Gastroenterology · USMLE Step 1 and Step 2

GERD song

GERD - Pathophysiology & Complications, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

GERD

Full song on YouTube ↗Spotify ↗

Key points in this song10

GERD results from transient lower esophageal sphincter relaxations (TLESRs) — the most common mechanism — allowing gastric acid to reflux into the esophagus.
A hypotensive LES (resting pressure <6 mmHg) is the key structural defect, seen especially in severe or refractory GERD.
Hiatal hernia impairs the esophagogastric junction barrier by displacing the LES above the diaphragm, eliminating the crural diaphragm's contribution to sphincter tone.
Delayed gastric emptying increases gastric volume and pressure, promoting reflux — a key mechanism linking obesity and GERD.
Intra-abdominal pressure elevation (obesity, pregnancy, ascites) overwhelms LES competence, driving acid retrograde into the esophagus.
Esophageal dysmotility reduces acid clearance, prolonging mucosal contact time and worsening injury even when reflux volume is modest.
Substances that lower LES tone include alcohol, caffeine, chocolate, fatty foods, calcium channel blockers, nitrates, and anticholinergics.
Refluxed contents damage the squamous esophageal epithelium via acid, pepsin, and bile salts — bile salts are particularly injurious at alkaline pH, relevant in post-gastrectomy patients.
Chronic acid exposure triggers metaplasia of squamous to columnar (intestinal-type) epithelium — Barrett's esophagus — the key premalignant complication driven by repeated injury-repair cycles.
Helicobacter pylori infection is NOT a cause of GERD; eradication can actually worsen GERD by increasing acid secretion in previously suppressed fundic mucosa.