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FPP 1 > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Alkylating agents MOA:

A

Introduce alkyl groups in DNA, and cause DNA crosslinks and strand breaks.

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2
Q

Alkylating agents CCS:

A

Cell-cycle-nonspecific, but cytotoxicity is enhanced in growing/dividing cells.

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3
Q

Mechlorethamine class and CCS:

A

Alkylating agent (nitrogen mustard); cell-cycle-nonspecific.

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4
Q

Mechlorethamine indications:

A

Hodgkin’s and non-Hodgkin’s lymphoma.

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5
Q

Cyclophosphamide class and CCS:

A

Alkylating agent (nitrogen mustard); cell-cycle phase-nonspecific.

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6
Q

Cyclophosphamide metabolism:

A

Activated by liver CYP450 system. Activation forms acrolein (bladder toxicity).

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7
Q

Cyclophosphamide indications:

A

Very broad spectrum of activity

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8
Q

Cyclophosphamide toxicity:

A

May cause sterile hemorrhagic cystitis. Can be partially prevented with the drug Mesna.

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9
Q

Carmustine class:

A

Alkylating agent (nitrosoureas)

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10
Q

Carmustine indication (important):

A

Treatment of brain tumors (rapidly crosses BBB)

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11
Q

Methotrexate class and MOA:

A

Folate analog; Binds to dihydrofolate reductase (DHFR) and prevents formation of tetrahydrofolate (THF).

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12
Q

Often co-administered with methotrexate:

A

Leucovorin (folinic acid; a fully reduced folate coenzyme that does not require reduction by DHFR.)

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13
Q

Methotrexate contraindication:

A

Binds to serum albumin so avoid other drugs that will displace it from albumin.

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14
Q

Methotrexate important toxicity:

A

Renal tubular necrosis.

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15
Q

Methotrexate indication:

A

Acute lymphocytic leukemia; choriocarcinoma (MTX is #1).

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16
Q

5-FU class and MOA:

A

Pyrimidine analog. Activated in cells to FUTP which inhibits RNA synthesis, to FdUMP which interferes with thymidylate synthetase and ultimately DNA synthesis.

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17
Q

5-FU CCS:

A

S phase

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18
Q

5-FU indications:

A

carcinoma of the stomach, COLON, pancreas, ovary, head and neck, BREAST, bladder. Also as a topical cream for basal cell carcinoma. Mostly GI cancers.

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19
Q

Cytarabine class and MOA:

A

Pyrimidine analog. Competes with cytidine for all 3 phosphorylation steps to dCTP. Cytarabine tri-phosphate then competes with dCTP for incorporation into DNA and causes DNA chain termination.

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20
Q

Cytarabine CCS:

A

S phase. Continuous infusion increases probability of killing tumor cells not initially in S phase.

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21
Q

Cytarabine toxicity:

A

Neurotoxicity.

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22
Q

Cytarabine indications:

A

Acute leukemias.

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23
Q

What is a nadir:

A

the lowest or deepest point in a WBC count-graph.

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24
Q

Mercaptopurine class and MOA:

A

Purine analog; is converted in cells to a ribonucleotide that inhibits RNA and DNA synthesis.

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25
Q

Mercaptopurine CSS:

A

S phase.

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26
Q

Mercaptopurine indications and important:

A

Acute leukemias.

*Need to check for mutations in TPMT which metabolizes 6-MP to inactive form. If there is 1 copy of nonfunctional TPMT, reduce dose to prevent serious bone marrow toxicity.

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27
Q

Hydroxyurea MOA:

A

Inhibits ribonucleotide reductase by blocking conversion of ribonucleotides to dNTPs, thereby preventing DNA synthesis. Causes cells to arrest at G1-S interface.

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28
Q

Hydroxyurea CSS:

A

S phase.

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29
Q

Hydroxyurea useful with….

A

radiation.

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30
Q

Hydroxyurea indications:

A

granulocytic leukemia, head and neck cancer.

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31
Q

Hydroxyurea toxicity:

A

Hematopoietic depression.

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32
Q

Vinblastine class:

A

Vinca alkaloid.

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33
Q

Vinca alkaloids CSS and MOA:

A

M phase specific. Binds to tubulin, inhibiting proper formation of MTs and mitotic spindle.

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34
Q

Vinblastine indications:

A

Breast cancer (also H and nonH lymphoma)

35
Q

Vinblastine toxicity:

A

Strongly myelosuppressive, EPITHELIAL ULCERATIONS.

36
Q

Vincristine class:

A

Vinca alkaloid.

37
Q

Vincristine indications:

A

Treatment of acute lymphocytic leukemia, Wilm’s tumor, neuroblastoma, rhabdomyosarcoma (also H and nonH).

38
Q

Vincristine toxicity:

A

Alopecia, significantly less myelosuppression than vinblastine, Neuromuscular abnormalities (ex: peripheral neuropathy).

39
Q

Paclitaxel class and CSS:

A

Taxane; blocks late in G2 phase (a phase more sensitive to radiation).

40
Q

Paclitaxel MOA:

A

Enhances assembly and stability of MTs by binding to B-subunit of tubulin. Polymerization is stabilized so MTs cannot dissociate.

Taxol can interfere with DNA repair, intensifying the effects of DNA damage by cisplatin or cyclophosphamide.

41
Q

Paclitaxel indications:

A

Refractory ovarian cancer; breast.

Can interfere with DNA repair so could be used with cisplatin or cyclophosphamide.

42
Q

Paclitaxel toxicity:

A

Dose-limiting leukopenia, peripheral neuropathy, myalgia/arthralgia.

43
Q

Doxorubicin class and MOA:

A

Antitumor antibiotics, cycle-specific phase-nonspecific.

  1. Intercalates between DNA base pairs, distorting DNA helix.
  2. Causes lipid peroxidation and free radical generation.
    3***. Binds to DNA and topoisomerase II.

Doxorubicin is one of the few drugs with some anti-angiogenic properties*.

44
Q

Doxorubicin indication:

A

H and nonH, breast, ovary, small-cell lung.

45
Q

Doxorubicin toxicity:

A

Cardiomyopathy***

46
Q

Bleomycin class and CSS:

A

Antitumor antibiotic; phase-specific for G2.

47
Q

Bleomycin MOA:

A

Iron is critical to its mechanism. Glycopeptides bind DNA, causes oxidative-like damage to DNA which leads to DNA strand breaks.

48
Q

Bleomycin indications:

A

Germ cell tumors of testes and ovaries.

49
Q

Bleomycin toxicity:

A

Dose-related PULMONARY TOXICITY.
Vesiculation of the skin, skin hyperpigmentation.

*Lungs and skin have lowest levels of bleomycin hydrolase (which inactivates bleomycin).

50
Q

Etoposide MOA:

A

Stabilizes DNA-topoisomerase II complexes, resulting in dsDNA breaks.

51
Q

Etoposide CSS:

A

Maximal effects in late G2 phase (also late S).

52
Q

Etoposide indications:

A

Lymphomas, acute nonlymphocytic leukemia, small cell carcinoma of the lung, testicular tumors.

53
Q

Etoposide toxicity:

A

Leukopenia

54
Q

Filgrastim MOA, use, side effect:

A

Stimulates granulocyte production by marrow.

Given after myelosuppressive agents to speed neutrophil recovery.

Bone pain.

55
Q

Trastuzumab MOA and use:

A

Monoclonal antibody that binds to HER2 receptor.

Use with metastatic breast cancers that overexpress HER2 (which tend to be less responsive to anti-estrogen strategies)

First line treatment with paclitaxel for breast cancer.

56
Q

Trastuzumab toxicity:

A

Cardiomyopathy, hypersensitivity, infusion reaction.

57
Q

Cisplatin MOA:

A

Platinum coordination complex. Activated species causes DNA crosslinks.

58
Q

Cisplatin CSS:

A

Cycle-specific, phase nonspecific.

59
Q

Cisplatin toxicity:

A

Nephrotoxicity, ototoxicity, electrolyte disturbances.

60
Q

Procarbazine MOA, CSS:

A

Activated in vivo to a methylating agent which causes chromosomal damage. Most effective in G1 and S phase.

Atypical alkylating agent; no cross resistance with other alkylating agents.

61
Q

Procarbazine indication:

A

H lymphoma.

62
Q

Prednisone MOA:

A

Binds to steroid receptors, depresses RNA synthesis of many growth-related genes. May arrest cells in G1.

Induces nucleases which may modulate cell lysis.

63
Q

Prednisone uses:

A

Anti-emetic effect. Palliative therapy.

Used for acute and chronic lymphocytic leukemia, H and nonH, breast cancer.

64
Q

Tamoxifen MOA:

A

Antiestrogen that blocks estrogen receptors. Activated by CYP2D6.

Generally cytostatic; tumor will grow back once therapy is stopped.

65
Q

Tamoxifen uses:

A

Breast cancer, breast cancer prophylaxis in women at high risk.

May prevent post-menopausal osteoporosis.

66
Q

Tamoxifen toxicity:

A

Hot flashes, fatigue, nausea, bone and other musculoskeletal pain.

*May increase rate of uterine/endometrial cancer.

67
Q

Letrozole MOA:

A

Aromatase inhibitor; inhibits conversion of androgens to estrogens in all tissues by binding to aromatase CYP19.

68
Q

Letrozole use:

A

1st line treatment of hormone receptor-positive or receptor-unknown breast carcinoma in post-menopausal women.

*Adjuvant therapy for postmenopausal women with advanced breast cancer who have received 5 years of adjuvant tamoxifen therapy.

69
Q

Letrozole toxicity:

A

Hot flashes, fatigue, nausea, bone and other musculoskeletal pain (no difference to tamoxifen).

70
Q

Leuprolide MOA:

A

Analog of gonadotropin-releasing hormone (GnRH). After 2-4 weeks it desensitizes GnRH signaling, inhibiting LH/FSH secretion thereby decreasing testosterone synthesis to castration levels.

71
Q

Leuprolide use and toxicity:

A

Advanced hormonally responsive prostate cancer.

Hot flashes, impotence.

72
Q

Flutamide MOA and use:

A

Non steroidal antiandrogen that blocks androgen receptors.

Metastatic prostate cancer.

73
Q

Flutamide toxicity:

A

Gynecomastia

74
Q

Imatinib (Gleevec) MOA and use:

A

CKIT tyrosine kinase inhibitor, blocks cell proliferation and increases apoptosis.

Approved for CML and GI stromal tumors.

75
Q

Sequential blockade:

A

Simultaneous action of two inhibitors acting on different enzymes of a linear metabolic pathway.

76
Q

Concurrent inhibition:

A

Inhibitors block two separate pathways that lead to the same end product.

77
Q

Complementary inhibition:

A

One of the inhibitors affects the function of an end product, the other inhibitor affects the synthesis of the end product.

78
Q

Rescue:

A

“Rescue” the patient’s normal cells from the treatment.

79
Q

Synchronization:

A

Tumor cells synchronized so they are in one phase and then use agent that is specific for that phase.

80
Q

Recruitment:

A

The mobilization of slowly proliferating or non-proliferating cells to more rapid proliferation.

81
Q

Antimetabolites CSS:

A

S phase specific.

82
Q

What are biological response markers?

A

Naturally occurring proteins or therapeutic molecules designed to mimic or impact natural proteins. Intent is to alter patient’s own biological response to tumor, less probability of serious toxicity.

83
Q

Procarbazine SEs:

A

Secondary malignancy if used too long.

84
Q

Prednisone SEs:

A

Immunosuppression.

FPP 1 (3 decks)

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