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MODHIII - Unit 3 > GI Drugs > Flashcards

Flashcards in GI Drugs Deck (75)
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1

Routes of acid stimulation

- histamine: from ECL cells
- gastrin: from G cells
- acetylcholine: nervous system (vagus nerve)

2

Histamine stimulated acid release is inhibited by

protanoids

3

Histamine acts on what receptor on parietal cell

H2

4

How is acid pumped into the stomach from parietal cells

K+/H+ ATPase antiporter

5

Proton Pump Inhibitors (PPIs): drugs

- Omeprazole
- Esomeprazole
- Lansoprazole

6

PPIs activation

- all are prodrugs that require acid activation

7

PPIs: action

- IRREVERSIBLY inhibit the proton pump
- enter parietal cells from the systemic circulation & activated withing the acidic environment around proton pump
- ineffective if activated in stomach by acid so they are put in gelatin capsules, coated, mixed with bicarb, or given parenterally

8

PPIs: administration

- gelatin capsules (omeprazole, esomperazole, lasoprazole)
- enteric coated tablets (pantoprazole, rabeprazole, omeprazole)
- mixed w/ bicarb (omeprazole)
- pantoprazole and lansoprazole can be give parenterally

9

PPIs: dose

- dosed daily
- active for about 2 hours but therapy relies on slow turnover of K+/H+ ATPase at the apical surface

10

PPIs: uses

- lower acid secretion 90%
- GERD, erosive esophagitis, peptic ulcers, zollinger-ellison syndrome, NSAID induced gastric ulcers, part of H. pylori treatment

11

PPIs: clearance

LIVER

12

PPIs: activity of proton pumps

- not all proton pumps are active at any one time
- only those that are active react with these drugs
- treatment requires 2-5 days

13

PPIs: adverse reactions

- nausea, abdominal pain, constipation, flatulence, diarrhea
- drug interactions through altered CYP activity: increase serum WARFARIN concentrations, decrease activation of clopidogrel

14

H2 receptor antagonists: drugs & duration

- cimetidine: 4-5 hrs
- ranitidine: 6-8 hrs
- famotidine: 10-12 hrs

15

H2 receptor antagonists: process and use

- block base level of acid secretion maintained by ECL cells
- use: NOCTURNAL acid secretion, duodenal ulcers, zollinger-ellison

16

H2 receptor antagonists: effectiveness

- decrease acid secretion 70% for 24 hours with daily dosing

17

H2 receptor antagonists: excretion

- RENAL via organic cation system

18

H2 receptor antagonists: adverse reactions

-

19

H2 receptor antagonists: adverse effects of cimetidine

- long term use of cimetidine at high doses decreases testosterone binding to androgen receptor and hydroxylation of estradiol causing galactorrhea in women and decreased sperm count, impotence and gynecomastia in men

20

H2 receptor antagonists: tolerance

- tolerance can develop in 3 days due to direct acid stimulation by gastrin

21

Prostaglandin analogs: Misoprostol

- synthetic analog of PGE1
- short acting, up to 3 hrs
- use: NSAID induced injury (less than PPIs and H2 antagonists though)
- adverse: diarrhea (30%), exacerbate IBD, increase uterine contractions

22

Sucralfate

- octasulfate of sucrose with Al(OH)3
- forms sticky neutral pH polymer coating that covers epithelium
- uses: stress ulcers (sticks better to duodenal than gastric ulcers)
- ACID activated, so take before food, and avoid antacids and PPIs
- adverse: constipation, block absorption of other drugs through stomach

23

Antacids: process & components

- neutralize pH of gastric contents
- Al(OH)3, Mg(OH)2, CaCO3 common components

24

Antacids: action

- fast acting: 15 min
- last up to 2-3 hours WITH food

25

Antacids: Mg vs. AL

Mg: fast acting, stimulates gastric emptying and motility
Al: slower acting, delays gastric emptying and slows motility

26

Antacids: gas

- surfactant simethicone is sometimes added to reduce gas

27

Antacids: adverse effects

- rebound acid secretion
- Mg contraindicated in RENAL disease
- interference with GI absorption of other drugs: take antacids 2 hrs before or after other drugs**********

28

Muscarinic antagonists

- pirenzepine: selective for M1 receptors
- blocks neurotransmission in ganglia resulting in less vagal stimulation of parietal and ECL cells
- reduce basal acid by 50%
- significant anticholinergic side effects

29

H. pylori infection

- 50% of all humans: 1/3 are pathogenic, difference is vacuolating endotoxin A
- associated with over half of peptic ulcer disease, gastritis, GERD
- bacteria need acid, which activates the toxin

30

H. pylori treatment

- combination of acid neutralization, cytoprotection, antibacterial agent