A/38. Drugs used in peptic ulcer diseases. Pharmacotherapy of peptic ulcer diseases. Flashcards
1
Q
Drugs need to know in this topic
A
(es)omeprazole
pantoprazole
famotidine
sucralfate
MgO magnesium oxide
Al2(OH)3
aluminum-hydroxide
2
Q
Magnesium hydroxide (Mg[OH]2)
Aluminum hydroxide (Al[OH]3)
A
Antacids Weak bases that neutralize stomach acid by reacting with protons in the lumen of the gut
- Oral
- Poorly absorbed from the bowel
Magnesium hydroxide (Mg[OH]2)
- Symptomatic relief of dyspepsia and heartburn Side
effects: diarrhea
Aluminum hydroxide (Al[OH]3)
- Symptomatic relief of dyspepsia and heartburn Side
effects: constipation
3
Q
Famotidine
A
- *H2-receptor antagonists**
1. Competitive inhibitors of H2-receptors → indirect effect on proton pump activity → decrease gastric acid secretion (mainly nocturnal acid secretion)
2. No H1, autonomic or anti-motion sickness effects (compared to H1 blockers)
3. Acid suppressing effect is milder compared to proton pump inhibitors
- Oral, parenteral
- Duration of action 12-24 h’
- Metabolism by hepatic CYP450
(affected by drugs that induce/inhibit hepatic metabolism) - Inhibitors of cytochrome P450 enzymes (cimetidine most potent)
- GERD
- Peptic ulcer disease (PUD)
- H. pylori associated ulcers (part of eradication regimen)
- NSAID’s induced ulcers
- Prophylaxis against stress-related mucosal injury
- Zollinger-Ellison syndrome
* *Side effects:** - GI distress
- Antiandrogenic effects (gynecomastia, decreased
libido) , mainly with cimetidine - Confusion, agitation (in the elderly)
- Milder drug-interactions, milder side effects
4
Q
Esomeprazole
Pantoprazole
Omeprazole (not in the list)
A
- *Proton pump inhibitors (PPI’s)**
1. Irreversible, direct inhibitors of the proton pump (K+/H+ antiport) in gastric parietal cells
2. 1st-line agents, most effective in reducing stomach acidity
- Oral, IV
(oral formulation should be administered on empty stomach) - Hepatic metabolism
- Prodrug; activation occurs inside parietal cell
**Omeprazole is an inhibitor of cytochrome P450 enzymes** (effect on: clopidogrel, warfarin, phenytoin, diazepam, cyclosporine) #Clopidogrel → bioactivation of prodrug is inhibited
- GERD
- Peptic ulcer disease (PUD)
- H. pylori associated ulcers (part of eradication regimen)
- NSAID’s associated ulcers
- Prophylaxis against stress-induced mucosal injury
- Zollinger-Ellison syndrome
Side effects: - Diarrhea, abdominal pain
- Headaches
- Decrease in oral bioavailability of vitamin-B12, iron, digoxin,
ketoconazole - Increased risk of respiratory and enteric infections
- Hypergastrinemia (loss of negative feedback of H+ on D-cells, may lead to ECL and parietal cells hyperplasia)
5
Q
Sucralfa
A
- *Mucosal-protective agents**
1. Aluminium sucrose sulphate; polymerizes on gastrointestinal luminal surface to form a protective gel-like coating of ulcer beds
2. Enhances PGE synthesis, stimulates mucus and bicarbonate secretion, enhances mucosal defense and repair
6
Q
Peptic ulcer disease – definition
A
- The term encompasses both gastric and duodenal ulcers.
- Ulcers are defined as breaks in the mucosal surface > 5 mm in size, with depth penetrating to the submucosa.
- May be acute or chronic, both penetrate the muscularis mucosae, but acute ulcer shows no evidence of fibrosis.
- Erosions do not penetrate the muscularis mucosae.
- Duodenal ulcers and gastric ulcers share many common features in terms of pathogenesis, diagnosis, and treatment.
7
Q
Therapy of H. pylori
A
Triple therapy
- Bismuth subsalicylate
- Metronidazole
- Tetracycline
- Omeprazole
- Clarithromycin
- Amoxicillin or Metronidazole
Quadruple therapy
- Bismuth subsalicylate
- Omeprazole
- Metronidazole
- Tetracycline