Pathogenesis and Prevention

Gastritis is a mucosal inflammation of the membrane lining of the stomach. It may result in an uncomfortable feeling in the stomach, distention of the abdomen, headache, nausea, coated tongue, and a bad taste in the mouth. In severe cases, all these symptoms will be worse, and there will be upper abdominal pain, tenderness, vomiting, fever, and sometimes bleeding from the stomach. Other causes of gastritis, asisde from aspirin misuse, are overeating, eating indigestible food, exposure to wet or cold weather, toxic infections, food poisoning, or allergy.

If the errors that caused the disease have been practiced so long that the stomach gland, when viewd with the use of medical microscopes, have completely degenerated and a real cure is not possible. In case the lining of the stomach is swollen and spongy rather than atrophic, the symptoms may be much like those of peptic ulcer, and the treatment should be the same.

The gross endoscopic diagnosis of gastritis correlates poorly with histologic findings when examined under laboratory microscopes, and is thus relatively useless as a diagnosis without confirmatory biopsy when tested with laboratory microscopes. Addi¬tionally, there is poor correlation between symptoms and histologic gastritis when samples are studied under laboratory microscopes. The most common cause of gastritis is H. pylori. Other causes of gastritis include alcohol, NSAIDs, Crohn’s disease, tu¬berculosis, and bile reflux (primary or secondary). These agents delay injury by a variety of different mechanisms. In general, the infectious and inflammatory causes result in immune cell infiltration and cytokine production, which damage mucosal cells when these tissues are examined under laboratory microscopes. The chem¬ical agents such as alcohol, aspirin, and bile generally work to disrupt the mucosal barrier, allowing mucosal damage by back-diffusion of luminal hydrogen ions and making them susceptible to bacteria such as H. pylori.

Stress gastritis is a peculiar entity that has all but disappeared from the clinical (if not endoscopic) help biology vocabulary, largely due to better critical care and acid suppression or agents that protect cell damage in the intensive care unit (ICU). Stress gastritis and stress ulcer are probably due to inadequate gastric mucosal blood flow during periods of intense stress. Adequate mucosal blood flow is important to maintain the mucosal barrier, as evidenced by microscopic studies, and to buffer any back diffused hydrogen ions. When blood flow is inadequate, these pro¬cesses fail and mucosal breakdown occurs. While it is still common to see small mucosal erosions when performing endoscopy in the ICU with the help of laboratory microscopes, it is rare for these lesions to coalesce into the larger bleeding erosions that plagued the ICU patient 30 years ago. In the extraordi¬narily rare patient requiring operation today for hemorrhagic stress gastritis, the surgical options include vagotomy and drainage with oversewing of the major bleeding lesions, or near total gastrectomy. The surgical introduction of various substances into the circulatory system to obstruct specific blood vessels and endoscopic haemostatic treatment should at least be considered as well.