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77 Cards in this Set
- Front
- Back
blood sampling should occur at least -- to -- hrs after dose
preferably should occur -- to --- hrs after dose |
6-8
12-24 |
|
what limits the bioavailabity of dig
|
p glycoprotein
|
|
where is dig absorbed
|
upper sm intestine
gi tract |
|
what can increase the F of dig
|
antibiotics: tetracycline and erythromycin
intestinal bacteria form dihydro metabolites |
|
usual desired tx range of dig
|
0.5 - 1.0 ng/ml
|
|
target range of HF
|
0.5-1.0 ng/ml
|
|
time to ss of dig
|
140-220 hrs
|
|
iv loading of dig
|
10 ug/kg
|
|
po loading dose of dig
|
10-15 ug/kg
|
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if the pt's renal cl is > 50ml/min what % of the normal recommended maintenance doe should be given
|
100
over 24 hrs |
|
if pt's Clcr is 10-50 ml/min what % of dose should be given
|
24-75%
over 24-36 hr |
|
time to ss of dig
|
140-220 hrs
|
|
iv loading of dig
|
10 ug/kg
|
|
po loading dose of dig
|
10-15 ug/kg
|
|
if the pt's renal cl is > 50ml/min what % of the normal recommended maintenance doe should be given
|
100
over 24 hrs |
|
if pt's Clcr is 10-50 ml/min what % of dose should be given
|
24-75%
over 24-36 hr |
|
if pt's renal cl is < 10 ml/min how much of the dose should be given?
|
10-25%
over 48 hrs |
|
dig cl equation
|
dig cl (L/hr)= 3 + (0.0546xCLcr)
x by 0.56 if pt also taking quinidine |
|
toxicities of dig
|
anorexia
nausea vomiting confusion altered color perception arrhythmias |
|
reason to measure sdc:
when there's question of --- |
toxicity
|
|
reason to measure sdc:
to investigate reasons for --- ---- |
poor response
|
|
reason to measure SDC:
pt started on --- --- known to interact |
concomittant drugs
|
|
reason to measure sdc:
pt w/ change -- --- |
renal fx
|
|
f/u w/ pts w/ hf
|
q 1-2 yrs
|
|
measurement of sdc w/ adequate respsonse and no evidence of toxicity " just ot see what the dig level is: is -- ---
|
not justified
|
|
desired range in HF
|
0.5 - 1 ng/ml
|
|
to minmize tox risk what should be the con of dig
|
< 2mg/ml
|
|
tx range that most labs will report
|
0.8-2.0 ng/ml
|
|
even if pt has no s/s, will the dose be reduced if dig level more than 2.0 ug/ml
|
yes
|
|
if pt's dig level is less than 0.8 ug/ml and well controlled should the dose be increased to meet tx range
|
no
|
|
what will affect Css
|
F
CL |
|
what should be monitored when taking dig
|
renal fx
dig clearance 70% renal |
|
what meds will reduce dig
|
oral antacids
bile acid sequestrants kaolin-pectin |
|
when to take meds that reduce dig
|
give dig 1 hr before or 2-3 hr after these drugs
|
|
what will increase the F of dig
|
antibiotics
|
|
what will increase the dig SDC by 2-3 fold
|
quinidine
|
|
quinidine causes a decrease in dig --- and ---- and an increase in dig ----
|
decrease Vd and CL
increase SDC |
|
with quinidine you will see an ------- increase in
and a new steady state will be achieved in -- to --- |
immediate
5-7 days |
|
w/ quinidine you may consider reducing dig dose by ---- upon initiation of quinidine and monitor
|
1/2
|
|
quinidine inibits --- ----
|
p-glycoprotein
|
|
--- will increase dig by 70 - 100%
|
amiodarone
|
|
w/ amiodarone reduce dig dose by ----%
|
25-50%
|
|
interaction of amiodarone and dig is -- ---
|
dose dependent
|
|
--- may increase dig by 60-90% due to decreased renal and nonrenal
|
verapamil
|
|
amiodarone and verapamil are ---- inhibitors
|
p glycoprotein
|
|
p-gp inhibitors will increase/decrease bioavailabilty and increase/decrease CL and thus lead to increased/decreased conc
|
increase
decrease increased |
|
inducer of p-gp
|
rifampin
will decrease plasma levels |
|
t/f
warfarin has high Vd |
f
small |
|
plasma protein binding of warfarin
|
>99%
|
|
which is more important in pharmcokinetics
|
S
|
|
t/f
protein binding of warfain diplament is clinically significant |
f
cuz the increase in free fraction is not associated w/ free warfacin drug. . . no increase in effect |
|
changes in protein binding ---- clinically relevant
|
rarely
|
|
metabolism of warfarin
|
hepatic
nearly 100% |
|
S metobolized by
|
CYP2C9
|
|
R metabolized by
|
CYP 1A2
CYP3A4 |
|
CYP2C9 inducers
|
barbituates
carbamazepine phenytoin primidone rifampin |
|
CYP2C9 inhibitors
|
amiodarone
fluconazole |
|
cyp1A2 inducers
|
smoking
|
|
cyp1A2 inhibitors
|
fluvoamine
|
|
cyp3A4 inducer
|
rifampim
|
|
cyp3A4 inhibitors
|
ketoconazole
ritonavir |
|
amiodarone has --, ---, --- absorption
|
slow
erratic variable |
|
amiodarone is ---- distributed
|
extensively
to most body tissues |
|
how is amiodarone excreted
|
almost entirely in feces as unchanged drug and metabolite (biliary excretion)
|
|
t1/2 of amiodarone
|
53 days
|
|
due to long t1/2 what's necessary of amiodarone
|
loading dose
|
|
most loading doses of amiodarone lasts
|
2-3 weeks
|
|
amiodarone inhibits --, -- and ---
|
p-gp
CYP2C9 CYP2D6 |
|
most significant interactions of amiodarone
|
warfarin
dig |
|
what do you do when starting amiodarone and pt on warfarin and dig
|
reduce dose by 1/2
|
|
why can drug interactios occur even after amiodarone d/ced
|
cuz of long t1/2
|
|
interactions of amiodarone can occure w/
|
bb
ccb's |
|
ae of statins
|
myalgia
serum creatine kinase elevation rhabdomyolysis |
|
about 50% of rhabo cases due to
|
drug-drug interaction w/ statins
|
|
what takes statin into hepatocyte
|
OAT
|
|
where do you find cyp3A and cyp2c9 that will affect statin
|
hepatocyte
|
|
which statin are hydrophillic
why is that significant |
pravastatin
rosuvastatin very small amount metabolized mainly eliminated unchaged |