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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
pharmacokinetics
required for excretion of toxic acetaminophen metabolit
glutathione
a drug that blocks a heroin overdose?
naloxone
programmed cell death
apoptosis
a sign of immune-complex disease
cutaneous vasculitis
database of national library of medicine
pubmed
result of penicillin hypersensitivity
urticaria
abbreciation for a genetic variation that occurs at a single nucleotide
SNP
ginkgo biloba is a..
herb
type of medicine that is the goal of pharmacogenetics...
individualized
a published compendium of drug product labels also available online
PDR
a drug that exhibits an interaction between pharmacodynamics and pharmacokinetic type of genetic variation
warfarin
uncontroled cell death resulting in attraction of inflammatory cells
necrosis
cancer agents that cause neurotoxicity frequently interfere with this cellular component
microtubules
a drug that is an antagonist in the breast cancer but an agonist in the endometrium (uterine cancer)
tamoxifen
an adverse effect of many drugs taken during pregnancy
teratogenesis
a class of drugs that somtimes causes myopathy due to a SNP
statins
sildenafil and nitroglycerin leading hypotensive crisis is an example of this type of drug-drug interaction
pharmacodynamics
prolonged glucocorticoid admin results in wasting of this type of tissue
muscle
the study of the role of inheritance in variation in drug response
pharmacogenomics
reslts of antibody-dependent cellular cytotoxicity
hemolysis
an adverse drug reaction of unknown cause
idiosyncratic
ginko biloba and NSAIDS inhibit the aggregation of..
platelets
a drug that blocks valium overdose
flumazenil
exacerbated when patient takes asprin
asthma
lb converted to Kg
2.2 lb = 1 kg
elimination 1/2 = ?
.693 x Vd / clearance
maintenance dose = ?
steady state concentration x clearance
loading dose = ?
desired plasma concentration x Volume of distribution
Volume of distribution = ?
total drug given / plasma concentration
initial concentration =
loading dose / volume of distribution
what can you do with knowledge of Volume of distribution for a given drug?
calculate a reasonable loading dose
what is the time needed to reach optimal drug blood level during constant rate infusion?
independent of the rate of infusion
dependent on the half life
volume of distribution?
a mathematical relationship between total amount of drug in the body and the concentration of drug in the blood
chart: if you are taking a substrate drug and you take another substrate drug what happens
they compete for binding
chart: if you are taking a substrate drug and you take an inhibitor drug
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)
chart: if you are taking a substrate drug and you take a inducer drug what happens
the inducer will cause a increase in metabolism of the substrate drug. resulting in a decrease in blood concentration
enzymes are saturated in _____ order elimination
zero order
steady state concentration is when?
rate of input = out put.

will take 4 half lifes to reach concentration steady state
why can apparent volume be higher then actual volume?
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
the ability of a drug to harm depends on 3 things
genetics, dose, other drugs patient is taking
intended tissue on target source of drug toxicity?
when you have a dose thats too high
can cause chronic activation or inhibition
intended tissue off target source of drug toxicity?
incorrect receptor is activated or inhibited by a drug
unintended tissue on target source of drug toxicity?
correct receptor but in the wrong tissue.
dose too high, can cause chronic activation or inhibition
unintended tissue off target source of drug toxicity?
incorrect receptor on incorrect tissue is activated
pharmacokinetic drug drug interaction (what the body does to the drug)
ketoconazole
pharmacokinetic drug drug interaction?
what the body does to the drug. this is an effected metabolism or elimination
pharmacodynamic drug drug interaction?
what the drug does to the body this refers to action at receptors
ketoconazole is a potent inhibitor of 3a4 this is a problem when..
another drug taken is metabolised by 3A4 , when you mix them the drug isnt metabolized and rises to toxic levels
pharmycodynamic drug-drug interaction example? with sildenafil (erectile drug)
sildenafil increases cGMP when thats used and you add something like nitroclycerin who does the same thing... you can cause severe dilation and hypotension
apoptosis benefit?
damaged cells are eliminated without damage to the surrounding tissue.
allergic reaction is what type of hypersensitivity
I
hemolysis is what type of hypersensitivity
2 antibody dependent cellular cytotoxicity
what type of hypersensitivity is drug-antibody reaction
what type of 3 immune complex disease
what type of hypersensitivity is cell mediated
4 delayed hypersensitivity
acetaminophen metabolism results in..
a toxin metabolite that can only be broken down when mixed with glutathione.
alcoholism effects what metabolism pathway?
that of glutathione, the toxic metabolite of acetaminophen accumulates and causes necrotic hepatic damage
if some one over doses on acetaminohen what are they given to increase glutathione
NAC N- acetylcysteine
drug induced renal toxicity cause by ______. they will cause specifically a nephrontoxicity
NSAIDS
What can be used to surpress the immune system... but also..
oral glucocorticoids but it also mobolizes glucose and contributes to wasting
how to treat someone with a drug induced toxcity
agonist, reduce or eliminate drug, alter metabolism of the drug
______ is the possibility that knowledge of a pateints dna seq. could be used to enhance pharmacotherapy
pharmacogenetics
enzyme with genetic polymorphisms resulting in differences in drug metabolism.. this can lead to
cyp 2d6

toxic drug concentrations or alter the production of active or toxic metabolites
why is it difficult to predict warfarin loading does
because of genetic variations in both the drug receptor and the drug metabolism
SNP can be used to predict who..
will have altered metabolism of statins (which causes increasing the frequency of statin induce myopathy)