Pathophysiology of Gastroesophageal Reflux Disease The fundamental abnormality in gastroesophageal reflux disease is excessive reflux of gastric contents into the esophagus. Reflux is controlled by the sphincter mechanism at the gastroesophageal junction, which consists anatomically of the lower esophageal sphincter, the crural diaphragm, the intra-abdominal location of the sphincter, the phrenoesophageal ligament, and the angle of His. These structurally complex components build the antireflux barrier in supine position, during abdominal straining and swallow-induced lower esophageal sphincter (LES) relaxation, while they also permit belching with a controlled opening of the sphincter. Gastroesophageal reflux is due to transient sphincter relaxation (tLESR), a mechanical incompetence of the LES, or presence of hiatal hernia. When the sphincter tonus is normal, most reflux episodes are attributed to tLESRs. Strain-induced reflux and free reflux are possible when the sphincter tonus is low and/or hiatal hernia is present. As a result of poor clearance function esophageal acid exposure is increased. Ineffective esophageal motility is a common finding in reflux disease. Moreover, hiatal hernias impair acid clearance by permitting reflux during swallow-induced LES relaxation. Variations in mucosal resistance may explain differences in acid sensitivity between individuals. Gastral malfunction such as increased acid secretion, excessive duodenogastric reflux or impaired gastric emptying can further aggravate gastroesophageal reflux disease.

No abstract