Flashcards in Pharm Small Group 5.1 Deck (20):
Which medications are used to treat GERD? (3)
2) H2 blockers
Which drugs should be used in patients with mild intermittent symptoms of GERD? (2)
1) H2 blockers
What is the MOA of H2 receptor blockers?
Decrease acid secretion by inhibiting the histamine 2 receptors in gastric parietal cells
Which drugs are proton pump inhibitors? (2)
What is the MOA of PPIs?
Block gastric acid secretion by inhibiting H+/K+ adenosine triphosphate in gastric parietal cells.
HOW do PPI's inhibit the H+/K+ ATPase?
Form covalent disulfide bonds, irreversibly inactivating it.
What is the effectiveness of PPI's?
90% reduction in 24/hour acid secretion in 1 dose.
What is the main use of PPI's?
Promote healing of gastric and duodenal ulcers and to treat GERD, including erosive esophagitis, which is either complicated or unresponsive to treatment with H2 antagonist.
Besides use in GERD treatment, what else are PPI's used for?
1) Combination therapy to treat H.Pylori
2) Superior to H2 antagonist and misoprostol in healing NSAID induced peptice ulcers
3) DOC for controlling acid in ZE syndrome
Which promotility agent is used in some patients with GERD as an adjunct to acid-supression therapy?
Metoclopromide, as an adjunct to acid-supression therapy, is not effect in patients with what?
Metoclopromide may cause what?
Tardive dyskinesia (esp with long term use)
What is the MOA of Metoclopromide?
1) Facilitates ACh release from enteric neurons, mediated either by antagonisms at 5-HT3 receptors or activation of 5-HT4 receptors.
Where does Metoclopromide act?
Both central and peripheral D2 antagonist.
-Central antidopaminergic action responsible for antinauseant and antiemetic properties
-Peripheral antidopaminergic action responsible for prokinetic .
What drug polymerizes and binds to ulcers, where it may act as a barrier to acid, pepsin, and bile, and is effective in healing of duodenal ulcers?
What does Sucralfate need to be activated?
What are the first line regimens for H.Pylori eradication? (3)
1) PPI + clarithromycin + amoxicillin
2) PPI + clarithromycin + metronidazole
3) Bismuth subalicylate + metronidazole + tetracycline + ranitidine or PPI
Why isn't conventional acid-suppressant therapy recommended for H.Pylori infections?
Most patients develop recurrent ulcer within 1 year.
What is the mechanism by which NSAIDs produce ulcers? (2)
1) Direct irritant effect
2) Synthetic effect mediated by COX inhibition leading to reduction of prostaglandin synthesis.