NSAIDS and Gout Treatment Flashcards
Salicylate drugs:
aspirin
salicylic acid
Non-specific NSAID drugs:
HIT BOTH COX1 and 2
- *aspirin
- *ibuprofen -
- *indomethacin - gout
- *ketorolac
- *naproxen
- *oxaprozin
- *piroxicam
- *sulindac
COX2 Inh drugs:
CeleCOXIB
EtorlCOXIB
Meloxicam
Analgesic/Antipyretic (not anti-inflammatory) drugs:
acetaminophen
Acute gout Tx drugs:
- NSAIDS=Indomethacin - primary for severe
- Colchicine
Gout prophylaxis drugs (lower uric acid levels):
1) xanthine oxidase inh (des UA production:
- allopurinol
- febuxostat
2) uricosuric drugs (inc renal excretion of UA):
- probenecid
- sulfinpyrazone
Classic inflammatory symptoms:
1) redness
2) swelling
3) heat
4) pain
Molecular inflammatory mediators:
1) kinins- BRADYKININ
2) neuropeptides- Substance P
3) vasoactive amines- Histamine & 5-HT
4) Arachidonic acid metabolites
- COX (prostaglandin, tromboxanes, prostacyclin)
5) Cytokines- TNF-alpha
- ACETAMINOPHEN IS NOT AN NSAID! –> NO ANTI-INFLAMMATORY PROPERTIES!
- ONLY HAS ANALGESIC AND ANTIPYRETIC PROPERTIES
- ACETAMINOPHEN IS NOT AN NSAID! –> NO ANTI-INFLAMMATORY PROPERTIES!
- ONLY HAS ANALGESIC AND ANTIPYRETIC PROPERTIES
NSAIDs - Functional Characteristics:
- analgesia
- antipyretic
- anti-inflammatory
NSAIDs -Primary target/MOA:
Dec prostaglandin production by inh COX1 and COX2
Products of arachodonic acid pathway that mediate inflammation & immunity?
PGE2 and PGI2 ==> Inc edema and vascular permeability
COX1:
always expressed and widely distributed–>keeping everything in check …such as in the stomach to protect mucosa via Prostaglandin production
–»PROTECTIVE!!!!
COX2:
- INDUCIBLE –> PRODUCTION OF INFLAMMATORY MOLECULES
- essential for kidney function
Leukotrienes primarily affect:
airways = inflammation = asthma and allergic rhinitis
NSAID uses:
pain (analgesic) fever (antipyretic inflammation (arthritis) -antithrombotic -->>bnch of other stuff
Original NSAID - prototype:
aspirin
Aspirin
-Pharmacokinetics:
- significant amount is hydrolyzed to salicylic acid (reversible COX inh) in the blood
- dose dependent uses (low=fever/pain and high=antiinflammatory)
Aspirin - why potential for drug interactions?
80% bound to plasma proteins
Low dose aspirin effects:
elimination?
- analgesic & antipyretic
- first order
High dose aspirin effects:
elimination?
Anti-inflammatory
-zero order
Aspirin works on primarily which enzyme?
COX2
Aspirin
-Antipyretic effect MOA?
- Inh of PGE2 via COX in the hypothalamus ==> resent temperature control
- drop in temperature causes dilation of superficial blood vessel + profuse sweating
Aspirin
-Anti-inflammatory MOA?
-inhibit COX2 –> no PG synthesis
== inh inflammatory cell migration