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Gastritis
Classification and external resources

Peptic ulcers may accompany gastritis
ICD-10 K29.0-K29.7
ICD-9 535.0-535.5
eMedicine emerg/820 med/852
MeSH D005756

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. Certain diseases, such as pernicious anemia, chronic bile reflux, stress and 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. 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

Causes and Treatment

Acute

Erosive gastritis is 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.[6] 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.[7] Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period of time are not typically dangerous. However, regular use can lead to gastritis.[8]

Chronic

If the esophageal sphincter fails to do its job properly, some stomach acid can escape up the esophagus. This causes very painful "heartburn" or "gastritis" in the chest as the esophageal walls are eroded by the hydrochloric acid. Chronic gastritis refers to a wide range of problems of the gastric tissues that are mainly the result of H. pylori infection.[2] The immune system makes proteins and antibodies that fight infections in the body to maintain a homeostatic condition. In some disorders, the body accidentally targets the stomach, believing it is a foreign protein or pathogen. It makes antibodies against, severely damages, and may even destroy the stomach and/or its lining.[8] In some cases, bile, normally used to aid digestion in the small intestine, will enter through the pyloric valve of the stomach, because it had been removed during surgery or may not work properly. This also leads to gastritis. Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease, certain connective tissue disorders, or liver/kidney failure.[9]

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), which 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).[10] 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.[11]

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.[12] 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. 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.[13]

Symptoms

Severe gastritis is possible when the stomach is viewed without symptoms being present and may be present despite only minor changes in the stomach lining. Seniors have a higher likelihood of developing painless stomach damage. They may have no symptoms at all, such as an absence of vomiting or pain, until they are suddenly taken ill with internal bleeding. Pain in the upper abdomen is the most common symptom. The pain is usually in the upper central portion of the abdomen, the "pit" of the stomach. Gastritis pain can occur in the left upper portion of the abdomen and in the back. The pain seems to travel from the belly to the back. The pain is typically vague, but can be a sharp pain. Belching either doesn't relieve pain or only relieves it for a moment. The vomit is either clear, green or yellow, has a bloody streak in it, or is completely bloody, depending on the severity of inflammation. Bloating and a feeling of fullness or burning in the upper abdomen are also signs of moderate gastritis. Severe gastritis presents pallor, sweating, rapid heart beat, feeling faint or short of breath, severe chest or stomach pain, vomiting large amounts of blood, or bloody or dark, sticky, foul-smelling bowel movements. [14]

Diagnosis

Typically, a diagnosis is made based on the patients description of his or her symptoms. If a diagnosis is not possible based on these symptoms, however, other methods are used. Tests for blood cell count, H. pylori, and pregnancy; and liver, kidney, gallbladder, and pancreas functions, may be ordered. Urinalysis may be used, or a stool sample taken, to look for blood in the stool. X-rays may be ordered, as well as ECGs. If none of these tests are able to be used for diagnosis, the patient may be recommended to a gastroenterologist. An endoscopy may be performed, where a flexible probe with a camera on the end is sent into the stomach to check for stomach lining inflammation and mucous erosion. At the same time, a stomach biopsy may be taken to test for gastritis and a variety of other conditions.[15]

References

  1. ^ "Gastritis". University of Maryland Medical Center (University of Maryland Medical System). 2002-12-01. http://www.umm.edu/altmed/articles/gastritis-000067.htm. Retrieved 2008-10-07. 
  2. ^ a b c d "Gastritis". Merck. January 2007. http://www.merck.com/mmpe/sec02/ch013/ch013c.html. Retrieved 2009-01-11. 
  3. ^ "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. ^ 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. 
  7. ^ 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. 
  8. ^ a b Siegelbaum, Jackson (2006). "Gastritis". Jackson Siegelbaum Gastroenterolgoy. http://www.gicare.com/pated/ecdgs46.htm. Retrieved 2008-11-18. 
  9. ^ "Gastritis". MayoClinic. April 13, 2007. http://www.mayoclinic.com/health/gastritis/DS00488/DSECTION=causes. Retrieved 2008-11-18. 
  10. ^ 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. 
  11. ^ 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. PMID 19048053. 
  12. ^ 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. 
  13. ^ "Gastritis: Treatment". CNN (CNN.com). 2008. http://www.cnn.com/HEALTH/library/DS/00488.html. Retrieved 2008-11-18. 
  14. ^ "Gastritis Symptoms". eMedicinHealth. 2008. http://www.emedicinehealth.com/gastritis/page3_em.htm. Retrieved 2008-11-18. 
  15. ^ "Exams and Tests". eMedicinHealth. 2008. http://www.emedicinehealth.com/gastritis/page3_em.htm. Retrieved 2008-11-18. 

See also


1911 encyclopedia

Up to date as of January 14, 2010

From LoveToKnow 1911

Medical warning!
This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead.

GASTRITIS (Gr. ryao-r ip, stomach), an inflammatory affection of the stomach, of which the condition of catarrh, or irritation of its mucous membrane, is the most frequent and most readily recognized. This may exist in an acute or a chronic form, and depends upon some condition, either local or general, which produces a congested state of the circulation in the walls of the stomach (see Digestive Organs: Pathology). Acute Gastritis may arise from various causes. The most intense forms of inflammation of the stomach are the toxic conditions which follow the swallowing of corrosive poisons, such as strong mineral acids of alkalis which may extensively destroy the mucous membrane. Other non-corrosive poisons cause acute degeneration of the stomach wall (see PolsoNs). Acute inflammatory conditions may be secondary to zymotic diseases such as diphtheria, pyaemia, typhus fever and others. Gastritis is also caused by the ingestion of food which has begun to decompose, or may result from eating unsuitable articles which themselves remain undigested and so excite acute catarrhal conditions. These give rise to the symptoms well known as characterizing an acute "bilious attack," consisting in loss of appetite, sickness or nausea, and headache, frontal or occipital, often accompanied with giddiness. The tongue is furred, the breath foetid, and there is pain or discomfort in the region of the stomach, with sour eructations, and frequently vomiting, first of food and then of bilious matter. An attack of this kind tends to subside in a few days, especially if the exciting cause be removed. Sometimes, however, the symptoms recur with such frequency as to lead to the more serious chronic form of the disease.

The treatment bears reference, in the first place, to any known source of irritation, which, if it exist, may be expelled by an emetic or purgative (except in cases due to poisoning). This, however, is seldom necessary, since vomiting is usually present. For the relief of sickness and pain the sucking of ice and counterirritation over the region of the stomach are of service. Further, remedies which exercise a soothing effect upon an irritable mucous membrane, such as bismuth or weak alkaline fluids, and along with these the use of a light milk diet, are usually sufficient to remove the symptoms.

Chronic Gastric Catarrh may result from the acute or may arise independently. It is not infrequently connected with antecedent disease in other organs, such as the lungs, heart, liver or kidneys, and it is especially common in persons addicted to alcoholic excess. In this form the texture of the stomach is more altered than in the acute form, except in the toxic and febrile forms above referred to. It is permanently in a state of congestion, and its mucous membrane and muscular coat undergo thickening and other changes, which markedly affect the function of digestion. The symptoms are those of dyspepsia in an aggravated form (see Dyspepsia), of which discomfort and pain after food, with distension and frequently vomiting, are the chief; and the treatment must be conducted in reference to the causes giving rise to it. The careful regulation of the diet, alike as to the amount, the quality, and the intervals between meals, demands special attention. Feeding on artificially soured milk may in many cases be useful. Lavage or washing out of the stomach with weak alkaline solutions has been used with marked success in the treatment of chronic gastritis. Of medicinal agents, bismuth, arsenic, nux vomica, and the mineral acids are all of acknowledged efficacy, as are also preparations of pepsin.


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Simple English

Gastritis
Classification and other resource links
Micrograph showing gastritis. H&E stain.
ICD-10 K29.0-K29.7
ICD-9 535.0-535.5
eMedicine emerg/820  med/852
MeSH D005756

Gastritis is an inflammation of the lining of the stomach. It has many possible causes.[1] The main causes are drinking too much alcohol, or using nonsteroidal anti-inflammatory drugs (also known as NSAIDs) such as aspirin or ibuprofen for too long. Sometimes gastritis starts after major surgery, serious injury, burns, or infections. People who have had weight loss surgery may also get gastritis. Long term causes are infection with bacteria, mainly Helicobacter pylori. Certain diseases, such as pernicious anemia, chronic bile reflux, stress and certain autoimmune disorders can cause gastritis as well. The most common symptom is abdominal pain. Other symptoms are indigestion, abdominal bloating, nausea, and vomiting. 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 faeces 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]

References

  1. "Gastritis". University of Maryland Medical Center (University of Maryland Medical System). 2002-12-01. http://www.umm.edu/altmed/articles/gastritis-000067.htm. Retrieved 2008-10-07. 
  2. "Gastritis". Merck. January 2007. http://www.merck.com/mmpe/sec02/ch013/ch013c.html. Retrieved 2009-01-11. 
  3. "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. 








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