10.5 : Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.

Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.

1. Helicobacter pylori Infection: Peptic ulcers result from H. pylori infections. This bacterium erodes the protective mucous layer, causing mucosal damage and inflammation.
2. Gastric Acid and Pepsin: While essential for digestion, excessive or prolonged exposure to these substances can damage the mucosa and lead to ulcers.
3. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Frequent NSAID use can lead to peptic ulcers by hindering prostaglandin production. Prostaglandins are crucial for the gastric mucosal barrier's maintenance, offering protection through mucus and bicarbonate secretion, regulating blood flow for nutrient supply and toxin elimination, curbing gastric acid production, and fostering cell repair. NSAIDs compromise these protective mechanisms.

On the protective side:

1. Mucosal Barrier: The mucosa of the stomach and duodenum has a protective barrier against acid and pepsin. Its impairment makes the tissue susceptible to ulcers.
2. Bicarbonate Secretion: Bicarbonate from the stomach and duodenal cells neutralizes gastric acid, shielding the mucosa.
3. Blood flow: Adequate blood flow is required to keep the mucosa healthy. Reduced blood flow can cause damage and lead to ulcers.

The interplay of these factors either heightens acid-pepsin levels or weakens the mucosal barrier's resistance. Damaged mucosa struggles to produce sufficient mucus as a defense, leading to inflammation, harm, and mucosal erosion.