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Sucralfate is a locally acting substance that in an acidic environment (pH < 4) reacts with hydrochloric acid in the stomach to form a cross-linking, viscous, paste-like material capable of acting as an acid buffer for as long as 6 to 8 hours after a single dose. [29]
Sucralfate is also effective in this role, as it coats the ulcer, thus protecting it from caustic stomach acid. Second, antibiotic therapy is used to eliminate the underlying bacterial infection. Clarithromycin and amoxicillin are commonly used in tandem, but antibiotic regiments may vary based on organism susceptibility , side effects, and ...
When antacids do not provide enough relief, medications such as H 2 blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed. [29] [30] Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. [31] They include the medications sucralfate and misoprostol.
Mucosal disruption in acid peptic disease patients can be caused by infection, barrier disruption, or gastric acid hypersecretion.Acid peptic diseases can arise due to various risk factors such as Helicobacter pylori infection, alcoholism, tobacco use, cocaine and amphetamine use, nonsteroidal anti-inflammatory drug use (NSAIDs), fasting, Zollinger-Ellison syndrome, angiogenesis inhibitor ...
Gastric acid or stomach acid is the acidic component – hydrochloric acid of gastric juice, produced by parietal cells in the gastric glands of the stomach lining. In humans, the pH is between one and three, much lower than most other animals, but is very similar to that of carrion eating carnivores , needing protection from ingesting pathogens .
Cimetidine was the prototypical histamine H 2 receptor antagonist from which later drugs were developed. Cimetidine was the culmination of a project at Smith, Kline & French (SK&F; now GlaxoSmithKline) by James W. Black, C. Robin Ganellin, and others to develop a histamine receptor antagonist that would suppress stomach acid secretion.