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Pathophysiology of reflux esophagitis

Peter J Kahrilas, MD
Section Editor
Nicholas J Talley, MD, PhD
Deputy Editor
Shilpa Grover, MD, MPH, AGAF


An essential concept in the pathogenesis of gastroesophageal reflux disease (GERD) is that the extent of symptoms and of mucosal injury is proportional to the frequency of reflux events, the duration of mucosal acidification, and the caustic potency of refluxed fluid. The integrity of the esophageal mucosa in normal individuals reflects the balance between injurious forces (acid reflux, potency of refluxate) and defensive forces (esophageal acid clearance, mucosal integrity). For one or more reasons, this balance becomes impaired in patients who develop GERD.

The pathophysiology of GERD will be reviewed here. The clinical manifestations and diagnosis of this disorder are discussed separately. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults".)


The primary event in the pathogenesis of gastroesophageal reflux disease (GERD) is movement of gastric juice from the stomach into the esophagus. The antireflux barrier at the gastroesophageal junction is anatomically and physiologically complex and vulnerable to several potential mechanisms of reflux. The three dominant pathophysiologic mechanisms causing gastroesophageal junction incompetence are:

Transient lower esophageal sphincter relaxations (tLESRs)

A hypotensive lower esophageal sphincter (LES)

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Literature review current through: Sep 2017. | This topic last updated: Jul 05, 2017.
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