10.2: Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.

In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.

In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.

Gastritis can stem from various causes, each with its distinct pathophysiology.

1. Medications like non-steroidal anti-inflammatory drugs or NSAIDs such as aspirin and indomethacin inhibit an enzyme called cyclooxygenase-1 or COX-1, which plays a vital role in producing prostaglandins. Prostaglandins are essential for maintaining mucus and bicarbonate secretion, mucosal blood flow, cell turnover, and repair, which are necessary for mucosal integrity. As a result, the inhibition of COX-1 by NSAIDs compromises these defense mechanisms, predisposing the gastric mucosa to injury from gastric acid. NSAIDs can trigger acute gastritis; however, they can also play a role in the development of chronic gastritis.
2. Alcohol, another common cause of acute gastritis, causes direct mucosal injury and increases gastric acid secretion while decreasing prostaglandin synthesis. Conversely, chronic gastritis develops over a more extended period and is often asymptomatic until later stages.
3. Helicobacter pylori (H. pylori), a gram-negative bacterium, is the primary cause of chronic gastritis worldwide. H. pylori generates an enzyme called urease, which converts urea to ammonia to survive in the stomach's acidic environment. Ammonia reduces the stomach acidity, making it a more hospitable environment for the bacterium.
   The spiral shape of H. pylori allows it to penetrate the mucus layer, which is less acidic than the stomach's inner lining. H. pylori can also attach itself to the cells that line the stomach's inner surface. When the immune system detects an H. pylori infection, immune cells gather at the site to kill the invading bacteria. However, they cannot prevent the erosion of the stomach lining caused by the bacterium.
4. Autoimmune gastritis is a less common type of chronic gastritis, where the body's immune system produces autoantibodies that target and attack the parietal cells in the stomach lining, leading to continuous destruction of parietal cells resulting in the atrophy or thinning of the stomach lining.