Acute gastritis and stress ulcers

Lesion

Painkillers, alcohol, bile and severe illness can strip the stomach's protective layer, leading to erosions, bleeding and small ulcers.

Updated Nov 12, 2026

Key points

NSAIDs block COX-1 and COX-2, removing prostaglandins E2 and I2 that drive mucus, bicarbonate, blood flow and repair; even selective COX-2 drugs can injure.
Other causes: alcohol, bile reflux, uraemia, chemotherapy, radiation, caustic ingestion, high altitude.
Neutrophils above the basement membrane mean active inflammation (gastritis); in the gut ‘acute’ refers to duration, not to the cell type.
Stress ulcers: multiple, small, anywhere in the stomach, in shock, sepsis or trauma; mainly ischaemic.
Curling ulcer: proximal duodenum or stomach after severe burns or trauma. Cushing ulcer: stomach, duodenum or oesophagus with intracranial disease, from vagal acid hypersecretion; perforates more often.
Other bleeding sources: Dieulafoy lesion (large submucosal arteriole) and gastric antral vascular ectasia (watermelon stomach).

What it is

The stomach survives an acid close to pH 1 thanks to layered defences: mucus and phospholipids, a bicarbonate-rich unstirred layer, tight epithelium that renews itself within days, prostaglandins, and a rich blood supply. When injury outweighs defence the mucosa is damaged. Pathologists call it gastritis when neutrophils are present and gastropathy when inflammatory cells are scarce. Severe physiological stress causes a distinct, ischaemic form: stress-related mucosal disease.

Structure

Reactive gastropathy: oedema, vascular congestion, foveolar hyperplasia with corkscrew pits, little inflammation.
Acute gastritis: neutrophils within the epithelium or gland lumens.
Erosion: loss of surface epithelium not passing the muscularis mucosae, with fibrin and neutrophils; with haemorrhage, acute erosive haemorrhagic gastritis.
Stress ulcer: round, usually under one centimetre, base stained brown-black by digested blood; sharp edges, normal adjacent mucosa, no scarring or thick vessels (unlike chronic peptic ulcer).

Step by step

An injurious agent or low blood flow weakens one or more defences.
Acid diffuses back into the lamina propria.
Epithelial cells die and capillaries leak; neutrophils may be recruited.
Surface erosions and haemorrhage form.
If the cause is removed, the mucosa re-epithelializes within days to weeks.

Ulcer	Setting	Main mechanism
Stress ulcer	Shock, sepsis, major trauma	Mucosal ischaemia from hypotension and splanchnic vasoconstriction
Curling ulcer	Severe burns or trauma	Ischaemia and hypovolaemia; proximal duodenum and stomach
Cushing ulcer	Intracranial disease or injury	Vagal stimulation and acid hypersecretion; higher risk of perforation

Clinical notes

Most patients in intensive care have some mucosal damage, but clinically significant bleeding is uncommon; acid suppression is used for prevention.
Watermelon stomach is associated with cirrhosis and systemic sclerosis and causes chronic iron deficiency.

Test yourself

Think of the answer, then tap the question to see it.

How do NSAIDs injure the gastric mucosa?

By blocking cyclooxygenase and so the prostaglandins that maintain mucus, bicarbonate, mucosal blood flow and epithelial repair.

What separates gastritis from gastropathy?

Gastritis has neutrophils (active inflammation); gastropathy is mucosal injury with few or no inflammatory cells.

Why are Cushing ulcers thought to form?

Intracranial disease stimulates vagal nuclei, causing gastric acid hypersecretion.

How do acute stress ulcers differ from chronic peptic ulcers?

They are multiple, anywhere in the stomach, and lack the scarring and thickened vessels of chronic ulcers.

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Peptic Ulcer Disease (StatPearls (NCBI Bookshelf), 2025); Upper Gastrointestinal Bleeding (StatPearls (NCBI Bookshelf), 2025).

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