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Pharm > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

what categories of drugs make up the classical chemotherapeutic agents?

A

DNA damaging agents
Antimetabolites
Inhibitors of mitosis

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2
Q

DNA cross-linking drugs include:

A

Nitrogen mustards - cycolphosphamdie
[ - mechlorethamine, ifsofamide, chloroambucil, melphalan]

platinum analogs - cisplatin

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3
Q

DNA cleaving agents include:

A

bleomycin

Doxorubicin

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4
Q

Antimetabolites include which categories of drugs?

A

folic acid analogs
pyrimidine analogs
purine analogs

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5
Q

folic acid analogs include:

A

methrotrexate

leucovorin

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6
Q

pyrimidine analogs include

A

5-fluorouracil

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7
Q

purine analogs include

A

mercaptopurine

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8
Q

inhibitors of mitosis include:

A

pacitaxel (taxol)

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9
Q

cross linking agents work by:

A

covalently binding to DNA bases causing cross-linking of DNA strands
- usually at N7 guanine

prevents DNA replication and RNA synthesis

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10
Q

cyclophosphamide is what kind of drug?

A

DNA cross linking agent (nitrogen mustard)

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11
Q

cisplatin is what kind of drug?

A

DNA cross linking agent (platinum analog)

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12
Q

cyclophosphamide - activation and toxicity

A

P450

bone marrow suppression

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13
Q

cisplatin - toxicity

A

renal toxicity

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14
Q

DNA cleaving agents work by:

A

cleaving DNA which stalls/disrupts replication and transcription

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15
Q

bleomycin is what kind of drug?

A

DNA cleaving agent

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16
Q

bleomycin - activation and toxicity

A

activated by microsomal reduction

pulmonary toxicity

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17
Q

doxorubicin is what kind of drug?

A

DNA cleaving agent

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18
Q

doxorubicin - action, activation, and toxicity

A

freezes topoisomerase II in strand cleavage and rejoining cycles –> DNA breaks
achieved with oxygen free radicals

activated by flavin centered reductase

bone marrow suppression and cardiac toxicity

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19
Q

antimetabolites work by:

A

enzyme inhibitors and nucleotide analog - interfere with metabolic pathways
competitive inhibition or incorporation into DNA, RNA that causes premature chain termination and an abnormal product

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20
Q

what is the theory behind folic analog therapy?

A

tumor cells rapidly divide which requires a large amount of folic acid to generate nucleotides and AAs

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21
Q

methotrexate is what kind of drug?

A

folic acid analog

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22
Q

what is the mechanism of methotrexate?

A
  • competitive inhibitor of dihydrofolate reductase (DHFR) which catalyzes FH2–>FH4
    can’t make thymine nucleotides from uracil –> pyrimidine shortage
  • inhibits enzymes required for de novo purine synthesis
  • impairs protein synthesis because it interferes with glycine and methionine synthesis
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23
Q

what is the major toxicity of methotrexate

A

bone marrow suppression

leukopenia and thrombocytopenia

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24
Q

leucovorin is what kind of drug?

A

folic acid analog (reduced)

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25
Q

what is the mechanism of leucovorin and why is it given?

A

used in the synthesis of purines and production of dTMP

functions to rescue normal cells by allowing them to partially recover after treatment with methotrexate

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26
Q

what is the theory behind pyrimidine and purine analogs as therapy?

A

become incorporated into nucleotides which results in DNA termination or an incorrect strand of DNA or RNA

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27
Q

fluorouracil is what kind of drug?

A

pyrimidine analog (uracil analog)

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28
Q

what is the mechanism of 5FU

A

uracil derivative is incorporated into RNA which prevents processing of rRNA into final product ==> 28 S ribosome
incorporation into DNA causes strand breaks
metabolite of 5FU (FdUMP) inhibits thymidylate synthase which prevents conversion of dUMP to dTMP

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29
Q

major toxicity of 5FU:

A

bone marrow suppression, oral and GI mucositis

30
Q

mercaptopurine is what kind of drug

A

purine analog

31
Q

what is the mechanism of mercaptopurine?

A

causes feedback inhibition of the first step in purine biosynthesis
results in decreased levels of purines available for nucleotide synthesis
also become incorproated in DNA causing strand breaks and inhibition of RNA synthesis

32
Q

what is the major toxicity of mercaptopurine?

A

bone marrow suppression

33
Q

Pacitaxel is what kind of drug?

A

mitosis inhibitor

34
Q

what is the mechanism of pacitaxel

A

stabilizes microtubule formation causing arrest in G2 or mitosis

35
Q

what is the major toxicity of pacitaxel?

A

neutropenia

36
Q

what combination of drugs are frequently used to treat cervical cancer

A

cisplatin
bleomycin
methotrexate

37
Q

what is the mechanism of selective estrogen receptor modulators (SERMs)

A

binds estrogen receptor (ER) on tumor cells that either mimics the effect of estrogen or has antiestrogenic effects

38
Q

what are the three classes of drugs used to treat ER+ breast cancer?

A 
SERMs
aromatase inhibitors (AIs)
Selective estrogen receptor downregulators (SERDs)
39
Q

SERMs include:

A

tamoxifen

raloxifen

40
Q

AIs include:

A

letrozole (femara)

41
Q

SERDs include:

A

fulvestrant

42
Q

what is the mechanism of tamoxifen

A

antiestrogenic effect - stops growth of tumor

in bone however, it mimics the effect of estrogen and promotes increased bone density

43
Q

what is the effect of tamoxifen on post menopausal women

A

promotes cell growth of uterus and is associated with increased incidence of endometrial cancer (2/1000)

44
Q

how can a tumor become resistant to tamoxifen

A

a mutation in P450 can prevent activation of tamoxifen

45
Q

what is the mechanism of raloxifen

A

estrogenic effect on bone, antiestrogenic effects on uterine and breast

not effective against lobular carcinoma in situ and ductal carcinoma in situ

46
Q

what is the mechanism of AIs

A

lower estrogen levels by inhibiting the aromatase that converts androstenedion to estrogen and estridiol

47
Q

when is letrozole used?

A

adjuvent therapy in post menopausal patients following surgery to remove tomor

also used to treat advanced metastatic breast cancer in post menopausal patients

not associated with increased blood clot formation or endometrial cancer

48
Q

when is letrozole NOT used?

A

premenopausal patients

49
Q

the adverse reactions of letrozole include:

A

osteoporosis
hot flashes
joint pain
muscle pain

50
Q

when is fulvestrant used

A

with ER+ post menopausal patients that no longer respond to tamoxifem or letrozole

51
Q

what are the two approaches of endocrine therapy for prostate cancer?

A

block androgens from interacting with receptor

block production of androgens

52
Q

what is the mechanism of leuprolide

A

GnRH superantagoinst - downregulates GnRH receptor

decreases secretion of LH and FSH and lowers androgen production by testes

53
Q

what is the problem with leuprolide?

A

blocks testicular production of androgens but not adrenal androgen production —> castration resistant tumors

54
Q

how is the problem with leuprolide solveD?

A

GnRH antagonist Flutamide is given to help prevent castration resistant tumors
–> causes a complete androgen blockade (CAB)

55
Q

how does abiraterone work?

A

inhibits CYP17 which inhibits androgen biosynthesis

56
Q

how do corticosteroids and adrenocortical suppression act as tumor chemotherapy?

A

glucocorticoids induce cell death in lymphoid tissues –> useful for treating lympholytic anemias, Hodgkins and nonHodgkins lymphomas

57
Q

what is the mechanism of cortiocosteroids and adrenocortical suppressants?

A

bind glucocorticoid receptor which initates apoptosis by caspases

58
Q

prednisone is a:

A

synthetic corticosteroid

59
Q

adverse reactions of prednisone include:

A

cushingoid features, sodium retension, muscle weakness, decreased glucose tolerance, acute tumor lysis syndrome

60
Q

targeted approaches include:

A

monoclonal antibodies
tyrosine kinase inhibitors
proteasome inhibitors
histone deacetylase inhibitors

61
Q

monoclonal antibodies include:

A

trustuzumab (herceptin)

bevacizumab (avastin)

62
Q

the mechanism of trustuzumab is

A

binds to exterior surface receptor on breast cancer cells (epidermal growth factor receptor type II, tyrosine kinase activity) and blocks binding of ligand

63
Q

the mechanism of bevacizumab is

A

binds to exterior surface of VEGF receptor, blocking the signal for proliferation and angiogenesis

64
Q

tyrosine kinase inhibitors include:

A

imatinib (gleevec)

lapatinib

65
Q

the mechanism of imatinib is

A

inhibitor of bcr-Able, KIT, PDGF
blocks catalytic activity of tyrosine kinase by binding to ATP binding domain
substrate for CYP34A cyp2c9 cyp2d6 so potential interactions can occur between drugs metabolized by these enzymes

66
Q

the mechanism of lapatinib is

A

inhibitor of epidermal growth factor receptor types I and II

67
Q

the mechanism of bortezomib (velcade) is

A

inhibits 26S proteosome

metabolized by 3A4

68
Q

brotezomib is used to treat

A

multiple myeloma

69
Q

the mechanism of vorinostat (zolinza) is

A

HDAC inhibitor

causes accumulation of acetylated histones and induces cell cycle arrest or apoptosis of cancer cells

70
Q

vorinostat is used to treat

A

cuaneous t-cell lymphoma (CTCL)

Pharm (11 decks)

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