Pharm NSAIDs part I Flashcards
what are the cox 2 selective NSAIDs
celecoxib
what are the non-narcotic analgesics
acetaminophen (tylenol)
what NSAIDs are propionic acids
ibuprofen, naproxen
what NSAIDs are indoleacetic acids
indomethacin, etodolac
what NSAIDs are herteroaryl acetic acids
ketoralac
3 major beneficial properties of NSAIDs
anti inflammatory
analgesic
anti-pyretic
All NSAIDs inhibit what
cyclooxygenase, enzyme needed to make PGs
prostacyclin works where
endothelium
kidney
platelets
brain
thromboxane A2 works where
platelets, vascular smooth muscle cells, macrophages, kidney
PG D2 works where
mast cells, brain, airways
PG E2 works where
brain, kidney, vascular smooth muscle, platelets
PG F2 works where
uterus, airways, vascular smooth muscle, eyes
how is aspirin unique
irreversibly inhibits COX enzymes
which PG sensitizes pain nerve endings
PGE2
What PG are important mediators of erythema and edema
PGE2 and PGI2
PG effect on apoptosis
inhibit it
PG role in GI
PGI2 inhibits gastric acid secretion
PGE2 and PGF2 stimulate synthesis of protective bicarb and mucus in stomach and small intestine
aspirin effects on platelet aggregation
irreversibly inhibits it
what occurs with higher doses of aspirin
inhibit PGI2 in endothelial cells which is a vasodilator and inhibitor of platelet aggregation
NSAID effects on renal function
decrease renal blood flow and rate of glomerular filtration
conditions assoc with NSAID induced acute kidney injury
volume depletion from emesis, diarrhea, sepsis or hemorrhage medications like diuretics, ACEI, ARBS, calcinuerin inhibitors cirrhosis CHF nephrotic syndrome hyperCa chronic kidney disease Renal a stenosis older age
CI to aspirin use
in children or adolescents with chicken pox or influenza because of Reyes syndrome
and patients with gout
What is recommended for NSAID use for chronic Tx
non aspirin because it is associated with more side effects and GI effects
what are NSAIDs used to Tx chronically
RA, osteoarthritis, SLE, seronegative spondyloarthropathy, arthralgia, myalgia