JAWAHARLAL NEHRU TECHNOLOGICAL UNIVERSITY HYDERABAD Pharm. D IV Year PHARMACOTHERAPEUTICS - III Previous Question Paper (June/July - 2022 - R08)

Peptic ulcer disease (PUD) refers to mucosal erosions in the stomach or duodenum, primarily resulting from an imbalance between aggressive factors (gastric acid, pepsin, bile salts) and defensive mucosal factors (mucus, bicarbonate, prostaglandins, blood flow). The two primary etiologies are Helicobacter pylori infection and the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs).

Etiopathology:

1. H. pylori infection: This bacterium produces urease, which neutralizes gastric acid and allows colonization. It induces inflammation, increases gastrin release, and decreases somatostatin, leading to hyperchlorhydria and mucosal damage.
2. NSAID-induced: NSAIDs inhibit cyclooxygenase (COX-1) enzymes, reducing the synthesis of cytoprotective prostaglandins. This diminishes mucus and bicarbonate secretion and reduces mucosal blood flow, making the lining vulnerable to acid-pepsin injury.
3. Other factors: Hypersecretion of acid (Zollinger-Ellison syndrome), smoking, alcohol, and stress-related mucosal damage contribute to the pathogenesis.

Pharmacotherapy:

The goal of therapy is to eradicate H. pylori, reduce acid secretion, and promote mucosal healing.

1. H. pylori Eradication: Triple therapy is the standard, typically consisting of a Proton Pump Inhibitor (PPI) twice daily, plus two antibiotics (e.g., Clarithromycin 500 mg and Amoxicillin 1 g) for 10–14 days. Bismuth-based quadruple therapy is used in areas of high resistance.
2. Acid-Suppressive Therapy:
   PPIs (e.g., Omeprazole, Pantoprazole) are the most effective agents for inhibiting the H+/K+-ATPase pump. H2-receptor antagonists (e.g., Ranitidine, Famotidine) are used for less severe cases or maintenance.
3. Mucosal Protective Agents: Sucralfate forms a physical barrier over the ulcer site. Bismuth subsalicylate provides both antibacterial effects against H. pylori and protective coating. Misoprostol, a synthetic prostaglandin E1 analog, is specifically indicated for preventing NSAID-induced ulcers.
4. Antacids: Magnesium or aluminum hydroxide salts provide rapid, short-term symptomatic relief by neutralizing existing gastric acid.