COX-2 is a ____ _______ enzyme. It mediates __________, ____, _____, and ___________. its' released in response to ____, _______, ____
pain inducing
inflammation, pain, fever, carcinogensis
Injury, illness, diet
T or F: NSAIDS are one the most widely used drugs in the US?
T
What are 4 properties of NSAIDS?
analgesic
Anti-inflammatory
antipyretic
platelet inhibition
What is the mechanism of action for NSAIDS:
COX inhibition
T or F: NSAIDS have a ceiling effect, but can decrease narcotic use up to 50%
T
T or F: NSAIDS are well absorbed from the GI tract?
Have limited first pass hepatic excretion?
Are highly protein bound?
have a low pK? (3-5)
T for all
Low pK of NSAIDS make them good for _____ and ____________ areas.
Gout
inflamed areas
Hepatocellular injury is most severe with what NSAID?
tylenol
Asthma exacerbation usually caused by which NSAID?
Aspirin- due to allergy
Ketoralac can inhibit what?
bone healing
NSAIDS are __________ with opioids
synergistic
What systems see the adverse fx of NSAIDS?
GI
Renal
Coagulation
Which NSAIDS are nonspecific, inhibiting both COX-1 and COX-2? INAAK
Ibuprofen
Naproxem
Aspirin
Acetaminophen
Ketorolac
when should you stop taking aspirin before surgery? Why?
7-10 days
allow platelets recovery, normal coag (fx last life of platelet)
ASA causes ____________ acetylation of COX enzyme. It is _______ ___________ by the GI tract. It can be _________ to prevent GI side fx, and can cause _______ __________