NSAIDS

Question 1

NSAIDS ADME

Answer 1

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

Question 2

Source of major biological effect

Answer 2

Inhibition of prostaglandin synthesis

Question 3

Low dose NSAIDS

Answer 3

analgesic, antipyretic

Question 4

High dose NSAIDS

Answer 4

Antiinflammatory, closure of PDA

Question 5

Prostacyclin

Answer 5

Synthesized by vascular endothelium, Vasodilates, and inhibits platelet aggregation

Question 6

Thromboxane

Answer 6

Platelet aggretation, vasoconstriction, bronchoconstriction. Mediator of inflammation

Question 7

PGE2

Answer 7

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

Question 8

COX-1 vs COX-2

Answer 8

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.

Question 9

Adverse effects of NSAIDS

Answer 9

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

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

Question 10

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

Answer 10

No. It is contraindicated

Question 11

Asprin mechanism

Answer 11

Irreversible inhibitor of COX 1 and COX 2

Question 12

Asprin hypersensitivity reaction

Answer 12

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

Question 13

Asprin is counterindicated in children because of the risk of?

Answer 13

Reye’s Syndrome

Question 14

Asprin and acid-base balance

Answer 14

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

Question 15

Ibuprofen - important info

Answer 15

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

Question 16

Naproxen - important info

Answer 16

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

Question 17

Celecoxib

Answer 17

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.

Question 18

GI protective agent

Answer 18

Omeprazole - Proton pump inhibitor - prodrug, enteric coating

Question 19

Acetaminophen

Answer 19

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

Question 20

Acetaminophen toxicity

Answer 20

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

Question 21

Acetaminophen overdose management

Answer 21

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