Upper Gastrointestinal Disorders: Dyspepsia, GERD, PUD & H. pylori

Upper Gastrointestinal Disorders: Dyspepsia, GERD, PUD & H. pylori

Dyspepsia & Clinical Evaluation

Dyspepsia is defined as epigastric pain or burning lasting at least 1 month, accompanied by postprandial fullness, early satiety, epigastric bloating, belching, or nausea. Clinical evaluation distinguishes functional (non-ulcer) dyspepsia from organic dyspepsia (peptic ulcer disease [PUD], GERD, gastric malignancy, medication toxicity).

Under Rome IV criteria, functional dyspepsia is subtyped into Epigastric Pain Syndrome and Postprandial Distress Syndrome. Joint American College of Gastroenterology (ACG) and Canadian Association of Gastroenterology guidelines establish diagnostic cutoffs:

• Patients Aged >= 60 Years: New-onset dyspepsia requires prompt diagnostic esophagogastroduodenoscopy (EGD) to exclude upper gastrointestinal malignancy.
• Patients Aged < 60 Years: In patients under age 60 without alarm features, non-invasive testing for Helicobacter pylori (stool antigen test or urea breath test) is recommended. If positive, eradication therapy is administered. If negative, an empiric 4- to 8-week PPI trial is initiated.

Gastroesophageal Reflux Disease (GERD)

GERD involves retrograde movement of gastric contents into the esophagus due to lower esophageal sphincter (LES) incompetence, transient LES relaxations, elevated intra-abdominal pressure, hiatal hernia, or smooth muscle relaxing medications (calcium channel blockers, nitrates, anticholinergics).

Clinical Presentation & Alarm Features

Classic symptoms include pyrosis (substernal burning pain) postprandially or when recumbent, and acidic regurgitation. Atypical extraesophageal manifestations include chronic non-productive cough, asthma, hoarseness, laryngitis, globus sensation, and dental enamel erosions.

In patients under age 60 without red flags, an empiric trial of lifestyle changes and once-daily PPI for 8 weeks is indicated. However, alarm features (red flags) mandate immediate referral for diagnostic EGD:

• Progressive dysphagia (difficulty swallowing) or odynophagia (painful swallowing).
• Unintentional weight loss (>5-10% of body weight).
• Gastrointestinal bleeding: Hematemesis, coffee-ground emesis, melena, or unexplained iron deficiency anemia.
• Persistent vomiting or palpable epigastric mass.

Management & PPI Safety (Beers Criteria 2023)

First-line lifestyle interventions include weight loss, elevating the head of the bed 6 to 8 inches using bed risers, avoiding meals within 3 hours of bedtime, eliminating trigger foods, and smoking cessation.

Pharmacologic therapy:

1. Mild GERD: H2-Receptor Antagonists (famotidine 20 mg BID or 40 mg at bedtime).
2. Moderate-to-Severe GERD: Proton Pump Inhibitors (omeprazole 20-40 mg daily or pantoprazole 40 mg daily) taken 30-60 minutes before breakfast to inhibit actively secreting H+/K+ ATPase pumps. Step-down therapy to the lowest effective dose should follow an 8-week course.

The AGS Beers Criteria (2023) recommends avoiding PPI use >8 weeks without high-risk indications (severe erosive esophagitis, Barrett's esophagus, chronic NSAID/anticoagulant use) due to documented systemic risks:

• Clostridioides difficile colitis and enteric infections.
• Osteoporosis and hip/spine fractures (impaired calcium ionization and intestinal absorption).
• Hypomagnesemia and Vitamin B12 deficiency.
• Acute interstitial nephritis and chronic kidney disease.

Complications of Uncontrolled GERD

• Erosive Esophagitis and fibrotic peptic strictures presenting as progressive solid-food dysphagia.
• Barrett's Esophagus: Metaplastic conversion of stratified squamous epithelium to specialized intestinal columnar mucosa with goblet cells, predisposing to Esophageal Adenocarcinoma. Surveillance EGD is required every 3 to 5 years for non-dysplastic lesions.

Peptic Ulcer Disease (PUD)

PUD involves mucosal defects extending through the muscularis mucosae, caused by H. pylori infection or chronic NSAID/aspirin use.

Gastric vs. Duodenal Ulcers

NSAID-induced PUD results from systemic inhibition of COX-1, suppressing mucosal prostaglandin E2 synthesis. Co-prescribing a PPI or choosing a selective COX-2 inhibitor (celecoxib) reduces ulcer risk. In refractory PUD without NSAID use or H. pylori, Zollinger-Ellison Syndrome (gastrinoma) should be evaluated with fasting serum gastrin levels.

H. pylori Diagnostics & Eradication Protocols

H. pylori is a microaerophilic Gram-negative bacterium that produces extracellular urease, buffering gastric acid to create a protective alkaline microenvironment.

Diagnostic Modalities & Critical Testing Rules

1. Urea Breath Test (UBT) and Stool Antigen Test (SAT): High sensitivity and specificity (>95%).
2. CRITICAL TESTING RULE: Patients must discontinue PPIs for at least 2 weeks and antibiotics/bismuth for at least 4 weeks prior to UBT or SAT to prevent false-negative results.
3. Serology (Anti-H. pylori IgG): Detects past exposure but cannot confirm active infection or verify post-treatment cure.

Eradication Regimens (2026 ACG Guidelines)

Due to widespread clarithromycin resistance exceeding 15-20%, 14-day Bismuth Quadruple Therapy is the preferred first-line empirical regimen:

• PPI BID (e.g., omeprazole 20 mg BID)
• Bismuth Subsalicylate 525 mg PO QID
• Metronidazole 500 mg PO TID/QID
• Tetracycline 500 mg PO QID

Alternatively, 14-day Non-Bismuth Quadruple (Concomitant) Therapy (PPI BID + Amoxicillin 1g BID + Clarithromycin 500mg BID + Metronidazole 500mg BID) may be used. Eradication must be verified >= 4 weeks post-treatment using UBT or SAT.