Tuesday, July 12, 2011

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Chronic gastritis/peptic ulcer - pathogenesis

Peptic ulcers are created by an imbalance between the gastroduodenal mucosal defenses and the damaging forces that overcome such defenses. It is very well depicted above.

H.pylori does not invade the tissues but it causes intense local inflammation. It has flagella that allows it to move in the viscous mucous. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucous, thus weakening the first line of mucosal defense. It also produces urease that breaks down endogenous urea to form ammonia. This causes the pH to increase locally. The H.pylori also has adhesins that make it bind to the cells and finally they elaborate toxins that cause further damage like metaplasia.

NSAIDs and aspirin are inhibitors of cyclooxygenase (COX). Thus they prevent the synthesis of prostaglandins. The latter is responsible for the promotion of mucin synthesis and vasodilation. In the absence of prostaglandins, the mucinous layer is depleted and the decreased vascular perfusion does not help in the regeneration of the damaged layer.

Ischaemia, shock and cigarette smoking also act by decreasing the blood flow.


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