NSAIDS 1 & 2 - 8/26/15

Question 1

Ibuprofen onset of action?

Answer 1

Rapid! 15-30 min

Question 2

Aspirin specific adverse effects (2)

Answer 2

Reye’s syndrome

Gout

Question 3

Aspirin + (what drug) = ameliorated GI toxicity?

Answer 3

Misprostol (careful! abortifacient!)

Omeprazole

Question 4

3 kidney diseases caused by aspirin/NSAID

Answer 4

(A) hemodynamically-mediated acute renal failure
(B) acute interstitial nephritis and nephrotic syndrome
(C) analgesic nephropathy/chronic interstitial nephritis

Question 5

Pre-op patient, or patient with platelet problems…should they take NSAIDs?

Answer 5

No - increased risk of bleeding

Question 6

ALL traditional NSAIDs are ________ inhibitors of ______

Answer 6

competitive, COX activity

Question 7

inhibition of which COX, 1 or 2, mediates therapeutic effect?

Answer 7

Cox2; Cox 1 inhibition mediates the bad effects

Question 8

Does acetaminophen inhibit peripheral COX1/2?

Answer 8

Very, very weakly

Question 9

Acetaminophen is a potent inhibitor of

Answer 9

CNS Cox2

Question 10

What is the breakdown product of acetaminophen, that also can block CNS Cox2, and bind cannabinoid receptors?

Answer 10

AM404

n-arachidonyl phenolamine

Question 11

T/F: Acetaminophen has no anti-inflammatory effects, no anti-platelet effects, and reduced adverse effects in the periphery

Answer 11

TRUE. This was emphasized.

Question 12

What is the toxic metabolite of acetaminophen?

Answer 12

N-acetylbenzoquinoneimine (NAPQI). Depletes hepatic glutathione.

Question 13

What is the antidote to acetaminophen overdose?

Answer 13

N-acetylcysteine (replenishes hepatic glutathione)

Question 14

Ibuprofen - key feature

Answer 14

rapid onset of action, ideal for fever and acute pain

Question 15

Naproxen – key feature

Answer 15

rapid onset of action, long serum half-life 14hrs- twice daily dosing

Question 16

Oxaproxin- key feature

Answer 16

long serum half life- 50-60 hrs, one daily dosing

Question 17

Indomethacin- key feature

Answer 17

potent anti-inflammatory, >toxicity; used to close patent ductus arteriosus

Question 18

Diclofenac- key features

Answer 18

relatively selective for COX-2; associated with increased risk of MI/stroke

Question 19

Ketorolac- key feature

Answer 19

mainly used as IV analgesic as a replacement for opioid analgesics

Question 20

Low dose aspirin is an effective ___________ agent as it permanently inhibits COX-1 in platelets blocking the production of pro-thrombotic thromboxane.

Answer 20

anti-thrombotic

Question 21

COX-1 is constitutively expressed and is primarily involved in ______

Answer 21

housekeeping functions

Question 22

Aspirin has a unique mechanism of action:

Answer 22

“it covalently attaches an acetyl group to the active site of COX enzymes irreversibly inhibiting COX-1 activity.”

note: aspirin inhibits COX2 also, but less potently`

Question 23

What are the 3 broad categories of NSAIDs?

Answer 23

A. aspirin and salicylates
B. Traditional NSAIDs
C. COX2 specific inhibitors

Question 24

NSAIDs are indicated for

Answer 24

Inflammation
Pain
Fever

Question 25

Inhibition of ______ is the cause of significant adverse effects of both Aspirin and the traditional NSAIDs

Answer 25

COX-1 in the stomach

Question 26

This fatal and rare side effect is seen only with aspirin, but not other NSAIDs

Answer 26

Reye’s syndrome

Question 27

Name 4 universal properties of NSAIDs

Answer 27

Reversible competitive COX inhibition.

Block prostaglandin production

Most are NON-SELECTIVE Cox 1 + 2 inhibitors

All exhibit anti-inflammatory, anti-pyretic and analgesic effects.