Pharm GI drugs 1 Flashcards by Abbey Phelps

what stimulates acid production?

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

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where is stomach acid made and what stimulates its release?

parietal cell - stimulated by histamine, gastrin, and acetylcholine

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how does acetylcholine stimulate the proton pump?

through Ca activating a protein kinase

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how does gastrin stimulate the proton pump?

through Ca activating a protein kinase

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how does histamine stimulate the proton pump?

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

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what has an inhibitory affect on acid release?

prostaglandin E2

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what is the approach to treating ulcers?

relief of symptoms (esp pain)
promotion of healing
prevention of complications such as perforation, hemorrhage, scar formation
prevention of recurrence

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

neutralize acid
decrease acid production
increase mucosal resistance

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what pharmacologic agents are used to neutralize acid?

antacids

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what pharmacologic agents are used to decrease acid production?

anticholinergics (antimuscarinic)
antihistamines
proton pump inhibitors

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what pharmacologic agents are used to increase mucosal resistance?

prostaglandins
sucralfate
bismuth

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what does acid neutralizing efficiency depend on?

neutralizing power of the antacid
the degree or rate of acid secretion
the rate of stomach emptying

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what are the characteristics of an ideal antacid?

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

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what are the antacids?

calcium carbonate
sodium bicarbonate
magnesium hydroxide and magnesium carbonate
aluminum hydroxide

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calcium carbonate therapeutics and side effects

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

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sodium bicarbonate therapeutics and side effects

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

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magnesium hydroxide and magnesium carbonate therapeutics and side effects

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

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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!)

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what are other common ingredients used in antacid preparations?

defoaming agent (antiflatulent effects)

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

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what do antacids cause enhanced absorption of?

dicumarol and L-dopa

what do antacids caused reduced absorption of?

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

what is a difficulty when prescribing antacids?

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

side effects of anticholinergic agents

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

what are the anticholinergics used to decrease acid production?

atropine sulfate, propantheline, metantheline bromide

when are anticholinergics administered?

30 min before meals and at bedtime

what are contraindications for anticholinergics?

pyloric obstruction, patients with hiatus hernia, peptic esophagitis

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

-tidines | cimetidine, ranitidine, famotidine, nizatidine

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

what is a disadvantage to using H2 blockers?

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

side effects of H2 blockers?

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

what are the proton pump inhibitors?

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

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

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

pantoprazole

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)

proton pump inhibitor clinical uses?

ulcer treatment, GERD

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

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

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)

which proton pump inhibitors have the most P450 interference?

omeprazole and lansoprazole

what is the prostaglandin E analog? what is its mechanism

misoprostol - decreases acid production, increase mucous and bicarbonate secretion

when is misoprostol used?

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

what mechanisms maintain mucosal integrity?

epithelial cells secreting mucus and bicarbonate | mucosal blood flow

what is a characteristic of duodenal ulcer patients?

acid stimulated bicarbonate production is reduced

what are factors impairing mucosal resistance to acid?

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

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

bismuth mechanism

mechanical protector: coats teh ulcer crater, increasing mucosal resistance

sucralfate mechanism

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

side effects of mechanical protectors (bismuth salts and sucralfate)

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

what is used to treat h pylori?

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