Peptic Ulcer And Gastric Mucosal Barrier

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Ulcers in the stomach or duodenum may be acute or chronic, both

penetrate the muscularis mucosal but acute ulcer shows no evidence of

fibrosis, erosions do not penetrate the muscularis mucosa.(

Patients with peptic ulcer often have a family history of the disease.

This is particularly the case with duodenal ulcers which develop below the

age of 20 yrs.


The gastric mucosa has an extraordinary capacity to secrete acid.

Peptic cells (or) chief cells which present in fundus of the stomach secrete

pepsin. Parietal cells scatered along the course of body and fundus secrete

HCl by a process involving oxidative phosphorylation.

The estimated concentration of HCl secreted by parietal cells is

approximately 160mm. Each secreted hydrogen ion (H+) is accompanied

by a chloride ion (Cl-). For each hydrogen ion secreted into the gastric

human, one bicarbonate ion is released in to the gastric venous circulation,

accounting for so called alkaline tide, bicarbonate is released from

carbonic acid generated from carbon dioxide by parietal cell carbonic


Several mechanisms protect the gastric mucosa from hydrogen ions

secreted into the lumen of the stomach. The surface epithelial cells

secrete bicarbonate which creates an alkaline tale at the surface of the

mucosa. This bicarbonate secretion is under the influence of mucosal

prostaglandins. The tight junctions between the epithelial cells and their

surface lipoprotein layer provide a mechanical barrier. The normal

turnover of epithelial cells and gastric mucus also has a protective function.

Collectively all these mechanisms can be described as the ‘Gastric

mucosal barrier’.

Peptic ulcer disease is thought to result from an imbalance between

gastric acid, pepsin and protective factors (mucosal barrier).


Several drugs, particularly those used in rheumatoid arthritis, will

disrupt the gastric mucosal barrier. When as a pH below 3.5 it is

undissociated and fat soluble, so that it is absorbed through the lipoprotein

membrane of the surface epithelial cells, during absorption it damages the

membrane and the tight junctions. It also inhibits prostaglandin shynthesis

thus reducing bicarbonate secretion by the surface epithelial cells. Aspirin

has been shown to be an important etiological factor in gastric ulcer in

Australia, and this may also be so in other countries where is a high

consumption of aspirin


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