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ABBEY MSII U6 > Pharm GI drugs 1 > Flashcards

Pharm GI drugs 1 Flashcards

1
Q

what stimulates acid production?

A
  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
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2
Q

where is stomach acid made and what stimulates its release?

A

parietal cell - stimulated by histamine, gastrin, and acetylcholine

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3
Q

how does acetylcholine stimulate the proton pump?

A

through Ca activating a protein kinase

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4
Q

how does gastrin stimulate the proton pump?

A

through Ca activating a protein kinase

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5
Q

how does histamine stimulate the proton pump?

A

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

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6
Q

what has an inhibitory affect on acid release?

A

prostaglandin E2

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7
Q

what is the approach to treating ulcers?

A
  1. relief of symptoms (esp pain)
  2. promotion of healing
  3. prevention of complications such as perforation, hemorrhage, scar formation
  4. prevention of recurrence
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8
Q

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

A
  1. neutralize acid
  2. decrease acid production
  3. increase mucosal resistance
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9
Q

what pharmacologic agents are used to neutralize acid?

A

antacids

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10
Q

what pharmacologic agents are used to decrease acid production?

A
  1. anticholinergics (antimuscarinic)
  2. antihistamines
  3. proton pump inhibitors
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11
Q

what pharmacologic agents are used to increase mucosal resistance?

A
  1. prostaglandins
  2. sucralfate
  3. bismuth
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12
Q

what does acid neutralizing efficiency depend on?

A
  1. neutralizing power of the antacid
  2. the degree or rate of acid secretion
  3. the rate of stomach emptying
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13
Q

what are the characteristics of an ideal antacid?

A
  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
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14
Q

what are the antacids?

A
  1. calcium carbonate
  2. sodium bicarbonate
  3. magnesium hydroxide and magnesium carbonate
  4. aluminum hydroxide
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15
Q

calcium carbonate therapeutics and side effects

A

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

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16
Q

sodium bicarbonate therapeutics and side effects

A

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

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17
Q

magnesium hydroxide and magnesium carbonate therapeutics and side effects

A

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

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18
Q

aluminum hydroxide therapeutics and side effects

A

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

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19
Q

what are other common ingredients used in antacid preparations?

A
  1. defoaming agent (antiflatulent effects)

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

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20
Q

what do antacids cause enhanced absorption of?

A

dicumarol and L-dopa

21
Q

what do antacids caused reduced absorption of?

A

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

22
Q

what is a difficulty when prescribing antacids?

A

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

23
Q

side effects of anticholinergic agents

A

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

24
Q

what are the anticholinergics used to decrease acid production?

A

atropine sulfate, propantheline, metantheline bromide

25
Q

when are anticholinergics administered?

A

30 min before meals and at bedtime

26
Q

what are contraindications for anticholinergics?

A

pyloric obstruction, patients with hiatus hernia, peptic esophagitis

27
Q

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

A

-tidines

cimetidine, ranitidine, famotidine, nizatidine

28
Q

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

A
  • 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
Q

what is a disadvantage to using H2 blockers?

A

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

30
Q

side effects of H2 blockers?

A

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

31
Q

what are the proton pump inhibitors?

A

-prazoles

omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole

32
Q

when are proton pump inhibitors (-prazoles) taken?

A

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

33
Q

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

A

pantoprazole

34
Q

what is the proton pump inhibitor mechanism?

A

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

35
Q

proton pump inhibitor clinical uses?

A

ulcer treatment, GERD

36
Q

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

A

omeprazole and lansoprazole

-triple therapy: add tetracycline, metronidazole, and clarithromycin

37
Q

adverse side effects of -prazoles

A

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

38
Q

which proton pump inhibitors have the most P450 interference?

A

omeprazole and lansoprazole

39
Q

what is the prostaglandin E analog? what is its mechanism

A

misoprostol - decreases acid production, increase mucous and bicarbonate secretion

40
Q

when is misoprostol used?

A

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

41
Q

what mechanisms maintain mucosal integrity?

A

epithelial cells secreting mucus and bicarbonate

mucosal blood flow

42
Q

what is a characteristic of duodenal ulcer patients?

A

acid stimulated bicarbonate production is reduced

43
Q

what are factors impairing mucosal resistance to acid?

A

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

44
Q

what are mechanisms to increase mucosal resistance?

A
  1. coat ulcer crater (bismuth salts and sucralfate)
  2. increase mucous and bicarb secretion (prostaglandin E2 analogs)
  3. eradicate H Pylori
45
Q

bismuth mechanism

A

mechanical protector: coats teh ulcer crater, increasing mucosal resistance

46
Q

sucralfate mechanism

A

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

47
Q

side effects of mechanical protectors (bismuth salts and sucralfate)

A

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

48
Q

what is used to treat h pylori?

A

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

ABBEY MSII U6 (18 decks)

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