Gastritis

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Gastritis
Classification and external resources

Micrograph showing gastritis. H&E stain.
ICD-10K29.0-K29.7
MedlinePlus001150
eMedicineemerg/820 med/852
MeSHD005756
 
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Gastritis
Classification and external resources

Micrograph showing gastritis. H&E stain.
ICD-10K29.0-K29.7
MedlinePlus001150
eMedicineemerg/820 med/852
MeSHD005756

Gastritis is an inflammation of the lining of the stomach, and has many possible causes.[1] The main acute causes are excessive alcohol consumption or prolonged use of nonsteroidal anti-inflammatory drugs (also known as NSAIDs) such as aspirin or ibuprofen. Sometimes gastritis develops after major surgery, traumatic injury, burns, or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract. Chronic causes are infection with bacteria, primarily Helicobacter pylori, chronic bile reflux, and stress; certain autoimmune disorders can cause gastritis as well. The most common symptom is abdominal upset or pain. Other symptoms are indigestion, abdominal bloating, nausea, and vomiting and pernicious anemia. Some may have a feeling of fullness or burning in the upper abdomen.[2][3] A gastroscopy, blood test, complete blood count test, or a stool test may be used to diagnose gastritis.[4] Treatment includes taking antacids or other medicines, such as proton pump inhibitors or antibiotics, and avoiding hot or spicy foods. For those with pernicious anemia, B12 injections are given.[5]

Contents

Signs and symptoms

A peptic ulcer may accompany gastritis. Endoscopic image.

Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp.[6] Pain is usually located in the upper central portion of the abdomen,[3] but it may occur anywhere from the upper left portion of the abdomen around to the back.

Other signs and symptoms may include:

Causes

Acute

Erosive gastritis is a gastric mucosal erosion caused by damage to mucosal defenses.[2] Alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.[7] NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming.[8] Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis.[9]

Chronic

Chronic gastritis refers to a wide range of problems of the gastric tissues.[2] The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining.[9] In some cases bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, and liver or kidney failure.[10]

Metaplasia

Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum, and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.[2]

Helicobacter pylori

Helicobacter pylori colonizes the stomach of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with Helicobacter pylori results in the development of chronic gastritis in infected individuals and in a subset of patients chronic gastritis progresses to complications (i.e. ulcer disease, gastric neoplasias, some distinct extra gastric disorders).[11] However, gastritis has no adverse consequences for most hosts and emerging evidence suggests that H. pylori prevalence is inversely related to gastroesophageal reflux disease and allergic disorders. These observations indicate that eradication may not be appropriate for certain populations due to the potentially beneficial effects conferred by persistent gastric inflammation.[12]

Diagnosis

Often, a diagnosis can be made based on the patient's description of his or her symptoms, but other methods which may be used to verify gastritis include:

Treatment

Over-the-counter antacids in liquid or tablet form are a common treatment for mild gastritis. Antacids neutralize stomach acid and can provide fast pain relief. When antacids don't provide enough relief, medications such as cimetidine, ranitidine, nizatidine or famotidine that help reduce the amount of acid the stomach produces are often prescribed. An even more effective way to limit stomach acid production is to shut down the acid "pumps" within acid-secreting stomach cells. Proton pump inhibitors reduce acid by blocking the action of these small pumps. This class of medications includes omeprazole, lansoprazole, rabeprazole, and esomeprazole. Proton pump inhibitors also appear to inhibit H. pylori activity.[14] Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate. Many people also drink milk to relieve symptoms, however the high calcium levels actually stimulate release of gastric acid from parietal cells, ultimately worsening symptoms. In addition to protecting the lining of stomach and intestines, bismuth preparations appear to inhibit H. pylori activity as well. Several regimens are used to treat H. pylori infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is also added to the regimen. The antibiotic aids in destroying the bacteria, and the acid blocker or proton pump inhibitor relieves pain and nausea, heals inflammation, and may increase the antibiotic's effectiveness.[15]

See also

References

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  2. ^ a b c d "Gastritis". Merck. January 2007. http://www.merck.com/mmpe/sec02/ch013/ch013c.html. Retrieved 2009-01-11. 
  3. ^ a b "Gastritis". National Digestive Diseases Information Clearinghouse (National Institute of Diabetes and Digestive and Kidney Diseases). December 2004. http://digestive.niddk.nih.gov/ddiseases/pubs/gastritis/. Retrieved 2008-10-06. 
  4. ^ "Gastritis: Diagnostic Tests for Gastritis". Wrong Diagnosis. December 30, 2008. http://www.wrongdiagnosis.com/g/gastritis/intro.htm. Retrieved 2009-01-11. 
  5. ^ "What is Gastritis?". Cleveland Clinic (WebMD). http://www.webmd.com/digestive-disorders/digestive-diseases-gastritis. Retrieved 2009-01-11. 
  6. ^ a b "Gastritis Symptoms". eMedicineHealth. 2008. http://www.emedicinehealth.com/gastritis/article_em.htm. Retrieved 2008-11-18. 
  7. ^ Wolff G (1989). "[Effect of alcohol on the stomach] [Effect of alcohol on the stomach]" (in German). Gastroenterol J 49 (2): 45–9. PMID 2679657. 
  8. ^ Dajani EZ, Islam K (August 2008). "Cardiovascular and gastrointestinal toxicity of selective cyclo-oxygenase-2 inhibitors in man" (PDF). J Physiol Pharmacol. 59 Suppl 2: 117–33. PMID 18812633. http://www.jpp.krakow.pl/journal/archive/0808_s2/pdf/117_0808_s2_article.pdf. 
  9. ^ a b Siegelbaum, Jackson (2006). "Gastritis". Jackson Siegelbaum Gastroenterolgoy. http://www.gicare.com/pated/ecdgs46.htm. Retrieved 2008-11-18. 
  10. ^ "Gastritis". MayoClinic. April 13, 2007. http://www.mayoclinic.com/health/gastritis/DS00488/DSECTION=causes. Retrieved 2008-11-18. 
  11. ^ Kandulski A, Selgrad M, Malfertheiner P (August 2008). "Helicobacter pylori infection: a clinical overview". Digestive and Liver Disease 40 (8): 619–26. doi:10.1016/j.dld.2008.02.026. PMID 18396114. 
  12. ^ Peek RM (2008). "Helicobacter pylori infection and disease: from humans to animal models". Disease Models & Mechanisms 1 (1): 50–5. doi:10.1242/dmm.000364. PMC 2561984. PMID 19048053. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2561984/. 
  13. ^ "Exams and Tests". eMedicinHealth. 2008. http://www.emedicinehealth.com/gastritis/page3_em.htm. Retrieved 2008-11-18. 
  14. ^ Boparai V, Rajagopalan J, Triadafilopoulos G (2008). "Guide to the use of proton pump inhibitors in adult patients". Drugs 68 (7): 925–47. doi:10.2165/00003495-200868070-00004. PMID 18457460. 
  15. ^ "Gastritis: Treatment". CNN (CNN.com). 2008. http://www.cnn.com/HEALTH/library/DS/00488.html. Retrieved 2008-11-18. [dead link]