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20 Cards in this Set

  • Front
  • Back
What are the MOA of NSAIDs?
All NSAIDs work by inhibiting COX

prevent conversion of Arachidonic Acid into Prostaglandins and Thromboxane

anti-inflammatory, analgesic, anti-pyretic, anti-platelet activity
What is the difference between COX-1 and COX-2?
always expressed in all tissues
maintains homeostasis
made in the ER
inhibited by Aspirin (irreversibly) and NSAIDs

Induced by inflammatory cytokines (TNFa, TGFb, IL-1, etc)
expressed at low levels in kidney, endothelium brain, uterus, ovaries, small intestines
inhibited by Aspirin, NSAIDs and COX-2 inhibitors
responsible for pro-inflammatory responses
Name the functions of prostaglandins in
COX-2 -> PGE2 and prostacyclin PGI2 cause increase edema, dilate blood vessels causing increased redness and enhance migration of phagocytes to the area

inflammatory cytokines induce COX-2 -> prostaglandins which act as pain neuromodulators in the spinal cord

inflammatory cytokines induce COX-2 which acts on the OVLT of the hypothalamus to cause fever
What are the homeostatic functions of prostaglandins?
COX-1 in the stomach and GI cause prostaglandin which protects the stomach against gastric acid.

When COX-1 is inhibited then there is no inhibition of gastric acid production.

Aspirin and NSAIDs cause ulcer

CV response
Platelets produce COX-1 produces TXA-2 which causes vasoconstriction and platelet activation and aggregation.

Endothelium produces COX-1 and COX-2 which produces PGI2 -> causes vasodilation and inhibits platelet activation

promotes vasodilation thereby increasing renal blood flow and preventing renal ischemia
increases the glomerular filtration rate
What is the MOA of low-dose aspirin?
permanently inhibits COX-1 preventing TXA2 production and inhibiting platelet aggregation
Why doesn't high dose aspirin work to treat CVD?
at high doses aspirin inhibits COX-1 and COX-2 which causes less TXA2-less platelet aggrevation but also causes less PGI2 producing less platelet inhibition
dimer of salicylic acid
converted to salicylic acid after absorption
competitive inhibitor of COX
used in treatment of mild to moderate pain, fever and inflammation
derivative of salicylic acid
not converted to salicylic acid
competitive inhibitor of COX
more potent anti-inflammatory than aspirin
cannot cross the BBB --> not antipyretic
cross BBB (except diflunisal)

protein-bound (affects Warfarin)

metabolized in the liver

excreted in the urine as free salicylic acid (10%) or conjugated (90%) low doses decreases uric acid excretion leading to gout

eliminated by first order kinetics at low doses

eliminated at zero order kinetics at high doses when its metabolic enzyme is saturaged....half-life then becomes greater than 15hrs.
equipotent with aspirin
rapid onset
20x more potent than aspirin
considered to be one of the safest NSAIDs
very long serum half-life of 50hrs allows once daily dosing

think.. oxen can work long hours so ox-aproxin can work long t1/2 is 50 hours
10-40X more potent than aspirin as an anti-inflammatory
most effective NSAID at reducing fever
not well tolerated
drug of choice to promote closure of patent ductus arteriosus
INDO= in doors close the patent duct
equipotent to aspirin
closely related to indomethacin- less potent
Dic lof enac
Dic lof enac

relatively selective for COX-2
increased heart/stroke risk similar to Vioxx (↑40%)

used as i.v. analgesic for moderate/severe post surgical pain
can be used to replace opiods eg. aspirin
increased incidence (>9.5X) of peptic ulcers and bleeding
preferentially inhibits COX-2
associated with fewer GI problems
associated with an increased risk of heart attach and stroke
Selective COX-2 inhibitors
Three selective COX-2 inhibitors
Celecoxib (Celebrex)
Rofecoxib (Vioxx)
Valdecoxib (Bextra)
anti-inflammatory, anti-pyretic and analgesic similary to NSAIDs

fewer GI side effects