Pathophysiology of gastroesophageal reflux disease.

From a pathophysiologic viewpoint, GERD results from the excessive reflux of gastric contents into the distal esophagus. Under normal conditions, this is prevented as a function of the antireflux barrier at the EGJ, the integrity of which is dependent on the delicate interplay of a host of anatomic and physiologic factors, including the integrity of the LES, TLESR, and anatomic degradation of the EGJ inclusive of but not limited to hiatus hernia. Considerable investigative focus is aimed at describing the subtle aberrations of the EGJ that may contribute to the root causes of GERD. The net result is an increased number of reflux events, an increasing diversity of potential mechanisms of reflux, and a diminished ability of the stomach to selectively vent gas, as opposed to gas and gastric juice, during TLESR. Once reflux occurs, 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 anatomic integrity of the EGJ. Approximately half of patients who have GERD have abnormal acid clearance and the major contributor to this is hiatus hernia. Abnormalities of acid clearance probably are the major determining factor influencing which patients who have GERD are most prone to developing esophagitis as opposed to symptomatic GERD. In summary, GERD is a multifactorial process involving physiologic and anatomic abnormalities. These abnormalities exhibit a complicated interplay that degrades the ability of the EGJ to contain gastric juice within the stomach and to clear the esophagus of gastric juice effectively once reflux has occurred.