Drugs for Upper GI Tract Flashcards
(30 cards)
Name the H2 receptor antagonists.
Cimetidine, Famotidine (more potent, better side effects, fewer drug interactions)
Describe the mechanism of action of H2 receptor antagonists.
They directly block histamine-stimulated gastric acid secretion and also blunt the parietal cell response to ACh and gastrin
What are the adverse side effects associated with H2 receptor antagonists?
Hormonal side effects, esp at high doses- gynecomastia, impotence in males, female galactorrhea
Discuss the pharmacokinetics of H2 receptor antagonists.
They are rapidly absorbed, peak quickly (~1 hour), are metabolized in the liver by CYP enzymes and are excreted by the kidneys.
What kind of patient should have a reduced dose when taking H2 receptor antagonists?
Renal insufficient patient
Name the proton pump inhibitor discussed in class.
Omeprazole
Describe the mechanism of action of PPIs.
Irreversible inhibition of parietal cell proton pump (H+/K+-ATPase). The drug gets through the stomach and accumulates in the cannaliculi of the parietal cells where it is protonated into its active form, so when the cell secretes acid the drug binds inhibiting the pump’s activity.
What are the clinical indications for PPIs?
First choice in Zollinger-Ellison syndrome (rare condition caused by gastrin-secreting tumors), peptic ulcers, and GERD.
*Also used w/ abx to treat H. pylori
Name the antacids discussed in lecture.
Mg(OH)2, Al(OH)3, CaCO3
Describe the mechanism of action of antacids.
They are weak bases that are poorly absorbed, thus they stay in the GI lumen and directly neutralize stomach acid
Which antacids cause constipation?
Al(OH)3 and CaCO3. They can be combined with Mg(OH)2 which may be diarrhea-producing, to balance things out.
Describe the drug interactions that can occur with antacids.
Many can increase/decrease absorption. Al and Ca can decrease absorption of tetracycline, isoniazid, ketoconazole…
When should you take antacids?
After the meal to neutralize acid
Name the mucosal protective agents discussed in lecture.
Sucralfate, Bismuth Subsalicylate (Pepto Bismol), and Misoprostol (a PG analog)
Describe the mechanism of action of sucralfate.
It forms a paste-like gel at low pH that adheres to positively charged proteins of epithelial cells and ulcer craters. This coating protects cells from acid and pepsin attack
Describe the mechanism of action of bismuth subsalicylate.
Not well understood, but It binds selectively to ulcers to protect against acid and pepsin, with antimicrobial properties
Describe the side effects associated with bismuth subsalicylate.
It may blacken the stool and tongue
Describe the mechanism of action of misoprostol.
It is a PGE1 analog, inhibiting acid secretion and augmenting mucus and HCO3 secretion
What should be avoided with sucralfate?
Do NOT co-admin with other antacids.
When is bismuth subsalicylate contraindicated?
In children (b/c of Reye’s syndrome, like aspirin)
When is misoprostol contraindicated?
In pregnancy, as it can induce uterine contractions
Which mucosal protective agent can adsorb other drugs?
Sucralfate
Name the antiemetics discussed in lecture.
Metoclopramide (aka Reglan), Odansetron (aka Zofran)
Describe the mechanism of action of metoclopramide.
It is a centrally acting dopamine receptor antagonist (D2 and 5-HT3 receptors) and a prokinetic agent (agonist at 5-HT4 peripherally). It enhances ACh release in myenteric plexus, improves intestinal smooth muscle response to ACh, and increases esophageal sphincter tone
