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49 Cards in this Set
- Front
- Back
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list 3 general properties of NSAIDS
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prevention of arachidonic acid release 1. anti-inflammatory2. anti-pyretic 3. analgesic
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what is the general mechanism of action of NSAIDS
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inhibiton of COX prevents the conversion of arachidonic acid to prostaglandins
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aspirn (acetylsalicylic acid) mechanism of action
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IRREVERSIBLE inhibitor of COX via acetylation of serine group
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aspirn (acetylsalicylic acid) is an IRREVERSIBLE inhibitor of the COX enzymes. What is the therapeutic implication of this in terms of anti-platelet therapy?
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Platelets express COX1 and produce TXA2 which promotes platelet aggregation. Plateles do not have a nuclues so when aspirin irreversibly inhibits COX, the effect lasts for several days until new platelets are synthesized. Endothelial cells express COX1 and COX2 but they synthesize PGI2 which inhibits platelet aggregation. Endothelial cells can make new COX after aspirin inhibits it. THis tips the prostaglandin balance to the PGI2/ anti-aggregation state
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list three unique effects of aspirin/ slicylates that are not releated to inhibition of COX
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1. uric acid excrestion: low doese=decrease, high dose=increase 2. CNS-delirium, psycoses, nausea, vom. toxicity 3. direct stimulation of respiratory center, increase rate, respiratory alkalosis, indirect stimultion via increase in oxygen consumtion and CO2 production in skeletal muscle
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describe the affect of aspirin on uric acid excretion
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1. low dose-aspirin cometes with uric acid for secretion by transporter into renal tubules, leads to decreased excretion 2. high dose= aspirin competes for both secretion and reabs, leads to increased excretion
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describe the GI side effects associated with NSAIDS
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inhibtion of COX leads to a decrease in the produciton of PGI2, PGE, prevents cytoprotective effects leading to ulcers and bleeding, can Tx w/ misoprostol a PGE analog
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describe the blood side effects associated with NSAIDS
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increased bleeding time, inhibiton of COX1 in platelet blocks produciton of TXA and decreases aggregation (note implication of aspirin as irreversible blocker, endothleial production of anti-aggregation PGI2)
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Describe the hypersensitivty reaciton associaited with NSAIDS
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bronchoconstriciton, edema, may be due to action of leukotrienes because of shunting of AA form COX to lipoxygenase pathway
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describe the renal side effects associated with NSAID use
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decreased renal blood flow and GFR, salt and water retention due to inhibiton of COX1= decrease PGI2, PGE2 vasodilatory effect, very important in pts with congestive heart failure, chornic renal disease, or liver disease
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describe the implications of NSAID use in pregnancy
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inhibition of COX= decrasein PGE, PGF can decrease uterine contracitons and prolong labor, also PGE matains patent DA, could have premature closure
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describe salicylism
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aspirin overdose, swtich to zero order kinetics, respiratory stimulation, nausea, vomiting, tinnitus deafness, confusion, fever, dehydration, electrolyte imbalance, metabolic acidodsis, Tx=gastric lavage, charcoal, replace fluid and electrolytes, alkalization of urine
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Describe Reye's syndrome
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unique to aspirin, in children link between viral infection and taking aspirin, can result in liver failure and death
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ibuprophen mechanism, use
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NSAID, reversible COX 1/2 inhibitor, shorter 1/2 life than naproxen, tx inflammatory disease, rehumatoid disorders, pain ,fever, injection to induce closure of PDA
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naproxen mechanism and use
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NSAID reversible, COX 1/2 inhibitor, longer t1/2 than ibuprophen, tx ankylosing spondylitis, osteoarthritis, rheumatoid disorders, acute goute, pain , tendonitis, bursitis, fever
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indomethacin mechanism and use
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NSAID, reversible COX 1/2 inhibitor, acute goutly athritis, burisits, tendonitis, osteoarthtis, AnkS. close PDA, decrease pre term labor
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ketorolac mechanism and use
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NSAID, reversible COX 1/2 inhibitor, manage of moderate to severe acute pain, opoid alternative
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nabumetone mechanism and use
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NSAID, reversible inhibitor of COX 2> COX1, prodrug-converted to active metabolite, used for osteoarthitis, rheumatoid arthitis
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Piroxicam mechanism and use
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NSAID, reversible COX 1/2 inhibitor, very long half life, tx rehumatoid and osteo arthtis
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sulfasalazine mechanism and use
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NSAID but effect is not relaed to inhibiton of COX, action= inhibiton of production of IL-1, TNFa, inhibit LOX pathway, scavenge free radicals/ oxidants, inhibit NFKB, azo linkage prevents abs in stomach and small intestine, effective delivery to distal GI, used for ulcerative colitis, rheumatoid arthritis, ANKS
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celecoxib mechanism and use
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seletive COX 2 inhibitor, decreased risk of GI side effects, Tx arthritis, dysmenorrhea, acute apin, reduce # of polyps in FAP
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acetaminophen mechanism and use
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inhibits reduction of COX enzyme to peroxidase for but No affinity for active site, analgesic and anti-pyretic but NOT ANTI-INFLAMMATORY, note toxicity esp w/ alcohol (occurs when metabolized by CYP450 and GST is exhausted)
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describe gout
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inflammatory reaction to sodium urate crystals that are deposited in the join, associated w/ hyperuricemia but not sole determinant
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how do NSAIDS (other than aspirin) treat gout
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usually indomethacin, provide symptomatic relief, decrease inflammation
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how do corticosteriods treat gout
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dramatic symptomatic relief by decreasing inflammation, useful for those with contraindication to nsaids
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how does colchicine treat gout
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exact mechanism not known, antimitotic effects arrest cell division in G1 by interfering with microtuble and spindle formation, decreases crystal induced secretion of chemotatcitc factors and SO2- by neutrophils, limits neutrophil adhesion to endotheilum
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colchicine mechanism and use
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treats goute, exact mechanism not known, antimitotic effects arrest cell division in G1 by interfering with microtuble and spindle formation, decreases crystal induced secretion of chemotatcitc factors and SO2- by neutrophils, limits neutrophil adhesion to endotheilum
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how does allopurinol treat gout
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competitive inhibitor of xanthine oxidase, decreases amount of uric acid
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allopurinol mechanism and use
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tx gout, competitive inhibitor of xanthine oxidase, decreases amount of uric acid
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probenecid mechanism and use
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inhibition of organic acid transport in renal tubule, tx gout
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how are NSAIDS used to treat RA
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anti-inflammatory changes if given in large doses for long periods of ime but no evidence that they effect the progression of the disease, symptomatic relief only
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Etanercept mechanism and use
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soluble recombinant TNF receptor fusion that binds endogenous TNF and inhibits its action, used to treat RA, other arthitis, and psoriasis
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infliximab mechanism and use
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chimeric IgG monoclonal Ab, binds TNFa, inhibits its action, used to treat RA, Chronn's, ulcerative colitis, psoriasis
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anakinra mechanism and use
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antagonist of IL-1 receptor, use to treat RA that has failed other drugs
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why should a pt with CHF use NSAIDS with caution
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NSAIDS decrease prostaglanins. PGE2 and I2 dilate the renal vasculature to maintain perfusion in the kidneys when AngII is constricting everything else. Ang II is high in pts with CHF, NSAID inibition of prostaglandins would cause a decrease in renal perfusion
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irreversible inhibitor of COX 1/2
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aspirin, acetylsalicylic acid
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reversible inhibitor of COX which t 1/2=2 hrs, can be used via IV to close PDA
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ibuprofen (premies, indomethacin is also used to close PDA)
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an NSAID that can manage pain at the opioid level
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ketorolac
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an NSAID that is a prodrug, has a higher affinity for COX 2 than COX1
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nabumetone
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an NSAID with an exceptionally long t1/2 (~50hrs)
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piroxicam
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an NSAID with effects that are not related to inibition of COX, contains an azo linkage that allows it to be delivered to the distal GI
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sulfasalazine
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an NSAID that is a selective COX 2 inhibitor
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celecoxib
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inhibits the reduction of COX to its peroxidase form, no anti-inflammatory properties
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acetaminophen
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a gout drug that has antimitotic effects
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colchicine
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a gout drug that is a competitive inhibitor of xanthine oxidase
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allopurinol
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a gout drug that inhibits the organic acid transporter in the renal tubule
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probenecid
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a soluble, recombinant TNF receptor fusion protein that binds and inhibits TNF
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etanercept
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a chimeric IgG that bins TNFa and inhibits its action
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infliximab
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an IL-1 receptor antagonist
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anakinra
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