The Pathophysiology of GERD

Abstract

The understanding of the pathophysiology of gastroesophageal reflux disease (GERD) has evolved in the last decade primarily by recognizing the multitude of factors that contribute to the emergence of the disorder (Fig. 1). These factors may overlap in some patients and differ in others. GERD is primarily considered a motility disorder, because dysfunction of the anti-reflux barrier is still considered as a prerequisite for the development of the disease. However, recent investigation into symptom generation in GERD disclosed the important role of altered esophageal sensation. Recent studies have demonstrated that peripheral and central factors are pivotal for the emergence of symptoms after gastroesophageal reflux had occurred; supporting the view that GERD is a sensory-motor disorder rather than motor disorder alone. The primary pathophysiologic event in GERD is the movement of acid, pepsin, and other injurious substances from the stomach into the esophagus. This event also occurs as part of normal physiology, but results in GERD when symptoms or tissue damage occurs. Esophageal mucosal injury in GERD results when mucosal defensive factors are overwhelmed by refluxate, occurring secondary to compromised anti-reflux barrier, decreased effective esophageal acid clearance, abnormal mucosal defensive factors and so on.