NSAIDs II Flashcards

1
Q

differentiate between COX 1 and COX 2

A
  • COX 2:
    • inducible
    • promotes inflammation
    • inhibits platelet aggregation (PGI2)
    • vasodilation (PGI2)
  • COX 1
    • inhibits gastric acid secretion -> protects against gastric irritation
    • promotes platelet aggregation (TXA2)
    • Vasoconstriction
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2
Q

MOA of Celecoxib

A
  • selective, reversible COX-2 inhibitors
    • less risk of GI bleeding
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3
Q

adverse reactions with Celecoxib

A
  • increased risk of cardiovascular diseases
    • platelet aggregation and constriction via unopposed COX-1
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4
Q

contraindications to Celecoxib

A
  • h/o heart problems
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5
Q

MOA of Ibuprofen (Motrin)

A
  • nonspecific reversible inhibitors of COX-1 and COX-2
  • first choice drug
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6
Q

toxicities of Ibuprofen

A
  • overall toxicity is low. It is better tolerated than aspirin
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7
Q

MOA of Indomethacin

A
  • Nonspecific COX inhibitor
  • inhibit phospholipase A (needed for arachidonic acid synthesis)
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8
Q

use of Indomethacin

A

used for patent ductus arteriosus, gout

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9
Q

MOA of Diclofenac

A
  • potent nonspecific COX inhibitor
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10
Q

Diclofenac is often combined with what to decrease GI side effects

A

Misoprostol

  • combined name: arthrotec
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11
Q

Use of Ketorolac (toradol)

A
  • Nonspecific COX inhibitor used mostly as an analgesic in postsurgical pain
  • may be combined with opiates
  • can’t use for more than 5 days -> GI ulcer
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12
Q

effect of patient taking ibuprofen while on long term ASA for anticoagulation

A

combination decreases the effect on platelet aggregation!

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13
Q

MOA of Naproxen

A
  • Nonspecific COX inhibitor
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14
Q

unique about naproxen

A
  • long half life!
  • mean plasma half-life = 13 hours
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15
Q

MOA of Piroxicam (Feldene)

A
  • Nonspecific COX inhibitors
  • inhibits PMN migration, lymphocyte function
  • decreases oxygen radical production
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16
Q

why is acetaminophen often preferred to aspirin

A
  • It is tolerated better
  • Not anti-inflammatory
  • No platelet effect
17
Q

overdose of acetaminophen can cause

A
  • fatal hepatic necrosis
18
Q

primary effects of acetaminophen

A
  • antipyretic action
  • analgesic action
  • no antiinflammatory action or platelet effects
19
Q

what eliminates the free radicals that acetaminophen produces

A
  • dose dependent free radical production - elimiated by GSH (reduced glutathione)
20
Q

why should a chronic alcoholic not take acetaminophen

A
  • alcohol induces P450 system which induces more free radicals
  • circulating metabolites exceed availability of reduced glutathione -> toxicity
21
Q

treatment of acetaminophen intoxication

A
  • specific antidote: N-acetylcysteine
    • parenterally within 10-12 hrs after intoxication