Pharm GI drugs 1 Flashcards Preview

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Flashcards in Pharm GI drugs 1 Deck (48):
1

what stimulates acid production?

1. gastrin (form antrum)
2. acetylcholine (vagal inputs, CNS)
3. histamine (stimulated by acetylcholine and gastrin from mast cells)
4. parietal cell H/K ATPase - final common pathway

2

where is stomach acid made and what stimulates its release?

parietal cell - stimulated by histamine, gastrin, and acetylcholine

3

how does acetylcholine stimulate the proton pump?

through Ca activating a protein kinase

4

how does gastrin stimulate the proton pump?

through Ca activating a protein kinase

5

how does histamine stimulate the proton pump?

through g couple protein causing increased cAMP which activates teh protein kinase

6

what has an inhibitory affect on acid release?

prostaglandin E2

7

what is the approach to treating ulcers?

1. relief of symptoms (esp pain)
2. promotion of healing
3. prevention of complications such as perforation, hemorrhage, scar formation
4. prevention of recurrence

8

what are the three mechanisms for pharmacologic interventions for treatment of ulcers?

1. neutralize acid
2. decrease acid production
3. increase mucosal resistance

9

what pharmacologic agents are used to neutralize acid?

antacids

10

what pharmacologic agents are used to decrease acid production?

1. anticholinergics (antimuscarinic)
2. antihistamines
3. proton pump inhibitors

11

what pharmacologic agents are used to increase mucosal resistance?

1. prostaglandins
2. sucralfate
3. bismuth

12

what does acid neutralizing efficiency depend on?

1. neutralizing power of the antacid
2. the degree or rate of acid secretion
3. the rate of stomach emptying

13

what are the characteristics of an ideal antacid?

1. elevate pH to at least 5
2. best taken about 1 hr after each meal (acidity at peak)
3. liquid formulations act more promptly and are more effective than tablet

14

what are the antacids?

1. calcium carbonate
2. sodium bicarbonate
3. magnesium hydroxide and magnesium carbonate
4. aluminum hydroxide

15

calcium carbonate therapeutics and side effects

therapeutics: ulcer and GERD
SE: milk-alkali syndrome, nephrocalcinosis, "rebound" acidity, digitalis antagonism

16

sodium bicarbonate therapeutics and side effects

therapeutics: ulcer and GERD
SE: systemic alkalosis (rarely used now)
also enhanced effects of amphetamine, quinidine, and cinchophen

17

magnesium hydroxide and magnesium carbonate therapeutics and side effects

therapeutics: ulcer and GERD
SE: diarrhea!, hypokalemia, hypermagnesemia, iron deficiency
*magnesium toxicity in renal disease

18

aluminum hydroxide therapeutics and side effects

therapeutics: ulcer and GERD
SE: phosphate depletion and sequelae (weakness, anemia, tetany, apnea), constipation!
*used in patients with renal failure (also helps eliminate phosphate!)

19

what are other common ingredients used in antacid preparations?

1. defoaming agent (antiflatulent effects)
2. sodium (can cause some salt and water retention - careful in cardiac failure, edema, ascites, HTN)

20

what do antacids cause enhanced absorption of?

dicumarol and L-dopa

21

what do antacids caused reduced absorption of?

phenothiazines, INH, nalidixic acid, nitrofurantoin, penicillin G, sulfonamides, calcium

22

what is a difficulty when prescribing antacids?

patient compliance (stop when pain stops and then ulcer relapses)

23

side effects of anticholinergic agents

dryness of mouth, blurred vision, atony of the bladder, constipation, drowsiness, mental confusionatropine

24

what are the anticholinergics used to decrease acid production?

atropine sulfate, propantheline, metantheline bromide

25

when are anticholinergics administered?

30 min before meals and at bedtime

26

what are contraindications for anticholinergics?

pyloric obstruction, patients with hiatus hernia, peptic esophagitis

27

what are the drugs that competitively inhibit the histamine H2 receptor?

-tidines
cimetidine, ranitidine, famotidine, nizatidine

28

why are the H2 receptors blockers good drugs to use for decreasing acid production?

-decrease basal and food stimulated acid secretion
-don't have to be administered in relationship to meals
-one large dose just as effective as frequent smaller doses
-can be used prophylacticly
-long-term maintenance, reducing relapse
-more convenient = better compliance

29

what is a disadvantage to using H2 blockers?

rebound hyperacidity (more acid output after stopping treatment) - need to taper dose

30

side effects of H2 blockers?

severe adverse effects uncommon. headache, lethargy, confusion, depression, hallucinations

31

what are the proton pump inhibitors?

-prazoles
omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole

32

when are proton pump inhibitors (-prazoles) taken?

~30 min before you eat - parietal cell has to be turned on in order to be turned off

33

which proton pump inhibitor can be given IV and has no P450 inhibition?

pantoprazole

34

what is the proton pump inhibitor mechanism?

non competitively inhibits more than 90% 24 acid secretion but requires acid environment to activate (can't take with antacids)

35

proton pump inhibitor clinical uses?

ulcer treatment, GERD

36

which -prazoles are effective at treating H pylori? what are they prescribed with?

omeprazole and lansoprazole
-triple therapy: add tetracycline, metronidazole, and clarithromycin

37

adverse side effects of -prazoles

headache, gynecomastia, inhibition of cytochrome P450 (delayed metabolism of diazepam, warfarin, dilantin), gastric hyperplasia long term (don't use long term)

38

which proton pump inhibitors have the most P450 interference?

omeprazole and lansoprazole

39

what is the prostaglandin E analog? what is its mechanism

misoprostol - decreases acid production, increase mucous and bicarbonate secretion

40

when is misoprostol used?

ulcer treatment when prostaglandin production is decreased (RA patients taking lots of NSAIDs)

41

what mechanisms maintain mucosal integrity?

epithelial cells secreting mucus and bicarbonate
mucosal blood flow

42

what is a characteristic of duodenal ulcer patients?

acid stimulated bicarbonate production is reduced

43

what are factors impairing mucosal resistance to acid?

smoking, genetics, stress, NSAIDs, H pylori leading impaired mucosal defense = ulcer

44

what are mechanisms to increase mucosal resistance?

1. coat ulcer crater (bismuth salts and sucralfate)
2. increase mucous and bicarb secretion (prostaglandin E2 analogs)
3. eradicate H Pylori

45

bismuth mechanism

mechanical protector: coats teh ulcer crater, increasing mucosal resistance

46

sucralfate mechanism

mechanical protector: an aluminum hydroxide complex of sucrose, binds to ulcerated tissue, activated in acid environment

47

side effects of mechanical protectors (bismuth salts and sucralfate)

no serious adverse effects - occasional constipation, aluminum toxicity, possible renal failure

48

what is used to treat h pylori?

triple therapy: PPI or ranitidine bismuth citrate plus 2 of : amoxicillin, clarithromycin, or metronidazole