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102 Cards in this Set
- Front
- Back
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aspirin
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nonspecific irreversible inhibition of cox 1 and 2
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nsaids
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nonspeifi reversible inhibition of cox 1 and 2
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coxibs
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selective reversible inhibition of cox2
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four principle uses for nsaids
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inflammation, analgesia, antipyretic, platelet aggregation
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inflammatory joint conditions
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arthritis, rheumatic fever, ostoearthritis, gout, psoriatic arthritis, arthrits assoc with ibs, inflammation assoc with mild bone and muscle trauma
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what do eicosanoids do to nociceptive signals
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amplify them
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mechanim for pain inhibition
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reduction of inflammation and inhibition of pain stimuli in neurons
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mechanism for antipyretic effects
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decrease elevated temperature, incease heat dissipation caused by supeficial vessel dilation
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fevers from infections are a result of what two events
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production of prostaglandins in cns, effects of il1 on the hypothalmus
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other clinical uses of nsaids
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inhibit platelet aggregation, neonatal patent ductus arteriosus, cancer chemoprevention, niacin tolerabilty
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which nsaid for platelet aggregation
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aspirin
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cox 2 inhibitors
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celecoxib, meloxicam
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Describe the absorption of aspirin
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rapid in stomach, peak plasma levels in 1-2 hours, raising gastric pH via buffereing slows absorption, slower in intestines
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describe the metabolism of aspirin
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rapidly hydrolyzed by exterase, saturable, rate of metabolism is constant above 600mg/d
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describe the protein binding of aspirin
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salicylate binds to albumin which is saturable. Increasing the concentration shifts to more unbound form
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describe the pharmokinetics of new nsaids
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most well absorbed, oral, highly metabolized, most have half life between .25-15 hours
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long half life means what
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once a day pill, examples include piroxicam, oxaprozin, nabumetone, meloxicam
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what is the most important route of elimination
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renal excretion
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what is a source of gi irritation
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biliary reabsorption and excretion
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where are they all found
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synovial fluid
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how often is naproxen given
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twice a day
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how often is ibuprophen given
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four times a day
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what two nsaids have the longest half lives
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piroxicam and oxaprozin
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what are the side effects of nsaids in
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….
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CNS
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Tinnitus and dizziness
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CV
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Fluid retention, hypertension, edema, CHF
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GI
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Abdominal pain, ulcers and bleeding
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Hematologic
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Thrombocytopenia , neutropenia, aplastic anemia, decreased platelet aggregation
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Hepatic
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Elevated liver enzymes
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Pulmonary
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Asthma
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Rashes
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pruritus
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Renal
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Renal insufficiency, renal failure, hyperkalemia and proteinuria
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describe salicylism
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tinnitis, vertigo, decrease hearing, headache, dimness of vision, mental confustion, lassitude, drowsiness, sweating thirst hyperventilation nausea vomiting and diarrhea
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what are the complications of aspirin
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direct effect on medulla, acidosis, depression of respiratory centers
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what does inhibition of cox 1 synthesized prosaglandin result in
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loss of gastric cytoprotection, vascular homeostasis, platelet aggreagation, and may effect cns
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why should you not give aspirin to children younger than 19
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reyes syndrome
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aspirin and nsaid adverse effect on liven
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mild asymptomatic hepatitis
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kidney
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–Prostaglandins synthesized by both COX1 and 2 promote renal vascular dilation and medullary blood flow
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what would blocking production of prostaglandins do
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unopposed vasoconstriction leading to renal ischemia, not an issue in well hydrated patients
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when would this be a problem
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patients with chf, elderly and hypotensive patients
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what else does nsaids, aspirin do to the kidney
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decrease glomerular filtration rate
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describe the dose dependent alterations in uric acid levels
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less than 2 g increase serum uric acid levels, greater than 2 g decrease urate levels
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adverse effects of aspirin and nsaids in pregnancy and laction
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contraindicated for pregnant women, effects labor and use in late term pregneny increases risk of postpartem hemorrhage
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when would the be ok to use
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preclampsia and eclampsia
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what else do they do
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increase hypersensitivity reactions in patients with asthma and nasal polyps cause bronchocostriction and shock
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gi effects
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gastric upset, 10-20 percent produced by undissolved tablets and decrease of cytoprotective prostaglandins
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how can they be minimized
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taking w meals and antacids, enteric coated tableds, proton pump inhibitors, recuded with cox 2 specific inhibitors,
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major and serious problems
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gastroduodenal ulceration and bleeding, avoid use in patients with peptic ulcer disease
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what would you take to protect against GI issues when taking nsaids
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proton pump inhibitor
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What are the high risk groups that would benefit from cox 2 inhibitors
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72 and above, history or ulders or gi bleeding, concomintant corticosteroid or anticoagulants use, smokers and alcoholics
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when should cox 2 inhibotors not be used
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in patients with a history of cardiovasular issues
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why
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cox 2 selective drugs are associaed with an increased risk of a cardiovascular event
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what is the chemical reason for this
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ihibiting cox 2 inhibits the production of pgi2 and shifts the balance to txa2 which causes platelet aggregation
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drug interactions of aspirin with nsaid
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reversible prevents irreversible from binding
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drug interactions of nsaid with glucocorticoids
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both cause gastric irritation so ulcers
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nsaids and warfarin interactions
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increased bleeding nsaids decrease warfarin metabolism and platelet aggregation
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is acetaminophen the same as nsaid and aspirin
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no
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how is it different
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no antiinflammatory, only fever
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what are the pharmokinetics of tylenol
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oral with toxic metabolites at high doses
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toxicity of tylenol
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increase in hepatic enzymes, high dose of 15g can be fatal
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in what patients is tylenol preferred
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hemophelia, history of peptic ulcer, children with viral infections, aspirin induced bronchospasm
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what is rheumatoid arthiritis
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body recognizes synovium as foreign
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describe the use of nsaids in r arthritis
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helpful in the first few weeks of patients symptoms, does not slow progression, should be used in combinaiton with dmards
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what is something to worry aout when using nsaids for ra
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gi bleeding but cox2 specific can help and so can proton pump inhibitors
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describe the use of glucocorticoids in ra
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stops inflammations and used as a bridge therapy while waiting for the dmards to kick in.
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adverse effects of glucocorticoids
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extensive such as cushings, fat redistribution, never exceed 10 mg daily
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dmards are
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immunosuppressive drugs that inhibit the function and division of immune cells
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when are dmards taken
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soon after ra diabnosis but may take several months to show effects
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what are the mechanisms of dmards
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antimetabolits, purine antagonists, agents that prevent cellular replication and suppress t and b cell funciton
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methotrexate MOA
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Folic acid analogue inhibits (low dose) ***AICAR transformylase and TS and (High dose) dihydrofolate reductase, which is required for new DNA synthesis
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methotrexate toxicity
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inhibits all fast growing cells (gut epithelium, bone marrow blood progenitor cells, teratogen—Cat X), hepatotoxicity (dose dependent). GI and hepatic toxicity reduced with leucovorin
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leflumonide moa
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Metabolite inhibits dihydro orate dehydrogenase inhibition de novo ribonucleotide synthesis, stops T cell proliferation and B cell function
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leflumonide toxicity
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Adverse effects: diarrhea (25%), rash and elevated liver enzymes and even hepatotoxicity (0.28%). Mild alopecia, weight gain, and increased blood pressure Fetal death, teratogen—Cat. X
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gold salts moa
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inhibits macrophage function
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Abatecept
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Endogenous ligand for CTLA-4--Prevents APC/antigen complex from activating T-Cells (see fig. 55-2)
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Etanercept
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TNF-a receptors linked to IgG1
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Rituximab
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MAB binds CD20 on B cells—compliment activation and B cell depletion
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Adalimumab
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monoclonal against TNF-a
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infliximab
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what is the toxicity of drugs that inhibit tnf a funciton
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increase in macrophage-dependent infections ( like TB and histoplasmosis) leukopenia and vasculitis, lupus, non h lymphoma, rituximab rash
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IL1 receptor antagonist
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anakinra
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pharmokinetcs of anakinra
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short half life daily injections
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adverse effects of anakinra
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injection site irritation and sepsis
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what medication can be used to treat ra in pregnancy
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low does glucocorticoids
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what are some considerations for dmards use
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start therapy immediately, monitor efficacy, combinations may be more efficatious, monitor liver function, cbc, measure serum creatinine, avoid pregnancy, administer flu and pneumonia vaccine
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gout
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hyperuricemia, recurrent episodes of acute arthirits, high serum uric acid levels
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Colchicine
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Prophylaxis for recurrent episodes. Treat acute gouty attacks
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Indomethacin
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Treat Acute gouty attacks
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Probenecid
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several acute attacks of gouty arthritis, evidence of tophi, or extremely high plasma levels
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sulfinpyrazone
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Allopurinol
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chronic tophaceous gout w/ elevated uric acid levels or in combo with
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Febuxostat
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Colchicine
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inhibits microtubule polymerization by binding to tubulin, inhibition of leukocyte migration
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Indomethacin
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nsaid
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Probenecid
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NSAID
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sulfinpyrazone
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decrease body pool of urate
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allopurinol and febuxostat
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inhibits xanthine oxidase
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