcer risk or corpus-associated gastric injury.
NSAID injury
Cyclooxygenase inhibition lowers protective prostaglandins, reducing mucus, bicarbonate and mucosal blood flow while platelet inhibition increases bleeding severity.
Uncommon drivers
Gastrinoma, Crohn disease, viral infection in immunosuppression, malignancy and severe physiological stress cause ulcers through distinct mechanisms requiring targeted treatment.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Barrier failure
Hydrogen ions and pepsin penetrate a compromised epithelial barrier, causing inflammation, necrosis and a defect extending through muscularis mucosae.
- 2Arterial erosion
Progressive ulcer depth can expose the gastroduodenal or left gastric arterial territory, converting superficial oozing into brisk life-threatening haemorrhage.
- 3Transmural extension
Continued digestion reaches serosa and releases gas and luminal contents, causing chemical peritonitis followed by bacterial contamination and sepsis.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Burning or gnawing epigastric discomfort may vary with meals, but timing cannot reliably determine location or benignity.
Fatigue, microcytosis and low ferritin can precede visible melaena from an intermittently oozing ulcer.
Haematemesis, coffee-ground vomit, melaena, syncope or shock requires acute upper-GI bleeding management.
Sudden severe epigastric pain with generalised guarding and loss of liver dullness suggests escape of gas and gastric contents.
Early satiety, succussion splash and recurrent non-bilious vomiting may reflect inflammatory oedema or chronic pyloroduodenal scarring.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Upper-GI endoscopyFirst step - Why
- Locate and photograph ulceration; obtain at least six targeted gastric-ulcer edge/base biopsies, or at least eight if malignancy is suspected.
- Interpretation and limitations
- BSG 2026 advises repeat endoscopy within two weeks when index gastric-ulcer biopsies were omitted, and healing review within twelve weeks, with further biopsy according to age, comorbidity and findings. A clean base or benign first sample does not alone exclude cancer.
- 02
Active H pylori testing - Why
- Identify an eradicable driver and later confirm cure.
- Interpretation and limitations
- Use biopsy, breath or stool antigen methods under valid drug conditions and document whether testing occurred before PPI exposure.
- 03
Full blood count and ferritin - Why
- Quantify acute or chronic blood loss and iron depletion.
- Interpretation and limitations
- Early haemoglobin can remain normal during acute haemorrhage, so interpret serial values with physiology and fluids.
- 04
CT abdomen - Why
- Identify free gas, penetration, collection or obstructing disease when complications are suspected.
- Interpretation and limitations
- CT does not replace endoscopic biopsy of a stable gastric ulcer and a small sealed perforation can be subtle.
- 05
Fasting gastrin in selected cases - Why
- Investigate recurrent, multiple or distal ulcers suggestive of hypersecretion.
- Interpretation and limitations
- PPIs and renal impairment raise gastrin; specialist preparation and gastric-acid context are needed before diagnosing gastrinoma.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Gastric adenocarcinoma
An ulcerated cancer can mimic benign peptic disease clinically and endoscopically, which is why gastric tissue and documented healing are essential.
Functional dyspepsia
Chronic upper-abdominal symptoms can occur without structural ulceration, but alarm features and treatment failure require reconsideration before applying this diagnosis.
Biliary or pancreatic pain
Gallstone pain and pancreatitis can produce severe epigastric symptoms, but liver tests, lipase, imaging and characteristic time course distinguish them.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Gastric ulcer healingProve benign resolutionFirst stepEndoscopy identifies an 18 mm antral ulcer in a stable NSAID user. Six targeted edge/base biopsies show inflammation without dysplasia; H pylori histology and urease testing are negative after valid medication washout.+
- 1Stop the NSAID and give omeprazole 20 mg orally once daily for eight weeks under the NICE NSAID-associated ulcer recommendation, after product safety checks. Confirm photographs, size, site and at least six edge/base samples. An ulcer suspicious for cancer needs at least eight targeted samples; if bleeding prevented any biopsy, repeat endoscopy within two weeks rather than waiting for healing.
- 2Book a six-to-eight-week healing examination in this patient: that appointment sits within the BSG 2026 twelve-week window and is proportionate to his fitness and lesion. NICE specifically recommends six to eight weeks for an H pylori-positive gastric ulcer; it is not a universal claim about this H pylori-negative case.
- 3At seven weeks, the ulcer has healed to a smooth scar and repeat targeted tissue is benign. If it had persisted, the next step would have been expert reassessment and further biopsy, irrespective of the initial benign report.
- 4AlternativeDocument the observed benign healing, reliable negative H pylori result and agreed alternative analgesia before closing follow-up; improvement in pain alone would not have supplied that evidence.
02Duodenal ulcerRemove recurrence biologyA clean-based duodenal ulcer is found after nocturnal epigastric pain and breath testing confirms H pylori.+
- 1Assess haemoglobin, bleeding history and medicine exposure before treating an apparently uncomplicated lesion.
- 2Give eradication therapy plus acid suppression using explicit doses and interaction checks.
- 3Confirm eradication six to eight weeks after treatment began. Use carbon-13 breath testing under NICE, or a validated laboratory monoclonal stool-antigen assay supported by the modern 2023 diagnostic consensus; allow two weeks off PPI and at least four weeks after antibiotics or bismuth.
- 4Investigate rather than repeatedly suppress if symptoms or ulceration recur despite proven clearance.
03Refractory ulcerRebuild the causal historyA gastric ulcer remains open after treatment and the first biopsy set was reported benign.+
- 1Check adherence, NSAIDs including over-the-counter products, aspirin, smoking and the validity of H pylori testing.
- 2Review the original photographs and tissue number: six edge/base samples are the general ulcer minimum, rising to at least eight targeted biopsies when malignant features are present. An unbiopsied gastric ulcer should already have triggered a repeat within two weeks.
- 3Arrange expert repeat endoscopy with adequate targeted sampling of the persistent edge, irregular base or abnormal scar; add CT staging when malignancy is suspected. Do not accept the first benign tissue result against persistent suspicious morphology.
- 4Consider rare inflammatory, infectious or hypersecretory causes only after common drivers and missed cancer are addressed.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Omeprazole for uncomplicated peptic-ulcer healing
Give omeprazole 20 mg orally once daily. Most active duodenal ulcers heal within 2 weeks and may receive a further 2 weeks if incomplete; most gastric ulcers heal within 4 weeks and may receive a further 4 weeks if incomplete. Use 40 mg once daily for a poorly responsive ulcer under the current SmPC while investigating the cause. Take the once-daily capsule in the morning, swallowed whole with half a glass of water; never chew or crush its enteric-coated pellets.Exclude alarm features and gastric malignancy rather than using symptom response as reassurance. In hepatic impairment the SmPC states 10–20 mg daily may be sufficient, so do not escalate automatically to 40 mg. Review the nelfinavir contraindication, clopidogrel and other CYP2C19 interactions, long-term magnesium and B12 risk, enteric infection and acute tubulointerstitial nephritis. Treatment duration does not replace repeat endoscopy when a gastric ulcer needs healing confirmation. No dose adjustment is required solely for renal impairment.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Upper-GI haemorrhage
Ulcer erosion into an artery produces haematemesis or melaena, hypovolaemia and rebleeding risk determined by physiology and endoscopic stigmata.
Perforation
Full-thickness penetration releases gastroduodenal contents into the peritoneum, causing abrupt pain, guarding, free gas and rapidly progressive sepsis.
Gastric outlet obstruction
Acute inflammatory oedema or chronic pyloroduodenal fibrosis narrows outflow, retaining food and causing vomiting, chloride loss, alkalosis and aspiration.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Follow pulse, blood pressure, stool colour and serial haemoglobin when bleeding is possible.
- Document ulcer site, diameter, biopsy number, histology and H pylori result together.
- Track NSAID cessation or the reason it must continue and the protective strategy chosen.
- Track gastric-ulcer healing endoscopy within twelve weeks under BSG 2026, tailored to age, comorbidity and further-biopsy need; bring an unbiopsied index ulcer back within two weeks. NICE six-to-eight-week healing review remains the specific H pylori-positive recommendation.
- Escalate sudden pain, persistent vomiting, syncope or recurrent melaena immediately.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Pain timing is imprecise
Meal association can suggest a mechanism but cannot replace endoscopic localisation or cancer exclusion.
Early haemoglobin can deceive
Acute whole-blood loss may initially preserve haemoglobin concentration before plasma refill or fluid resuscitation.
Healing is diagnostic evidence
A gastric ulcer that disappears with treatment provides reassurance that one benign biopsy set cannot supply alone.
Refractory means unexplained
Persistent ulcer should trigger review of cause, adherence, resistance and histology rather than an automatic longer prescription.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling a smooth-edged gastric ulcer benign without adequate biopsy and healing follow-up.
- 02
Using normal initial haemoglobin to dismiss ongoing melaena.
- 03
Eradicating H pylori without a correctly timed active test of cure in ulcer disease.
- 04
Continuing an over-the-counter NSAID while escalating PPI dose for non-healing.