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Foundations 2 > Antineoplastic drugs > Flashcards

Antineoplastic drugs Flashcards

1
Q

Three main clinical setting of chemotherapy?

A

Primary induction treatment, neoadjuvant, adjuvant post surgical treatment

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2
Q

Log Kill

A

fixed proportion of cancer cells that are killed

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3
Q

What drugs do you use in G1

A

Steroid hormones and Asparaginase

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4
Q

What drugs do you use in S phase

A

Antimetabolites: Methotrexate, 5-flurorouracil, 6-Mercaptopurine

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5
Q

What drugs do you use in G2

A

Bleomycin and Etoposide

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6
Q

What drugs do you use in M phase

A

Vincristine and Paclitaxel

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7
Q

What are some alkylating agents?

A

Nitrogen mustards (Cyclophosphamide) and Nitrosoureas (Carmustine(

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8
Q

What are some Anthracycline antibiotics?

A

Doxorubicin and Daunorubicin

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9
Q

What monoclonal antibodies are used?

A

Rituximab

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10
Q

What RTK inhibitors?

A

Imatinib

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11
Q

Schedule dependent –duration of exposure for anti-tumor and toxicity

A

Cell-cycle specific (CCS) agents

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12
Q

Cumulative dose for anti tumor and toxic results

A

Non-cell cycle specific agents (NCCS)

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13
Q

What is myelosuppression associated with?

A

Alkylating agents and anti-metabolites

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14
Q

CCS agents, Glucocorticoid types (hormone)

A

Prednisone and dexamethasone

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15
Q

Mechanism of Glucocorticoid

A

G1 phase, cell death in lymphoid illness by apoptosis

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16
Q

Adverse effects of Glucocorticoid

A

Hyperglycemia, weight gain, body fluid retention, euphoria, depression, confusion

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17
Q

When do you use glucocorticoid?

A

Blood cancer (leukemia, lymphoma, myeloma), breat cancer, brain metastasis, spinal cord compresion

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18
Q

CCS agents, Gonadal (hormone)

A

Diethylstillbestrol and testosterone

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19
Q

Mechanism of Gonadal (hormone)

A

G1, longer term administration, cytostatic

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20
Q

Adverse effect of Gonadal (hormone)

A

cholestatic jaundice (androgen), hypercalcemia, uterine bleeding, hypercoagulable state (estrogen)

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21
Q

When do you use Gonadal (hormone)

A

breast cancer and prostrate cancer

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22
Q

CCS agents, Gonadal (hormone) anatgonist

A

Tamoxifen and flutamide

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23
Q

Mechanism of tamoxifen

A

g1, estrogen Receptor blocker –estrogen positive cell growth stopped

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24
Q

Mechanism of Flutamide

A

g1, androgen receptor blocker

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25
Q

Adverse effects of Gonadal (hormone) anatgonist

A

hot flashes, fluid retention (tamoxifen), gynecomastia (flutamide)

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26
Q

When do you use Gonadal (hormone) anatgonist?

A

Breast cancer (tamoxifen) and prostrate cancer (flutamide)

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27
Q

CCS agents, Gonadotropin-releasing (hormone) analogs

A

Leuprolide and Goserelin

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28
Q

Mechanism of Gonadotropin-releasing (hormone) analogs

A

g1, decrease FSH and LH if used constantly

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29
Q

Adverse effects of Gonadotropin-releasing (hormone) analogs

A

transient flare of symptoms with bone metastasis

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30
Q

When do you use Gonadotropin-releasing (hormone) analogs

A

prostate cancer

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31
Q

CCS agents Aromatase inhibitors (hormone)

A

Anastrazole

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32
Q

Mechanism of Aromatase inhibitors (hormone)

A

g1, inhibits estrogen and androstenedione formation

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33
Q

Adverse effects of Aromatase inhibitors (hormone)

A

nausea, asthenia, headache, hot flashes

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34
Q

When do you use Aromatase inhibitors (hormone)?

A

advanced breast cancer

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35
Q

CCS miscellaneous Antineoplastic agent

A

L-Asparaginase

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36
Q

Mechanism of L-Asparaginase

A

g1, catalyze Asn to Asp and NH3, decreases serum Asn which is necessary for growth of certain lymphoid cells

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37
Q

Adverse effects of L-Asparaginase

A

hypersensitivity, inhibits protein synth–decrease clotting factors, hypoalbuminemia

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38
Q

When do you use L-Asparaginase?

A

Lymphoid malignancy, Acute lymphoblastic leukemia, T-cell leukemia, T-cell lymphoma (so Lymphocytes issue–specifically T cells)

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39
Q

Types of antometabolites used to kill cells in S phase of cell cycle

A

Methotrexate (MTX), 6-mercaptopurine, cytarabine (Ara-c) and 5-Flurouracil (5-Fu)

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40
Q

Mechanism of MTX

A

S phase, analog of folic acid, inhibit DHFR so decrease A,G,T in cell

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41
Q

Adverse effects of MTX

A

myelosuppression, GI toxicity

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42
Q

When do you use MTX

A

acute leukemia, breast cancer, non-hodgkin’s and T-cell lymphomas

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43
Q

Mechanism of 6-mercaptopurine

A

S phase, inhibits purine metabolism after activation of HGPRT , a purine analogue –affect replication, transcription and stability

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44
Q

Adverse effects of 6-mercaptopurine

A

bone marrow suppression

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45
Q

When do you use 6-mercaptopurine ?

A

Acute leukemias (ALL and AML)

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46
Q

Mechanism of cytarabine (Ara-c)

A

S phase, tumor cell kinase activate it to form nucleotide that suppresses pyrimidine metabolism

47
Q

Adverse effects of cytarabine (Ara-c)

A

bone marrow suppression, N/V, mucositis

48
Q

When do you use cytarabine (Ara-c) ?

A

in acute leukemias

49
Q

Mechanism of 5-Flurouracil (5-Fu)

A

S phase, activated to metabolite, inhibits thymidylate synthase–thymine less death of tumors, a pyrimidine analog –affects of DNA/RNA stability, elongation, transcription

50
Q

Adverse effects of 5-Flurouracil (5-Fu)

A

diarrhea, bone marrow suppression, ulcerative stomatitis

51
Q

When do you use 5-Flurouracil (5-Fu)?

A

in solid tumors

52
Q

CCS for G2 phase?

A

Bleomycin (antobiotics) and Etoposide (plant alkaloid, podophyllotoxin)

53
Q

Mechanism for Bleomycin (antobiotics)

A

G2, glycopeptide mixture alters nucleic acid functions via free radical form

54
Q

Adverse effects of Bleomycin (antobiotics)

A

bone marrow sparing, pulmonary fibrosis, skin thickening, hypersensitivity reactions

55
Q

When do you use Bleomycin (antobiotics)?

A

Hodgkin’s and other lymphomas, squamous cell and testicular cancers

56
Q

Mechanism for Etoposide (plant alkaloid, podophyllotoxin)

A

late S/early G2, topoisomerase II inhibitor

57
Q

Adverse effects of Etoposide (plant alkaloid, podophyllotoxin)

A

Neutropenia, N/V, diarrhea, hepatic dysfunction (high dose)

58
Q

When do you use Etoposide (plant alkaloid, podophyllotoxin)?

A

Testicular, small cell carcinoma, and prostate cancer

59
Q

CCS-M phase drugs

A

Vincristine and Vinblastine (Vinca alkaloids) and Paciltaxel (Taxane)

60
Q

Mechanism for Vincristine and Vinblastine (Vinca alkaloids)

A

M phase, binds tubulin and block mitotic spindle activity–destabilizes microtubule complex –enhance depolymerization

61
Q

Adverse effects of Vincristine and Vinblastine (Vinca alkaloids)

A

neurotoxic (Vincristine) and bone marrow suppression (Vinblastine)

62
Q

When do you use Vincristine and Vinblastine (Vinca alkaloids)?

A

Acute leukemias, Hodgkin’s and other lymphomas, kaposi’s sarcoma, neuroblastoma and testicular cancer

63
Q

Mechanism for Paciltaxel (Taxane)

A

M phase, block mitotic spindles disassembly, stabilze microtubule ad inhibit depolymerization–opposite of vinca alkaloids but same effect

64
Q

When do we use Paciltaxel (Taxane)?

A

Advanced breast and ovarian cancer

65
Q

What are some cell cycle non-specific agents

A

Cisplatin (alkylating agents: platinum coordination compound), Cyclophosphamide (Alkylating agents: Nitrogen mustard), Cartmustine (alkylating agents, non classical, nitrosourea), Procarbazine (Alkylating agents: non classical)

66
Q

Mechanism for Cisplatin (alkylating agents: platinum coordination compound)

A

CCNS, covalent bonds with DNA, inhibits DNA replication and transcription, miscoding

67
Q

Adverse effects of Cisplatin (alkylating agents: platinum coordination compound)

A

Bone marrow sparing, peripheral neuropathy, renal insufficiency, N/V

68
Q

When do you use Cisplatin (alkylating agents: platinum coordination compound)?

A

Bladder cancer, lung, ovaries, testicles

69
Q

Mechanism for Cyclophosphamide (Alkylating agents: Nitrogen mustard)

A

CCNS, covalently bond with DNA, activated via hepatic cytochrome P-450

70
Q

Adverse effect of Cyclophosphamide (Alkylating agents: Nitrogen mustard)

A

forms acrolein, causing bladder toxicity

71
Q

When do you use Cyclophosphamide (Alkylating agents: Nitrogen mustard)?

A

Breast and ovarion cancers; non-hodgkin’s lymphoma

72
Q

Mechanism for Cartmustine (alkylating agents, non classical, nitrosourea)

A

CCNS, highly lipid soluble

73
Q

Adverse effects of Cartmustine (alkylating agents, non classical, nitrosourea),

A

leukopenia, pulmonary fibrosis, N/V

74
Q

When do you use Cartmustine (alkylating agents, non classical, nitrosourea)?

A

adjunctively in brain tumors (glioblastoma; lymphoma)

75
Q

Mechanism for Procarbazine (Alkylating agents: non classical)

A

CCNS, activation by hepatic cyp450 in liver for active metabolites–similar effects on DNA as classic alkylating agents

76
Q

Adverse effects of Procarbazine (Alkylating agents: non classical)

A

may cause leukemia, bone marrow suppression, N/V

77
Q

When do you use Procarbazine (Alkylating agents: non classical)?

A

Hodgkin’s lymphoma; glioma

78
Q

What are some anthracycline antibiotics used in CCNS

A

Doxorubicin, Daunorubicin

79
Q

Mechanism for Doxorubicin

A

CCNS, inhibits topiosomerase II, intercalate with DNA, form free radicals

80
Q

What are the adverse effects of Doxorubicin

A

Breast, endometrial, lung, and ovarion cancers, Hodgkin’s lymphoma

81
Q

When do use Doxorubicin?

A

Brest, endometerial, lung, and ovarian cancers; Hodgkin’s lymphoma

82
Q

Mechanism for Daunorubicin

A

CCNS, inhibit topiosomerase II , intercalate with DNA, form free radicals

83
Q

What are the adverse effects of Daunorubicin

A

Myelosuppression, cardiotoxicity is dose-limiting

84
Q

When do you use Daunorubicin?

A

Leukemias

85
Q

What are other antibiotics used in CCNS

A

Dantinomycin and mitomycin

86
Q

Mechanism for Dantinomycin

A

CCNS, inhibits DNA-dependent RNA synthesis

87
Q

What is the adverse effects of Dantinomycin

A

bone marrow suppression

88
Q

When do you use Dantinomycin?

A

Choriocarcinoma, Wilm’s tumor, rhabdomysocarcoma, testicular, Ewing sarcoma

89
Q

Mechanism of mitomycin

A

CCNS, biotransformed alkylating agent

90
Q

Adverse effects of mitomycin

A

Bone marrow suppression

91
Q

When do you use mitomycin

A

Colon cancer, superficial bladder, stomach, pancreatic cancer

92
Q

Interferon-alpha although no longer used, for test purpose it is used in?

A

it is used for T-cell lymphoma

93
Q

Miscellaneous Antineoplastic agents

A

Monoclonal antibodies (Rituximab) and Imatinib

94
Q

Mechanism of Monoclonal antibodies (Rituximab)

A

interact with CD-20 of normal and malginant B-lymphocytes

95
Q

What is the adverse effect of Monoclonal antibodies (Rituximab)?

A

myelosuppression, hypersensitivity

96
Q

When do you use Monoclonal antibodies (Rituximab)?

A

non Hodgkin’s lymphoma

97
Q

Mechanism of Imatinib

A

inhibits abnormal Tyrosine kinase created by philidelphia chromosome in CML

98
Q

What is the adverse effect Imatinib ?

A

Diarrhea, nausea, cramps, fatigue

99
Q

When do you use Imatinib ?

A

Philadelphia positive CML

100
Q

Mechanism of Alkylating agent drug resistance

A

increased DNA repair and formation of trapping agents

101
Q

Mechanism of 5-fluorouracil and 6-mercaptopurine drug resistance

A

decreased activation of pro-drug

102
Q

Mechanism of Alkylating agent, Dactinomycin, MTX, drug resistance

A

decreased drug accumulation via increase in transporters

103
Q

Mechanism of Vinca alkaloids, MTX, Etoposide and gonadal hormones drug resistance

A

change in target enzymes or receptors

104
Q

Mechanism of pyrimidine and purine analogs drug resistance

A

formation of drug-inactivating enzymes

105
Q

Drug toxicities: Vincristine

A

Peripheral neuropathy

106
Q

Drug toxicities: Bleomycin

A

pulmonary fibrosis, fever, blisters, anaphylaxis

107
Q

Drug toxicities: MTX

A

Myelosuppresion, mucositis, crystalluria

108
Q

Drug toxicities: Cisplatin

A

nephrotoxicity, acoustic, and peripheral neuropathy

109
Q

Drug toxicities: Doxo-Daunorubicin

A

cardiomyopathy

110
Q

Drug toxicities: Cyclophosphamide

A

hemorrhagic cystitis

111
Q

How can multiple anticancer drugs may occur?

A

increased expression of MDR1 –increase cell surface glycoproteins involved in drug efflux –drive out drug molecules through ATP usage

112
Q

Various drug resistance mechanism:

A

increased drug efflux, mutation of drug target, DNA damage repair, activation of alternative signalling pathways or evasion of cell death

113
Q

What can drug resistance do to cancer treatments?

A

limit effectiveness of therapies, amount of drugs that can be administered and limit the amount of drugs that reaches the tumor

Foundations 2 (15 decks)

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