Stress-Induced Gastritis Medication
- Author: Rohan C Clarke, MD; Chief Editor: BS Anand, MD more...
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
PPIs have not been fully evaluated in the role of prophylaxis for this disease.
Shown to be effective in the prevention of stress-induced gastritis.
Binds with positively charged proteins in exudates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. Primary agent for prophylaxis of stress gastritis.
Histamine H2 antagonists
These agents block H2 receptor binding. The primary indication is to reduce symptoms and to accelerate healing of gastric ulcers. In the acutely bleeding patient, they are of limited benefit. Some have also been used for prophylaxis (eg, famotidine).
Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Competitively inhibits histamine at H2 receptors of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.
Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.
Inhibits histamine stimulation of the H2 receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Proton Pump Inhibitor
Proton pump inhibitors are inhibitors of the gastric H+/K+ -ATPase (proton pump) enzyme system, which catalyzes the exchange of H+ and K+.
S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+ -ATPase enzyme system at secretory surface of gastric parietal cells.
Used in severe cases of and patients not responding to H2 antagonist therapy.
Used for up to 4 wk to treat and relieve symptoms of active duodenal ulcers; may be used up to 8 wk to treat all grades of erosive esophagitis.
Pantoprazole suppresses gastric acid secretion by specifically inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells. Use of the intravenous preparation has only been studied for short-term use (ie, 7-10 d).
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