NSAIDs, analgesics, gout Flashcards
first line tx for OA
Tylenol + non-drug tx
If NSAID side effects are likely in OA what should you use
opioids + tylenol
How to tx acute gout? (4)
high-dose NSAIDs, colchicine, steroids, and/or opioids
How to tx frequent/severe gout or tophaceous gout?
xanthine oxidase inhibitor or probenecid
Up to what dose of tylenol is safe qid (4x/day)
1000mg qid (4000mg)
APAP activites (3)
Potent antipyretic and analgesic. (weak anti-inflammatory
WHat is APAP converted to in liver?
NAPQI
Minimum toxic dose of APAP
= 10-12 grams or 20 pills
Non-acetylated salicylates
Choline magnesium trisalicylate, salsalate
How should NSAIDs be dosed
on a schedule, not prn
NSAID MOA
Inhibit both COX1/2
COX-1 regulates what processes (4)
cellular processes: gastric protection, vascular homeostasis, plt aggregation, kidney function
COX-2 regulates what processes (3)
Mediates pain, inflammation, fever
naproxen shows a huge drop in what activity
platelet aggregation (TXA2)
Indomethacin: greater inhibtion of COX-1 or 2
Meloxicam: greater inhibtion of COX-1 or 2
APAP: greater inhibtion of COX-1 or 2
Indomethacin: greater inhibtion of COX-1
Meloxicam: greater inhibtion of COX-2
APAP: greater inhibtion of COX-2
If you have a CV risk but no GI risk, what should you take
naproxen
If you have a GI risk but no CV risk, what should you take (general class)
COX-2 inghibitor
If you have both GI and CV risk what is tx (2)
PPI + NSAID
NSAID not effective against what type of condition? why?
Compression neuropathies : carpal tunnel, etc
they aren’t inflammatory
ADEs of aspirin (3)
tinnitus, hearing loss, and gastric intolerance .
ASA MOA
COX-1 inhibitor
What is ASA not used as?
anti-inflammatory
define Tophi:
nodules comprised of monosodium urate crystals in a matrix of lipids, protein, and mucopolysaccharides
Colchicine MOA
Prevents microtubule formation and resultatnt inflammatory cell chemotaxis