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PH-GI13

Precancerous changes of the stomach

How long-standing Helicobacter pylori or autoimmune gastritis wears away the stomach’s glands, how intestinal metaplasia and dysplasia follow (the Correa cascade), which gastric polyps can turn malignant, and what losing acid does.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Describe the normal gastric mucosa of the body and antrum and how it renews itself.
  • Compare Helicobacter pylori gastritis and autoimmune gastritis: where they sit, how they injure the mucosa and what they do to acid and gastrin.
  • Explain the sequence from chronic gastritis through atrophy, intestinal metaplasia and dysplasia to intestinal-type adenocarcinoma, and why it is not inevitable.
  • Distinguish fundic gland polyps, hyperplastic polyps and gastric adenomas by their background mucosa and malignant potential.
  • Relate anaemia, high gastrin and low pepsinogen to the loss of specialised glands.
  • Recognise the classic appearances, staging concepts (Correa cascade, OLGA and OLGIM) and tests of precancerous gastric changes, and explain how H. pylori eradication, acid suppression, endoscopic resection and vitamin replacement act on them.

What it is

Precancerous changes of the stomach are mucosal states from which gastric adenocarcinoma can arise. Most begin with chronic gastritis, from Helicobacter pylori or autoimmunity, which can lead to atrophy (loss of glands), intestinal metaplasia and then dysplasia, the directly precancerous change. Some gastric polyps, above all adenomas, also carry malignant potential.

4 types to tell apart
Helicobacter pylori gastritis
The commonest cause worldwide; begins in the antrum and can spread through the body as multifocal atrophic gastritis.
Autoimmune gastritis
Immune destruction of parietal cells, confined to the body and fundus; causes loss of acid and intrinsic factor and very high gastrin.
Intestinal metaplasia and dysplasia
Metaplasia replaces lost glands with intestinal-type cells; dysplasia is neoplastic epithelium that has not yet invaded, graded low or high.
Gastric polyps
Fundic gland polyps (negligible risk when sporadic), hyperplastic polyps (rare dysplasia) and adenomas (true neoplasms).

Normal function

Pits, glands and a lining renewed every few days

The stomach lining is a columnar mucosa folded into . Mucus-secreting surface cells line the pits and cover the surface with mucus and bicarbonate. Below them, tubular glands reach down through the to the . The healthy stomach has no goblet cells.

The glands differ by region. In the body and fundus, oxyntic glands hold parietal cells, which secrete acid and intrinsic factor, chief cells, which secrete pepsinogen, and enterochromaffin-like (ECL) cells, which release histamine. In the antrum, mucous glands hold G cells, which secrete gastrin, and D cells, which secrete somatostatin. Gastrin drives acid; acid in the antrum turns gastrin down through somatostatin, a negative feedback loop.

Stem cells in the neck of each gland renew the surface cells every few days and the gland cells more slowly. This constant renewal repairs daily wear, but it also means that years of injury force a great many cell divisions.

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