GN Cancer Chemotherapies and Flipped Classroom Flashcards Preview

Genetics and Neoplasia > GN Cancer Chemotherapies and Flipped Classroom > Flashcards

Flashcards in GN Cancer Chemotherapies and Flipped Classroom Deck (101)
Loading flashcards...
1

What is pharmacodynamics?

How drugs affect the body

2

How are the vinca drugs excreted?

Biliary excretion

3

Why are alkylating not a preferential treatment in pediatrics patients?

There many secondary malignancies that arise as a result of alkylating agent chemo. (This concern is inversely proportional to age of patient)

4

What are the acute adverse effects of mechlorethamine?

Nausea, vomiting

5

Are alkylating agents CCNS or CCS? What type of cells are more sensitive to alkylating agents?

CCNS; replicating cells

6

Cardiotoxicity is the signature adverse effect of what drug?

Anthracyclines: doxorubicin and daunorubicin

7

Topo I in inhibited by what drug?

Irinotecan

8

What does 5-FU inhibit? What required to aid in this inhibition?

Thymidylate synthase; enhanced by leucovorin (folinic acid) - inactivation requires both 5-FU and folinic acid

9

How can methotrexate be administered?

Orally, IV, or intrathecally

10

How is cis-platin administered? and cleared?

Intravenous, cleared in urine

11

Most alkylating agents are bifunctional. What is meant by bifunctional?

They are able to bind and cross-link adjacent bases or they can bind and cross-link bases on opposite strands

12

What inactivates SN-38 (the active metabolite of irinotecan)?

Glucouronidation by UGT1A1

13

How have STIs (single transduction inhibitors) transformed cancer?

From "curable" disease to a "manageable" disease

14

What drug blocks growth factor signaling in chronic myelogenous leukemia (CML)?

(Buzz association: CML = philadelphia chromosome)

Imatinib (inhibits Bcr-Abl and other tyr kinases)

15

When would an alkylating agent be ill-advised?

If the a cell has a p53 mutation (like Li Fraumeni), then inducing DNA damage wouldn't result in apoptosis which is the desired effect.

16

What are 3 ways to classify drugs?

Chemical structure, mechanism of action, and therapeutic use

17

What are the four branches of pharmacology?

pharmacokinetics, pharmacodynamics, adverse effects, and pharmaacotherapeutics

18

What might cause a patient have a fatal myelosuppression incident when administered a standard dose of 6-mercaptopurine?

A defect in one or both TMPT

19

Though alkylating agents and antitumor antibiotics are CCNS what are they most effective against?

Rapidly proliferating cells

20

What is used as a "rescue" to prevent the cytotoxicity of methotrexate to normal cells?

Leucovorin (folinic acid)

21

Patient is given FOLFIRI which is made up of 5-FU, Leucovorin, and Irinotecan. The patient is genotyped and found to be UGT1A1*3*7. What would be the appropriate response to this genotype?

Decreasing irinotecan dosing to decrease the amount of toxic metabolites

22

What does gefitinib inhibit?

EGF-R tyr kinase

23

What drug is a cytosine analog and inhibits polymerase and is a chain terminator?

Gemcitabine

24

How are doxorubicin and daunorubicin administered?

intravenous, metabolized in liver

25

What causes the cystitis that results from cyclophosphamide? What drug can be administered to almeloriate these effects?

Acrolein; Mesna

26

Which isomerase does irinotecan inhibit?

Topo I

27

To which class do doxorubicin daunorubicin belong?

Antitumor antibiotics: anthracyclines; block Topo II

28

What specific cancer is gefitinib indicated for? What are some factors that can better the outcome?

Non-small cell lung cancer; better when pt is an Asian non-smoking woman

29

45 year old female pt will be treated with a combination of Doxorubicin, docetaxel, and cyclophosphamide. Desrazoxane may be added in order to?

Protect against doxorubicin cardiotoxicity. Doxorubicin generates free radicals and desrazoxane acts as a free radical scavenger.

30

sterile hemorrhagic cystitis is the hallmark side effect of what?

Cyclophosphamide