Esophageal & Gastric Disorders

ESOPHAGEAL AND GASTRIC DISORDERS

GERD, Barrett's Esophagus, H. pylori, and Peptic Ulcer Disease

LEARNING OBJECTIVES

Upon completion, the participant will be able to:

Differentiate between erosive and non-erosive GERD and explain the role of the lower esophageal sphincter

Compare proton pump inhibitors (PPIs) and H2 receptor antagonists in acid suppression therapy

Describe Barrett's esophagus surveillance and dysplasia management protocols

Explain diagnostic methods for Helicobacter pylori infection

Apply current H. pylori eradication regimens including first-line and salvage therapies

Identify risk factors and complications of peptic ulcer disease

Implement nursing care for patients with upper GI bleeding from ulcer disease

SECTION 1: GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Pathophysiology and Classification

GERD occurs when gastric contents reflux into the esophagus causing symptoms and/or complications. The primary mechanism is transient lower esophageal sphincter (LES) relaxation or a hypotensive LES. Contributing factors include hiatal hernia, delayed gastric emptying, impaired esophageal clearance, and mucosal resistance abnormalities.

EROSIVE ESOPHAGITIS (EE): Visible mucosal breaks on endoscopy. Classified by Los Angeles (LA) Classification: Grade A (≤5mm mucosal breaks), Grade B (>5mm, non-confluent), Grade C (confluent <75% circumference), Grade D (≥75% circumference).

NON-EROSIVE REFLUX DISEASE (NERD): Typical GERD symptoms without visible esophageal injury on endoscopy. Accounts for 60-70% of GERD patients.

Pharmacotherapy

PROTON PUMP INHIBITORS (PPIs): First-line therapy for moderate-severe GERD. Irreversibly inhibit H+/K+-ATPase (proton pump) in gastric parietal cells. Take 30-60 minutes before meals. Examples: omeprazole, esomeprazole, pantoprazole, lansoprazole, rabeprazole, dexlansoprazole.

PPI LONG-TERM CONCERNS: C. difficile infection, hypomagnesemia, vitamin B12 deficiency, hip fracture risk, chronic kidney disease, and fundic gland polyps. Benefits generally outweigh risks when indicated. Use lowest effective dose for shortest duration.

H2 RECEPTOR ANTAGONISTS: Block histamine H2 receptors on parietal cells. Less potent than PPIs. Useful for mild/intermittent symptoms or nocturnal acid breakthrough. Examples: famotidine, nizatidine. Ranitidine withdrawn due to NDMA contamination.

SECTION 2: BARRETT'S ESOPHAGUS

Definition and Cancer Risk

Barrett's esophagus is a premalignant condition in which normal squamous epithelium of the distal esophagus is replaced by specialized intestinal-type columnar epithelium (intestinal metaplasia) containing goblet cells. It develops in approximately 10-15% of patients with chronic GERD. Risk factors: chronic GERD symptoms (>5 years), male sex, age >50, Caucasian race, central obesity, smoking, and family history.

CANCER PROGRESSION: Barrett's → Low-grade dysplasia (LGD) → High-grade dysplasia (HGD) → Esophageal adenocarcinoma. Annual progression rate to cancer: Non-dysplastic Barrett's ~0.5%/year, LGD ~1%/year, HGD ~5-10%/year.

Surveillance and Management

NON-DYSPLASTIC BARRETT'S: EGD with systematic 4-quadrant biopsies every 2cm (Seattle protocol). PPI therapy to optimize healing. Surveillance every 3-5 years.

HIGH-GRADE DYSPLASIA: Endoscopic eradication therapy recommended. Options: radiofrequency ablation (RFA), endoscopic mucosal resection (EMR), cryotherapy. Esophagectomy reserved for failed endoscopic therapy or cancer.

SECTION 3: HELICOBACTER PYLORI INFECTION

Epidemiology and Significance

Helicobacter pylori is a gram-negative, spiral-shaped bacterium that colonizes the gastric mucosa. It affects approximately 50% of the world's population. H. pylori is the primary cause of peptic ulcer disease (90% of duodenal ulcers, 70% of gastric ulcers), a WHO Class I carcinogen for gastric adenocarcinoma, and associated with MALT lymphoma and atrophic gastritis.

Diagnostic Methods

NON-INVASIVE TESTS:

• Urea Breath Test (UBT): Patient ingests 13C or 14C-labeled urea. H. pylori urease splits urea releasing labeled CO2 detected in breath. High sensitivity/specificity (>95%).

• Stool Antigen Test: Detects H. pylori antigens in stool. Monoclonal antibody tests preferred. Good for diagnosis and confirmation of eradication.

• Serology: Detects anti-H. pylori IgG antibodies. Cannot distinguish active from past infection. Not useful for confirming eradication.

INVASIVE TESTS (via endoscopy):

• Rapid Urease Test (CLO test): Biopsy placed in urea-containing medium. Color change indicates urease activity. Results in 1-24 hours.

• Histology: Biopsy with special stains (Giemsa, Warthin-Starry). Also assesses inflammation, atrophy, metaplasia.

• Culture: Allows antibiotic sensitivity testing. Technically demanding, not widely available.

IMPORTANT: Stop PPIs for ≥2 weeks and antibiotics/bismuth for ≥4 weeks before testing (except serology) to avoid false negatives.

Eradication Therapy

FIRST-LINE (in areas with low clarithromycin resistance <15%):

• PPI + Clarithromycin + Amoxicillin (PCA) x 14 days

• PPI + Clarithromycin + Metronidazole (PCM) x 14 days if penicillin allergic

FIRST-LINE (in areas with high clarithromycin resistance ≥15% or unknown):

• Bismuth Quadruple Therapy: PPI + bismuth subsalicylate + metronidazole + tetracycline x 14 days

• Concomitant Therapy: PPI + clarithromycin + amoxicillin + metronidazole x 14 days

CONFIRM ERADICATION: UBT or stool antigen at least 4 weeks after completing therapy. Do NOT use serology for eradication confirmation.

SECTION 4: PEPTIC ULCER DISEASE

Etiology and Pathophysiology

Peptic ulcer disease (PUD) involves mucosal defects extending through the muscularis mucosa. Primary causes: H. pylori infection (most common worldwide) and NSAID use (most common in developed countries). Other causes include Zollinger-Ellison syndrome (gastrinoma), Crohn's disease, and stress ulcers in critically ill patients.

DUODENAL ULCERS: Pain typically 2-3 hours after meals ('hunger pain'), relieved by eating. Anterior wall perforation, posterior wall bleeding (gastroduodenal artery).

GASTRIC ULCERS: Pain often worsened by eating. Higher malignancy concern requires biopsy. Multiple biopsies from ulcer margin to rule out cancer.

Complications and Nursing Care

UPPER GI BLEEDING: Most common complication. Presents with hematemesis, melena, or hematochezia with hemodynamic instability. Nursing priorities: Airway protection, two large-bore IVs, type and crossmatch, NPO status, IV PPI therapy (80mg bolus then 8mg/hr continuous), hemodynamic monitoring, prepare for emergent EGD.

PERFORATION: Surgical emergency. Sudden severe abdominal pain, rigid abdomen, free air on imaging. Immediate surgical consultation.

GASTRIC OUTLET OBSTRUCTION: From edema, scarring, or malignancy. Presents with early satiety, vomiting undigested food, succussion splash. Requires NG decompression, endoscopic dilation or surgery.