Peptic Ulcer: Causes and Treatment

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10 Questions

What is the primary cause of peptic ulcer?

Imbalance between the damaging effects of gastric acid and pepsin, and the defense mechanisms

What is the effect of prostaglandin E2 on gastric acid secretion?

Inhibits adenylyl cyclase

What is the role of somatostatin in gastric acid secretion?

Diminishes gastric acid production

What is the primary target of treatment for peptic ulceration?

Neutralizing gastric acid

What is the mechanism of action of histamine on gastric acid secretion?

Activates adenylyl cyclase

What is the primary mechanism by which proton pump inhibitors irreversibly inactivate the Na+/K+ ATPase enzyme?

By binding to sulphydryl groups on the enzyme

What is the recommended timing for taking proton pump inhibitors to maximize their effect?

30 minutes before breakfast or the largest meal of the day

Why should H2-receptor antagonists be taken after proton pump inhibitors?

To reduce the activity of the proton pump

What is a potential long-term consequence of prolonged hypochlorhydria induced by proton pump inhibitors?

Increased susceptibility to gastrointestinal infections

What is a unique endocrine effect of cimetidine that is not seen with other H2-receptor antagonists?

Increased prolactin levels

Study Notes

Peptic Ulcer

  • Occurs due to an imbalance between aggressive factors (gastric acid and pepsin) and defensive mechanisms (gastric and duodenal mucosa)
  • Major causes: NSAIDs use, especially in the elderly, and smoking
  • Smoking is a major environmental factor, and patients should be advised to quit

Gastric Acid Secretion

  • Secreted by parietal cells in gastric mucosa
  • Stimulated by gastrin, histamine, and acetylcholine, which bind to receptors on basolateral membranes
  • Inhibited by prostaglandin E2 and somatostatin
  • Acetylcholine and gastrin increase intracellular calcium levels, while histamine activates adenylyl cyclase

Inhibition and Neutralization of Gastric Acid

  • Proton pump inhibitors (PPIs): omeprazole, esomeprazole, lansoprazole, pantoprazole, and rabeprazole
  • Mode of action: irreversibly inhibit Na+/K+ ATPase, reducing acid secretion
  • Therapeutic uses: erosive esophagitis, active duodenal ulcer, Zollinger-Ellison syndrome, GERD, and H. pylori eradication

Proton Pump Inhibitors (PPIs)

  • Omeprazole is a prodrug, which becomes ionized in acidic media and binds to sulphydryl groups on Na+/K+ ATPase
  • Given in enteric-coated tablets due to degradation at low pH
  • Adverse effects: nausea, headache, diarrhea, constipation, rash, and interactions with warfarin, diazepam, carbamazepine, and phenytoin
  • Long-term use may increase risk of gastric carcinoid tumors, reduce vitamin B12 absorption, and increase susceptibility to GIT infections

H2 Receptor Antagonists

  • Examples: cimetidine, ranitidine, famotidine, nizatidine
  • Therapeutic uses: peptic ulcers, acute stress ulcers, and gastroesophageal reflux disease
  • Adverse effects: headache, dizziness, diarrhea, muscular pain, CNS effects (confusion, hallucinations), and endocrine effects (antiandrogenic effects)

Test your knowledge on peptic ulcers, its causes, symptoms, and treatment options. Learn about the imbalance between gastric acid and defense mechanisms, and how NSAIDs and smoking contribute to the disease. Explore the different approaches to treating peptic ulceration.

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