Pharmacology Flashcards
What are the four H2 receptor antagonist drugs?
(Ranitidine, famotidine, cimetidine, and nizatidine)
What is the mechanism of action of H2 receptor antagonist drugs (Reversible? Non-competitive? Location?)?
(Reversible, competitive inhibitors of H2 receptors on gastric parietal cells → reduces the amount of gastric acid present in gastric secretions)
When is intravenous administration of an H2 receptor antagonist indicated? Two answers.
(Vomiting patients or ruminant patients)
(T/F) Cimetidine is also used to treat melanomas in horse patients.
(T)
Although there is such a large cost difference between IV famotidine ($55/day) and IV ranitidine ($264/day), why might a practitioner choose to use ranitidine in a horse with ileus?
(Ranitidine is also a prokinetic)
Of the H2 receptor antagonists, which is the most potent?
(Famotidine)
Of the H2 receptor antagonists, which is the least potent?
(Cimetidine)
Why should you taper doses when taking an animal off of an H2 receptor antagonist?
(Rebound gastric hyperacidity)
What are the two proton pump inhibitor [PPI] drugs?
(Omeprazole and pantoprazole)
What is the mechanism of action of proton pump inhibitors?
(Irreversibly inhibit active H+/K+ ATPase pumps)
Which of the PPIs can be administered to ruminants and by what route that makes it actually useful in those species?
(Pantoprazole can be administered to ruminants parenterally)
What two characteristics of the inactive form of PPIs allows for them to readily cross the parietal cell membrane to then be activated within the cell?
(Unionized and lipophilic)
Which of the PPIs takes longer to reach equilibrium within the cells?
(Omeprazole)
Should omeprazole be administered on an empty stomach or with a full meal?
(Empty stomach)
Effects of omeprazole are blunted in horses on what type of diet?
(All hay diets)
Do PPIs also need to be tapered for the same reason that you taper H2 receptor antagonists?
(Yes)
What adverse effect of PPIs increases an animal’s risk of non-ulcer GI complications when administered with NSAIDs?
(PPI alteration of small intestinal microbiome which play a protective role against adverse GI effects of NSAIDs)
How do PPIs increase bioavailability of themselves?
(PPIs are broken down by acids but they also block acid production, as they are continually used, block acid production and leads to less drug breakdown)
What is the mucosal protectant drug?
(Sucralfate)
Sucralfate is a complex of sucrose and aluminum hydroxide; in a pH of <4 (so in the stomach), what occurs to the sucrose and aluminum hydroxide?
(Sucrose dissociates allowing AlOH to bind to damaged GI epithelial cell membranes)
Sucralfate also stimulates local protective factors such as prostaglandins, what two effects do prostaglandins have on the GI tract?
(Increases mucosal blood flow and has negative feedback on acid production)