Drugs Employed in GI Disease 1 Flashcards

1
Q

the 2 causes for ulcers

A

increased acid production and decreased mucosal resistance

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2
Q

3 interventions for ulcers

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

calcium carbonate

A

antacid. reacts w/ HCl to make calcium chloride and carbonic acid. side effect is constipation. use in combo with magnesium compounds

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4
Q

sodium bicarbonate

A

antacid. rarely used because of systemic alkalosis. high sodium content

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5
Q

magnesium hydroxide/magnesium carbonate

A

antacid. may cause magnesium toxicity in presence of renal disease. adverse effects include diarrhea. can cause bradycardia with renal problems.

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6
Q

aluminum hydroxide

A

antacid. combines with HCl to make aluminum chloride and water. aluminum Cl -> aluminum phosphate which cant be absorbed. doesnt disturb serum electrolyte or pH. useful in renal failure patients. may have protective effect on mucosa. causes constipation

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7
Q

simethicone

A

defoaming agent in antacids. decreases gas bubbles/bloating

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8
Q

sodium

A

used with antacids. small amounts, but can cause concern in patients with edema and hypertension.

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9
Q

anticholinergic agents effect

A

vagotomy type of effect. reduction of HCl secretion, spasmolytic effect. adverse effects include dry mouth, blurry vision, atony of bladder, constipation, drowsiness, confusion.

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10
Q

anticholinergic drugs + when you take them

A

atropine, propantheline, dicyclomine. administered 30 minutes before meals and at bedtime.

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11
Q

blockade of histamine H2 receptor

A

lower acid secretion by blocking H2 histamine receptors on parietal cells. decrease basal and food stimulated acid secretion. dont need to be given in relationship to meals

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12
Q

H2 receptor antagonists list

A

cimetidine, ranitidine, famotidine, nizatidine. inhibi 50-80% of 24 hour acid secretion.

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13
Q

other use for H2 receptor antagonists

A

can be used prophylactically to decrease stress ulcers in ICU and burn patients.

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14
Q

what happens if you abruptly stop h2 blockers?

A

hyperproduction of acid! ween off slowly

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15
Q

H2 blocker adverse effects

A

messes with p450 so can interfere with metabolism of other drugs. headache, lethargy, confusion, depression. severe side effects uncommon

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16
Q

list the 6 H/K ATPase inhibitors (proton pump inhibitors)

A

omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole, dexlansoprazole

17
Q

which proton pump inhibitors can be given IV

A

pantoprazole. doesn’t mess with p450.

18
Q

proton pump inhibitor mechanism of action

A

accumulate selectively in the highly acid environment of the canniliculus. protonated to a reactive thiophillic sulfenamide that binds to cysteine 813 in the alpha subunit of the enzyme. non competitive inhibitors. better pain relief and faster ulcer healing rates than with H2 antagonists. will heal H2 refractory ulcers

19
Q

adverse effects of PPIs

A

headache, gynecomastia, inhibition of P450, gastric hyperplasia possible in long term stuff.

20
Q

factors impairing mucosal resistance to acid

A

smoking, genetics, stress, NSAIDs, H. pylori

21
Q

bismuth salts

A

in acid environment it forms crystals that precipitate on the ulcer crater. lower ulcer recurrence rate than with h2 antagonists

22
Q

sucralfate

A

aluminum hydroxide complex, activates in acid environment, binds to ulcerated tissue. as effective as H2 antagonists.

23
Q

what type of ulcers are prostaglandin E2 analogs

A

used in people with NSAID ulcers, because duodenal ulcer patients already hyperproduce E2 prostaglandins

24
Q

misoprostol

A

prostaglandin E2 analog. decrease acid production, increase mucous and bicarb secretion. less effective than H2 blockers when used solo. approved for prevention of NSAID ulcers. can cause diarrhea, dont use in pregnant bitches!

25
Q

preferred therapies for H. pylori infection

A

twice a day PPI or ranitidine bismuth citrate triple therapies (PPI or bismuth + 2 of antobiotics)

quadruple therapy: PPI twice a day, tetracycline, bismuth, metronidazole