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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
what criteria must be met for the target concentration method to be effective
reliable conc-response relationship population PK information reliable analytic assays available
26
5 steps for target concentration strategy
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
27
types of solid tumors
carcinomas, sarcomas
28
types of hematologic cancer
lymphoma, leukemia
29
use of medication to treat cancer
chemotherapy
30
what is the mechanism of chemo
affects every step of making DNA, RNA, and protein
31
newer treatment that uses drugs more precisely to identify and attack cancer cells with little damage to normal cells
targeted therapy
32
what do small and large molecules target in targeted therapy
small -- receptors for cellular processes large -- specific Ab mediated processes
33
treatment that uses your body's own immune system to fight cancer
immunotherapy
34
given prior to surgery to shrink cancer
neoadjuvant
35
given to destroy leftover cells that may be present after a tumor is removed
adjuvant
36
given in low doses to assist in prolonging remission
maintenance
37
determined to have the best probability of treating a given cancer
1st line
38
given if a disease has not responded or reoccurred after 1st line, also called salvage therapy
2nd line
39
addresses cancer symptom management
palliative
40
what decreases absorption of cancer drugs? increases?
dec -- NV, prior treatment affecting GI, DDI, dec. peristalsis inc -- DDI, inc. peristalsis
41
what decreases cancer drug distribution? increases?
dec -- weight loss and dec. body fat inc -- hypoalbumin, protein binding, peritoneal or pleural effusions
42
what decreases cancer agent elimination? increases?
dec -- renal or hepatic dysfunction inc -- induction of metabolism
43
what correlates with toxicity and therapeutic effect of cancer agents
AUC, Css, Cmax, drug exposure time above a certain threshold concentration
44
what are affected by DDIs with cancer agent
PD but NOT PK
45
the reaction between 5-FU and folinic acid (leucovorin) is a
positive PD reaction folinic acid enhances effect of 5-FU
46
carboplatin administered with paclitaxel leads to
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
methods for dose individualization of cancer drugs (3)
BSA based priori dose determination based on patient characteristics dose adaptation by LSM and TDM
48
dose adaptation of cancer drugs for renal & liver function
renal- base on eGFR, calvert formula for carboplatin liver- depends on drug
49
how to dose adjust cancer agents based on patient history
assess propensity for toxicity
50
should TBW or IBW be used for cancer agent dosing? why?
IBW, toxicity can occur if using TBW for obese patients
51
does pharmacogenetics play a role is cancer dose adjustment? which enzymes?
yes 5-FU catabolized by DPD 6-MP inactivated by TPMT
52
how is population PK used for cancer agents
find covariates that change the dose-conc relationship and adjust dose
53
dose adaptation method done to limit frequency of blood sampling
Limited sampling methods (LSMs)
54
limitations of LSM
need to be applied prospectively and validated in treatments using the same agent, dose, admin schedule, and infusion duration as the original study
55
which drug frequently uses TDM for cancer
methotrexate
56
warfarin binds with high affinity to receptors and enzymes, which affects
PK of the drug
57
warfarin has what type of binding and distribution
reversible binding target mediated drug disposition
58
which form of warfarin is more active
S > R
59
S warfarin is metabolized by what enzyme? is it affected by genetics
CYP2C9-- has genetic polymorphism
60
what type of PD response does warfarin have
indirect PD response indirect MOA -- effect delayed on the prothrombin complex since it changes production for the complex's activity
61
genetic polymorphisms of warfarin occur with what 2 enzymes
CYP2C9 and VKORC1
62
when is warfarin dose proportional
on multiple doses
63
what happens with Css with low dose IV warfarin infusion
time lag to Css
64
how does genomic dosing compare to TDM
genomic modeling is NOT superior trials assessed therapy initiation not management
65
what do you need for bayesian dose individualization of warfarin
PKPD model, patient info, observed drug response, the dose, and schedule
66
what does the bayesian model do
uses a bayesian algorithm to predict the drug response using individualized parameter estimates
67
what is the most common type of anemia
iron deficiency anemia
68
absorption of erythropoietin follows
flip flop kinetics
69
bioavailability of EPO is
dose dependent
70
what is the dose dependent half life of EPO following IV INJECTION
8 hours
71
what is the most important clinical marker for EPO administration
hemoglobin
72
will Hgb spike immediately after EPO administration? if not when?
no immediate spike after dose 1 rise may take 5 days with multiple dosing
73
what does steady state of Hgb depend on?
lifespan of RBCs
74
are higher levels of Hgb seen in males or females?
males
75
which administration method of EPO is more effective?
SC >>>> IV

Misc. Pharm Exams (6 decks)

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