NSAIDS Flashcards Preview

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Flashcards in NSAIDS Deck (21)
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1
Q

NSAIDS ADME

A

A - generally PO
D - Highly protein bound, found in synovial fluid.
M - extensive metabolism, enterohepatic circulation
E - Renal

2
Q

Source of major biological effect

A

Inhibition of prostaglandin synthesis

3
Q

Low dose NSAIDS

A

analgesic, antipyretic

4
Q

High dose NSAIDS

A

Antiinflammatory, closure of PDA

5
Q

Prostacyclin

A

Synthesized by vascular endothelium, Vasodilates, and inhibits platelet aggregation

6
Q

Thromboxane

A

Platelet aggretation, vasoconstriction, bronchoconstriction. Mediator of inflammation

7
Q

PGE2

A

Produced by COX-2, Increases body temperature and inflammation.

8
Q

COX-1 vs COX-2

A

COX 1 constituitively expressed in most tissues - used for gastric protection. - Inhibition leads to GI side effects. COX 2 is expressed by stress - growth factors, cytokines, and inflammatory mediators.

9
Q

Adverse effects of NSAIDS

A

GI - pain, nausea, diarrhea, ulcers, hemorrhage,

Renal - Renal insufficiency/failure, hyperkalemia, proteinuria, nephropathy

10
Q

If a patient is allergic to asprin, can you use other NSAIDS

A

No. It is contraindicated

11
Q

Asprin mechanism

A

Irreversible inhibitor of COX 1 and COX 2

12
Q

Asprin hypersensitivity reaction

A

Vasomotor rhinitis, angioedema, generalized urticaria, bronchial asthma, hypotension, shock

13
Q

Asprin is counterindicated in children because of the risk of?

A

Reye’s Syndrome

14
Q

Asprin and acid-base balance

A

At therapeutic doses, respiration increases leading to respiratory alkalosis. At toxic doses, metabolic acidosis due to accumulation of lactic acid.

15
Q

Ibuprofen - important info

A

Approved for IV admin. used to close PDA. Co-administration with asprin decreases effects.

16
Q

Naproxen - important info

A

Long T 1/2 - 14 hours. More common GI side effects than ibuprofen

17
Q

Celecoxib

A

Selective COX-2 inhibitor - less GI toxicity, but doesn’t work better than any of the other NSAIDS.
Also risk of thrombosis, hypertension, atherogenesis. Not first choice. Cross-reactivity with sulfa drugs.

18
Q

GI protective agent

A

Omeprazole - Proton pump inhibitor - prodrug, enteric coating

19
Q

Acetaminophen

A

Weak anti-inflammatory. No effect on respiratory, CV, hemostasis, GI system.

20
Q

Acetaminophen toxicity

A

Hepatotoxic at a single dose of 10-15g- nausea, abdominal pain, anorexia, elevated LFT’s

21
Q

Acetaminophen overdose management

A

N-Acetylcysteine (mucomyst) - detoxifies NAPQI - also use activated charcoal to reduce absorbtion, and supportive care.