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.
ACID – PEPSIN THEORY : VERSUS MUCOSAL RESISTANCE
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
Peptic ulcer disease is thought to result from an imbalance between
gastric acid, pepsin and protective factors (mucosal barrier).
FACTORS REDUCING MUCOSAL RESISTANCE & NSAIDS
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