domingo, 25 de marzo de 2007

Fisiopatologia Ulcerosa

Pathophysiologic defects in some patients with:

A. Peptic ulcer disease/gastric ulcer disease

Decreased acid secretion, decreased parietal cell mass (PCM), back-diffusion of acid

Chronic superficial and atrophic gastritis

Increased concentration of bile acids and pancreatic juice in stomach (duodenogastric reflux)

Delayed gastric emptying

Inappropriately decreased pyloric sphincter pressure under basal conditions and in response to
acid (secretin) or fat (cholecystokinin) in the duodenum

B. Duodenal ulcer disease

Increased parietal cell mass

Increased sensitivity of parietal cells to gastrin and secretagogues

Increased secretory drive

Decreased acid-induced inhibition of meal-stimulated gastrin release

Increased gastric emptying

Increased duodenal acid/pepsin loads

Chronic active gastritis

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