Heartburn pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
[[Heartburn]] is the burning [[pain]] caused by the reflux of [[gastric acid]] and [[pepsin]] from the [[stomach]] into the [[esophagus]]. These substances enter the [[esophagus]] due to a dysfunctional [[lower esophagus sphincter]], which in normal conditions should now allow the occurrence of such reflux. This can happen due to many causes such as [[hiatal hernia]], use of medications which causes relaxation of the [[lower esophagus sphincter]] or due to abnormal relaxation or weakening of the [[lower esophagus sphincter]] which causes the [[gastroesophageal reflux disease]]. | |||
The [[gastric acid]] and the [[pepsin]] damages the epithelium and causes an inflammatory response mediated by [[IL-8]] and [[IL-1B]]. These [[cytokines]] stimulate inflammation and sensitizes the [[peripheral nerves]] in the [[mucosa]] which mediates the [[pain]]. It is believed that the release of such [[cytokines]] is mediated by an increased production of [[PGE2]] and [[ATP]] by the [[epithelium]]. | |||
With the most recent research findings, it is believed that the [[gastric acid]] does not directly cause [[heartburn]], but causes it using a myriad of [[inflammatory]] mechanisms which are being elucidated and may be targets of new [[therapeutic]] drugs in the future.<ref name="pmid27206157">{{cite journal| author=Miwa H, Kondo T, Oshima T| title=Gastroesophageal reflux disease-related and functional heartburn: pathophysiology and treatment. | journal=Curr Opin Gastroenterol | year= 2016 | volume= 32 | issue= 4 | pages= 344-52 | pmid=27206157 | doi=10.1097/MOG.0000000000000282 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27206157 }} </ref> | |||
==References== | ==References== | ||
Revision as of 15:50, 1 September 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The sensation of heartburn is caused by exposure of the lower esophagus to the acidic contents of the stomach. Normally, the lower esophageal sphincter (LES) separating the stomach from the esophagus is supposed to contract to prevent this situation. If the sphincter relaxes for any reason (as normally occurs during swallowing), stomach contents, mixed with gastric acid, can return into the esophagus. This return is also known as reflux, and may progress to gastroesophageal reflux disease (GERD) if it occurs frequently. If this is the case, the gastric acid and pepsin now located in the esophagus can injure the tight junction proteins in the esophageal epithelium. This results in increased paracellular permeability and dilated intercellular space and edema in the submucosa, which is amplified by an immunological mechanism mediated by inflammatory cytokines.[1]
Pathophysiology
Heartburn is the burning pain caused by the reflux of gastric acid and pepsin from the stomach into the esophagus. These substances enter the esophagus due to a dysfunctional lower esophagus sphincter, which in normal conditions should now allow the occurrence of such reflux. This can happen due to many causes such as hiatal hernia, use of medications which causes relaxation of the lower esophagus sphincter or due to abnormal relaxation or weakening of the lower esophagus sphincter which causes the gastroesophageal reflux disease. The gastric acid and the pepsin damages the epithelium and causes an inflammatory response mediated by IL-8 and IL-1B. These cytokines stimulate inflammation and sensitizes the peripheral nerves in the mucosa which mediates the pain. It is believed that the release of such cytokines is mediated by an increased production of PGE2 and ATP by the epithelium. With the most recent research findings, it is believed that the gastric acid does not directly cause heartburn, but causes it using a myriad of inflammatory mechanisms which are being elucidated and may be targets of new therapeutic drugs in the future.[1]
References
- ↑ 1.0 1.1 Miwa H, Kondo T, Oshima T (2016). "Gastroesophageal reflux disease-related and functional heartburn: pathophysiology and treatment". Curr Opin Gastroenterol. 32 (4): 344–52. doi:10.1097/MOG.0000000000000282. PMID 27206157.