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192 Cards in this Set
- Front
- Back
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what are the four routs arachidonic acid is oxygenated
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cyclooxygenase, lipoxygenase, P450 epoxygenase, isoprostane
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COX 1 is always what
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present in most cells in the body
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COX 2 is what
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inducible as an early response product in inflammatory cells responsible for prostaglandin production
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effects of prostacyclin
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vasodilator, platelet aggregation inhibition
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effects prostaglandins
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important in may process most are not inflammatory variety of effects of blood vessels, nerve endings, and cells
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effects of thromboxane
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vasoconstrictor and promotes aggregation of platelets
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thrombaxne is a smooth muscel what
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smooth muscle mitogen
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prostaglandins are not what
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non-mitogenic constricts or dilates depends on compound
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effects of PGE, E2, I2 in the airway
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resp smooth muscle relaxants
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effects of TXA, PGF2a in the airway
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contracts airway
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effects of TXA and PG in GI
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both activate GI smooth muscle
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effects of PGE2 and PGF2a in GI
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colicky cramps
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TXA2
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platelet aggregator
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Prostaglanding E1 and I2 effects on platelets
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inhibit aggregation
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what are the products of arachodonic acid metabolism via the lipoxygenase pathway
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hydroperosyeicosatetraenoic acids which rapdily convert to hydroxyderivatives and leukotrienes
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leukotrines are powerful what
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chemotatic agents on inflammatory cells
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leukotrines promote what effects that are associated with what
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promote bronchoconstriction and alter vascular permeability associated with asthma and anaphylactic shock
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what do corticosteroids block
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all pathways of eicosanoid synthesis
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what do NSAIDs block
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prostaglandin and thromboxane formation
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what are primary goals in treating inflammation
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relief of pain and termination of the tissue damaging process
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this drug does not reduce inflammation
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acetaminophen
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what is ultimate drug in inflammatory processes
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glucocorticoids
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when is peak salicylate levels reached with aspirin
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1-2hrs
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what does acid do to salicylate
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promotes absorption
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salicylate binds to what
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albumin
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what is aspirin metabolized to
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hydrolyzed to acetic acid and salicylate by esterases
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how would you increase excretion of free salicylate
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alkalinize urine
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what is elimination of aspirin in low doses
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first order elimination
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what is elimination of aspirin in higher doses
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zero order
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what is MOA of aspirin
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inhibit cyclooxygenase and may scavenge oxygen free radicals, irreversible block of COX
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aspirin decreases formation of what
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PG, and TXA2
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aspirin does not decrease formation of what
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leukotrines
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what are anti-inflammatory effects of aspirin
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reduce eicosanoids and other mediators, granulocye adherence to damaged blood vessels, inhibit migration of neutrophils and macrophages to site
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mild arthritis may be managed with what
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salicylates alone
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aspirin is effective for what type of pain
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mild to moderate pain
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what types of pain is aspirin good for
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muscular, vascular, dental, post partum pain, arthritis, bursitis
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aspirin is not good for what pain
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visceral pain
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anti-inflammatory effects of aspirin are synergistic with what
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opiods to increase effectiveness
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what temp is aspirin effective against
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elevated body temp
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MOA of aspirin for temperatures
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dissipation of heat through vasodilation of superficial blood vessels, blocks both production of PG and CNS response to IL-1
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aspirin blocks what to decrease temperature
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blocks production of PG and CNS response to IL-1
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what is the order of fever reducers in infection form best to worse
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aspirin, ibuprofen, acetaminophen
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when should aspirin be stopped prior to surgery
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1 wk
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aspirin inhibits what for platelet effects
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inhibits TXA synthesis
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how long do aspirins anti-coagulation effects last
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8 days until new platelets can be made
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what is the therapeutic anti-coag uses of aspirin
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decrease incidence of transient ischemic attacks and unstable angina, decrease incidence of artery bypass graft loss, preempt or decreased severity of evolving MI
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what are the therapeutic results of 325mg every other day
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40% reduction of MI
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what are some of the other uses of aspirin
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may reduce cataract formation, long-term low dose may lower incidence of colon cancer
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buffered aspirin doesn't contain what
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enough buffer to modify gastric irritation
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what are the effects of enteric coated aspirin
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decreases gastritis
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what are the adverse effects of aspirin
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gastric upset, erosive gastritis and ulcers, upper GI bleeding, vomiting, small increase in fecal bleeding
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salicylism
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tinnitus, decreased hearing and vertigo
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how is salicylism reversed
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by reducing the dose of aspirin
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what are CNS side effects of aspirin
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salicylism, hyperpnea, acidosis and then central respiratory depression
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what does hyperpnea from aspirin cause
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respiratory alkalosis
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what is acidosis from asprin caused by and what does it cause
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it is caused by accumulation of salicylic acid derivatives and then central respiratory depression
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aspirin is contraindicated in what
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patients with hemophilia
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aspirin is not recommended for who
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pregnant women
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aspirin can be used when
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during breast feeding
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reyes syndrome
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fatty infiltration of the liver and brain <18yrs
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what is reyes syndrome associated with
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some viral infections like chickenpox and use of APAP
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what is overdose amount of aspirin
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150-175mg/kg of body weight
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what is treatment for aspirin overdose
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gastric lavage, alcohol sponges, ice packs for hyperthermia, maintain urine output, Na bicarb to facilitate excretion
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what are drug intercations that enhance salicylate intoxication
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acetazolamide and ammonium chloride
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what is the effect of alcohol with salicylates
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alcohol increases GI bleeding produced by salicylates
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what drugs are displaced by aspirin
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tolbutamide, chlorpropamide, NSAIDs, metotrexate, phenytoin, and probenecid
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what is the effect of corticosteroids on salicylate
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decrease salicylate concentration
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what is the effect of aspirin on spirolactone
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spirolactone is decreased by ASA
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What competes with aspirin for renal tubular secretion
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penicillin G
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what effects are inhibited by aspirin
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sulfinpyrazone and probeneciduricosuric
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what are the effects of inhibition of COX 1 by NSAIDs
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GI toxicity and nephrotoxicity
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what is the function of COX 2
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produce prostaglandins at sites of inflammation
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what are the effects of inhibition of COX 2 by NSAIDs
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decrease pain and inflammation
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COX 2 selective agents
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rofecoxib, valdecoxib, celecoxib, diclofenac, etodolac, meloxicam, nabumetone
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nonacetylated salicylates
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magensium choline salicylate, sodium salicylate, salicylsalicylate
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nonacetylated salicylates are better for whom
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asthmatics, those for whom bleeding could be a problem, or renal dysfunction
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diflunisal
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newer NSAID chemically derived from salicylic acid
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diflunisal is used for what
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OA, RA, pain
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effects of diflunisal
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analgesic, anti-inflammatory, little anti-pyretic
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NSAID ADME
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A-food does not effect
D-protein bound all found in synovial fluid M-some phase 1 some phase 2 E-renal, biliary excretion and reabsorption |
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anti-inflammatory MOA for NSAIDs
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reduced by decreasing rls of mediators from granulocytes, basophils, and mast cells
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drugs with shorter half life are usually used for what
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musculoskeletal pain
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drugs with longer half life are usually used for
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RA and other chronic conditions
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to varying degrees all newer NSAIDs are what
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anti-inflammatory, antipyretic, analgesic, and all inhibit platelet aggregation
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what are adverse effect of NSAIDs on GI
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all are gastric irritants, dyspepsia, NV,
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what is the the order of gastric irritants with NSAIDs from most to least
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piroxicam>indomethacin>naproxen>sulindac>diclofenac>ketoprofen>ibuprofen
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what are risk factors for GI adr's with NSAID use
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over 60, history of gastric or duodenal ulcer, cardiovascular disease, inflammatory disease disability, concurrent steroid use
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what is most common reason for stopping NSAID therapy
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GI effects
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NSAIDs are not at risk for what
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ulceration
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always give the what with NSAIDs
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lowest possible dose
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H2 antagonist may do what with NSAIDs
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reduce NSAID related dyspepsia
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all currently available NSAIDs induce what
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nephrotoxicity
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what is usually the duration limit with NSAIDs
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1-2 wk limit
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NSAID induced nephrotoxicity is most likely in what patients
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CHF, cirrhosis, intrinsic renal disease
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there is an occasional increase in what with NSAIDs
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serum LFT's
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diclofenac can cause what
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clinical hep
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what shoudl be done if patient is on Diclo+Flurbi
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check LFTs after 8wks
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there is an increased risk of what with sulindac
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acute liver injury
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when is liver dysfunction from naproxen more common
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in OA or RA
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what are the CNS ADRs from NSAIDs
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aseptic meningitis, psychosis, cognitive dysfunction, tinnitus
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when should NSAIDs be stopped prior to surgery
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5 half lives
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NSAIDs should be avoided in what patients
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patients with platelet defects or thrombocytopenia
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what is the cardiovascular adr of NSAIDs
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water retention and increased blood pressure
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NSAIDs antagonize what
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loop diuretics and antihypertensives
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what needs to be monitored when on NSAIDs
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baseline SCr if increased the at higher risk
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what are opthalmic ADR for NSAIDs
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drug crystals in cornea, corneal edema
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NSAIDs can cause what in pregnancy
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increased uterine contractility
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what are NSAIDs interactions with probenecid (anticoagulant)
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increased levels of NSAIDs
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what are NSAIDs interactions with Thiazides
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decrease diuretic effectiveness except sulindac
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what are interactions with antihypertensives
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antihypertensives may work less well
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what are interactions with digoxin
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increase digoxin levls
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what are interactions with MTX
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increase MTX levels
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what are interactions with Li, CSA, phenytoin
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increases levels of these drugs
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what are the effects of ibuprofen
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analgesic, antipyretic, anti-inflammatory
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what is equivalent dose of ibuprofen and ASA
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2.4g Ib=4g ASA
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what is effect of using IBU with ASA
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can decrese total anti-inflammatory effect
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when is IBU contraindicated
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asthma, nasal polyps
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what are renal effects of IBU
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acute renal failure
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IBU is good for what
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bone pain
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antacids delay absorption of what
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naproxen
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naproxen competes with what for protein binding sites
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ASA
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naproxen prolongs what
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prothrombin time
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what NSAID is most likely to cause interstitial nephritis
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fenoprofen
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Flurbiprofen is similiar to what for RA, OA, and ankylosing spondylitis
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ASA
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what is a special formulation of flurbiprofen
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topical ophthalmic
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what should be checked with flurbiprofen
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LFTs 8 wks after
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what does ketoprofen inhibit
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both cyclooxygenase and lipoxygenase
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ketoprofen does not alter what
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warfarin or digoxin activity
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what are the effects of porbenecid on ketoprofen
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increase ketoprofen and prolong half life
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ADR of ketoprofen
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GI mild 30% and may increase serum Cr
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Oxaprozin is mildy what
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mildly uricosuric
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oxaprozin is more useful in what than other NSAIDs
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gout
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dosing for oxaprozin
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once a day
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when are dose adjustments made with oxaprozin
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5 days to 2 wks
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oxaprozin does not interfere with what
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INR
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high concentrations of diclofenac are reported to do what
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inhibit formation of leukotrines but not through direct inhibition
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what are uses of diclofenac
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RA, OA, long term/short term dysmenorrhea
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ADR of diclofenac
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GI irritation, severe hepatic reactions
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uses for sulindac
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RA, OA, gout
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sulindac is a what
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prodrug
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ADR for sulindac
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GI, Stevens johnson, epidermal necrolysis syndrome, thrombocytopenia, agranulocytosis, and nephrotic syndrome
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Tometin is approved for use where
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in peds
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tolmetin is similar to ASA in what conditions
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JRA, RA, OA, but better tolerated
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tolmetin has no what
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enterohepatic circulation
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etodolac has what effects
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selective Cox 2
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when is etodolac used
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post-op analgesia, OA, RA, relief of symptoms of JRA
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meloxicam is structurally related to what
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piroxicam
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Cox 2 selectivity of meloxicam is what
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dose dependent and less at higher doses
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what is the risk with meloxicam
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hepatotoxicity
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what is dosing with nabumetone
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once daily
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nabumetone is a what
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prodrug
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meclofenamate and mefenamic acid are less effective than what
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ASA
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what is time limit on meclofenamate and mefenamic acid
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no more than one week
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meclofenamate and mefenamic acid enhance what
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oral anticoagulant activity
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when should meclofenamate and mefenamic acid be stopped
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hemolytic anemia, diarrhea, skin rashes,
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what is dosing on piroxicam
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once daily
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what are adr's of piroxicam
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dizziness, tinnitus, headache, and rash
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one of the most potent inhibitors of PG synthesis
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indomethacin
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what does indomethacin antagonize
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furosemide
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when should indomethacin be cautioned
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asthma, angioedema, nasal polyps, peptic ulcer, psych disorders
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what are uses of indomethacin
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gouty arthritis, ankylosing spondylitis, pericarditis, and pleurisy
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indomethacin can replace what are intial drug in acute gout
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colchicine
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what can indomethacin be used for in premature infants
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management of patent ductus arteriosus
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what are GI adr's of indomethacin
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ABD pain, diarrhea, GI hemorrhage, pancreatitis
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what are CNS adr's of indomethacin
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headache, dizziness, confusion
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what are other ADR's of indomethacin
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hyperkalemia, inhibits PG in kidney, thrombocytopenia, aplastic anemia
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what is use of ketorolac
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analgesic esp post op
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ketorolac not really used for what
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anti-inflammatory effect
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what is the only NSAID used parenterally or pain
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ketorolac
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what is max term with ketorolac
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5 days
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what can ketorolac cause with long term use
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peptic ulceration, renal dysfunction, and bleeding
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celecoxib is what type of inhibitor
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selective cox 2 inhibitor
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what are effects of celecoxib
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analgesic and anti-inflammatory
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celecoxib may be protective against what
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colon cancer
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what are uses for celecoxib
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RA and OA
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when should celecoxib be used with caution
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hepatic and renal impairment
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celecoxib is not for use in what patients
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asthmatic or those allergic to sulfas
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celecoxib does not effect what
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platelet aggregation or bleeding time
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celecoxib has no effect on what drugs
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INR or warfarin
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celecoxib causes retention of what
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Na and K
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what are indications for valdecoxib
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osteoarthritis, adult RA, primary dysmenorrhea
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what are ADR of valdecoxib
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HTN, peripheral edema, dizziness, headache, diarrhea, dyspepsia, flatulence, myalgias, sinusitis, and rash
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valdecoxib has no significant effect on what
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platelet aggregation
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acetaminophen has no significant what
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anti-inflammatory effects
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what are indications for acetaminophen
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pain and fever
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what are adverse effects of acetaminophen
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GI upset, rash, neutropenia, pancytopenai, leukopenia, hepatic necrosis with overdose, renal injury with chronic use, increased hepatotoxicity with chronic use
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Tramadol is not what
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not NSAID, not true opioid, not seddative
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tramadol binds to what
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Mu receptors, analgesic
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tramadol has less what than opioids
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respiratory depression
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tramadol is partially antagonized by what
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naloxone
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tramadol is as effective as what and more effective than what
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as=tylenol 3
more=propoxyphene |
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tramadol has a what
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active metabolite that increases half life
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