GI pharm Flashcards
H2 antagonists (drugs)
Cimetidine (major one)
ranitidine
famotidine
H2 antagonists - MOA
Works on parietal cells to decrease HCl secretion caused by vagally or gastrin-induced release of histamine from enterochromaffin-like cells
No effect on gastric emptying time
H2 antagonists - uses
Less effective the PPIs Used in: PUD, GERD, ZE syndrome
Cimetidine - what is it? Side effect profile?
H2 antagonist
SE:
- major inhibitor of certain cyp450s –> elevated levels of other drugs
- anti-androgenic effects –> decreases androgens –> gynecomastia and decreased libido
Proton pump inhibitors (PPIs)
Omeprazole and related “-prazoles” are irreversible, direct PPIs (K+/H+ antiport) in gastric parietal cell
PPIs - clinical uses
More effective than H2 blockers in everything
- PUD (peptic ulcer disease)
- GERD
- ZE syndrome
- eradication regime for H. pylori
Misoprostol
PGE1 analog – cytoprotective increasing mucus and bicarbonate secretion
also decreases HCl secretion
Misoprostol - clinical uses
previously used for NSAID-induced ulcers, but PPIs are now used
Sucralfate
Polymerizes GI luminal surface to form protective, gel-like coating of ulcer beds – basically coats the ulcer and protects from further damage
Requires acid pH (antacids may interfere)
Uses: increased healing and decreased ulcer recurrence
Sucralfate - biggest problem with this drug?
can’t really take it with any other GI drugs (anti-cholinergics, H2 blockers, or PPIs)
Requires an acidic environment to work, so any of the other drugs may interfere with that
Bismuth subsalicylate
Similar to sucralfate MOA: binds selectively to ulcer, coating and protecting it from acid and pepsin main component of peptobismol
Bismuth subsalicylate - clinical uses
combined with metronidazole and tetracycline to eradicate H. pylori (BMT regimen)
Most rapid way to relieve the pain associated with peptic ulcers
Antacids – aluminium hydroxide, magnesium hydroxide or calcium carbonate neutralizes protons in the gut lumen
Antacids
aluminium hydroxide, magnesium hydroxide or calcium carbonate neutralizes protons in the gut lumen
ionization states and absorption
ionized –> harder to absorb (remember best characteristics of absorption is: small, nonpolar, noncharged)
Antacid + weak base drug || what happens to the absorption?
weak base drug is increased. antacid –> increased pH –> neutral form of drug –> increased uptake
Antacid + weak acid drug || what happens to the absorption?
weak acid drug is decreased. antacid –> increased pH –> ionized form of drug –> decreased uptake
Interaction between antacids and tetracyclines or fluoroquinolones
Decreased activity of the antibiotics because of chelation. The metals chelate up the antibiotics and are excreted
Major 2 receptors in the chemoreceptor trigger zone (CTZ) responsible for vomiting
D2
5HT3
chemoreceptor trigger zone – receptors
D2
5HT3
CB1 (cannaboid receptor 1) – normally inhibitory effect on emesis
Emetic pathways
Antagonists
- 5HT3
- D2
- M1 (muscarinic)
- NK1
Agonists
- CB1 (cannaboid)
antiemetic 5HT3 antagonists
“-setrons”
- ondansetron (used in cancer chemotherapy)
- granisetron
antiemetic DA antagonists
Work on D2 receptors
- prochlorperazine (weak anti-psychotic effects)
- metoclopramide (used in cancer chemo; also prokinetic GI motility in GERD)
antiemetic DA antagonists – SE profile
anti-psychotic effects –> pseudo Parkingson disease found especially with chronic use
