Gastroesophageal reflux disease begins with failure of the barrier that normally keeps gastric contents in the stomach.
A minimal amount of gastric juice reflux is normal and physiological, and it is needed for belching. In GERD, however, the relaxation of the lower esophageal sphincter (LES) — the ring of muscle at the junction of the esophagus and stomach — is more than enough, and repeated episodes let gastric contents damage the gastroesophageal junction.
Why the barrier fails
Three mechanisms make the sphincter incompetent, and they often coexist. Transient LES relaxations are brief, inappropriate openings of the sphincter that are not triggered by swallowing; they account for more than 90% of reflux in normal patients without an anatomical problem such as a hiatal hernia, and they are the dominant mechanism. LES hypotension, a resting sphincter pressure that is too low, allows reflux without a specific relaxation. Distortion of the gastroesophageal junction, such as in a hiatal hernia, pulls the sphincter out of position so it no longer closes effectively.
What raises acid exposure
Some foods lower LES pressure and so predispose to reflux: chocolate, mint and lipids (fats). Other factors increase the exposure of the esophageal mucosa in a different way. Abdominal obesity and pregnancy both raise the pressure inside the abdomen and push gastric contents upward. A hypersecretory state of the stomach is not a dominant cause of esophagitis and GERD, except in Zollinger-Ellison syndrome, in which a gastrin-producing tumour drives acid output so high that more than 50% of cases develop esophagitis. Delayed transit time of the stomach leaves contents in the stomach longer, giving them more opportunity to reflux.
Clearing the refluxate
After reflux reaches the esophagus, two mechanisms normally clear the acid: peristalsis, the wave of contraction that returns the refluxate to the stomach, and saliva, whose bicarbonate raises the pH. When either is impaired, acid remains in contact with the mucosa for longer.
Acid is not the only damaging component of the refluxate. Pepsin, a protein-digesting enzyme, and pancreatic enzymes travel with it, and bile has an important effect on the pathogenesis of Barrett esophagus and esophageal adenocarcinoma.