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PH-GI24

Gastritis

How NSAIDs, alcohol and critical illness erode the stomach lining within hours, how Helicobacter pylori and autoimmunity inflame it for decades in different regions, how chemical gastropathy differs, and how the Sydney system describes it.

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  • 6 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Distinguish acute from chronic gastritis by the cells present, and gastritis from gastropathy.
  • Explain how NSAIDs, alcohol, bile and poor mucosal blood flow in critical illness breach the mucosal barrier and cause erosions and bleeding.
  • Compare Helicobacter pylori gastritis, autoimmune gastritis and reactive gastropathy by site, histology and effect on acid, gastrin and absorption.
  • Explain why the site of chronic gastritis predicts high or low acid and which complications follow.
  • Describe a gastritis with the updated Sydney system, recognise its tests and classic biopsy appearances, and explain how acid suppression, mucosal protectants, H. pylori eradication and vitamin B12 act on the mechanism.

What it is

Gastritis is inflammation of the stomach lining (gastric mucosa). Acute gastritis is short-lived, with neutrophils, oedema and often erosions and bleeding; chronic gastritis lasts months to decades, with lymphocytes and plasma cells, and is mainly caused by Helicobacter pylori or autoimmunity. Injury and regeneration with little inflammation, as from bile or long-term NSAIDs, is called gastropathy.

5 types to tell apart
Acute erosive (haemorrhagic) gastritis
Chemical injury (NSAIDs, alcohol, corrosives) or poor mucosal blood flow in critical illness (stress gastritis); erosions and bleeding within hours to days.
Chronic Helicobacter pylori gastritis (type B)
The commonest gastritis worldwide: a chronic active gastritis that starts in the antrum and can spread through the body.
Autoimmune gastritis (type A)
Immune destruction of parietal cells in the body and fundus, sparing the antrum; leads to loss of acid and intrinsic factor and to pernicious anaemia.
Reactive (chemical) gastropathy (type C)
Repeated injury from bile reflux, long-term NSAIDs or alcohol; regenerating, hyperplastic pits with few inflammatory cells.
Uncommon forms
Lymphocytic and eosinophilic gastritis, granulomatous gastritis (Crohn’s disease, sarcoidosis), infections such as cytomegalovirus in people with weak immunity, and radiation injury.

US spelling: oedema → edema.

Normal function

A barrier over a quiet lamina propria

The surface of the stomach is a sheet of mucus-secreting cells over . Its defences, described in peptic ulcer disease, are a mucus–bicarbonate layer, tight junctions, rapid renewal and a rich blood flow, all sustained by prostaglandins. Together they form the gastric mucosal barrier: they keep hydrogen ions in the lumen, and blood flow carries away any acid that enters the tissue.

In the healthy stomach the between the glands holds only scattered lymphocytes and plasma cells, with no neutrophils and no lymphoid follicles. Pathologists read gastritis against this baseline: neutrophils mark acute or active injury, an excess of lymphocytes and plasma cells marks chronic gastritis, and fewer glands above the mark atrophy.

The regions differ. The body and fundus carry oxyntic glands with acid-secreting parietal cells; the antrum carries mucous glands with gastrin-secreting G cells. Because each cause of gastritis prefers one region, biopsies from both are needed to name the type.

Point to it on the model