Pathophysiology of gastroesophageal reflux disease

Gastroesophageal reflux disease (GERD) is likely the most prevalent condition afflicting the GI tract in the USA. However, most GERD patients do not have esophagitis, and as esophagitis has become less of a problem, largely because of more effective treatments, the issue of symptom control has become a more substantial one. From a pathophysiological viewpoint, GERD results from the excessive reflux of gastric contents into the esophagus which is normally prevented as a function of the esophagogastric junction (EGJ), the integrity of which is dependent upon both physiological and anatomical factors, inclusive of, but not limited to, hiatus hernia. The net result is of an increased number of reflux events, an increasing diversity of potential mechanisms of reflux. Once reflux has occurred, the duration of resultant esophageal acid exposure is determined by the effectiveness of esophageal acid clearance, the dominant determinants of which are peristalsis, salivation, and, again, the anatomical integrity of the EGJ. About half of GERD patients have abnormal acid clearance and the major contributor to this is hiatus hernia. Abnormalities of acid clearance are probably the major determinant of developing esophagitis as opposed to symptomatic GERD. In summary, GERD is a multifactorial disease involving both physiological and anatomical abnormalities.