GERD

Gastroesophageal reflux disease (GERD) results from the pathological retrograde movement of gastric contents (acid, pepsin, bile acids) into the esophagus, causing symptoms and/or mucosal injury. The primary anti-reflux barrier is the lower esophageal sphincter (LES), a 3-4 cm zone of tonically contracted smooth muscle at the gastroesophageal junction (GEJ), normally maintaining a resting pressure of 10-30 mmHg above intragastric pressure. The dominant mechanism of GERD is transient LES relaxations (TLESRs) — vagally mediated, non-swallow-related relaxations lasting 10-60 seconds that occur independently of esophageal peristalsis, accounting for >70% of reflux episodes in GERD patients. Additional mechanisms include a hypotensive LES (basal pressure <10 mmHg, allowing free reflux), hiatal hernia (which disrupts the extrinsic crural diaphragm reinforcement of the LES and creates an acid pocket above the diaphragm), and impaired esophageal clearance (reduced peristaltic amplitude and salivary bicarbonate buffering). At the mucosal level, refluxed hydrochloric acid (pH <4) and activated pepsin cause epithelial injury by disrupting intercellular tight junctions, allowing acid penetration into the submucosa where it activates nociceptors (producing heartburn) and triggers an inflammatory cascade. Chronic acid exposure induces adaptive metaplasia...