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PHC 532- Exam 4 > Anticancer PK/PD > Flashcards

Anticancer PK/PD Flashcards

1
Q

How are cancer cells generated?

A

Multiple gene mutations

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2
Q

Solid tumors

A

Carcinomas and sarcomas

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3
Q

Hematological tumors

A

Lymphomas, leukemias

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4
Q

Treatment types

A

Surgery, radiation therapy, chemo, targeted therapy, immunotherapy, blood product donation and transfusion, stem cell transplant, vaccine, hyperthermia, photodynamic therapy, lasers

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5
Q

Neoadjuvant therapy

A

Given before the surgical procedure to shrink cancer and procedure doesn’t have to be as extensive

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6
Q

Adjuvant therapy

A

Destroy leftover cancer cells that may be present after the tumor is removed to prevent reoccurrence

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7
Q

First-line

A

Treatment best to treat a certain cancer

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8
Q

Second-line

A

Use if first-line doesn’t work, aka salvage therapy

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9
Q

Palliative

A

Supportive care

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10
Q

Cell cycle phase-specific agents

A

Appear to be most active during a particular phase but can be active in another phase

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11
Q

Cell cycle phase-nonspecific agents

A

May have greater activity in one phase than another but not to the degree of cell cycle phase-specific agents

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12
Q

PK of anticancer agents

A

Most have a narrow TI and wide inter-individual PK –> TDM

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13
Q

Consequence of not being able to predict anticancer PK

A

Increased toxicity or sub-therapeutic dosing

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14
Q

Effects/causes of decreased absorption of anticancer agents

A

N/V, prior surgery, radiotherapy, chemo affecting GI tract, DDI, decreased peristalsis

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15
Q

Effects/causes of increased absorption of anticancer agents

A

DDI, increased peristalsis

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16
Q

Effects/causes of decreased distribution of anticancer agents

A

Weight loss, decreased body fat

17
Q

Effects/causes of increased distribution of anticancer agents

A

Hypoalbuminemia, protein binding, peritoneal or pleural effusions

18
Q

Effects/causes of decreased elimination of anticancer agents

A

Decreased renal and/or hepatic dysfunction

19
Q

Effects/causes of increased elimination of anticancer agents

A

Induction of metabolism

20
Q

Indicator of efficacy

A

Toxicity

21
Q

Efficacy of MTX is associated with what?

A

Cmax

22
Q

PD drug interaction between 5-FU and leucovorin

A

Leucovorin enhances the effect of 5-FU by inhibiting thymidylate synthase

23
Q

PD DDI between cisplatin/carboplatin and paclitaxel/docetaxel

A

Administration of paclitaxel followed by carboplatin lead to a decrease in the formation of platinum adducts in patient DNA (aka decreasing the toxicity of carboplatin)

24
Q

Dose individualization: BSA-based

A

BSA has minimal clinical value in achieving consistent drug exposure but using BSA to dose adjust is still widely used

25
Q

A priori dose adjustment: renal function

A

Carboplatin is the only drug that’s dosed based on GFR

26
Q

A priori dose adjustment: propensity for toxicity

A

Based on history of chemo and physiological status of patients, their propensity to manifest the known toxicity can be predicted and adjusted

27
Q

A priori dose adjustment: elderly and obesity

A

Aging can’t be considered as an independent feature (can’t be used to adjust doses alone)

Limitation of calculated BSA at 2.2m^2 recommended for obese patients

28
Q

A priori dose adjustment: pharmacogenetics

A

5-FU is catabolized by DPD and patients who don’t have much of this enzyme are at risk of life-threatening toxicity

6-MP is inactivated by TPMT and there’s polymorphic populations that have different dose adjustments

29
Q

Dose adjustment based on population PK

A

Run a trial and get the PK, put it into some software and it builds a population model

30
Q

Limitation of LSM

A

Need to be applied and validated in treatments using the same anticancer agents, doses, administration schedules, and duration of infusion as the original study the LSM was established

31
Q

Rescue therapy for MTX toxicity

A

Leucovorin

32
Q

PK matrixes used to establish a correlation with efficacy/toxicity

A

AUC, Css, Cmax, time above a threshold concentration

PHC 532- Exam 4 (5 decks)

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