• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/77

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

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
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