BackgroundGastritis refers to an array of entities that cause inflammation in the gastric mucosa (Feldman, et al. 2002). The clinical presentation of gastritis differs in histologic characteristics. The inflammation may present in the whole stomach or part of the stomach. The most common symptom of gastritis is epigastric discomfort. Loss of appetite, bloating, nausea, vomiting and sometimes abdominal pain is also symptoms associated with gastritis. Gastritis accounts for as many as 2 million doctor’s office visits each year in the US. Gastritis is common especially in individuals over the age of 60 (Jensen, et al., 2016).
Pathophysiology
Gastritis can be caused in a number of ways including from bile, infections, stress, radiation, drugs and alcohol, food poisoning and trauma. The most common cause of gastritis is from the bacterium called H pylori. (Sonnenberg, & Genta, 2016). The prevalence of this bacterium varies depending on country of origin, socioeconomic class and age and typically, the number of people infected with this bacterium increases with age in the Western world.
The H. pylori infection is found in approximately 20% of people under the age of 40 years and 50% in people older than aged 60. The transmission of this bacterium is not fully understood, although transmission occurs from ingesting contaminated food or water and through oral-fecal transmission. This explains the high prevalence of this bacterium in lower socioeconomic areas. This bacterium is attributed to 60% and 80% of gastritis and duodenal ulcers, respectively.
Bacterium associated gastritis usually begins as a gastritis in the antrum which causes an individual to have intense inflammation and with time may involve the whole gastric mucosa.
Acute gastritis associated with this bacterium does not typically present with symptoms. The bacterium is protected from a layer of mucous and is protected from stomach acid through a production of an enzyme that is responsible for breaking down urea into ammonia and carbon dioxide. This ammonia neutralizes acid in the area of the bacterium providing protection.
Diagnosis and Treatment
Gastritis is diagnosed through a review of patient history and through a physical examination and recommended tests (Anderson, 2007). One test is an upper endoscopy. In this process, a small camera is inserted into the stomach lining. The physician will assess inflammation and may perform a biopsy. Gastritis can also be diagnosed through a blood test to assess red blood cell counts to assess anemia. A blood test can also screen for bacterium H. pylori . A fecal occult blood test, or commonly called a stool test is another method of diagnosing gastritis.
A variety of treatments exist for gastritis which involves taking antacids and medications such as H-2 blockers to reduce the amount of acid in the stomach. People with gastritis should avoid eating hot or spicy food. For gastritis that is a result of a bacterium infection acid blocking medications are recommended. If the gastritis is caused by anemia, vitamin B12 shot are indicated. The prognosis for gastritis is good as most people improve rapidly once diagnosed and treated.
Conclusion
Gastritis refers to an array of entities that cause inflammation in the gastric mucosa. The most common symptom of gastritis is epigastric discomfort. Loss of appetite, bloating, nausea, vomiting and sometimes abdominal pain is also symptoms associated with gastritis. Gastritis can be caused in a number of ways including from bile, infections, stress, radiation, drugs and alcohol, food poisoning and trauma. The most common cause of gastritis is from the bacterium called H pylori. The number of people infected with this bacterium increases with age in the Western world. Gastritis is diagnosed through a review of patient history and through a physical examination and recommended tests. The prognosis for gastritis is good as most people improve rapidly once diagnosed and treated. The Appendix provides an illustration of the epidemiology, diagnosis, treatment and physiology of gastritis.
- Andersen, L.P. (2007) Colonization and infection by Helicobacter pylori in humans. Helicobacter, 12(2), 12-15
- Jensen, E.T, Martin, C.F., Kappelman, M.D., & Dellon, E.S. (2016). Prevalence of eosinophilic gastritis, gastroenteritis, and colitis: estimates from a national administrative database. J Pediatr Gastroenterol Nutr. 62(1), 36-42
- Feldman, S., Sleisenger, P. & Fordtran, M. (2002). Gastrointestinal and Liver Disease (7th ed.). 810-823.
- Sonnenberg, A.,& Genta, R.M(2016). Inverse association between Helicobacter pylori gastritis and microscopic colitis. Inflamm Bowel Dis. 22(1):182-6.
