NSAIDs Flashcards
what are the non-pharmacological interventions to reduce inflammation
1) rest
2) heat/cold
3) weight loss
4) surgery
what are the 2 pharmacological interventions to reduce inflammation
1) NSAIDS
2) GLUCOCORTICOIDS
what is the mechanism of aspirin action
inhibition of prostaglandin synthesis
what is the oldest NSAID
aspirin
T/F NSAIDs are a family of chemically similar drugs
F
what are the three main benefits of all NSAIDs
1) anti-inflammatory
2) antipyretic
3) analgesic
prostaglandins are synthesized from ________________ by ______ and _____ enzymes
arachidonic acid; COX 1; COX 2
what are the 3 main prostaglandins
thromboxane, prostacyclin, other PGs
which of the COX enzymes is a housekeeping enzyme present at low levels in most tissues
COX1
what is COX2 important for
homeostasis of renal medulla and gastric mucosa
what is the role of:
1) thromboxane (TXA2)
2) other PGs (PGD2, PGE2, etc)
3) prostacyclin (PGI2)
1) made in platelets; promotes platelet aggregation
2) maintain tissue blood flow
3) inhibit platelet aggregation; vasodilation; gastric mucosa protection
what happens to the COX enzymes when there is inflammation
COX2 is locally upregulated -> prostacyclin produces vasodilation -> cardinal signs of inflammation
what are the signals of inflammation to the COX enzymes
plasma membrane damage or inflammatory mediator release
T/F most enzymes inhibit both COX1 and COX2
T
how to NSAIDS limit the cardinal signs of inflammation
block COX enzymes -> inhibition of production of prostaglandins -> no vasodilation (because prostacyclins blocked) -> no cardinal signs
a major benefit of NSAIDs is ___________ to ___________
reduction in blood flow; site of injury
what is the most common adverse effect of NSAIDs and why
gastric bleeding +/- ulceration; inhibition of prostaglandin synthesis means decreased secretion of bicarb/mucus, increased acid secretion and decreased blood flow to gastric mucosa (from prostacyclin and PGE2)
what are the 3 main adverse effects of NSAIDs
1) gastric bleeding
2) increased general tendency to bleed
3) renal medullary hypoxia and necrosis
What is the key takeaway of NSAIDs that preferentially target COX2
they produce fewer adverse GI affects as long as GI lesions are not already present (in which case they would be exacerbated)
T/F coxibs cause more bleeding
F; they cause less because platelet aggregation is not inhibited
what are the 4 shared pharmacokinetic properties of NSAIDs
1) weak acids
2) highy protein bound
3) hepatic metabolism (phase 2 conjugation)
4) variable elimination
T/F NSAIDs are associated with decreased uterine motility
T
what are some contraindications of NSAIDS
renal disease, gastric ulcers, hepatic disorders, hypoproteinemia, dehydration, cardiac disease
what is the shared clinical use of all NSAIDs
to reduce musculoskeletal and inflammatory pain
