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GI > Drugs > Flashcards

Drugs Flashcards

1
Q

How do PG’s protect the mucosa?

A
  • inhibit cAMP
  • decreased activity of H/K ATPase
  • stim production of mucus and bicarb
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2
Q

How is omeprazole processed in the body?

A
  • prodrug
  • absorbed and secreted into acidic canaliculi
  • acid converts drug by protonation to OM-sulfenamide
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3
Q

What is the active form of omeprazole? Function?

A
  • OM-sulfenamide
  • covalently (IRREVERSIBLE) binds H/K ATPase on cell surface (these pumps move to membrane surface when GI system is activated)
  • blocks basal and stimulated acid production 80-95%
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4
Q

How is half life of omeprazole affected?

A
  • covalently binds pump so it is irreversible

- elicits effects for turnover time of pump = 24 hours

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5
Q

What protects the oral omeprazole from acid?

A

enteric coating

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6
Q

What metabolizes omeprazole?

A

CYP2C19 - metabolized by and inhibit this CYP

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7
Q

What drug interactions should you be concerned about with omeprazole?

A

any drugs that require acidic environment (ketoconazole) = decreased availability

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8
Q

Two competitive H2 receptor antagonists?

A

cimetidine, rimetidine - higher potency, 1x a day

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9
Q

How much do H2 blockers reduce acid secretion?

A

70% - greater effect on basal than stimulated

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10
Q

What may cause a reduction in effect of H2 blockers?

A
  • blocking the receptor results in upregulation of receptor production
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11
Q

Who needs IV PPI?

A
  • patients receiving parenteral nutrition
  • if not eating food and still producing acid, need additional protection
  • before surgery (aspiration concerns)
  • chronic illness
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12
Q

How are H2 blockers excreted? Concerns in elderly?

A
  • renally in inactive and active forms

- decrease dose in elderly with dec renal function

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13
Q

What allows large 1x day dosing of H2 blockers?

A

large therapeutic window - short half life but can give large doses

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14
Q

3 minor AE’s of H2 blockers?

A

confusion, depression, hallucinations

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15
Q

What is are 3 additional AE concerns with cimetidine?

A
  • inhibits CYP’s
  • dec testosterone binding (gynecomastia, impotence)
  • inhibits estradiol hydroxylation (galactorrhea)
  • not used much anymore
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16
Q

What is a concern with discontinuing PPI and H2 blockers?

A

rebound hypersecretion

17
Q

What kind of drug is dicyclomine?

A

NON-selective muscarinic receptor antagonist

18
Q

Uses of dicyclomine?

A
  • IBS (anti-spastic effects)

- NOT anti-acid

19
Q

What are antacids used for?

A

rapid relief of dyspepsia and GERD (not effect at treating peptic ulcer disease)

20
Q

What is the antacid chemical reaction?

A

acid + antacid – salt + water

21
Q

What is an adverse effect of bicarb antacids?

A
  • Bicarb is converted to CO2

- belching

22
Q

What are two effects of Magnesium at high doses?

A

CNS depression and kidney failure (diarrhea at low dose)

23
Q

AE of Al at normal and high doses?

A
  • constipation

- dec phosphate absorption

24
Q

What analog is used to increase mucosal defense?

A

PGE agonist misoprostol

25
Q

5 effects of PGE agonists?

A
  • inhibits acid secretion
  • inc mucus secretion
  • inc bicarb production
  • inc blood flow
  • promotes healing
26
Q

Three AE’s of misoprostol?

A
  • diarrhea in 30%
  • abdominal pain (may trigger IBD)
  • abortifacient
27
Q

What is Pepto Bismol? Function?

A
  • bismuth subsalicylate
  • bismuth is cytoprotective = coats erosions, may stimulate PGE, minor anti-bact action (H. pylori)
  • salicylate is anti-inflamm
28
Q

AE of bismuth salicylate?

A
  • black color to oral cavity and feces

- be careful with ASA dosing (don’t drink by the gallon)

29
Q

What is sucralfate? Function?

A
  • Al hydroxide complex of sulfated sucrose
  • in acidic pH, forms viscous coating (dec function with PPI, H2 blockers)
  • combines with protein exudate at base of ulcer and stim PGE production
30
Q

When is sucralfate used?

A

dyspepsia/GERD in pregnant women (but PPI’s are still recommended because they are most effective)

31
Q

Treatment approach to H. pylori?

A

2 antibiotics that work by different MOA to minimize resistance development + PPI or H2 blocker

32
Q

How long does H. pylori need to be treated? Cure rate?

A

14 days

80%

GI (5 decks)

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