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.
| Factor | Effect on reflux |
|---|---|
| Obesity, pregnancy | ↑ intra-abdominal pressure |
| Hiatal hernia | Loss of the diaphragm's support of the LES |
| Smoking, alcohol, fatty meals, caffeine, chocolate | ↓ LES tone or ↑ transient relaxations |
| Systemic sclerosis | Fibrosis 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.
Hiatal hernias and GERD mimics
Know which disorders cause dysphagia or chest pain and how they look on studies.
| Condition | Key feature |
|---|---|
| Sliding hiatal hernia | GE junction displaced upward; "hourglass stomach"; causes reflux |
| Paraesophageal hernia | GE junction normal; fundus beside the esophagus; may strangulate |
| Achalasia | Loss of myenteric (Auerbach) inhibitory neurons (NO, VIP) → incomplete LES relaxation, absent peristalsis; dysphagia to solids and liquids |
| Eosinophilic esophagitis | Atopy; stacked rings and furrows; ≥ 15 eosinophils per high-power field |
| Mallory-Weiss vs Boerhaave | Mucosal 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.
| Drug | Mechanism | Adverse effects |
|---|---|---|
| PPIs (-prazole) | Irreversible H⁺/K⁺-ATPase inhibition in parietal cells | C. difficile, pneumonia, hypomagnesemia, ↓ B₁₂/iron/Ca²⁺ absorption, fractures |
| H₂ blockers (-tidine) | Reversible H₂ receptor block → ↓ acid | Cimetidine: CYP450 inhibition, antiandrogenic effects, crosses placenta |
| Antacids | Neutralize acid | Al(OH)₃ constipation, hypophosphatemia; Mg(OH)₂ diarrhea; CaCO₃ hypercalcemia, rebound acid |
| Sucralfate | Coats ulcer base in acid environment | Needs 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.
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?
- Chronic acid exposure injures the normal stratified squamous epithelium.
- It is replaced by intestinal-type columnar epithelium with goblet cells: metaplasia (Barrett esophagus).
- Metaplasia can progress to dysplasia and then carcinoma.
- The cancer arises in the distal esophagus and is glandular.
Answer. Barrett esophagus (intestinal metaplasia), with increased risk of esophageal adenocarcinoma.