GI Pharmacology (Mid-term exam content) Flashcards
What stimulates gastric acid secretions?
- Acetylcholine (A).
- Histamine (H).
- Gastrin (G).
How can you treat peptic ulcers?
Decrease the acid secretion.
Neutralize acid.
Promote mucosal defense.
Modify risk factors.
Which NSAID won’t cause peptic ulcers?
COX2 inhibitors, because they don’t inhibit PG in the stomach.
What does antacids form when the weak bases react with gastric hydrochloric acid?
Salt and water
Sodium bicarbonate Alka Seltzer (what does it form? in which patients its contraindicated? its SE’s?)
- produce carbon dioxide and sodium chloride.
- In a patient w/peptic ulcer (weak stomach wall), if it’s bloated it can rupture/ perforate! Don’t use sodium bicarbonate in peptic ulcer patients! + heart failure, hypertension, and renal insufficiency
- Stomach bloating.
Calcium carbonate Tums (what does it form? effect? SE’s?)
- form carbon dioxide and calcium chloride (CaCl2).
- Not very strong antacid.
- belching (due to CO2, which is a gas)
How does antacids affect the absorption of other medications?
- Binding the drug.
- Antacids decrease stomach acidity, some drugs need that acidity to act better/be absorbed.
H2-receptor antagonists examples?
Cimetidine
Ranitidine
Nizatidine
Famotidine
MOA of H2-receptor antagonists? it’s PK? Any warnings?
- Competitive antagonists of histamine and are fully reversible.
1. Histamine (ECL or vagal stimulation) is blocked from binding to the parietal cell H2 receptor.
2. Direct stimulation of the parietal cell by gastrin or acetylcholine has a diminished effect on acid secretion - inhibit nocturnal acid secretion.
- Suppress basal and meal-stimulated acid secretion.
PK: - undergo first-pass hepatic metabolism, glomerular filtration, and renal tubular secretion.
- Serum half-lives of range from 1.1 to 4 hours.
- Distribute to breast milk and across the placenta.
- Excreted mainly in urine.
- Carful: when prescribing it to pregnant ladies.
carful when prescribing it to elderly patients.
H2 blocker clinical uses?
- (GERD).
- Peptic ulcer disease.
- Non-ulcer dyspepsia.
- Prevention of bleeding from stress-related gastritis.
Cimetidine MOA? SE’s? CI? IV method?
- Inhibits binding of dihydrotestosterone to androgen receptors, inhibits metabolism of estradiol, and increases serum prolactin levels.
- Gynecomastia, galactorrhea, confusion and altered mentation, endocrine effects.
- CI: Not for pregnant women! (cross the placenta)
- Slow intravenous infusion, if rapid may cause bradycardia and hypotension. (blockade of cardiac H2 receptors)
Cimetidine inhibits which cytochrome isoenzymes?
Cytochrome P450 isoenzymes (Can interfere with the metabolism of many other drugs).
Proton-pump inhibitors (PPIs) MOA?
- Block the final common pathway of acid secretion, the proton pump.
Proton-pump inhibitors (PPIs) SE’s?
- SE’s: No more acids, patient is prone to infections! Hypergastrinemia (promote the growth of GI tumors), hypomagnesemia, nausea, abdominal pain, constipation, flatulence, and diarrhea, Subacute myopathy, arthralgias, headaches, and skin rashes, increased risk of bone fracture, (Chronic treatment with omeprazole decreases the absorption of vitamin B12).
Proton-pump inhibitors (PPIs) Metabolized by which hepatic CYPs?
- Metabolized by hepatic CYPs, particularly CYP2C19 and CYP3A4
