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Misc. Pharm Exams > PKPD Exam 4 > Flashcards

PKPD Exam 4 Flashcards

1
Q

4 applications of antibodies include

A
  1. alteration of toxin disposition
  2. elimination of cells
  3. alteration of cell function
  4. drug delivery
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2
Q

nonspecific and slow mechanism of antibody elimination where proteins are taken up and broken down into component amino acids

A

fluid phase endocytosis and catabolism

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3
Q

size specific mechanism of antibody elimination that is a primary mechanism when MW <50 kDa

A

renal filtration and catabolism or excretion

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4
Q

what is a primary determinant of interindividual variability for antibody elimination

A

renal clearance

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5
Q

size specific mechanism of antibody elimination for proteins and aggregates > 400 kDa

A

phagocytosis

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6
Q

component specific mechanism of antibody elimination where sugars interact with receptors allowing proteins to be taken up into cells

A

receptor mediated endocytosis

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7
Q

receptor that is a part of receptor mediated endocytosis that protects all IgG antibodies from elimination

A

FcRn

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8
Q

how does the presence of FcRn affect antibody half life?

A

prolongs t1/2

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9
Q

FcRn is saturable, so elimination is…

A

concentration dependent
as drug concentration increases, CL increases

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10
Q

component specific mechanism of antibody elimination through target mediated drug disposition where the interaction between drug and receptor determines plasma PK (saturable)

A

receptor mediated protection

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11
Q

according to target mediated drug disposition for antibodies, as drug concentration increases…

A

clearance decreases when receptor binding leads to drug elimination

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12
Q

drug specific mechanism of antibody elimination with drug specific uptake into receptors for target mediated disposition

A

receptor mediated endocytosis

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13
Q

drug specific uptake receptors for elimination are saturable, so as dose increases…

A

CL decreases due to saturation of target mediated clearance

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14
Q

how do anti-drug antibodies affect elimination of protein drugs

A

lead to rapid increase in elimination

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15
Q

mechanism of distribution for proteins where they move into the ISF via paracellular pores, fluid then gets back into the blood via lymph

A

convection

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16
Q

are antibody drug concentrations greater in plasma or tissue? why?

A

css plasma > css tissue
small Vd since drug moving from blood to tissue is less efficient than moving from tissue to lymph

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17
Q

what makes it difficult to assess Vd of antibody drugs

A

elimination via proteolysis
includes elimination from sites that are not in rapid equilibrium with plasma

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18
Q

distribution of antibodies of nonlinear, so binding is…

A

saturable in tissue

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19
Q

variability in the FcYR (gamma receptor) may cause

A

interindividual effects on PD but NOT PK
may contribute to elimination of circulating antibodies

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20
Q

does ADA impact interindividual variability? what does it effect?

A

yes, impacts PK (increased drug CL)

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21
Q

what can DDIs affect when it comes to antibody therapy

A

disposition through effects on FcRN, TMD, convection, and ADA

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22
Q

how does diabetic nephropathy affect antibody therapy

A

higher urinary levels of IgG
increases drug clearance

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23
Q

strategy where initiation and management of therapy is done through an individualized dosage regimen

A

target concentration strategy

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24
Q

concentration value with the greatest probability of therapeutic success

A

target concentration

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25
Q

what criteria must be met for the target concentration method to be effective

A

reliable conc-response relationship
population PK information
reliable analytic assays available

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26
Q

5 steps for target concentration strategy

A
  1. estimate likely PK parameter values
  2. estimate plasma conc expected at time of sampling
  3. compare observed and expected conc
  4. if observed are different, revise PK parameters
  5. make recommendation based on dose level and or interval adjusting according to desired target conc
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27
Q

types of solid tumors

A

carcinomas, sarcomas

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28
Q

types of hematologic cancer

A

lymphoma, leukemia

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29
Q

use of medication to treat cancer

A

chemotherapy

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30
Q

what is the mechanism of chemo

A

affects every step of making DNA, RNA, and protein

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31
Q

newer treatment that uses drugs more precisely to identify and attack cancer cells with little damage to normal cells

A

targeted therapy

32
Q

what do small and large molecules target in targeted therapy

A

small – receptors for cellular processes
large – specific Ab mediated processes

33
Q

treatment that uses your body’s own immune system to fight cancer

A

immunotherapy

34
Q

given prior to surgery to shrink cancer

A

neoadjuvant

35
Q

given to destroy leftover cells that may be present after a tumor is removed

A

adjuvant

36
Q

given in low doses to assist in prolonging remission

A

maintenance

37
Q

determined to have the best probability of treating a given cancer

A

1st line

38
Q

given if a disease has not responded or reoccurred after 1st line, also called salvage therapy

A

2nd line

39
Q

addresses cancer symptom management

A

palliative

40
Q

what decreases absorption of cancer drugs?
increases?

A

dec – NV, prior treatment affecting GI, DDI, dec. peristalsis
inc – DDI, inc. peristalsis

41
Q

what decreases cancer drug distribution?
increases?

A

dec – weight loss and dec. body fat
inc – hypoalbumin, protein binding, peritoneal or pleural effusions

42
Q

what decreases cancer agent elimination?
increases?

A

dec – renal or hepatic dysfunction
inc – induction of metabolism

43
Q

what correlates with toxicity and therapeutic effect of cancer agents

A

AUC, Css, Cmax, drug exposure time above a certain threshold concentration

44
Q

what are affected by DDIs with cancer agent

A

PD but NOT PK

45
Q

the reaction between 5-FU and folinic acid (leucovorin) is a

A

positive PD reaction
folinic acid enhances effect of 5-FU

46
Q

carboplatin administered with paclitaxel leads to

A

dec formation of platinum adducts, which is the drug effect of carboplatin

higher AUC needed to achieve same toxicity when paclitaxel is added vs less needed when carboplatin given alone

47
Q

methods for dose individualization of cancer drugs (3)

A

BSA based
priori dose determination based on patient characteristics
dose adaptation by LSM and TDM

48
Q

dose adaptation of cancer drugs for renal & liver function

A

renal- base on eGFR, calvert formula for carboplatin
liver- depends on drug

49
Q

how to dose adjust cancer agents based on patient history

A

assess propensity for toxicity

50
Q

should TBW or IBW be used for cancer agent dosing? why?

A

IBW, toxicity can occur if using TBW for obese patients

51
Q

does pharmacogenetics play a role is cancer dose adjustment?
which enzymes?

A

yes
5-FU catabolized by DPD
6-MP inactivated by TPMT

52
Q

how is population PK used for cancer agents

A

find covariates that change the dose-conc relationship and adjust dose

53
Q

dose adaptation method done to limit frequency of blood sampling

A

Limited sampling methods (LSMs)

54
Q

limitations of LSM

A

need to be applied prospectively and validated in treatments using the same agent, dose, admin schedule, and infusion duration as the original study

55
Q

which drug frequently uses TDM for cancer

A

methotrexate

56
Q

warfarin binds with high affinity to receptors and enzymes, which affects

A

PK of the drug

57
Q

warfarin has what type of binding and distribution

A

reversible binding
target mediated drug disposition

58
Q

which form of warfarin is more active

A

S > R

59
Q

S warfarin is metabolized by what enzyme? is it affected by genetics

A

CYP2C9– has genetic polymorphism

60
Q

what type of PD response does warfarin have

A

indirect PD response
indirect MOA – effect delayed on the prothrombin complex since it changes production for the complex’s activity

61
Q

genetic polymorphisms of warfarin occur with what 2 enzymes

A

CYP2C9 and VKORC1

62
Q

when is warfarin dose proportional

A

on multiple doses

63
Q

what happens with Css with low dose IV warfarin infusion

A

time lag to Css

64
Q

how does genomic dosing compare to TDM

A

genomic modeling is NOT superior
trials assessed therapy initiation not management

65
Q

what do you need for bayesian dose individualization of warfarin

A

PKPD model, patient info, observed drug response, the dose, and schedule

66
Q

what does the bayesian model do

A

uses a bayesian algorithm to predict the drug response using individualized parameter estimates

67
Q

what is the most common type of anemia

A

iron deficiency anemia

68
Q

absorption of erythropoietin follows

A

flip flop kinetics

69
Q

bioavailability of EPO is

A

dose dependent

70
Q

what is the dose dependent half life of EPO following IV INJECTION

A

8 hours

71
Q

what is the most important clinical marker for EPO administration

A

hemoglobin

72
Q

will Hgb spike immediately after EPO administration?
if not when?

A

no immediate spike after dose 1
rise may take 5 days with multiple dosing

73
Q

what does steady state of Hgb depend on?

A

lifespan of RBCs

74
Q

are higher levels of Hgb seen in males or females?

A

males

75
Q

which administration method of EPO is more effective?

A

SC&raquo_space;» IV

Misc. Pharm Exams (5 decks)

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