Peptic ulcer causes: Difference between revisions
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==Overview== | ==Overview== | ||
==Comon Cuases== | |||
A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic [[inflammation]] due to ''[[Helicobacter pylori]]'' that colonizes (''i.e.'' settles there after entering the body) the [[Pyloric antrum|antral]] [[mucosa]]. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the [[bacterium]] can cause a chronic active [[gastritis]] (type B gastritis), resulting in a defect in the regulation of [[gastrin]] production by that part of the stomach, and gastrin secretion is increased. [[Gastrin]], in turn, stimulates the production of [[gastric acid]] by parietal cells. The acid erodes the [[mucosa]] and causes the ulcer. | |||
Another major cause is the use of [[NSAID]]s (see above). The gastric mucosa protects itself from [[gastric acid]] with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of [[cyclooxygenase]] 1 (''cox-1''), which is essential for the production of these prostaglandins. Newer NSAIDs ([[celecoxib]], [[rofecoxib]]) only inhibit''cox-2'', which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration. | |||
[[Tobacco smoking]], [[Blood type|blood group]], spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.<ref>For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids.[http://digestive.niddk.nih.gov/ddiseases/pubs/hpylori/ National Digestive Diseases Information Clearinghouse]</ref> | |||
*[[Glucocorticoid]]s | |||
*[[Burn (injury)|Burns]] | |||
*[[Head trauma]] | |||
*[[Mechanical ventilation]]. | |||
*[[Tobacco smoking|Smoking]] | |||
*[[Overuse of laxatives]] | |||
A [[Family history (medicine)|family history]] is often present in duodenal ulcers, especially when [[ABO blood group system|blood group O]] is also present. Inheritance appears to be unimportant in gastric ulcers. | |||
[[Gastrinoma]]s ([[Zollinger-Ellison syndrome]]), rare gastrin-secreting tumors, cause multiple and difficult to heal ulcers. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
Revision as of 12:26, 19 August 2012
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Peptic ulcer Microchapters |
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Diagnosis |
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Treatment |
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Surgery |
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Case Studies |
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2017 ACG Guidelines for Peptic Ulcer Disease |
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Guidelines for the Indications to Test for, and to Treat, H. pylori Infection |
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Guidlines for factors that predict the successful eradication when treating H. pylori infection |
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Guidelines to document H. pylori antimicrobial resistance in the North America |
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Guidelines for evaluation and testing of H. pylori antibiotic resistance |
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Guidelines for when to test for treatment success after H. pylori eradication therapy |
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Guidelines for penicillin allergy in patients with H. pylori infection |
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Peptic ulcer causes On the Web |
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American Roentgen Ray Society Images of Peptic ulcer causes |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Comon Cuases
A major causative factor (60% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes (i.e. settles there after entering the body) the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion is increased. Gastrin, in turn, stimulates the production of gastric acid by parietal cells. The acid erodes the mucosa and causes the ulcer.
Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. Newer NSAIDs (celecoxib, rofecoxib) only inhibitcox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.
Tobacco smoking, blood group, spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.[1]
A family history is often present in duodenal ulcers, especially when blood group O is also present. Inheritance appears to be unimportant in gastric ulcers.
Gastrinomas (Zollinger-Ellison syndrome), rare gastrin-secreting tumors, cause multiple and difficult to heal ulcers.
References
- ↑ For nearly 100 years, scientists and doctors thought that ulcers were caused by stress, spicy food, and alcohol. Treatment involved bed rest and a bland diet. Later, researchers added stomach acid to the list of causes and began treating ulcers with antacids.National Digestive Diseases Information Clearinghouse
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