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76 Cards in this Set
- Front
- Back
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What are the 3 A's of NSAIDs?
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antipyretic, analgesic, and antiinflammatory
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What is the primary MOA of NSAIDs?
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inhibits COX enzymes, resulting in inhibition of PG synthesis
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How are PGs and LTs formed?
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phospholipase A2 will break cell membrane phospholipids into arachidonic acids, which form LTs and PGs
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What enzyme is needed to convert arachidonic acids to LTs? PGs?
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lipoxygenase; cyclooxygenase (COX)
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What are the functions of COX1, COX2, and COX3?
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1. protective/maintenance
2. proinflammatory 3. CNS |
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Which COX isoenzyme is inducible?
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COX2
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What is the MOA of aspirin?
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non-selective COX inhibitor (irreversible)
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How does aspirin's analgesic effect occur?
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PGs intensify pain response; ASA decreases PG production
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How does aspirin's antipyretic effect occur?
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interferes with hypothalamic control mechanisms
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What is unique about ASA's pharmacokinetics? What about its metabolism?
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hydrolyzed by esterases in tissue & blood to salicylate; at high doses, metabolism and protein binding are saturable
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What are some adverse effects of ASA?
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GI problems; hemorrhage; asthma attacks due to excessive production of LTs; rare renal/hepatic toxicity
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What are symptoms of acute, mild salicylism?
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headache, dizziness, tinnitus
hearing loss, drowsiness, NVD mental confusion, and sweating |
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What are symptoms of chronic, severe salicylism?
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dehydration, loss of electrolytes, hyperthermia,
uncoupling of oxidative phosphorylation, energy lost as heat, CNS effects |
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What are the CNS effects of chronic, severe salicylism?
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irritability and psychosis, convulsions and coma, cardiovascular collapse, respiratory failure
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Does salicylism normally occur in children or adults? What is the treatment?
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children; supportive
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What are some therapeutic uses of ASA?
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anti-thrombolytic; fever; pain; RA and OA; colon cancer possibly
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What are some drug interactions of ASA?
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1. warfarin/coumadin-increased bleeding
2. hypoglycemia in patients on insulin 3. interferes w/probenecid 4. reyes syndrom in kids |
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What drug is basically a chemically modified ASA? What is the main difference between this and ASA?
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Diflunisal; no antipyretic effect
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Why would you use diflunisal instead of ASA?
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fewer adverse effects
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What is the MOA of non-salicylate NSAIDs?
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All inhibit COX to decrease synthesis of PG
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T or F: non-salicylate NSAIDs share the 3 A's?
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true
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What are the general effects of non-salicylate NSAIDs?
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1. decrease capillary permeability
2. decrease lysosomal enzyme release 3. decrease release of mediators from neutrophils, basophils, and mast cells 4. affect lymphokine release from T cells 5. have a limited effect on lipoxygenase |
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Which has higher potential for drug-drug interactions: highly bound or not highly bound
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highly bound
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Non-salicylate NSAIDs are extensively bound to what?
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plasma albumin
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Which has fewer adverse effects, ASA or non-salicylate NSAIDs?
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non-salicylate NSAIDs
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What are the only 2 OTC non-salicylate NSAIDs?
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ibuprofen and naproxen
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Do non-salicylate NSAIDS inhibit platelet aggregation reversibly or irreversibly
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reversibly
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T or F: non-salicylate NSAIDS can block benefits of ASA
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true
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What are some adverse effects of non-salicylate NSAIDs?
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gastric irritants, nephrotoxicity, acute renal failure, hepatotoxicity, CNS effects, and cartilage damage
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Chronic use of non-salicylate NSAIDs can result in what condition?
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analgesic nephropathy
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What drug interactions occur in non-salicylate NSAIDs?
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diuretics, beta blockers,
cyclosporin, methotrexate lithium, leflunamide, and warfarin |
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What are the 2 COX II selective NSAIDs left on the market?
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celecoxib and meloxicam
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What are the therapeutic uses for non-salicylate NSAIDs?
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dysmenorrhea, OA, RA, ankylosing spondylitis, and acute gout
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What is one of the most toxic NSAIDs?
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indomethacin
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In addition to treating gout, RA, and tendonitis, what is a very special use for indomethacin?
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closing a patent ductus arteriosus
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Which NSAID will produce the most potent CNS effects?
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indomethacin
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What contraindications are specific to indomethacin?
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don't use in patients with epilepsy and psychosis
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What are the 4 NSAIDs that are listed as having the lowest toxicity?
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ibuprofen, naproxen, ketoprofen, and fenoprofen
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Why is ibuprofen not good at treating RA?
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rapid half life requires QID dosing
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Why is ibuprofen not used in conjunction with ASA?
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it blocks ASA's anti-platelet effecct
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What is the advantage in using naproxen compared to ibuprofen?
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longer half-life allows for BID dosage
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What additional use is naproxen given for that other NSAIDs are not?
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post-op pain
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What is the only non-acid NSAID in use?
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nabumetone
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What are some special features of nabumetone?
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1. half-life allows for QD dosage
2. prodrug converts to active form 3. reduce dose in kidney disease 4. less effect on GI |
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Celecoxib and meloxicam carry what kind of warnings?
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black box
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COX II inhibitors have what major adverse effect? These may be useful in treating what unusual condition?
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1. MI
2. treating some cancers |
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GI toxicity is lowest in which NSAIDs?
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celecoxib, nabumetone, etodolac, sulindac, salsalate
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What drug can be useful in combination with NSAIDs to reduce GI toxicity?
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misoprostol (PG analog)
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T or F: acetaminophen is an NSAID
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false
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Which of the 3 A's does acetaminophen lack?
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anti-inflammatory
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Acetaminophen is mostly eliminated by what reactions?
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phase II
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A small portion of acetaminophen is eliminated through what system? What is the enzyme that converts it to a non-toxic metabolite?
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cytochrome p450; glutathione
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Which COX does acetaminophen inhibit?
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COX II and COX III
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If given within 24 hours of toxic acetaminophen dosage, what drug can protect the liver? How?
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NAC (N-acetylcysteine); acts like glutathione
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What effects may result from acute acetaminophen toxicity?
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N&V, anorexia, abdominal pain, hypoglycemia, renal necrosis
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What are the therapeutic uses of acetaminophen?
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pain and fever relief, especially on people who can't take ASA
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Which is more toxic, NSAIDs or DMARDs?
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DMARDs
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What is the MOA thought to be in DMARDs?
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interfere with lymphocyte function
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DMARDs have been shown to be especially useful in doing what?
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slowing progression of RA
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What is the gold standard of DMARDs for RA?
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methotrexate
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Which DMARD may have an anti-cancer effect?
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MTX
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What are the adverse effects of MTX?
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hepatic problems (cirrhosis), pneumonitis, and mucosal ulcers
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Hydroxychloroquine is an antimalarial and DMARD that can cause what problem?
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irreversible retinopathy
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How do gold salts work? How long does it take to see results?
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inhibition of macrophage function; several months
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What drug can be used to treat copper poisoning and Wilsons disease (too much copper in blood)?
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pencillamine (chelating agent)
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What is the problem with gold salts and pencillamine?
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toxicity
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What is the MOA for leflunamide? When would you use it?
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1. Inhibits de novo pyrimidine synthesis to produce anti-proliferative effect in lymphocytes
2. option for those that don’t respond to MTX or can’t tolerate it |
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What is the major adverse effect of leflunamide?
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hepatotoxicity
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What is etanercept? What is its MOA?
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synthesized TNF-alpha receptor; competes with endogenous TNF-alpha receptors
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Etanercept is used in conjunction with what DMARD?
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MTX
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What is the most common adverse effect of etanercept? What are less likely effects?
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injection site inflammation; activation of latent TB and CNS demylinating disorders
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How is leflunomide given? Etanercept? Infliximab?
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PO, SQ, IV
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What is the MOA of infliximab?
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monoclonal antibody to TNF-alpha
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What is the major adverse effects of infliximab?
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risk of heart failure
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What is the MOA of abatacept?
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inhibits T-cell activation, thus decreasing the production of TNFα
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What is the MOA of capsacin? Where does this come from?
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stimulates release of substance P from afferents, depleting stores which decreases pain sensation; cayenne pepper
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