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...