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Pathology Anti-Neoplastics > Anti-Neoplastics > Flashcards

Anti-Neoplastics Flashcards

1
Q

cell cycle nonspecific alkylating agents

A

mechlorethamine, carmustine

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2
Q

cell cycle specific phase nonspecific alkylating agents

A

cyclophosphamide

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3
Q

least selective of the anti-neoplastics

A

alkylating agents

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4
Q

typical side effects of anti-neoplastics

A

myelosuppression, GI effects (nausea/vomiting), alopecia

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5
Q

nitrogen mustards

A

mechlorethamine, cyclophosphamide

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6
Q

nitrosoureas

A

carmustine

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7
Q

non-Hodgkins lymphoma drug

A

mechlorethamine

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8
Q

cyclophosphamide: mechanism, cell cycle specificity, side effects, uses

A

prodrug activated by liver cytochrome P450s, cell cycle specific phase nonspecific, bladder toxicity, broad uses

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9
Q

carmustine: cell cycle specificity, uses

A

cycle-nonspecific, brain tumors (crosses blood-brain barrier)

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10
Q

treats brain tumors

A

carmustine

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11
Q

methotrexate: mechanism

A

binds to dihydrofolate reductase and prevents formation of tetrahydrofolate

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12
Q

followed by “rescue” of host cells by leucovorin

A

methotrexate

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13
Q

methotrexate: side effects and uses

A

myelosuppression, GI damage, renal tubular necrosis, displaces other drugs from serum albumin; acute lymphocytic leukemia (ALL)

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14
Q

pyrimidine analogs

A

5-FU, cytarabine

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15
Q

5-FU: mechanism, uses

A

pyrimidine analog that inhibits RNA and DNA synthesis; broad spectrum of uses but mostly for GI cancers

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16
Q

cytarabine: mechanism, side effects, uses

A

pyrimidine analog that causes chain termination of DNA, myelosuppression and neurotoxicity, acute myelocytic leukemia (AML)

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17
Q

has neurotoxicity and myelosuppression as side effects

A

cytarabine

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18
Q

pyrimidine analog that causes chain termination of DNA

A

cytarabine

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19
Q

treats acute myelocytic leukemia (AML)

A

cytarabine, 6-MP, etoposide

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20
Q

6-mercaptopurine: mechanism, metabolism, use

A

purine analog, inhibits RNA and DNA synthesis; metabolized by TPMT; acute leukemias

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21
Q

patients with no functional TPMT cannot tolerate what drug?

A

6-mercaptopurine

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22
Q

hydroxyurea: mechanism

A

inhibits ribonucleotide reductase, prevents DNA synthesis, arrests cells at G1-S interface

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23
Q

hydroxyurea: use

A

granulocytic leukemia

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24
Q

inhibits ribonucleotide reductase

A

hydroxyurea

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25
Q

treats granulocytic anemia

A

hydroxyurea

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26
Q

binds to tubulin, inhibiting proper formation of microtubules and mitotic spindle

A

vincristine, vinblastine

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27
Q

major differences between vincristine and vinblastine

A

vinblastine is strongly myelosuppressive and treats breast cancer, vincristine treats acute lymphocytic leukemia (ALL)

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28
Q

vinca alkaloids: mechanism

A

binds to tubulin, inhibiting proper formation of microtubules and mitotic spindle

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29
Q

enhances assembly and stability of microtubules

A

taxanes (paclitaxel)

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30
Q

paclitaxel mechanism

A

enhances assembly and stability of microtubules, interferes with DNA repair

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31
Q

paclitaxel: use, side effect

A

refractory ovarian cancer; peripheral neuropathy

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32
Q

treats refractory ovarian cancer

A

paclitaxel

33
Q

antitumor antibiotic

A

doxorubicin

34
Q

only drug with some anti-angiogenic properties

A

doxorubicin

35
Q

doxorubicin: cell cycle specificity

A

cycle-specific phase non-specific

36
Q

multi-faceted mechanism of doxorubicin

A
  1. intercalates in DNA, distorting DNA helix 2. causes lipid peroxidation and free radical generation 3. binds to DNA + topoisomerase II
37
Q

doxorubicin: unique side effect

A

cardiomyopathy (cardiotoxicity)

38
Q

cardiomyopathy (cardiotoxicity) as a side effect

A

doxorubicin

39
Q

pulmonary toxicity as a side effect

A

bleomycin

40
Q

bleomycin: mechanism

A

iron-containing glycopeptides that bind to DNA, makes site-specific DNA breaks, phase-specific for G2

41
Q

bleomycin: unique side effect

A

pulmonary toxicity

42
Q

etoposide: mechanism

A

stabilizes DNA-topoisomerase II complexes, results in dsDNA breaks that cannot be repaired

43
Q

goal is to limit chemotherapy-induced neutropenia

A

filgrastim (G-CSF)

44
Q

filgrastim (G-CSF): unique side effect

A

bone pain

45
Q

filgrastim (G-CSF): mechanism

A

promotes progenitor of neutrophils

46
Q

treats breast cancers that overexpress HER2

A

trastuzumab

47
Q

trastuzumab: mechanism

A

monoclonal antibody that binds HER2 receptor and blocks proliferation of cells

48
Q

has nephrotoxicity as a side effect

A

cisplatin

49
Q

cisplatin: mechanism; cycle specificity

A

platinum coordination complex, causes DNA crosslinks; cycle-specific phase-nonspecific

50
Q

cisplatin: unique side effect

A

nephrotoxicity

51
Q

revolutionized treatment of testicular cancer

A

cisplatin

52
Q

procarbazine: mechanism

A

activated in vivo by liver enzymes to methylating agent which causes chromosomal damage

53
Q

procarbazine: use

A

Hodgkin’s lymphoma

54
Q

treats Hodgkin’s lymphoma

A

procarbazine

55
Q

prednisone: mechanism

A

binds to steroid receptors, depress expression of many growth related genes, induce nucleases which may modulate cell lysis

56
Q

prednisone: uses, palliative effects

A

lymphoma, leukemia, breast cancer; anti-emetic, anti-inflammatory, stimulates appetite

57
Q

estrogen receptor antagonist

A

tamoxifen

58
Q

tamoxifen: mechanism, uses

A

estrogen receptor antagonist that competitively blocks estrogen receptors in breast tissue, cytostatic (stops cell growth without killing the cells); pre-menopausal metastatic breast cancer and advanced post-menopausal breast cancer, breast cancer prophylaxis for those at higher risk

59
Q

breast cancer prophylaxis for those at higher risk

A

tamoxifen

60
Q

tamoxifen: metabolism

A

activated by CYP2D6

61
Q

tamoxifen: unique side effects

A

bone and other musculoskeletal pain, may increase rates of uterine/endometrial cancer

62
Q

may increase rates of uterine/endometrial cancer

A

tamoxifen

63
Q

blocks conversion of angdrogens to estrogens by inhibiting aromatase

A

letrozole

64
Q

letrozole: mechanism, use

A

blocks conversion of angdrogens to estrogens by inhibiting aromatase; first line treatment of post-menopausal advanced or metastatic breast cancer

65
Q

analog of GnRH

A

leuprolide

66
Q

leuprolide: mechanism, use, side effects

A

analog of GnRH, desensitizes GnRH signaling and decreases testosterone; advanced hormonally responsive prostate cancer; hot flashes and impotence

67
Q

treats advanced hormonally responsive prostate cancer

A

leuprolide

68
Q

has side effects of hot flashes and impotence

A

leuprolide

69
Q

antiandrogen that blocks androgen receptors

A

flutamide

70
Q

flutamide: mechanism and use

A

antiandrogen that blocks androgen receptors; metastatic prostate cancer

71
Q

3 drugs that lack significant bone marrow toxicity

A

vincristine, prednisone, bleomycin

72
Q

treats metastatic prostate cancer

A

flutamide

73
Q

define concurrent inhibition

A

inhibitors block two separate pathways that lead to the same end product

74
Q

define complementary inhibition

A

one drug affects the function of an end product, the other drug affects the synthesis of that end product

75
Q

define the synchronization strategy of antineoplastic therapy

A

synchronize cells so they are in one phase and then use a drug that is specific for that phase

76
Q

define the recruitment strategy of antineoplastic therapy

A

bring cells out of G0 and back into cell cycle via therapy with cell cycle-nonspecific drugs and then hit them with cycle-specific drugs

77
Q

which drug has bladder toxicity (cystitis) as a side effect and what drug prevents this?

A

cyclophosphamide; mesna

78
Q

inhibits BCR-ABL tyrosine kinase in CML

A

imatinib mesylate (Gleevec)

79
Q

imatinib mesylate (Gleevec): mechanism, net effect

A

inhibits BCR-ABL tyrosine kinase in CML, net effect blocks cell proliferation and increases apoptosis

Pathology Anti-Neoplastics (1 decks)

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