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Review
. 2001 Oct 27;323(7319):980-2.
doi: 10.1136/bmj.323.7319.980.

ABC of the upper gastrointestinal tract: Pathophysiology of duodenal and gastric ulcer and gastric cancer

J Calam, J H Baron
Review

ABC of the upper gastrointestinal tract: Pathophysiology of duodenal and gastric ulcer and gastric cancer

J Calam et al. BMJ. .
No abstract available

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Figures

Figure
Figure
Relation of H pylori infection to upper gastrointestinal conditions
Figure
Figure
Autoregulation of acid secretion. Food stimulates release of gastrin from antral G cells (G). Gastrin stimulates enterochromaffin-like cells (ECL) to release histamine, which stimulates parietal cells (P) in the gastric corpus to secrete acid. Acid stimulates release of somatostatin from somatostatin cells (S) in the antrum, inhibiting further gastrin release
Figure
Figure
With acid hyposecretion (left), the main effect of H pylori gastritis affecting the gastric body is to suppress parietal cells, leading to low acid secretion, which is associated with gastric cancer. With acid hypersecretion (right), antral H pylori gastritis increases acid secretion by suppressing somatostatin and elevating gastrin release, increasing the risk of duodenal ulceration. Orange areas indicate extent and location of gastritis
Figure
Figure
Intestinal metaplasia of antral mucosa. Inset shows large goblet cells packed with mucin (shown by Alcian blue staining)
Figure
Figure
Duodenum with gastric metaplasia and mild inflammation. Inset shows H pylori adhering to surface epithelial cells
Figure
Figure
Transmission electron micrograph of duodenal gastric metaplasia with H pylori attached to the apical surface (arrows)
See this image and copyright information in PMC

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