NSAIDS Flashcards
common uses for NSAIDS
acute and chronic pain conditions
cancer-associated pain syndromes
treatment of dysmenorrhea
prevention of thrombosis
example of carboxylic acid
acetylated: ASA
nonacetylated: sodium salicylate, salicylamide, difunisal
examples of acetic acids
indomethicin, sulindac, tolmetin
examples of proprionic acids
ibuprofen, naproxen, COX 2 inhibitors
examples of enolic acids
phenylbutazone, piroxicam
examples of pyrrolopyrrole
ketorolac
common therapuetic actions of NSAIDS
analgesic, antiinflammatory, antipyretic, platelet inhibitory effects
MOA of COX inhibition
resulting in decrease in peripheral synthesis of prostaglandins, inhibition of prostaglandin synthesis decreases inflammatory response to surgical trauma, thus decreases peripheral nocioception and pain perception
Two forms of COX
COX-1 is present in all tissues
COX-2 inhibitor-specific dugs reduced likelihood of GI toxicity. Is produced primarily at the site of inflammation
NSAID pharmacokinetics
- well absorbed from the GI tract
- low first pass hepatic extraction
- highly bound (>95%) to plasma albumin
- exhibit small volumes of distribution
- most are weakly acidic. with pK of 3-5
NSAID adverse reactions
dyspepsia, renal problems, skin reactions, CNS issues, inhibition of platelet aggregation
rare NSAID reactions
blood dyscrasias, erythema, uticaria, pneumonitis, aseptic meningitis, aplastic anemia
NSAIDS and gastric acid
prostaglandins go to the paraietal cells and block gastric acid production. If COX is blocked so is prostaglandins, so acid will keep building up causing dyspepsia
NSAID and renal
rarely have effects on renal function in healthy individuals.
Renal toxicity can occur, which is likely due to NSAID induced inhibition of prostaglandin synthesis, which inhibits the compensatory mechanism response for renal medullary ischemia.
What NSAID can be prescribed with absolute safety with respect to renal effects
ASA
NSAIDS and HTN
prostaglandins modulate systemic BP by effects on vascular tone in arteriolar smooth muscle and control of extracellular fluid volume.
Prostaglandins counteract response to vasoconstrictor hormones and can influence sodium balance
NSAIDS may interfere with the pharmacologic control of HTN
Usually clinically insignificant
NSAIDS and coags
due to the reversable inhibition of COX NSAIDS inhibit platelet aggregation, lasts about 5 elimination half times (24-96hrs)
Increasing period use, especially ketorolac has sparked debates among surgeons regarding postop bleeding…
conversely- useful after microvascular surgery
ASA and coags
ASA induces irreversible inactivation of platelet COX
NSAIDS and aseptic meningitis
may follow systemic drug administration especially ibuprofen and H2 receptor agonists
Syndrome is greater in females with underlying autoimmune or collagen vascular disease.
S/S appear within hours but may delay for weeks
Most patietns recover fully when drug is discontinued
Fever is common
Other usual features of meningitis, periorbital edema, conjunctivitis, hypotension, parotitis, fatigue, and seizure
NSAIDS and drug reactions
elderly patients are at greatest risk:
most common- oral anticoags and NSAIDS= increased risk of GI hemorrhage
Potassium sparing diuratics + NSAIDS= increased risk of hyperkalemia
NSAID induced decrease in renal function may interfere with clearance of:
digoxin, lithium, amoniglycoside antibiotics