Medicine chapters
Gastritis, H. pylori and peptic ulcer disease
Types of gastritis, how Helicobacter pylori and NSAIDs cause ulcers, the tests for H. pylori, eradication regimens, and the recognition and management of bleeding, perforation and gastric outlet obstruction.
- Helicobacter pylori and NSAIDs cause most peptic ulcers; duodenal ulcers are commoner, cause hunger and night pain, and are linked to high acid, while gastric ulcers must be biopsied to exclude cancer.
- Non-invasive tests (urea breath test, stool antigen) need the patient off PPIs for 2 weeks; first-line eradication is a PPI + two antibiotics or bismuth quadruple therapy where clarithromycin resistance is high.
- Complications are bleeding (commonest), perforation (sudden pain, board-like rigidity, gas under the diaphragm) and gastric outlet obstruction (hypochloraemic hypokalaemic metabolic alkalosis).
On this page
Overview
A peptic ulcer is a break in the lining of the stomach or duodenum that goes through the muscularis mucosae. An erosion is shallower and stays in the mucosa.
The two big causes are Helicobacter pylori and NSAIDs (including aspirin). H. pylori is very common in Pakistan, where most adults are infected, so peptic ulcer and its complications are everyday problems in medical and surgical wards.
Gastritis and gastropathy
- Gastritis = inflammation of the stomach lining with mucosal injury.
- Gastropathy = epithelial damage without much inflammation (NSAIDs, alcohol, bile reflux, portal hypertension).
| Type | Cause | Site | Key consequences |
|---|---|---|---|
| H. pylori gastritis (type B) | H. pylori | Usually antrum; may spread to the body | Duodenal ulcer, gastric ulcer, intestinal metaplasia, gastric adenocarcinoma, MALT lymphoma |
| Autoimmune gastritis (type A) | Antibodies to parietal cells and intrinsic factor | Body and fundus | Atrophy, achlorhydria, B12 deficiency (pernicious anaemia), high gastrin, gastric cancer and carcinoid risk |
| Acute erosive / haemorrhagic gastropathy | NSAIDs, alcohol, severe stress | Diffuse | Bleeding |
| Stress ulcers | Shock, sepsis, ICU patients | Stomach | Bleeding; prevented with PPI in high-risk ICU patients |
| Curling ulcer | Major burns | Stomach/duodenum | Bleeding |
| Cushing ulcer | Head injury, raised ICP | Stomach/duodenum | Bleeding, perforation |
| Portal hypertensive gastropathy | Cirrhosis | Fundus/body | Chronic blood loss |
Anti-intrinsic factor antibodies are more specific for pernicious anaemia than anti-parietal cell antibodies, which are common and non-specific.
Autoimmune gastritis = A for Acid gone (achlorhydria) and Anaemia (B12). Bacterial gastritis = B for antrum-to-Bulb (duodenal ulcer).
Helicobacter pylori
The organism
- Gram-negative, spiral, flagellated, slow-growing rod.
- Lives under the mucus layer of the gastric antrum, and in patches of gastric metaplasia in the duodenum.
- Produces urease, which splits urea into ammonia and CO2; ammonia buffers acid around the organism. This is also the basis of the urease and breath tests.
- Virulence factors CagA and VacA are linked to more inflammation, ulcers and cancer.
- Acquired in childhood, probably by faecal–oral or oral–oral spread; prevalence is 80–90% in developing countries.
How it causes duodenal ulcer
Antral infection reduces somatostatin (D cells), so gastrin release from G cells rises. More gastrin means more acid from the parietal cells, which damages the duodenum. In contrast, pangastritis (body involvement) lowers acid output and favours gastric ulcer and cancer.
Diseases linked to H. pylori
- Chronic antral gastritis.
- Duodenal and gastric ulcers.
- Gastric adenocarcinoma (distal stomach; H. pylori is classed as a class 1 carcinogen).
- Gastric MALT lymphoma: early disease can regress after eradication alone.
- Also iron deficiency anaemia and immune thrombocytopenia in some patients.
Tests for H. pylori
| Test | Type | Points |
|---|---|---|
| 13C-urea breath test | Non-invasive | Accurate; good for diagnosis and for confirming eradication |
| Stool antigen test | Non-invasive | Accurate; good for diagnosis and confirming eradication; now widely used |
| Serology (IgG) | Non-invasive | Stays positive for many months after cure, so useless to confirm eradication |
| Rapid urease (CLO) test | Invasive, at endoscopy | Antral biopsy in urea + phenol red; turns yellow to red/pink; quick result |
| Histology | Invasive | Giemsa or immunostaining; also shows gastritis, atrophy, metaplasia |
| Culture | Invasive | For antibiotic sensitivity after repeated treatment failure |
PPIs and antibiotics suppress the organism and give false-negative breath, stool, urease and histology results. Stop PPIs for 2 weeks and antibiotics for 4 weeks before testing. H2 blockers can be continued.
Serology cannot confirm eradication, because antibodies remain for up to a year.
Peptic ulcer disease
Duodenal versus gastric ulcer
| Feature | Duodenal ulcer (DU) | Gastric ulcer (GU) |
|---|---|---|
| Frequency | 2–3 times commoner | Less common |
| Usual site | First part of duodenum (duodenal cap) | Lesser curve near the incisura |
| Acid output | Normal or high | Normal or low |
| Pain | Epigastric; hunger pain, wakes at night, often eased by food | Epigastric; often worse with food |
| Weight | Usually maintained | Anorexia and weight loss more common |
| Cancer risk | Practically none | Must biopsy; gastric cancer can look like a benign ulcer |
| Typical complication | Bleeding (posterior DU erodes the gastroduodenal artery), perforation (anterior DU) | Bleeding (left gastric artery) |
Duodenal ulcers outnumber gastric ulcers by about 2–3 to 1, but it is the gastric ulcer that must always be biopsied.
The link between pain and meals is unreliable. Back pain suggests a posterior penetrating ulcer. Many patients with bleeding or perforation have no previous ulcer symptoms, especially those on NSAIDs.
NSAIDs and ulcers
- NSAIDs block COX-1, reducing protective prostaglandins (mucus, bicarbonate, blood flow).
- Ulcers are more often gastric and frequently painless.
- H. pylori and NSAIDs act together and multiply the risk.
- High-risk patients: over 65, previous ulcer (especially with bleeding), also taking steroids, anticoagulants or antiplatelets, serious illness.
Management: stop the NSAID if possible; give a PPI; test and eradicate H. pylori. If an NSAID must continue, use the lowest dose with PPI cover; misoprostol (a prostaglandin E1 analogue) also protects but causes diarrhoea and is contraindicated in pregnancy. COX-2 selective drugs cause fewer ulcers but carry cardiovascular risk.
Other causes
- Zollinger–Ellison syndrome (gastrinoma, often with MEN 1): multiple, recurrent or distal (post-bulbar, jejunal) ulcers, diarrhoea, very high fasting gastrin. Suspect when ulcers recur despite eradication.
- Smoking (delays healing), steroids with NSAIDs, Crohn disease, hypercalcaemia.
Investigation
- Under about 55 with no alarm features: "test and treat" for H. pylori with a breath or stool test.
- Older patients or anyone with alarm features (dysphagia, weight loss, anaemia, vomiting, bleeding, epigastric mass, family history of gastric cancer): endoscopy.
- Endoscopy is the diagnostic investigation of choice for ulcers.
- Every gastric ulcer is biopsied, and endoscopy is repeated about 6 weeks later to confirm healing.
Treatment
H. pylori positive ulcer: eradication therapy, then confirm cure.
| Regimen | Drugs | Duration |
|---|---|---|
| Triple therapy (where clarithromycin resistance is low) | PPI (e.g. omeprazole 20 mg) + clarithromycin 500 mg + amoxicillin 1 g, all twice daily | 7 or 14 days |
| Penicillin allergy | PPI + clarithromycin + metronidazole 400 mg, twice daily | 7 or 14 days |
| Bismuth quadruple therapy (first-line where clarithromycin resistance is high, and for failures) | PPI + bismuth + tetracycline + metronidazole | 14 days |
| Rescue options | Levofloxacin-based or rifabutin-based regimens, guided by culture | Specialist |
- In Pakistan, metronidazole and clarithromycin resistance are high (metronidazole is widely used for gut infections), so bismuth quadruple or longer regimens are often preferred. Follow current national or hospital guidance, as resistance patterns change.
- Bismuth turns the stool and tongue black; metronidazole with alcohol causes a disulfiram-like reaction.
- Confirm eradication with a urea breath test or stool antigen after the course has finished (off PPI for 2 weeks); after a complicated ulcer this is done about 6 weeks after treatment. Checking cure is essential after a complicated ulcer (bleeding or perforation).
H. pylori negative / NSAID ulcer: stop the NSAID and give a full course of PPI until healing.
Stopping smoking speeds healing. Elective surgery (vagotomy, partial gastrectomy) is now rarely needed.
Complications
1. Bleeding (commonest)
- Haematemesis and/or melaena; may cause shock.
- Resuscitate (IV access, fluids, blood), risk-score (Glasgow–Blatchford before endoscopy, Rockall after), and do endoscopy within 24 hours.
- Endoscopic therapy for high-risk stigmata (active bleeding, visible vessel): adrenaline injection plus clips or thermal coagulation.
- High-dose IV PPI after endoscopic haemostasis.
- Repeat bleeding: repeat endoscopy, angiographic embolisation, or surgery.
Bleeding is the commonest complication of peptic ulcer; an anterior duodenal ulcer is the one that typically perforates.
2. Perforation
- Duodenal ulcers perforate more often than gastric, usually the anterior wall.
- Sudden severe epigastric pain spreading over the abdomen, board-like rigidity, absent bowel sounds, shoulder-tip pain; may be painless in the elderly or on steroids.
- Erect chest X-ray: gas under the diaphragm; CT is more sensitive.
- Treatment: resuscitation, nasogastric tube, IV antibiotics and PPI, then laparoscopic or open closure with an omental patch and peritoneal washout. Conservative care only for unfit patients with a sealed perforation.
3. Gastric outlet obstruction (pyloric stenosis)
- From scarring or oedema of a pyloric or duodenal ulcer; today gastric cancer is also a common cause.
- Large-volume projectile vomiting of undigested food eaten many hours earlier, without bile; weight loss; visible peristalsis; succussion splash.
- Biochemistry: hypochloraemic, hypokalaemic metabolic alkalosis. The kidney later swaps H+ for Na+ to save sodium and water, so the urine becomes acidic: paradoxical aciduria.
- Treatment: IV 0.9% saline with potassium, nasogastric drainage, IV PPI; endoscopy and biopsy; balloon dilatation or surgery (gastrojejunostomy) if it does not settle.
Do not correct the alkalosis with acid. Replace chloride and potassium with normal saline plus KCl; the kidney then corrects the alkalosis.
4. Penetration
Into the pancreas (back pain, raised amylase) or other organs.
Long-term effects of old ulcer surgery
Dumping (early: fluid shift after meals; late: reactive hypoglycaemia), diarrhoea after vagotomy, iron and B12 deficiency, weight loss, recurrent ulcer (exclude H. pylori and Zollinger–Ellison).
Expect: features of H. pylori (urease, spiral Gram-negative, CagA), autoimmune versus H. pylori gastritis, DU versus GU features, the test of choice to confirm eradication (breath or stool, not serology), stopping PPIs before testing, triple and bismuth quadruple regimens, black stool with bismuth, NSAID ulcer prevention with PPI or misoprostol, biopsy of all gastric ulcers, MALT lymphoma regression after eradication, Zollinger–Ellison, and the three complications: bleeding, perforation (gas under diaphragm) and outlet obstruction (hypochloraemic hypokalaemic alkalosis with paradoxical aciduria).
Quick revision
- H. pylori: spiral Gram-negative, urease, antrum; very common in Pakistan.
- Antral infection → high gastrin → high acid → DU.
- Autoimmune gastritis: body/fundus, achlorhydria, pernicious anaemia.
- DU commoner, cap, hunger and night pain; GU lesser curve, always biopsy.
- Breath or stool test to confirm cure; stop PPI 2 weeks before.
- Triple: PPI + clarithromycin + amoxicillin twice daily; quadruple adds bismuth + tetracycline + metronidazole.
- NSAID ulcer: stop NSAID, PPI; misoprostol alternative.
- Bleeding commonest complication; DU perforates more often; outlet obstruction gives hypochloraemic hypokalaemic alkalosis.
- Recurrent, distal or multiple ulcers with diarrhoea: gastrinoma.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine; Bailey & Love's Short Practice of Surgery).
FAQ
Which test confirms that H. pylori has been eradicated?
A urea breath test or stool antigen test done after treatment has finished (about 6 weeks later after a complicated ulcer), with PPIs stopped for 2 weeks beforehand; serology is not suitable.
Why is a gastric ulcer biopsied but a duodenal ulcer usually not?
Gastric cancer can look exactly like a benign gastric ulcer, whereas duodenal ulcers are almost never malignant.
What is paradoxical aciduria in gastric outlet obstruction?
Despite a metabolic alkalosis, the kidney excretes acid urine because, with low potassium and volume depletion, it retains sodium by exchanging it for hydrogen ions.
Why is bismuth quadruple therapy often preferred in Pakistan?
Resistance to clarithromycin and metronidazole is common, which makes standard triple therapy fail more often.