Pathophysiology of Gastroesophageal Reflux Disease (GERD)

Core Pathophysiologic Mechanisms

• The American Gastroenterological Association notes that GERD results from abnormal reflux of gastric contents into the esophagus due to failure of the antireflux barrier, primarily through transient lower esophageal sphincter relaxations (TLESRs) and incompetence of the lower esophageal sphincter (LES), combined with impaired esophageal clearance mechanisms 1

The Refluxate Composition

• The damaging potential of refluxed material depends on multiple factors, including gastric acid concentration, proteolytic enzymes, and bile acids, with the volume and frequency of reflux episodes determining total esophageal exposure 1

Mucosal Integrity and Symptom Perception

• The American Medical Association recommends considering that macroscopic changes, such as erosive esophagitis, strictures, and Barrett esophagus, can occur due to refluxate, and microscopic alterations can occur without visible erosions, explaining symptoms in non-erosive reflux disease 2, 3

Extraesophageal Manifestations

• The American College of Chest Physicians states that GERD can cause symptoms through three distinct mechanisms beyond direct esophageal injury, including esophageal-bronchial reflex, microaspiration or macroaspiration, and laryngopharyngeal reflux 5, 6, 7

Pediatric Considerations

• The American Academy of Pediatrics notes that in infants and children, physiologic GER occurs through transient LES relaxations in up to 50% of healthy infants daily and typically resolves with maturation, while pathologic GERD develops when reflux causes troublesome symptoms or complications 8