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123 Cards in this Set
- Front
- Back
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AAA
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Anti-inflam;analgesic;antipyretic
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Effect of NSAIDs (ASA prototype)
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Inhibit PG synthesis by inhibiting COX
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Efficacy of various NSAIDs
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Differs by tissue
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NSAIDS affect specific points on the ...
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Arachidonic acid pathway
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The arachidonic acid pathway splits into what two pathways?
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Cyclooxygenase and Lipoxygenase
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NSAIDS act ___ for pain and ___ for fever
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Locally, centrally
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NSAID antypyretic effects via?
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PGE2
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NSAIDs for treatment of what pain
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Low to moderate
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NSAIDs on pain relative to opioids
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Not as effective but lack respiratory and dependence side effects
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Prolonged use of NSAIDs
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Possible toxicity
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Primary NSAID use
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Anti-inflammatory agent
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Musculoskeletal disorder for NSAID use
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RA, OA, ankylosing spondylitis (spinal bones hardened into place - pain, immobilizing)
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"other" NSAID use
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Close ductus arteriousus (open during gestation may fail to close), pyrexia, dysmenorrhea, renal colic. Symptomatic relief.
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NSAID don’t'
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Arrest progression of disease
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NSAIDS interfere with PG biosynthesis
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By inhibiting COX
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COX enzymes forms & roles
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1: protective role in supporting platelets and protecting stomach mucosa, and kidney; 2: primarily expressed in inflammation; 3: CNS inflammation and fever production
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Selectivity of COX
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Not a lot of selectivity, but some have more selectivity for COX1 - therefore bleeding time increased.
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COX2 & LOX versus the GI
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Equally mild on gastric (celecoxib v diclofenac)
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COX2 vs. non-spec COX
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Vioxx more gentle than Aleve
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AAA
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Anti-inflam;analgesic;antipyretic
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First step after arachidonic
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LOX or COX; most NSAIDS do not inhibit LOX so leukotrienes can still form
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Effect of NSAIDs (ASA prototype)
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Inhibit PG synthesis by inhibiting COX
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NSAIDs and platelets
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COX1 needed for thromboxane - a potent aggregating agent. ASA covalently bonds with COX1 & COX2 so affects last for the life of the platelet. Other NSAIDs are reversible.
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Efficacy of various NSAIDs
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Differs by tissue
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Primary adverse SE of NSAIDS
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GI problems and related: blood loss, nausea, anemia, dyspepsia. Direct and indirect: (ind= inh of COX1 protective properties for stomach mucosa)
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NSAIDS affect specific points on the ...
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Arachidonic acid pathway
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four families of eicosanoids
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prostaglandins, prostacyclins, the thromboxanes and the leukotrienes
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NSAID renal effects
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Decreased renal blood flow - lower filtration rate, bad if have CHF or are hypovolemic (don't have as much blood anyway.)
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The arachidonic acid pathway splits into what two pathways?
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Cyclooxygenase and Lipoxygenase
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NSAIDS act ___ for pain and ___ for fever
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Locally, centrally
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NSAID platelet effect
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Disturb function due to inhibition of thromboxane
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NSAID antypyretic effects via?
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PGE2
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NSAID and pregnancy
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Premature closure of ductus arteriosus so not recommended especially during third trimester. Prostaglandins role in initiation and progression of labor & delivery; uterotropic effect - their biosynth in uterus increases dramatically during birth so NSAIDs can interfere
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NSAIDs for treatment of what pain
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Low to moderate
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Photosensitivity SE in which NSAIDs
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Ibuprofen, naproxen, piroxicam, diclofenac
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NSAIDs on pain relative to opioids
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Not as effective but lack respiratory and dependence side effects
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ASA/NSAID intolerance
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Looks like allergic/anaphalactc, but not immunological. If sensitive to one, probably sensitive to others. It's unclear why.
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Prolonged use of NSAIDs
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Possible toxicity
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Aspirin Common usage
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Analgesia/antipyresis
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Primary NSAID use
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Anti-inflammatory agent
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Aspirin not effective for
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Deep pain, visceral pain
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Musculoskeletal disorder for NSAID use
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RA, OA, ankylosing spondylitis (spinal bones hardened into place - pain, immobilizing)
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"other" NSAID use
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Close ductus arteriousus (open during gestation may fail to close), pyrexia, dysmenorrhea, renal colic. Symptomatic relief.
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Aspirin specific pains
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Headache, join, muscle, nerve
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Aspirin benefits
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No tolerance, dependence, addition, or CNS depression
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NSAID don’t'
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Arrest progression of disease
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Problem with ASA and specific syndrome
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Reye's, causes encephalapathy.
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NSAIDS interfere with PG biosynthesis
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By inhibiting COX
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Dose dependent effects of ASA
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Low dose for analgesia, high dose/chronic for antirheumatic
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COX enzymes forms & roles
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1: protective role in supporting platelets and protecting stomach mucosa, and kidney; 2: primarily expressed in inflammation; 3: CNS inflammation and fever production
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Large doses of ASA
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CNS effects
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Selectivity of COX
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Not a lot of selectivity, but some have more selectivity for COX1 - therefore bleeding time increased.
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Salicylism
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Tinnitus, hearing loss, vertigo, (reversible)
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COX2 & LOX versus the GI
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Equally mild on gastric (celecoxib v diclofenac)
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SE of ASA (some)
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Hypersensitivity, GI effects, inhibits platelets, overdose in children can be fata.
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COX2 vs. non-spec COX
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Vioxx more gentle than Aleve
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APAP lacks
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Peripheral anti-inflammatory action (compared to ASA)
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First step after arachidonic
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LOX or COX; most NSAIDS do not inhibit LOX so leukotrienes can still form
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APAP vs ASA
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Lower incidence of SE and toxicity (except liver); more effective than ASA for dysmenorrhea; probably acting on COX-3, no effect of Reye's syndrome, no effects on platelets and bleeding time. But, the liver thing...
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NSAIDs and platelets
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COX1 needed for thromboxane - a potent aggregating agent. ASA covalently bonds with COX1 & COX2 so affects last for the life of the platelet. Other NSAIDs are reversible.
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APAP & liver
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Highly toxic intermediary is detoxified by glutathione. If glutathione is depleted, the toxic compound binds to hepatic macromolecules causing necrosis. Six grams over two days can cause tosicity.
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Primary adverse SE of NSAIDS
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GI problems and related: blood loss, nausea, anemia, dyspepsia. Direct and indirect: (ind= inh of COX1 protective properties for stomach mucosa)
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What are the propionic acids?
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Ibuprofen, naproxen
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four families of eicosanoids
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prostaglandins, prostacyclins, the thromboxanes and the leukotrienes
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Ibuprofen strengths
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Strong analgesic and moderate anti-inflammatory action (>= 600 mg needed for anti-inflammatory)
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NSAID renal effects
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Decreased renal blood flow - lower filtration rate, bad if have CHF or are hypovolemic (don't have as much blood anyway.)
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Naproxen strengths
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Longer 1/2 life than ibuprofen, AAA activity
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NSAID platelet effect
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Disturb function due to inhibition of thromboxane
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Long term (up to 3 years) naproxen use
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May be associated with increased CV risk
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NSAID and pregnancy
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Premature closure of ductus arteriosus so not recommended especially during third trimester. Prostaglandins role in initiation and progression of labor & delivery; uterotropic effect - their biosynth in uterus increases dramatically during birth so NSAIDs can interfere
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Other NSAIDS
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Fill this in…?
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Photosensitivity SE in which NSAIDs
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Ibuprofen, naproxen, piroxicam, diclofenac
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Acetic acid NSAIDs
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Indomethacin, diclofenac, etodolac
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ASA/NSAID intolerance
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Looks like allergic/anaphalactc, but not immunological. If sensitive to one, probably sensitive to others. It's unclear why.
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Fenamate NSAIDs
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Mefenamic acid, meclofenamic acid, no clear advantages over other NSAIDs, frequent side effects, tosicity limits usage
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Aspirin Common usage
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Analgesia/antipyresis
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Pyrzalone NSAIDs
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Phenylbutazone (mostly vet), azapropazone (weak COX inh, effective anti-inflammatory - good for RA and OA and gout)
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Aspirin not effective for
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Deep pain, visceral pain
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Oxicam NSAIDs
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Piroxicam (selective COX2) & meloxicam
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Aspirin specific pains
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Headache, join, muscle, nerve
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Piroxicam
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An oxicam NSAID, long 1/2 life, inhibits PG and activation of neutrophils
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Aspirin benefits
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No tolerance, dependence, addition, or CNS depression
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Alkanone NSAIDs
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Nabumetone is the only example given, has less GI effects, but not COX-2 selective. Active metabolite is AAA
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Problem with ASA and specific syndrome
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Reye's, causes encephalapathy.
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Coxibs
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COX-2 selective - should reduce GI problems
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Dose dependent effects of ASA
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Low dose for analgesia, high dose/chronic for antirheumatic
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Large doses of ASA
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CNS effects
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NSAIDS with GI SE
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Indomethacin, ketoprofen and piroxicam > Ibuprofen and diclofenac
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NSAIDs with hepatic problems
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Pyrazolone, propionic acid, and acetic acid
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Salicylism
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Tinnitus, hearing loss, vertigo, (reversible)
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NSAIDs with psychotic episode SE
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Sulindac and indomethacin
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SE of ASA (some)
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Hypersensitivity, GI effects, inhibits platelets, overdose in children can be fata.
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APAP lacks
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Peripheral anti-inflammatory action (compared to ASA)
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NSAIDs with renal function SE
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Monitoring still needed for COX-2 drugs
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Acquired immunity
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Develops when body is exposed to various antigens, and body builds a defense that is specific to those antigens.
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APAP vs ASA
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Lower incidence of SE and toxicity (except liver); more effective than ASA for dysmenorrhea; probably acting on COX-3, no effect of Reye's syndrome, no effects on platelets and bleeding time. But, the liver thing...
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Passive Immunity
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Antibodies produced in smebody's body other than your own. Antibodies transferred through placenta (last six months then disapper) and Immunoglobulin injections provide , rubella, hepatitis protections
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APAP & liver
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Highly toxic intermediary is detoxified by glutathione. If glutathione is depleted, the toxic compound binds to hepatic macromolecules causing necrosis. Six grams over two days can cause tosicity.
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What are the propionic acids?
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Ibuprofen, naproxen
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Inappropriate Immune response
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Usually it's desired, but can be lacking,
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Ibuprofen strengths
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Strong analgesic and moderate anti-inflammatory action (>= 600 mg needed for anti-inflammatory)
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Autoimmune disorders can have what problematic effect
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Destroy normal body tissues
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Naproxen strengths
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Longer 1/2 life than ibuprofen, AAA activity
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Why are steroids used
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To suppress some inappropriate immune responses
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Immunodeficiency disorders
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Like AIDS, when there is a failure in one or part or all of the immune system
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Long term (up to 3 years) naproxen use
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May be associated with increased CV risk
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Other NSAIDS
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Fill this in…?
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Inflammatory response occurs when
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Tissue injury by bacteria, trauma, toxins, heat, etc
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Acetic acid NSAIDs
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Indomethacin, diclofenac, etodolac
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Diesel can cause
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Vapor inhalation is huge contributor to inflammatory response, central effects, interferes with developing fetus.
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Fenamate NSAIDs
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Mefenamic acid, meclofenamic acid, no clear advantages over other NSAIDs, frequent side effects, tosicity limits usage
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Primary physical effect of inflammatory response
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Circulation to increase around the affected area, in particular the blood vessels around the site of infection - they dilate - causing increase in body heat.
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Pyrzalone NSAIDs
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Phenylbutazone (mostly vet), azapropazone (weak COX inh, effective anti-inflammatory - good for RA and OA and gout)
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Heat associated with inflammation
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Antibiotic effect in favor of the host organism
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Released in inflammatory response
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A laundry list of chemicals that causes blood to leak into tissue
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Oxicam NSAIDs
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Piroxicam (selective COX2) & meloxicam
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Piroxicam
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An oxicam NSAID, long 1/2 life, inhibits PG and activation of neutrophils
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Alkanone NSAIDs
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Nabumetone is the only example given, has less GI effects, but not COX-2 selective. Active metabolite is AAA
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Coxibs
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COX-2 selective - should reduce GI problems
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|
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NSAIDS with GI SE
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Indomethacin, ketoprofen and piroxicam > Ibuprofen and diclofenac
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NSAIDs with hepatic problems
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Pyrazolone, propionic acid, and acetic acid
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NSAIDs with psychotic episode SE
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Sulindac and indomethacin
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NSAIDs with renal function SE
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Monitoring still needed for COX-2 drugs
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