OIA2004 PUD & GERD MANAGEMENT

Definition of PUD

Ulceration in the GI mucosa exposed to acid and pepsin, typically in the stomach or duodenum

Main Causes of PUD

H. pylori infection

NSAID use

Stress, smoking, chronic disease

Gastric vs. Duodenal Ulcers

Gastric ulcer: Pain worsens with food; weight loss

Duodenal ulcer: Pain relieved by food; weight gain

Complications of PUD

Bleeding, perforation, gastric outlet obstruction, peritonitis

H. pylori Pathogenesis

Secretes urease, protease, and lipopolysaccharide → disrupts mucosa, causes inflammation and ulceration

Triple Therapy (H. pylori Eradication)

PPI + Amoxicillin + Clarithromycin (for 14 days)

Quadruple Therapy (if resistance)

PPI + Bismuth + Metronidazole + Tetracycline

Monitoring after H. pylori Therapy

Urea breath test (after 4 weeks)

Stool antigen test (after 8 weeks)

Prophylaxis in NSAID users

Omeprazole 20–40 mg od, or Lansoprazole 15–30 mg od

Surgical Options PUD (If refractory/complications)

Vagotomy, Antrectomy, Pyloroplasty

Definition of GERD

Reflux of gastric contents into the esophagus, causing symptoms or complications

Common GERD Symptoms

Heartburn, regurgitation, dysphagia

Atypical: chronic cough, sore throat, chest pain

GERD Risk Factors

Fatty foods, alcohol, caffeine, obesity, smoking, tight clothing

Diagnostic Tools for GERD

Clinical trial of PPI, 24-hour esophageal pH monitoring

Treatment Goals in GERD

Symptom relief, healing, prevention of relapse and complications

Lifestyle Modifications for GERD

Smaller meals, avoid lying down after eating, smoking cessation, avoid triggers (e.g., chocolate, citrus)

Examples of Antacids

Aluminum hydroxide, Magnesium trisilicate, Calcium carbonate

Mechanism of Antacids

Neutralize gastric acid, onset within 15 mins, duration 1–3 hrs

Timing of Antacids

Best taken 1 hour after meals

Alginates (e.g., Gaviscon)

Forms a “raft” that floats on stomach contents, preventing reflux

Examples of H2RAs

Cimetidine, Famotidine

Mechanism of Action (H2RAs)

Reversibly inhibit H2 receptors on gastric parietal cells → ↓ acid secretion

Adverse Effects of Cimetidine

Gynecomastia, galactorrhea, inhibits CYP450 → drug interactions

Limitation of H2RAs

Tolerance may develop with long-term use

Examples of PPIs

Omeprazole, Pantoprazole, Esomeprazole

Mechanism of Action (PPIs)

Irreversible inhibition of H⁺/K⁺-ATPase pump in gastric parietal cells

Dosing Tip

Take 30–60 mins before meals for optimal efficacy

Treatment Duration

2–8 weeks depending on indication

Common Side Effects of PPIs

Headache, diarrhea, long-term: ↓ B12, ↑ fracture risk, C. difficile infection

Drug Interactions (PPIs)

Omeprazole inhibits CYP2C19 → may reduce clopidogrel effectiveness

Examples of PCABs (potassium-competitive acid blockers)

Vonoprazan, Tegoprazan, Fexuprazan

Mechanism of PCABs

Compete with K⁺ for binding on the proton pump → fast, reversible acid suppression

Advantages of PCABs

Faster onset, food-independent absorption, alternative in PPI-resistant GERD

Examples of Pro kinetics

Domperidone, Metoclopramide, Itopride

Mechanism of Action (Prokinetics)

Enhance GI motility, increase LES tone, promote gastric emptying

Side Effects (Metoclopramide)

Extrapyramidal symptoms (EPS), sedation, tardive dyskinesia with long-term use

NSAID-related Ulcers

Prefer paracetamol or add PPI/Misoprostol in high-risk patients

Misoprostol

PGE1 analog, protects mucosa

Side effect: Diarrhea, CI in pregnancy

Monitoring PUD Treatment

Check hemoglobin, stool guaiac test, H. pylori status post-treatment

Preventive Therapy Candidates

Elderly (>60 years), chronic NSAID/steroid users, history of GI bleeding/PUD