How GERD is tested on Step 1

Vignettes describe burning chest pain after meals or when lying down, then ask about mechanism, complication, histology, or drug.

ProgressionLES failureTransient relaxations or low resting toneAcid refluxHeartburn, regurgitationEsophagitisErosions, ulcers, strictureBarrett esophagusColumnar epithelium with goblet cellsDysplasiaPrecursor lesion; endoscopic surveillanceAdenocarcinomaDistal third of the esophagus
The reflux sequence. Barrett esophagus is metaplasia, an adaptation, and is reversible in principle; dysplasia is the precursor lesion.
FactorEffect on reflux
Obesity, pregnancy↑ intra-abdominal pressure
Hiatal herniaLoss of the diaphragm's support of the LES
Smoking, alcohol, fatty meals, caffeine, chocolate↓ LES tone or ↑ transient relaxations
Systemic sclerosisFibrosis of esophageal smooth muscle → weak LES and poor peristalsis
Anticholinergics, calcium channel blockers, nitrates↓ LES tone

The LES is a high-pressure zone of smooth muscle maintained by intrinsic tone and the crural diaphragm.

Barrett esophagus and esophageal cancer

Metaplasia is the most-tested pathology concept in GERD.

AdenocarcinomaDistal thirdGERD, Barrett esophagusObesity; more common in the USGlandular histologyArises from Barrett dysplasiaSquamous cell carcinomaUpper and middle thirdsSmoking and alcoholHot liquids, nitrosamines, achalasiaKeratin pearlsMost common worldwidevs
Esophageal cancer. Both present with progressive dysphagia (solids, then liquids) and weight loss.

Hiatal hernias and GERD mimics

Know which disorders cause dysphagia or chest pain and how they look on studies.

Esophageal disordersAchalasiaLost inhibitoryneurons; bird beakEosinophilicesophagitisAtopy, rings, foodimpactionPillesophagitisDoxycycline, NSAIDs,bisphosphonatesInfectiousCandida, HSV, CMV
GERD mimics. Infectious esophagitis suggests immunosuppression: Candida (white plaques), HSV (punched-out ulcers), CMV (linear ulcers).
ConditionKey feature
Sliding hiatal herniaGE junction displaced upward; "hourglass stomach"; causes reflux
Paraesophageal herniaGE junction normal; fundus beside the esophagus; may strangulate
AchalasiaLoss of myenteric (Auerbach) inhibitory neurons (NO, VIP) → incomplete LES relaxation, absent peristalsis; dysphagia to solids and liquids
Eosinophilic esophagitisAtopy; stacked rings and furrows; ≥ 15 eosinophils per high-power field
Mallory-Weiss vs BoerhaaveMucosal tear with hematemesis vs transmural rupture with mediastinitis

Chagas disease (Trypanosoma cruzi) can cause secondary achalasia.

Acid-suppressing drugs

Mechanisms and adverse effects are high yield.

DrugMechanismAdverse effects
PPIs (-prazole)Irreversible H⁺/K⁺-ATPase inhibition in parietal cellsC. difficile, pneumonia, hypomagnesemia, ↓ B₁₂/iron/Ca²⁺ absorption, fractures
H₂ blockers (-tidine)Reversible H₂ receptor block → ↓ acidCimetidine: CYP450 inhibition, antiandrogenic effects, crosses placenta
AntacidsNeutralize acidAl(OH)₃ constipation, hypophosphatemia; Mg(OH)₂ diarrhea; CaCO₃ hypercalcemia, rebound acid
SucralfateCoats ulcer base in acid environmentNeeds acid to work; separate from PPIs

Surgical option for refractory GERD: Nissen fundoplication (fundus wrapped around the distal esophagus).

Worked example

Link chronic reflux to histology.

functions Worked example — long-standing heartburn

A 58-year-old man with obesity and 15 years of heartburn has salmon-colored mucosa extending up from the GE junction on endoscopy. Biopsy shows columnar epithelium with goblet cells. What is the process, and what cancer is he at risk for?

  1. Chronic acid exposure injures the normal stratified squamous epithelium.
  2. It is replaced by intestinal-type columnar epithelium with goblet cells: metaplasia (Barrett esophagus).
  3. Metaplasia can progress to dysplasia and then carcinoma.
  4. The cancer arises in the distal esophagus and is glandular.

Answer. Barrett esophagus (intestinal metaplasia), with increased risk of esophageal adenocarcinoma.