Gastritis-II: Pathophysiology

NSAIDs inhibit cyclooxygenase-1, an enzyme essential for prostaglandin production. Prostaglandins maintain mucosal integrity, mucus and bicarbonate secretion, and mucosal blood flow. When NSAIDs reduce prostaglandin levels, the stomach lining becomes vulnerable to gastric juice damage, leading to inflammation and erosion of the gastric mucosa.

H. pylori produces urease, an enzyme that converts urea to ammonia, creating a less acidic environment favorable for bacterial survival. This adaptation allows the bacterium to penetrate the mucus layer and attach to stomach cells. Once established, H. pylori triggers an immune response and releases toxins, resulting in mucosal inflammation and damage.

Acute gastritis causes the gastric mucosa to become hyperemic and edematous with superficial erosion, potentially leading to bleeding. Chronic gastritis develops over an extended period from persistent or repeated insults, causing chronic inflammatory changes and eventual thinning or atrophy of gastric tissue. Chronic gastritis is often asymptomatic until later stages.

Alcohol causes direct mucosal injury to the stomach lining and increases gastric acid secretion while decreasing prostaglandin synthesis. This dual mechanism compromises the stomach's protective mechanisms, making the mucosa more susceptible to damage from digestive juices and triggering acute gastritis.

In autoimmune gastritis, the immune system produces autoantibodies that target and attack parietal cells in the stomach lining. This continuous destruction of parietal cells leads to atrophy or thinning of the gastric tissue. Autoimmune gastritis is a less common type of chronic gastritis with progressive mucosal damage.

The mucosal barrier protects stomach tissue from digestive juices through mucus and bicarbonate secretion, mucosal blood flow, cell turnover, and repair mechanisms. When this barrier is disrupted by NSAIDs, alcohol, H. pylori, or autoimmune attack, the gastric mucosa becomes hyperemic and edematous, leading to inflammation and erosion.

The spiral shape of H. pylori allows it to penetrate the mucus layer, which is less acidic than the stomach's inner lining. This morphology enables the bacterium to reach and attach to cells lining the stomach's inner surface, establishing chronic infection. Understanding these mechanisms helps explain gastritis iii clinical manifestations and management in clinical practice.