Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores in the mucosa of the stomach or duodenum.

The mucosal epithelium houses acid-secreting parietal and gastrin-secreting G cells.

The vagus nerve releases acetylcholine and GRP.

GRP stimulates antral G cells to secrete gastrin that binds to gastrin-cholecystokinin receptors on parietal and enterochromaffin-like cells. Acetylcholine binds to muscarinic receptors on these cells.

Acetylcholine or gastrin binding in ECL cells stimulates the histamine release, which attaches to H₂ receptors, initiating the cyclic AMP pathway and activating the proton pump for acid production.

In the parietal cells, gastrin and acetylcholine binding activates the Ca²⁺-dependent pathway and increases cytosolic calcium levels, stimulating gastric acid secretion.

In a healthy stomach, the antral D cells produce somatostatin, which inhibits gastrin secretion.

However, H. pylori infection decreases D cell count, reducing somatostatin production. This increases gastrin secretion and acid production, further contributing to ulcer development.