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SBL > CA Pharm > Flashcards

CA Pharm Flashcards

1
Q

Five main classes of cancer drugs

A

alkylating agents, antimetabolites, natural products, antibodies, miscellaneous

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2
Q

Oncogene

A

gene that positively influences tumor growth

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3
Q

Tumor suppressor

A

gene that negatively influences tumor growth

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4
Q

Activation of oncogenes overrides which check point?

A

G1 arrest

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5
Q

Inactivation of tumor suppressor genes overrides which check point?

A

G2 arrest

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6
Q

Treatment process for primary chemotherapy

A

chemo! for advanced CA and metastatic disease

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7
Q

Goals of primary chemotherapy

A

relieve tumor-related symptoms, improve quality of life, prolong time to tumor progression

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8
Q

CAs curable by primary chemotherapy

A

Hodgkin’s and NHL, Burkitt’s lymphoma, Wilms tumor, embyonal rhabodmyosarcoma, choriocarcinoma, germ cell cancer, acute lymphoblastic leukemia

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9
Q

Neoadjuvant chemotherapy treatment process

A

chemo -> surgery -> chemo

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10
Q

Goal of neoadjuvant chemo

A

reduce tumor size to make resection easier and more effective, follow up with chemo to prevent relapse

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11
Q

Adjuvant chemotherapy treatment process

A

surgery -> chemo

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12
Q

Goal of adjuvant chemo

A

reduce incidence of local and systemic recurrence, improve survival of patients

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13
Q

Growth fraction definition

A

ratio of proliferating to G0 cells

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14
Q

Growth fraction can determine what about a tissue?

A

responsiveness to chemotherapy; higher growth fraction, more curable

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15
Q

Cell types with high growth fraction

A

bone marrow, GI tract, hair follicles, sperm-forming cells

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16
Q

How can growth fraction of solid tumors be increased?

A

reducing tumor burden via surgery or radiation

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17
Q

Main challenge in achieving therapeutic balance during treatment

A

therapeutic without being too toxic

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18
Q

Pharmacokinetics of antineoplastic therapy

A

first-order, given dose of a drug destroys a constant fraction of cells rather than an absolute number

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19
Q

High-dose intermittent therapy allows what for normal tissues

A

recovery

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20
Q

Common routes of chemo administration

A

IV and PO

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21
Q

Why should alternative drug administration routes be considered for some patients?

A

can reduce systemic toxicity and increase drug delivery

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22
Q

Pharmacologic sanctuaries

A

regions where tumor cells are less susceptible to antineoplastic drugs (CNS)

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23
Q

Alternative chemo admin routes

A

intracavity, intrathecal, intraventricular, intraarterial, topical, isolated limb perfusion

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24
Q

Advantages of combination chemotherapy

A

provides maximal cell killing, effective against a broader range of cell lines in heterogenous tumors, may delay or prevent development of drug-resistant tumors

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25
Q

Primary chemotherapeutic drug resistance

A

occurs in the absence of prior exposure, often due to the genetic instability of CA and p53 mutations

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26
Q

Acquired chemo drug resistance

A

develops in response to exposure to a given drug, due to genetic change

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27
Q

Examples of acquired drug resistance

A

decreased drug transport into cells, reduced drug affinity due to mutations in target, increased expression of enzyme that inactivates drug, increased expression of DNA repair enzymes for drugs that damage DNA

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28
Q

P-glycoprotein is present in which tissues?

A

tissues with barrier functions such as kidney, liver, GI tract; blood-brain barrier and placental-blood barrier

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29
Q

Role of PGP

A

pumps drug out of a cell, may indicate inherent or primary resistance or acquired resistance

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30
Q

Rapidly proliferating tissues that demonstrate major sites of toxicity

A

bone marrow, GI tract, hair follicles, oral mucosa, sperm forming cells

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31
Q

How can adverse drug effects be minimized?

A

choosing a route that minimizes systemic toxicity and providing pharmacologic agents that can decrease adverse effects

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32
Q

Hematopoietic agents can decrease what adverse effects?

A

neutropenia, thrombocytopenia, anemia

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33
Q

Serotonin receptor antagonists can decrease what adverse effects?

A

emetegoenicity

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34
Q

Bisphosphonates can delay what complications?

A

skeletal complications

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35
Q

Five major types of alkylating agents

A

nitrogen mustards, nitrosoureas, alkyl sulfonates, methylhydrazine derivatives, triazines **also platinum compounds

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36
Q

What type of alkylating agent is cyclophosphamide?

A

nitrogen mustard

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37
Q

What type of alkylating agent is carmustine?

A

nitrosourea

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38
Q

What type of alkylating agent is busulfan?

A

alkyl sulfonates

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39
Q

What type of alkylating agent is procarbazine?

A

methylhydrazine derivative

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40
Q

What type of alkylating agent is dacarbazine?

A

tirazines

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41
Q

What type of alkylating agent is cisplatin?

A

platinum compounds

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42
Q

Most widely used alkylating agent

A

cyclophosphamide

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43
Q

MOA of alkylating agents

A

form covalent linkages within DNA, prevents the unwinding of DNA so cells cannot make RNA and DNA; non cell cycle specific

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44
Q

What enzyme activates cyclophosphamide?

A

CYP2B

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45
Q

What are the cytotoxic metabolites of cyclophosphamide?

A

acrolein, phosphoramide mustard

46
Q

Side effect of acrolein

A

hemorrhagic cystitis

47
Q

Drug that inactivates acrolein

48
Q

Acute toxicity of alkylating agents

A

nausea and vomiting (may pretreat with zofran) and delayed toxicities such as bone marrow depression, alopecia, nephrotoxicity, mucosal ulceration, intestinal denudation

49
Q

AE associated with cisplatin

A

renal tubular damage, ototoxicity

50
Q

AE associated with busulfan

A

pulmonary fibrosis

51
Q

Main categories of antimetabolites

A

folic acid analogs, pyrimidine analogs, purine analogs

52
Q

MOA of antimetabolites

A

block or subvert pathways involved in cell replication, cell cycle specific

53
Q

Methotrexate is an analog of what?

A

folic acid

54
Q

Fluorouracil is an analog of what?

A

pyrimidines

55
Q

Mercaptopurine is an analog of what?

56
Q

What enzyme does methotrexate inhibit?

A

dihydrofolate reductase

57
Q

What other diseases can methotrexate be used to treat?

A

rheumatoid arthritis and psoriasis

58
Q

What drug is used in combination therapy with methotrexate?

A

leucovorin, used to rescue normal cells

59
Q

Leucovorin is an analog of what?

A

methylene FH4

60
Q

Active compound of fluorouracil

61
Q

FdUMP action

A

covalently binds thymidylate synthetase and blocks synthesis of thymidylate; incorporated into DNA synthesis

62
Q

Enzyme that metabolizes mercaptopurine

A

hypo-xanthine-guanine phosphoribosyl transferase (HGPRT)

63
Q

Active form of mercaptopurine

A

6-thioinosinic acid

64
Q

Enzyme that biotransforms 6-thioinosinic acid

A

xanthine oxidase

65
Q

What drug should be used in supportive care of leukemia to prevent hyperuricemia?

A

allopurinol

66
Q

What portion of the cell cycle are antimetabolites specific to?

67
Q

Common administration routes of antimetabolites

A

oral, IV, intrathecal

68
Q

Common toxicities of antimetabolites

A

diarrhea, myelosuppression, nausea, vomiting, immunosuppression, thrombocytopenia, leukopenia, hepatotoxicity

69
Q

Where are natural antineoplastic agents found?

A

extracted from plants/trees, isolated from cultures of bacteria, enzymes

70
Q

Vinca alkaloids MOA

A

bind to beta-tubulin and inhibit microtubule assembly (depolarization), specific to M phase

71
Q

Common AE of vinca alkaloids

A

alopecia and bone marrow depression

72
Q

AE of vinblastine vs vincristine

A

Vinblastine - myelosuppression

Vincristine - cumulative neuro toxicities

73
Q

Taxanes MOA

A

Binds to beta-tubulin and stabilize microtubule formation, mitosis inhibition

74
Q

Paclitaxel AE

A

hypersensitivity in hands and toes, change in taste

75
Q

Docetaxel AE

A

hypersensitivity, neutropenia, hair loss

76
Q

Function of topoisomerase I

A

cut one strand to dsDNA to relax and reanneal strand

77
Q

Function of topoisomerase II

A

cut both strands of double-stranded DNA, coil and uncoil DNA supercoils

78
Q

Drugs that inhibit topoisomerase I

A

camptothecins

79
Q

Drugs that inhibit topoisomerase II

A

epipodophyllotoxins and anthracycline abx

80
Q

What bacteria produce anticancer antibiotics?

A

Streptomyces

81
Q

Anthracyclins MOA

A

topoisomerase II inhibitor and DNA intercalation, cell cycle nonspecific

82
Q

Anthracyclins AE

A

Produces free radicals that can lead to cardiotoxicity – dysrhythmias and heart failure

83
Q

Bleomycin MOA

A

single and dsDNA breaks

84
Q

Bleomycin AE

A

pulmonary toxicity resulting in pneumonitis with cough, dyspnea and inspiratory crackers

85
Q

Dactinomycin MOA

A

intercalation of DNA

86
Q

MOA asparaginase and pegaspargase

A

hydrolyzes circulating L-asparagine into aspartic acid and ammonia, inhibiting protein synthesis, works at G1

87
Q

Toxicities associated with asparaginase and pegaspargase treatment

A

acute hypersensitivity (fever, chills, N/V, skin rash), increased risk of clotting and bleeding, pancreatitis, CNS toxicity

88
Q

Acute promyelocytic leukemia translocation

A

t(15;17), creates PML-RARa fusion protein

89
Q

Tretinoin MOA

A

binds PML-RARa and antagonizes inhibitory effect on gene transcription

90
Q

BCR-ABL fusion protein results from which translocation?

91
Q

MOA Imatinib

A

inhibits ABL tyrosine kinase, inhibit RTKs PDGFR and KIT

92
Q

MOA Erlotinib and gefitinib

A

inhibitors of EGFR, used for lung and pancreatic CA

93
Q

Toxicities caused by erlotinib and gefitinib

A

dermatologic

94
Q

Tyrosine kinase and growth factor inhibitors MOA

A

inhibit tyr kinase activity and growth factor receptor signaling

95
Q

AE tyrosine kinase and growth factor inhibitors

A

acneform skin rash and hypersensitivity, N/V

96
Q

Functions of interferons in CA response

A

inhibit cell growth, alter cell differentiation, interfere with oncogene expression, increase macrophage activity

97
Q

AE of interferon therapy

A

bone marrow depression, neutropenia, anemia, renal toxicity, edema, arrhythmias

98
Q

IL-2 MOA

A

increases cytotoxic killing by T cells and NK cells

99
Q

Toxicity of IL-2

A

capillary leak syndrome

100
Q

Rituximab antigen and ag function

A

CD20, proliferation and differentiation

101
Q

Rituximab CA

102
Q

Most active cytotoxic agents to malignant melanoma

A

dacarbazine, temozolomide, cisplatin

103
Q

Biological agents used to treat malignant melanoma

A

IFN-a and IL-2

104
Q

Nivolumab and pembrolizumab CA

A

malignant melanoma

105
Q

Mucositis is commonly caused by which chemotherapies?

A

methotrexate, melphalan

106
Q

Pulmonary fibrosis is commonly caused by which chemotherapies?

A

Bleomycin, busulfan

107
Q

Peripheral neuropathy is commonly caused by which chemotherapies?

A

Vincristine

108
Q

Ototoxicity is commonly caused by which chemotherapies?

109
Q

Cardiotoxicity is commonly caused by which chemotherapies?

A

doxorubicin, daunorubicin

110
Q

Nephrotoxicity is commonly caused by which chemotherapies?

A

cisplatin, cyclophosphamide

111
Q

Hemorrhagic cystitis is commonly caused by which chemotherapies?

A

cyclophosphamide, ifosfamide

SBL (21 decks)

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