GI Drugs Flashcards
1
Q
examples of antacids
A
- sodium bicarbonate
- calcium carbonate
- magnesium hydroxide
- aluminum hydroxide
2
Q
moa of antacids
A
- weak bases react with gastric hcl to form salt and water (neutralizing)
- inhibit peptic activity
- can increase acid production
- liquids > chewables
- onset 5-15 mins, duration 2 hrs
3
Q
clinical use of antacids
A
- fast relief of gastric discomfort
- dyspepsia
- peptic ulcer and ger
4
Q
side effect of antacids
A
- less absorption of other medications
- dont give with tetracyclines, fluoroquinolones, itraconazole, and iron
5
Q
moa to h2 receptor antagonists
A
- histamine from enterochromaffin like cells is blocked
- decreased acid secretion
- bid or at bedtime
6
Q
clinical use of h2 receptor antagonists
A
- pud
- gerd
- erosive esophagitis
- non0ulcer dyspepsia
7
Q
side effects of h2 receptor antagonists
A
- most seen in elderly: constipation, mental status change
- cimetidine: most adverse effects, drug interactions
- avoid in pregnant and breastfeeding
8
Q
moa of protein pump inhibitors
A
- inhibit h+ secretion by irreversible inhibition of k/h proton pumps in parietal cells
- inhibit meal stimulated acid and basal acid
- give 30 mins to 1 hour before meals
9
Q
examples of ppis
A
omeprazole, lansoprazole, pantoprazole, esomeprazole
“prazole”
10
Q
clinical uses of ppis
A
- pud (h pylori, nsaid-related, stress, gastrinoma)
- gerd
11
Q
moa of mucosal resistance enhancers
A
- provide physical barrier over ulcer
- increase secretion of protectants (mucus, prostaglandin, bicarbonate)
12
Q
examples of mucosal resistance enhancers
A
- sucralfate
- bismuth chelate
- carbenoxolone
- misoprostol
13
Q
moa of sucralfate
A
- stimulates mucus, bicarbonate, and prostaglandin
- for gastric, duodenal, and oral ulcers, gi bleed, and stress ulcer
14
Q
moa of bismuth
A
- increases mucus
- reduces peptic activity
- eliminates h pylori
15
Q
moa of misoprostol
A
- stable analog of pge1
- augments secretion of mucus and bicarbonate
- prevention and treatment of nsaid ulcers
