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PKPD II > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Lecture 1: Applied PK:Digoxin

digoxin molecular weight

A

780.95

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2
Q

Lecture 1: Applied PK:Digoxin

bioavailability of diff dosage forms

A

tabs: 0.7
elixir: 0.8

Lanoxicaps: 1

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3
Q

Lecture 1: Applied PK:Digoxin

digoxin binding

A

high tissue binding

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4
Q

Lecture 1: Applied PK:Digoxin

digoxin distribution

A

binds very tightly to Na/K atpASE, IN COMPETITION WITH K+.

high tissue binding

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5
Q

Lecture 1: Applied PK:Digoxin

digoxin pk variability

Absorption

A

increased:
erythromycin
tetracycline

decreased:
diarrhea

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6
Q

Lecture 1: Applied PK:Digoxin

digoxin pk variability

distribution

A

increased:
hypokalemia

decreased:
hyperkalemia
renal failure

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7
Q

Lecture 1: Applied PK:Digoxin

digoxin pk variability

elimination

A

increased:–
decreased: renal fialure
p-GP substrates

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8
Q

Lecture 1: Applied PK:Digoxin

therapeutic range for digoxin

A

0.5-2.0 ng/mL

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9
Q

Lecture 1: Applied PK:Digoxin

digoxin adverse effects

A

cardiac effect: av block, premature ventricular contractions (PVCs), atrial tachycardia, sinus bradycardia

etc.

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10
Q

Lecture 1: Applied PK:Digoxin

why use pk individualization for digoxin?

A

high interpt. variability in disposition

low TI

poor accuracy in prediction of pk PARAMETERS FROM PATIENT CHARACTERISTICS

Limitations:

  • poor correlation of Cp to effect/ toxicity
  • poor selectivity inclniical assay

Goals: achieve desired Css, av concentration

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11
Q

Lecture 1: Applied PK:Digoxin

estimation of volume of distribution equations

A

A. from ‘pt characteristics

if renal insufficiency(when CrcL<30 mL/min):
V(L)= 3.8xTBWxCLcr(in ml/min)

no renal sufficiency(when CrCL>30 ml/min, or is not available):
V=7.3L/kg x TBW

B: from plasma conc: NEVERRR!!!

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12
Q

Lecture 1: Applied PK:Digoxin

estimation of CL prior to dosing

A

if pt doesn’t have CHF:
0.8 mL/min/kg x TBW + CLcr (in mL/min)

if pt has CHF: 0.33 ml/kg/min x TBW + CLcr x 0.9

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13
Q

Lecture 1: Applied PK:Digoxin

estimation of CL: pk analysis of Cp

A
  1. determine if pt is at steady state (have they been on it for >/= 1 week?
  2. determine if the plasma conc. was collected greater than 6 hrs after the last dose.
  3. use Css av eq. to determine CL:
  4. if want to calculate a new dose to get a new (desired) Css, rearrange css eq. to solve for dose
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14
Q

Lecture 1: Applied PK:Digoxin

method of superposition for atypical dosing. what is it?

A

loading dose is calculated

pt given 50% of dose as IV bolus

pt given next 25% dose

then pt given next 25%

then starts maintenance dose

used to find remaining concentration of drug in blood before initiation of maintenance dose

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15
Q

Lecture 1: Applied PK:Digoxin

how to calculate cp using method of superposition for atypical dosing

A
  1. calculate PK parameters:
    CL: (use eq.. based on whether pt has CHFor not)

V: (use eq. based on if pt has renal failure or not)

K: CL/V

  1. create a table with dose/ admin times.

titles for each column:
Dose, ug, time, hrs, t(time from last dose to measurement), F (consider different F for different dosage forms)

  1. calculate the cp for each dose given after decay using eq.
    Cp= (Dose x F)/V x e ^-kt
  2. add up the concentrations
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16
Q

Lecture 2: Applied PK:Digoxin pt 2

evaluation of digoxin toxiicity

when do we use ADF (antidigoxin immune fab)

A

LIFE THREATENING digoxin intoxication…

  1. V. tachycardia, or V. fib
  2. 2nd/3rd degree block (not responsive to atropine)
  3. acute ingestion of > 10 mg digoxin (adults), > 4 mg children)
  4. K+> 5 mEq (in setting of digoxin intoxication
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17
Q

Lecture 2: Applied PK:Digoxin pt 2

info on ADF

A

specific activity: 0.8

18
Q

Lecture 2: Applied PK:Digoxin pt 2

how to calculate ADF dose

A
  1. estimate V
  2. calculate amount of digoxin in body (in ug): AB= Cp/V
  3. convert to molar quantity using molecular weight (780.95 g/mol)(must first convert from ug to g )
  4. calculate equimolar quantity of ADF using specific activity (0.8)
    Active quantitiy[[of digoxin in moles]= dose x specific acttivity
    solve for dose (answer is in mol)
  5. convert mol to mg using ADF molecular weight of 50000 g/mol.
19
Q

when do you give a repeat dose of ADF?

A

only if life threatening symptoms return or got worse following first ADF. if pt is feeling better, do not give ADF again.

20
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

dosage forms of phenytoin

A

phenytoin sodium:IV or capsules. has 92% phenytoin by weight

Phenytoin acid: chewable tablets, oral suspension

fosphophenytoin: only parenteral(IV).

21
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

how to increase solubility of phenytoin sodium

A

ethanol and propylene glycol assed to admin vehicle

22
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

phenytoin infusioin rate

A

limit of infusion for adults and pets, with lower and children

23
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

side effect of phenytoin sodium injection

A

hypotension and ready cardia

24
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

fosphenytoin dosing

A

to avoid confusion, fosphenytoin is prescribed in terms of phenytoin sodium equivalents (PE)

25
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

VM
KM:

A

Vm: max rate of elimination

km: concentration at which saturation is likely to occur

26
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

therpeutic range of phenytoin

target phenytoin fup:

A

10-20 mg/mL

1-2 mg/L

27
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

affect of 10% chain in max depends on what

A

depends on Km and steady state.

As css becomes much greater than km, the maintenance dose approaches max, and a small change in either the maintenance dose or max can result in disproportionate changes in the new Css

28
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

phenytoin skin special situations

Pregnancy

liver disease:

A

serum phenytoin conc. tend to fal; during pregnancy due to enhanced metabolism

Liver disease: increased conc. due to impaired metabolism

renal disease: reduced phenytoin conc due to binding to serum proteins is reduced

29
Q

Lecture 3: Phenytoin 1: ADME and PK-PD

why do TDM for phenytoin

A

undergoes saturable metabolism

TI is narrow

great interpt. variability

30
Q

Lecture 4: Phenytoin calculations

Estimation of pk parameters proper to dosing

A

V: always = 0.65

Vm: use 7 mg/kg/day

Km: use 4mg/day

31
Q

Lecture 4: Phenytoin calculations

note about fup

A

fun of phenytoin is fup=0.1

total=bound+unbound

32
Q

Lecture 4: Phenytoin calculations

how to find out true phenytoin conc. w. decreased protein binding

A

normal albumin is 4.4

if albumin is below that, must rearrange and find the conc if the person had normal protein binding.

use those 2 eq.
1. if pt has low albumin and CrcL>25mL/min

  1. if pt has normal or low albumin and pt receiving dialysis
33
Q

Lecture 4: Phenytoin calculations

how to decide regimen of pt who has not received phenytoin

A

start with a low dose and increase based on pt response and plasma concentrations.

not able to predict pk parameters from pt characteristics

initial calculated doses are probably not gonna yield safe effective ocncentrations

34
Q

Lecture 4: Phenytoin calculations

when increasing phenytoin, how to do so

A

never increase more than 25% when vm and km not known

35
Q

Lecture: Carbamezapine and Valproic Acid

Carbamezapine as a drug

A

used for tonic clinic (grand mal), partial or secondarily generalized

prophylactic agent

moa: blocks Na channels in their inactive conformation, which prevents repetitive and sustained firing of an action potential

36
Q

Lecture: Carbamezapine and Valproic Acid

carbamezapine absormption

A

no first pass metabolism

rate of absorption is slow, erratic, and unpredictable, due to slow rate of dissolution and or/ anticholinergic properties

also circadian variation: evening doses absorb more slowly than morning dose

secondary peaks in drug conc. due to slow and constant rate of absorption in the upper and lower intestine

37
Q

Lecture: Carbamezapine and Valproic Acid

carbamezapine distribution

A

distributes rapidly and uniformly to various organs

crosses placenta and accumulates in fetal tissues of

38
Q

Lecture: Carbamezapine and Valproic Acid

carbamezapine metabolism

A

met. by cyp3a4

metabolite is therapeutically active and toxic as well. it is a potent inducer and can induce its own enzyme, causing auto induction

that’s why you must start low

39
Q

Lecture: Carbamezapine and Valproic Acid

cl of carbamezapine in initial conc. vs chronic doising

A

different clearance

40
Q

Lecture: Carbamezapine and Valproic Acid

carbamezapine ddi

A

induces cyp3a4, (own enzyme)

and inhibit cyp219

41
Q

Lecture: Carbamezapine and Valproic Acid

tDM

A

tdm not usually done, but conc. of >15 is associated with toxic effects. start low and go slow

42
Q

Lecture: Carbamezapine and Valproic Acid

carbamezapine dosing rate and titration

A

no loading dose

short dosing intervals.

PKPD II (4 decks)

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