NSAIDS Flashcards
Aspirin
- NSAID: analgesic, antipyretic, anti-inflammatory, antiplatelets
- Irreversible COX1/2 inhibitor,
- Biphasic effects on respiration (stim then depress), uric acid excretion (prevent secretion then reabsorption). GI issues, asthma, Reyes syndrome, nephrotoxicity.
- Lots of interactions, big ones are anticoagulants or anything that binds to plasma proteins.
- Can have hypersensitivity
- CI in gastric ulcers, hypoprothrominemia, vit k def, hemophilia. Stop 1wk prior to surgery.
Sodium salicylate, methyl salicylate (oil of wintergreen), Diflunisal
Sodium salicylate: nonacetylated salicylate; no platelet effects, no irreversible cox inhibition, effective anti-inflammatory, less analgesic than ASA.
Methyl Salicylate (Oil of wintergreen): irritating to skin/mucosa, fatal dose is 4-5 mL in children
Diflunisal: little antipyretic effects (poor CNS penetration), less GI irritation than ASA, not metabolized to salicylic acid but is a derivative of it.
Analgesics and PUD
No history of PUD: any NSAID
PUD history but not active: celecoxib w/ or w/out antacid or some NSAIDs w/misoprostal or “prazols” (but not aripiprazole)
Active PUD: acetaminophen and/or opioids (codeine) only!
Celecoxib
- Reversible Cox2 inhibitor
- No inhibitory effects on platelet aggregation
- Inc risk of CV disease. GI disease, asthma, renal failure
- CI in pregnancy/breast feeding, GI disease, asthma, renal fialure
- Less risk of GI bleeding/gastropathy
Indomethacin
- Inhibits Phospholipase A
- Very potent, reduces PMN migration, used to close PDA
- Worst side effects of NSAIDs, particularly upper GI/CNS effects
Sulindac
- NSAID
- Long t1/2, less nephrotoxic
- Severe GI effects including pancreatitis
Meclofenamate
- NSAID
- No advantages over other drugs
- Frequent SE, DIARRHEA
Diclofenac
- NSAID, potent COX inhibitor, also dec arachidonic acid availability.
- Oral admin, liver metabolism
- GI side effects (combined with misoprostol (arthrotec is the combination drug) to avoid GI SE)
Ketorlac
- NSAID: highest potency NSAID
- Analgesic post op, often combined w/opiates
- Get GI SE after 5 days of use, dont use longer than 5 days
Ibuprofen
- NSAID DOC: best SE profile, probably least potent
- Anti-inflammatory, antipyretic, analgesic. Better tolerated than ASA –> less SE. Less platelet effects than ASA.
- GI SE common, inc in alkaline phosphatse (indicates liver damage). Hyperuricemia possible.
- If combined with ASA the effects will decrease.
- Used in RA and osteoarthrits
Naproxen
- NSAID: longest t1/2, used in RA, osteoarthritis
- Extensively bound to plasma proteins
- Crosses placenta (CI in pregnancy), typical GI effects, bleeding not as bad as w/ASA
Piroxicam
- Inhibits PMN migration/lymphocyte function-dec radical production
- long t1/2
- GI effects very common
Nabumetone
- NSAID
- Prodrug: must be metabolized to active form, long t1/2, once daily dosing
- fewer GI SE
Acetaminophen
- Antipyretic and analgesic, not anti-inflammatory
- Not a COX inhibitor, tolerated better than ASA
- Fatal hepatic necrosis at high doses (if all reduced glutathione is used up), elevated serum transaminase and LDH indicate hepatic damage. No blood clotting defects, acid-base intolerance or auditory toxicity.
- Chronic EtOH consumption inc toxicity due to induction of CYP2E1.
- Tx of toxicity: gastric lavage (if w/in 4 hrs), forced dialysis (furosemide), admin antagonist (n-acetylcysteine (mucomyst)-paraenteral) hemodialysis. Preffered over ASA for those with ASA allergies, coagulation disorders, peptic ulcers, gout, children (reye’s). Not anti-rheumatic.