Heartburn pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The sensation of heartburn is caused by exposure of the lower [[esophagus]] to the [[acid]]ic contents of the [[stomach]]. Normally, the lower esophageal [[cardia|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.<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> | The sensation of heartburn is caused by exposure of the lower [[esophagus]] to the [[acid]]ic contents of the [[stomach]]. Normally, the lower esophageal [[cardia|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]].<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> | ||
==Pathophysiology== | |||
==References== | ==References== | ||
Revision as of 15:30, 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
References
- ↑ 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.