Gastritis

On this page
  1. Direct answer
  2. What you must remember
  3. Common confusion
  4. Exam-focused takeaway
  5. Frequently asked questions
  6. Related topics

Direct answer

Gastritis is inflammation of the gastric mucosa, of which Helicobacter pylori infection is the commonest cause worldwide, followed by autoimmune gastritis. H. pylori — a urease-producing, curved Gram-negative rod colonising the antrum — causes neutrophilic and lymphoplasmacytic gastritis that underlies most peptic ulcers, and through CagA-driven chronicity predisposes to gastric adenocarcinoma and MALT lymphoma. Autoimmune gastritis destroys the acid-secreting body-fundus mucosa with anti-parietal cell and anti-intrinsic factor antibodies, producing pernicious anaemia, achlorhydria with hypergastrinaemia and enterochromaffin-like cell hyperplasia.

What you must remember

  • Helicobacter pylori: spiral, urease-positive Gram-negative bacilli beneath the mucus layer; diagnosed by biopsy urease test, histology, urea breath test or stool antigen; eradication with acid suppression plus antibiotics per current guidance.
  • H. pylori gastritis: antral-predominant disease spares acid secretion and drives duodenal ulceration, whereas pangastritis with atrophy and intestinal metaplasia lowers acid and raises gastric cancer risk; CagA-positive strains are the most virulent.
  • Autoimmune gastritis: body and fundus mucosa destroyed with lymphoplasmacytic inflammation; anti-parietal cell and anti-intrinsic factor antibodies; achlorhydria and raised gastrin cause enterochromaffin-like hyperplasia with carcinoid tumour risk; vitamin B12 malabsorption gives megaloblastic pernicious anaemia with neurological sequelae.
  • Acute (erosive) gastritis: NSAIDs, alcohol, stress ulcers in burns and neurosurgery (Cushing) and extensive trauma (Curling), uraemia and bile reflux cause neutrophil-rich mucosal erosions and haemorrhage.
  • Menetrier disease: massive foveolar hyperplasia yielding giant cerebriform rugal folds, protein-losing enteropathy with hypoalbuminaemia and hypochlorhydria; a premalignant condition needing surveillance.
  • Complications of chronic gastritis: peptic ulcer disease, gastric adenocarcinoma (intestinal type) and extranodal marginal zone (MALT) lymphoma that may regress after H. pylori eradication.
  • Reactive (chemical) gastropathy: bile reflux after gastrectomy and chronic NSAID exposure cause foveolar hyperplasia without prominent inflammation — a recognised mimic.

Common confusion

Antral versus body disease decides the mechanism: H. pylori antral gastritis leaves acid high and ulcers duodenal, while autoimmune body gastritis leaves acid absent and B12 low — a distinction constantly retested. Do not confuse Menetrier disease (giant folds with protein loss) with gastritis of H. pylori; nor MALT lymphoma (antibiotic-responsive in early stage) with diffuse large B-cell lymphoma of the stomach. Stress ulcer names are also mixed: Curling for burns and intensive-care stress, Cushing for intracranial disease.

Exam-focused takeaway

Vignettes show epigastric pain with a positive urea breath test (H. pylori), a middle-aged woman with glossitis, paraesthesiae and macrocytic anaemia (pernicious), or hypoalbuminaemia with giant folds on endoscopy (Menetrier). Questions ask the antibody pair, the tumour risks of chronic gastritis, and which tests confirm infection. Link organism to ulcer and to cancer in one chain — H. pylori, gastritis, ulcer, adenocarcinoma, MALToma.

Frequently asked questions

Which organism causes most chronic gastritis?

Helicobacter pylori, a urease-positive curved Gram-negative rod that colonises the gastric antrum beneath mucus.

What antibodies define autoimmune gastritis?

Anti-parietal cell and anti-intrinsic factor antibodies, causing achlorhydria and vitamin B12-deficient pernicious anaemia.

Why does autoimmune gastritis raise gastrin?

Loss of acid secretion removes feedback on antral G cells, so gastrin rises continuously and drives enterochromaffin-like hyperplasia with carcinoid risk.

What is Menetrier disease?

A hyperproliferative gastropathy with giant rugal folds, foveolar hyperplasia, protein-losing enteropathy and hypoalbuminaemia.

Which malignancies complicate chronic H. pylori gastritis?

Intestinal-type gastric adenocarcinoma and gastric MALT lymphoma — the latter often regressing after bacterial eradication.

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