Pathophysiology of Chronic Gastritis

Pathophysiology of Chronic Gastritis
Chronic gastritis can be classified as type A or type B.

Type A (often referred to as autoimmune gastritis) resulting from changes in parietal cells, leading to atrophy and cell infiltration. It is associated with autoimmune diseases, such as pernicious anemia and occurs in the fundus or corpus of the stomach.

Type B (sometimes referred to as Helicobacter pylori, also known as H. pylori) is associated with the bacteria H. pylori, dietary factors such as heat or spicy drink, use drugs and alcohol, smoking or reflux of intestinal contents into the stomach. H. Pylori includes bacteria that are not acid resistant, but this kind of bacteria are able to secure himself in the mucosal lining of the stomach. The presence of this bacterium in gastric mucosa of the stomach lining causing weakening and brittle so that stomach acid can penetrate the layer. Thus both gastric acid and the bacteria causing wound or ulcer. The immune system will respond to bacterial infection H. Pylori by sending beads of leukocytes, killer T cells, and other infection-fighting. However, it is not able to fight infection H. The reason pylori can not penetrate the stomach lining. But also can not be removed so that the immune response continues to increase and grow. Polymorph die and release of superoxide radicals damaging compounds in the cells lining the stomach. Extra nutrients are sent to strengthen the leukocyte cells, but nutrition is also a source of nutrients for H. Pylori. Finally, the state of the damaged epithelium of the stomach, forming a superficial ulceration and can cause hemorrhage (bleeding). Within a few days gastritis and even peptic ulcers are formed.

Related Articles :