Overview
Clinical Meaning
Gastroesophageal reflux disease (GERD) results from failure of the anti reflux barrier at the gastroesophageal junction (GEJ), allowing gastric acid and pepsin to contact esopha...
WHNP
WHNP
Gastroesophageal reflux disease (GERD) results from failure of the anti-reflux barrier at the gastroesophageal junction (GEJ), allowing gastric acid and pepsin to contact esophageal squamous epithelium not designed to withstand prolonged acid exposure. The anti-reflux barrier consists of the lower esophageal sphincter (LES), the crural diaphragm, and the angle of His. Transient LES relaxations (TLESRs) — vagally mediated, non-swallow-related relaxations triggered by gastric distension — account for approximately 70% of reflux episodes. Prolonged acid contact (pH <4) activates pepsin, which proteolyzes the esophageal mucosal barrier, causing inflammation ranging from non-erosive reflux disease (NERD, with intact mucosa but acid-sensitive nerve fiber sensitization) to erosive esophagitis (mucosal breaks classified by the Los Angeles system, Grades A-D). Chronic acid injury induces a metaplastic adaptation in the distal esophagus: stratified squamous epithelium is replaced by specialized intestinal-type columnar epithelium with goblet cells (Barrett esophagus), which represents a premalignant condition with a 0.5% annual risk of progression to esophageal adenocarcinoma through a dysplasia sequence. Diagnostic criteria distinguish typical GERD (heartburn and regurgitation amenable to empiric PPI trial) from atypical presentations requiring objective testing. Ambulatory pH...
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