3.1 Esophageal & Gastric Disorders (GERD, PUD)
Key Takeaways
- GERD diagnosis is typically clinical, but 24-hour pH monitoring is the gold standard, and upper endoscopy (EGD) is required for any alarm symptoms.
- Barrett's esophagus involves a metaplastic shift from stratified squamous to simple columnar epithelium with goblet cells, carrying a significant risk of esophageal adenocarcinoma.
- Duodenal ulcers are most commonly caused by H. pylori and characteristically improve with food, whereas gastric ulcers worsen with food and carry a higher risk of malignancy.
- Boerhaave syndrome is a transmural esophageal rupture presenting with pneumomediastinum and Hamman's crunch, requiring emergent surgical repair, whereas Mallory-Weiss tears are superficial mucosal lacerations that are usually self-limiting.
- H. pylori eradication requires combination therapy: triple therapy consists of a PPI, amoxicillin, and clarithromycin, while quadruple therapy includes bismuth, metronidazole, tetracycline, and a PPI.
Esophageal and Gastric Disorders
Gastroesophageal reflux disease (GERD) and peptic ulcer disease (PUD) are among the most common gastrointestinal conditions encountered on the PANCE. A clear understanding of their clinical presentations, diagnostic algorithms, and pharmacotherapeutic strategies is essential for exam success.
GERD Pathophysiology and Clinical Presentation
GERD is characterized by the retrograde flow of gastroduodenal contents into the esophagus, causing symptoms or mucosal damage. The primary pathophysiologic mechanism is transient lower esophageal sphincter relaxations (TLESRs) or a hypotensive lower esophageal sphincter (LES). Other contributing factors include sliding hiatal hernias, delayed gastric emptying (gastroparesis), and increased intra-abdominal pressure due to obesity or pregnancy. Typical symptoms include pyrosis (heartburn), which is characteristically retrosternal and worsens postprandially or in a recumbent position, and acid regurgitation. Extraesophageal (atypical) symptoms include chronic dry cough, adult-onset asthma, laryngitis, hoarseness, and globus sensation, which occur due to microaspiration of gastric acid or vagal-mediated bronchospasm.
Diagnostic Workup and Alarm Symptoms
Uncomplicated GERD is a clinical diagnosis. An empirical trial of lifestyle modifications and acid suppression is the standard initial step. However, the presence of any "alarm symptoms" warrants immediate evaluation with upper endoscopy (esophagogastroduodenoscopy or EGD) to rule out malignancy, strictures, or severe ulceration. The primary alarm symptoms are:
- Dysphagia (difficulty swallowing) or odynophagia (painful swallowing)
- Unintentional weight loss
- Persistent vomiting
- Hematemesis or melena
- New-onset dyspepsia in patients older than 55 years
The gold standard diagnostic test for refractory GERD or for pre-operative planning is 24-hour ambulatory pH monitoring.
Clinical Management and Barrett Esophagus
Management follows a stepped care approach. Lifestyle modifications include elevating the head of the bed (6-8 inches), losing weight, avoiding recumbency within three hours of a meal, and eliminating dietary triggers (caffeine, alcohol, chocolate, peppermint, and fatty foods). For mild, intermittent symptoms (<2 times per week), low-dose H2-receptor antagonists (H2RAs) like famotidine are appropriate; they work by reversibly blocking H2 receptors on parietal cells, reducing histamine-stimulated acid secretion. For moderate-to-severe symptoms (>=2 times per week) or suspected erosive esophagitis, daily proton pump inhibitors (PPIs) like omeprazole or pantoprazole are first-line. PPIs irreversibly bind to and inhibit the active hydrogen-potassium ATPase pump (H+/K+-ATPase) on parietal cells, representing the most potent class of acid suppressants. PPIs must be taken 30-60 minutes before the first meal of the day to maximize efficacy because they only inhibit active pumps. Barrett esophagus is a metaplastic complication of chronic GERD where the normal stratified squamous epithelium of the distal esophagus is replaced by simple columnar epithelium with goblet cells (specialized intestinal metaplasia). This metaplasia is a precursor to esophageal adenocarcinoma, which primarily affects the distal third of the esophagus. In contrast, squamous cell carcinoma of the esophagus is associated with alcohol and tobacco use and is typically found in the proximal and middle thirds. Endoscopic surveillance guidelines are based on dysplasia grade:
- No dysplasia: Repeat EGD in 3 to 5 years.
- Low-grade dysplasia: Repeat EGD in 6 to 12 months, or undergo endoscopic ablation.
- High-grade dysplasia: Endoscopic mucosal resection or radiofrequency ablation.
Peptic Ulcer Disease Pathophysiology
PUD is characterized by mucosal breaks in the stomach or duodenum extending through the muscularis mucosae. The two dominant etiologies are Helicobacter pylori infection and the use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs). NSAID-induced PUD results from the systemic inhibition of the cyclooxygenase-1 (COX-1) enzyme, which decreases cytoprotective prostaglandin synthesis (specifically PGE2 and PGI2). Prostaglandins normally stimulate the secretion of mucus and bicarbonate, maintain mucosal blood flow, and inhibit gastric acid secretion. When NSAIDs inhibit the COX-1 pathway, this protective barrier is compromised, making the gastric mucosa highly vulnerable to the damaging effects of hydrochloric acid.
| Feature | Gastric Ulcer | Duodenal Ulcer |
|---|---|---|
| Pain with Food | Worsens (leads to weight loss) | Improves (leads to weight gain) |
| H. pylori Association | ~70% of cases | ~90% of cases |
| Malignancy Risk | High (must be biopsied) | Very low (no routine biopsy) |
| Typical Patient Age | Older (50–70 years) | Younger (30–55 years) |
Diagnostic Testing for H. pylori
Diagnostic modalities are categorized by invasiveness. Non-invasive testing includes the Urea Breath Test (where H. pylori urease converts labeled urea to carbon dioxide, which is measured in exhaled breath) and the Stool Antigen Test (highly sensitive and specific for active infection and confirming eradication). Serology (IgG antibodies) indicates lifetime exposure but cannot differentiate active from past infection. Next-step invasive testing includes endoscopic biopsy with histopathology (the gold standard) and the rapid urease test (CLOtest). Crucially, to prevent false-negative urea breath and stool antigen tests, PPIs must be held for 2 weeks, and bismuth/antibiotics must be held for 4 weeks before testing.
PUD Complications
Gastrointestinal hemorrhage is the most common complication. Bleeding from a posterior duodenal ulcer typically involves the gastroduodenal artery, which lies directly behind the duodenal bulb. Perforation is a medical emergency that presents with sudden, severe, generalized abdominal pain and a rigid, board-like abdomen with rebound tenderness. Upright chest radiograph reveals pneumoperitoneum (free air under the diaphragm). Gastric outlet obstruction, due to edema or scarring of the pylorus, presents with early satiety, abdominal bloating, and projectile vomiting of undigested food.
Gastritis
Gastritis is mucosal inflammation of the stomach and appears under the GI/Nutrition blueprint. It is categorized as acute or chronic.
- Acute Gastritis: Sudden mucosal inflammation, most commonly caused by NSAIDs, alcohol, stress (Curling ulcers in severe burns, Cushing ulcers in head trauma), and Helicobacter pylori. Presents with epigastric pain, nausea, vomiting, and hematemesis.
- Chronic Gastritis:
- Type A (Autoimmune): Autoantibodies against parietal cells and intrinsic factor. Affects the fundus and body. Causes pernicious anemia (B12 deficiency) and achlorhydria. Associated with other autoimmune disorders.
- Type B (Bacterial): Caused by H. pylori infection. Affects the antrum. Associated with peptic ulcer disease and MALT lymphoma.
- Diagnostic Workup: Upper endoscopy with biopsy is the gold standard. Test for H. pylori (urea breath test, stool antigen, or biopsy histology). For autoimmune gastritis, check anti-parietal cell and anti-intrinsic factor antibodies and vitamin B12 levels.
- Management:
- Stop offending agents (NSAIDs, alcohol).
- Proton pump inhibitor (PPI) for acid suppression.
- H. pylori eradication with triple therapy (PPI + clarithromycin + amoxicillin or metronidazole) for 14 days.
- Vitamin B12 replacement for autoimmune (pernicious anemia).
- PANCE Trap — Stress Ulcer Prophylaxis: Critically ill ICU patients are at risk for stress-related mucosal disease. Indications for prophylaxis (PPI or H2 blocker) include mechanical ventilation for >48 hours and coagulopathy. Curling ulcers (burns) and Cushing ulcers (head trauma) are classic stress ulcer associations.
A 62-year-old male presents to the clinic complaining of a three-month history of burning epigastric pain that is exacerbated approximately 30 minutes after eating a meal. He also notes a 10-pound unintentional weight loss over the same period due to fear of eating. Which of the following is the most appropriate next step in the management of this patient?
A 45-year-old female presents to the emergency department with sudden-onset, severe, retrosternal chest pain that began immediately after a prolonged episode of forceful retching. On physical examination, she is tachycardic, tachypneic, and febrile. Auscultation of the chest reveals a crackling sound synchronous with her heartbeat. Which of the following diagnostic studies is most appropriate to confirm the suspected diagnosis?