antacids Flashcards
1. Describe the syndromes involving gastric acid production and the pharmacological approaches used to modulate gastric acidity 2. List the prototype proton pump inhibitors, H2 antagonists, anti-muscarinics, antacids and mucosal protective agents, describe their mechanism of action, pharmacokinetics, clinical uses, and significant side effects 3. Define peptic ulcers, describe the role that Helicobacter pylori play in inducing peptic ulcers, list the two therapeutic approaches for treatment of
how stomach acid is formed
1) meal, or anticipation of a meal relases gastrin
2) gastrin induces the release of histamin from ECL cells
3) histamine deffuses to paritel cells and acts on H2 receptors to produce cAMP
4) cAMP actiavtes the proton pump to secrete H+
acid protective factor released by epithelial cells
prostaglandin
recurrence rate of h pylori caused ulcers if the bug is not eliminated
100%
PPIs
-prazole
MOA of PPI
suicide inhibitor of H+/K+ pase
long acting antiacids
PPI
reason PPIs are long active
recovery requires sythethis of new enzyme and instertion into the cell membrane
requires an acidic environment for activation
PPI
cleared by hepatic metabolism
PPI
best taken before meals
PPI
inhibits CYP2C19 the least
pantoprazole
uses for PPI
1st line for GERD, best for peptic ulcers, ZOllinger-ellison
best drug for peptic ulcers
PPI
DOC for zollinger-ellison
PPI
potential serious side effect of PPI
bacterial bloom
drug intereaction with PPI
clopidogrel, ketoconazole, ampiclillin esters
drug regimen for H pylori
PPI+amoxicillin + clarithromycin (PAC)
H2 receptor antagonists
-tidine
uses for H2 receptor agonists
non-ulcer indigestion, duodenal ulcer, gastric ulcer, GERD
more effective antiacid
PPI
MOA of H2 RAs
inhibits secretion by gastrin and muscaric agonists. Inhibits basal and meal-induced gastric HCL secretion
decreases intrinsic factor production
H2 RA
absorbed by the SI
H2 RA
excreted unchanged by the kidney
H2 RA
