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65 Cards in this Set
- Front
- Back
ketoconazole inhibition of a 3A4 metobiled drug is what type of drug-drug interation
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pharmacokinetics
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required for excretion of toxic acetaminophen metabolit
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glutathione
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a drug that blocks a heroin overdose?
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naloxone
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programmed cell death
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apoptosis
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a sign of immune-complex disease
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cutaneous vasculitis
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database of national library of medicine
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pubmed
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result of penicillin hypersensitivity
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urticaria
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abbreciation for a genetic variation that occurs at a single nucleotide
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SNP
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ginkgo biloba is a..
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herb
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type of medicine that is the goal of pharmacogenetics...
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individualized
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a published compendium of drug product labels also available online
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PDR
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a drug that exhibits an interaction between pharmacodynamics and pharmacokinetic type of genetic variation
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warfarin
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uncontroled cell death resulting in attraction of inflammatory cells
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necrosis
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cancer agents that cause neurotoxicity frequently interfere with this cellular component
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microtubules
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a drug that is an antagonist in the breast cancer but an agonist in the endometrium (uterine cancer)
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tamoxifen
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an adverse effect of many drugs taken during pregnancy
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teratogenesis
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a class of drugs that somtimes causes myopathy due to a SNP
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statins
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sildenafil and nitroglycerin leading hypotensive crisis is an example of this type of drug-drug interaction
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pharmacodynamics
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prolonged glucocorticoid admin results in wasting of this type of tissue
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muscle
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the study of the role of inheritance in variation in drug response
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pharmacogenomics
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reslts of antibody-dependent cellular cytotoxicity
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hemolysis
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an adverse drug reaction of unknown cause
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idiosyncratic
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ginko biloba and NSAIDS inhibit the aggregation of..
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platelets
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a drug that blocks valium overdose
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flumazenil
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exacerbated when patient takes asprin
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asthma
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lb converted to Kg
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2.2 lb = 1 kg
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elimination 1/2 = ?
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.693 x Vd / clearance
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maintenance dose = ?
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steady state concentration x clearance
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loading dose = ?
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desired plasma concentration x Volume of distribution
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Volume of distribution = ?
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total drug given / plasma concentration
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initial concentration =
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loading dose / volume of distribution
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what can you do with knowledge of Volume of distribution for a given drug?
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calculate a reasonable loading dose
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what is the time needed to reach optimal drug blood level during constant rate infusion?
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independent of the rate of infusion
dependent on the half life |
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volume of distribution?
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a mathematical relationship between total amount of drug in the body and the concentration of drug in the blood
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chart: if you are taking a substrate drug and you take another substrate drug what happens
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they compete for binding
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chart: if you are taking a substrate drug and you take an inhibitor drug
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the inhibitor drug will block the metabolism of the substrate drug. and the substrate drug will increase in blood concentration (cause its breakdown is blocked)
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chart: if you are taking a substrate drug and you take a inducer drug what happens
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the inducer will cause a increase in metabolism of the substrate drug. resulting in a decrease in blood concentration
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enzymes are saturated in _____ order elimination
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zero order
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steady state concentration is when?
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rate of input = out put.
will take 4 half lifes to reach concentration steady state |
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why can apparent volume be higher then actual volume?
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cause when you calculate the apparent volume you are calculating how much volume that drug must be in to be that concentration that was measured. but since some drug is lost to distribution... the apparent volume measured is actually higher saying that the drug is diluted in more volume then it realy is. cause the volume isnt raised its actually the mass of drug that is lost
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the ability of a drug to harm depends on 3 things
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genetics, dose, other drugs patient is taking
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intended tissue on target source of drug toxicity?
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when you have a dose thats too high
can cause chronic activation or inhibition |
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intended tissue off target source of drug toxicity?
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incorrect receptor is activated or inhibited by a drug
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unintended tissue on target source of drug toxicity?
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correct receptor but in the wrong tissue.
dose too high, can cause chronic activation or inhibition |
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unintended tissue off target source of drug toxicity?
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incorrect receptor on incorrect tissue is activated
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pharmacokinetic drug drug interaction (what the body does to the drug)
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ketoconazole
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pharmacokinetic drug drug interaction?
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what the body does to the drug. this is an effected metabolism or elimination
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pharmacodynamic drug drug interaction?
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what the drug does to the body this refers to action at receptors
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ketoconazole is a potent inhibitor of 3a4 this is a problem when..
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another drug taken is metabolised by 3A4 , when you mix them the drug isnt metabolized and rises to toxic levels
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pharmycodynamic drug-drug interaction example? with sildenafil (erectile drug)
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sildenafil increases cGMP when thats used and you add something like nitroclycerin who does the same thing... you can cause severe dilation and hypotension
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apoptosis benefit?
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damaged cells are eliminated without damage to the surrounding tissue.
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allergic reaction is what type of hypersensitivity
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I
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hemolysis is what type of hypersensitivity
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2 antibody dependent cellular cytotoxicity
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what type of hypersensitivity is drug-antibody reaction
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what type of 3 immune complex disease
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what type of hypersensitivity is cell mediated
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4 delayed hypersensitivity
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acetaminophen metabolism results in..
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a toxin metabolite that can only be broken down when mixed with glutathione.
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alcoholism effects what metabolism pathway?
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that of glutathione, the toxic metabolite of acetaminophen accumulates and causes necrotic hepatic damage
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if some one over doses on acetaminohen what are they given to increase glutathione
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NAC N- acetylcysteine
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drug induced renal toxicity cause by ______. they will cause specifically a nephrontoxicity
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NSAIDS
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What can be used to surpress the immune system... but also..
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oral glucocorticoids but it also mobolizes glucose and contributes to wasting
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how to treat someone with a drug induced toxcity
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agonist, reduce or eliminate drug, alter metabolism of the drug
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______ is the possibility that knowledge of a pateints dna seq. could be used to enhance pharmacotherapy
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pharmacogenetics
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enzyme with genetic polymorphisms resulting in differences in drug metabolism.. this can lead to
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cyp 2d6
toxic drug concentrations or alter the production of active or toxic metabolites |
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why is it difficult to predict warfarin loading does
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because of genetic variations in both the drug receptor and the drug metabolism
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SNP can be used to predict who..
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will have altered metabolism of statins (which causes increasing the frequency of statin induce myopathy)
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