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19 Cards in this Set

  • Front
  • Back

what are the traditional NSAIDS and non narcotic analgesics

aspirin (aka acetyl salicyclic acid) and acetaminophen

what are the cox-2 selective agents

celecoxib (celebrex)

general mechanism of NSAIDS

they act by inhibiting the cyclooxygenase (COX) enzyme; inhibition of the COX enzyme blocks the production of the prostaglandin's which mediate the pathogenesis of inflammation and fever; so their actions are= ANTI INFLAMMATORY, ANALGESIC (this is why they're also called non-narcotic analgesics), AND ANTIPYRETIC

what are the roles of prostaglandins in inflammation

vasodilation, vascular permeability, sensitizes nerve receptors to other inflammatory mediators, fever

so where does the inhibition of cyclooxygenase (COX) fit in with the inflammatory process

arachidonic acid is first acted on by COX on it's way to making prostaglandins, thromboxanes (prothrombotic compound), or prostacyclines (antithrombotic compounds); have to be a little carful blocking COX through because then arachidonic acid can be pushed into its alternate route of leukotrienes (can cause bronchospams)

what effect do prostaglandins have on the stomach

increase mucous secretion, increase bicarb secretion, inhibit gastric secretion

what effect does thromboxane have on the blood

inducer of platelet aggregation

what effect do prostaglandins have on the kidney

modulates the production of renin, and of renal blood flow (causes vasodilation)

what effect do prostaglandins have on inflammation

vasodilation and increased vascular permeability; cause pain; cause the hypothalamus to increase body temp (fever)

when aspirin interacts with COX where does it act

on serine 530; it acetylates it; THIS IS UNIQUE AMONG TH NSAIDS BECAUSE BY ACETYLATING THE ACTIVE SITE IT IRREVERSIBLY INACTIVATED THE ENZYME; this means that the platelets are no longer able to make any of the arachidonic break down products (except the leukotrienes) until their death and therefore clearance of the drug (will have blood thinning effect for many days)

so what is the difference between this COX-1 and COX-2

we didn't know that there were these 2 isoforms; COX-2 is only expressed in the BRAIN and parts of the KIDNEY, AND ENDOTHELIUM (AND OVARY); otherwise it is very similar to COX-1 and inhibited by the same things (but could we make one that is specific to COX-2? and why would that be helpful?)

stress in the kidney leads to what

dehydration leads to an increase in COX-2 expression which produces prostaglandins that play an important role in preserving renal function; this example is just to show that COX-2 does have some specific functions different from that of COX-1

COX-2 in the brain

in the hypothalamus the production of prostaglandins by COX-2 is what is responsible for resetting the body's thermostat during fever

overall responsibilities of COX-1 and COX-2

COX-1 is responsible for the homeostatic functions of prostaglandins (ex. stomach mucin) while COX-2 is responsible for the inflammatory response as well as some homeostatic functions

side effects of our standard NSAIDS

the blocking of the homeostatic functions of COX-1 as well as the inflammatory of COX-2; gastric ulcers, blockade of platelet agg, inhibition of uterine motility, inhibition of prostaglandin mediated renin production, inhibition of fever, inhibition of pain, inhibition of inflammation

examples of some COX (in general) inhibitors (NSAIDS)

aspirin, indomethacin, ibuprofen, acetaminophen, diclofenac, naproxen

the COX-2 inhibitor that we will study

CELECOXIB aka celebrex (way more specific for COX-2 than for COX-1)

what is the problem with Vioxx and Bextra

they are also COX-2 inhibitors and so they inhibited the formation of PGI2 (an antithrombotic agent) so basically they increased the risk of thrombosis (people were having heart attacks) and they were taken off the market; why doesn't celebrex do this? it probably does do this but they stopped the studies (protect their product) (don't give it to a pt that even has a slight risk of MI); also it has slightly less specificity for COX-2 than the others (so maybe some COX-1 thrown in is good)

a 62 y/o women has recently become a pt of your and you havediagnosed her as having rheumatoid arthritis (RA). This pt also has a history of coronary heartdisease. In discussing treatment optionsfor her RA, in addition to prescribing a DMARD (disease modifyinganti-rheumatic drug), you express a hesitation in prescribing celecoxib(celelbrex). In your explanation to heryou point out that this drug is a COX-2 selective inhibitor and like anotherCOX-2 selective inhibitor (Rofecoxib, Vioxx) that was taken off the market,over time it may inhibit the production of WHICH EICOSANOID that is thenassociated with an increase in the risk of a cardiovascular event (e.g.myocardial infarction)?A. thromboxane A2(TXA2)B. prostaglandin E1(PGE1)C. prostacyclin I2(PGI2)D. Prostaglandin F2(PGF2)E. Leukotriene (LTB4)

C. prostacyclin I2 (PGI2)