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MF2 Conditions & Drugs > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

Describes the proportion of cancer cells that are actively proliferating

A

Tumor growth fraction

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2
Q

Model that describes how tumor growth changes with tumor size
Small tumor has large growth fraction
Growth fraction decreases as tumor gets larger due to limited availability of nutrients and oxygen

A

Gompertzian Growth Model

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3
Q

A model for effect of cytotoxic chemotherapy on tumor size
States that a given dose kills the same fraction regardless of tumor size
E.g. a dose that reduces 10^7 to 10^5 will also reduce that tumor from 10^5 to 10^3

A

Log-kill hypothesis

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4
Q

What is the Gompertzian growth model?

A

States that tumor growth changes with tumor size
E.g. small tumor has large growth fraction

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5
Q

A given dose that reduces 10^7 tumor cells to 10^5, will also reduce that tumor from 10^5 to?

A

10^3 cells

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6
Q

Shared toxicity of cancer mediations that involves acute inflammation in irradiated tissues when chemotherapy is administered after radiation

A

Radiation recall

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7
Q

Is this a reproductive toxicity of alkylating agents or methotrexate:
Multiple birth defects

A

Alkylating agents

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8
Q

Is this a reproductive toxicity of alkylating agents or methotrexate:
Neural tube defects

A

Methotrexate

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9
Q

What component of nucleosides (sugars and bases) can act as a nucleophile?

A

Both

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10
Q

Outcome of treatment with alkylating agents that is less repairable/higher cytotoxicity

A

Irreversible crosslinking of two guanines (within and between chains)

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11
Q

A less repairable/higher cytotoxic outcome of alkylating agents is the irreversible crosslinking of these

A

Two guanines

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12
Q

Cisplatin, Carboplatin, Oxaliplatin, and Cyclophosphamide are this type of antineoplastic agent

A

Alkylating agents

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13
Q

Cisplatin is this type of antineoplastic agent

A

Alkylating agent

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14
Q

Carboplatin is this type of antineoplastic agent

A

Alkylating agent

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15
Q

Cyclophosphamide is this type of antineoplastic agent

A

Alkylating agent

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16
Q

Busulfan is this type of antineoplastic agent

A

Alkylating agent

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17
Q

Primary toxicity of busulfan (an alkylating agent)

A

Pulmonary fibrosis (“Busulfan lung”)

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18
Q

Carmustine, lomustine, and semustine are this type of neoplastic agent

A

Alkylating agents

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19
Q

Alkylating agent with pulmonary fibrosis as a primary toxicity

A

Busulfan

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20
Q

Primary toxicity of carmustine, lomustine, and semustine (alkylating agents)

A

Bone marrow depression that may be delayed and prolonged

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21
Q

Alkylating agents with bone marrow depression that may be delayed and prolonged as a primary toxicity

A

Carmustine, lomustine, semustine

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22
Q

2 primary toxicities associated with ciplastin, carboplatin, and oxaliplatin (alkylating agents)

A

Nephrotoxicity and Ototoxicity

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23
Q

Alkylating agent that causes powerful nausea and vomiting

A

Cisplatin

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24
Q

Primary toxicity of cisplatin (alkylating agent)

A

Powerful nausea and vomiting
(also nephrotoxicity and ototoxicity)

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25
Q

Nephrotoxicity and ototoxicity are toxicities associated with these alkylating agents

A

Cisplatin, carboplatin, oxaliplatin

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26
Q

2 Alkylating agents with toxicities involving hemorrhagic cystitis caused by acrolein (a CYP metabolite)

A

Cyclophosphamide, ifosfamide

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27
Q

Primary toxicity associated with cyclophosphamide and ifosfamide (alkylating agents)

A

Hemorrhagic cystitis
caused by acrolein (a CYP metabolite)

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28
Q

Hemorrhagic cystitis may be reduced in patients taking cyclophosphamide or ifosfamide with these

A

Mesna or amifostine (scavenger compound for acrolein)

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29
Q

CYP metabolite that causes hemorrhagic cystitis in patients taking cyclophosphamide or ifosfamide

A

Acrolein

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30
Q

Mesna or amifostine (scavenger compound for acrolein) reduces hemorrhagic cystitis and is required for this alkylating agent

A

Ifosfamide

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31
Q

Dacarbazine and mechlorethamine are alkylating agents with this effect

A

Vesicant (blistering agents)

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32
Q

Alkylating agent that uses phenylalanine transporter to enter cells (should be taken on an empty stomach)

A

Melphalan

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33
Q

Melphalan is an alkylating agent that uses this to enter cells

A

Phenylalanine transporter

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34
Q

Diabetes is a primary toxicity associated with this alkylating agent

A

Streptozocin
action is specific for beta cells of pancreas

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35
Q

Streptozocin is an alkylating agent with this primary toxicity

A

Diabetes
Action is specific for pancreas beta cells

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36
Q

Alkylating agent with risk of opportunistic infections, especially of the lungs

A

Temozolomide

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37
Q

Methotrexate, pemetrexed, and pralatrexate are this type of antimetabolite

A

Antifolates

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38
Q

6-mercaptopurine, Fludarabine, and Cladribine are this type of antimetabolite

A

Purine analogs

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39
Q

5-fluorouracil, capecitabine, cytarabine, azacitidine, and gemcitabine are this type of antimetabolite

A

Pyrimidine analogs

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40
Q

Methotrexate is this type of antineoplastic agent

A

Antifolate

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41
Q

6-Mercaptopurine is this type of antineoplastic agent

A

Purine analog (antimetabolite)

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42
Q

5-fluorouracil is this type of antineoplastic agent

A

Pyrimidine analog (antimetabolite)

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43
Q

Gemcitabine is this type of antineoplastic agent

A

Pyrimidine analog (antimetabolite)

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44
Q

Antifolates are specific for this cell cycle phase

A

S phase

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45
Q

Why are antifolates describes as self-limiting?

A

Inhibition of protein synthesis delays or stalls cancer cell cycle progression by preventing them from entering the vulnerable S phase
Referred to as self-limiting because the agent actually limits its own cell kill rate by delaying cell progression

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46
Q

MOA of methotrexate and pralatrexate

A

Inhibition of dihydrofolate reductase

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47
Q

Methotrexate inhibits this

A

Dihydrofolate reductase

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48
Q

2 antifolates that inhibit dihydrofolate reductase

A

Methotrexate and Pralatrexate

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49
Q

MOA of pemetrexed

A

Inhibition of dihydrofolate reductase and thymidylate synthase

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50
Q

Pemetrexed inhibits these 2 enzymes

A

Dihydrofolate reductase
Thymidylate synthase

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51
Q

Antimetabolite that inhibits dihydrofolate reductase and thymidylate synthase

A

Pemetrexed

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52
Q

Main toxicity of antifolates

A

Bone marrow depression

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53
Q

Bone marrow depression, neurotoxicity, and nephrotoxicity are toxicities of this type of antineoplastic agent

A

Antifolates

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54
Q

Reduced folate that uses the same entry mechanism as methotrexate

A

Leucovorin

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55
Q

Leucovorin is used as rescue for this

A

Overcoming methotrexate resistance
Normal cells with normal permeability of methotrexate allow leucovorin to “rescue” normal cells from high dose methotrexate while cancer cells die

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56
Q

Cancer cell resistance mechanism of antifolates prevents rescue by this

A

Leucovorin

57
Q

Reduced folate that is used as a “rescue” for normal cells from high dose methotrexate while cancer cells die

A

Leucovorin

58
Q

Leucovorin rescues normal cells from high doses of this antineoplastic agent while cancer cells die

A

Methotrexate (antifolate)

59
Q

Purine analog whose dose should be reduced by 50-70% with concurrent use of allopurinol or febuxostat

A

6-Mercaptopurine

60
Q

6-mercaptopurine is this type of anti-cancer agent

A

Purine analog

61
Q

6-mercaptopurine dose should be reduced by 50-70% with concurrent use of either of these

A

Allopurinol or Febuxostat

62
Q

Allopurinol and febuxostat are inhibitors of xanthine oxidase, which normally inactivates this purine analog

A

6-mercaptopurine

63
Q

Allopurinol and Febuxostat are inhibitors of this enzyme which normally inactivates 6-mercaptopurine

A

Xanthine oxidase

64
Q

Fludarabine is this type of anti-cancer agent

A

Purine analog

65
Q

Toxicity of Fludarabine (purine analog)

A

Neurologic toxicity

66
Q

Purine analog that is not for oral use; gut bacteria convert it to a toxic product

A

Fludarabine

67
Q

Purine analog with neurologic toxicity

A

Fludarabine

68
Q

Cladribine is this type of anti-cancer agent

A

Purine analog

69
Q

Cladribine has this toxicity

A

Immunosuppression
and neurotoxicity

70
Q

Purine analog with immunosuppression as a toxicity

A

Cladribine

71
Q

Pyrimidine analogues inhibit DNA synthesis by blocking this enzyme

A

Thymidylate synthase

72
Q

Pyrimidine analog with these toxicities:
Myelosuppression, coronary vasospasm, ‘foot/hand’ syndrome

A

5-Fluorouracil

73
Q

5-Fluorouracil is this type of anti-cancer agent

A

Pyrimidine analog

74
Q

Pyrimidine analog that is a powerful radiosensitizer (radiation recall)

A

Gemcitabine

75
Q

Antibiotics with the suffix “-rubicin” have this toxicity

A

Intercalate with calcium channels –> Cardiotoxicity

76
Q

Why do antibiotics with the suffix “-rubicin” cause cardiotoxicity?

A

Because they intercalate with calcium channels

77
Q

Antibiotics for cancer that have cumulative lifetime limits

A

Daunorubicin, Doxorubicin, Epirubicin, Idarubicin
“-rubicin”
Due to cardiac toxicity

78
Q

Cancer antibiotic with pulmonary fibrosis and mucocutaneous reactions as toxicities

A

Bleomycin

79
Q

Primary toxicity of Bleomycin

A

Pulmonary fibrosis
“Bleomycin lung”

80
Q

Bleomycin is inactivated by this

A

Hydrolase
Low activity in skin and lungs

81
Q

This should be monitored in patients taking Bleomycin

A

Pulmonary function

82
Q

Cardiac toxicity and radiation recall are toxicities of this cancer antibiotic

A

Daunorubicin

83
Q

Cardiac toxicity with -rubicin use can be reduced by concurrent use of this

A

Iron chelator (dexrazoxane)

84
Q

-rubicin concurrent use of iron chelator (dexrazosane) can reduce this

A

Cardiac toxicity

85
Q

MOA of Vincristine, Vinblastine and Vinorelbine

A

Block formation of mitotic spindles by inhibition of polymerization

86
Q

MOA of Paclitaxel and Docetaxel

A

Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)

87
Q

3 drugs with this MOA:
Block formation of mitotic spindles by inhibition of polymerization

A

Vincristine, Vinblastine, Vinorelbine

88
Q

2 drugs with this MOA:
Promote microtubule polymerization and stabilization, preventing their disassembly leading to accumulation of nonfunctional microtubules (mitosis freezes in metaphase)

A

Paclitaxel, Docetaxel

89
Q

3 microtubule inhibitors that are vesicants

A

Vincristine, Vinblastine, Vinorelbine

90
Q

2 microtubule inhibitors with hypersensitivity reactions

A

Paclitaxel, Docetaxel

91
Q

Microtubule inhibitor with neurotoxicity

A

Vincristine

92
Q

Microtubule inhibitor with myelosuppression

A

Vinblastine
(also vinorelbine)

93
Q

3 toxicities of Paclitaxel and Docetaxel

A

Myelosuppression, Neurotoxicity, Alopecia

94
Q

Primary toxicity of Vincristine

A

Neurotoxicity

95
Q

Primary toxicity of Vinblastine

A

Myelosuppression

96
Q

2 S-phase specific inhibitors of topoisomerase I
Do not relieve torsional strain in DNA, leading to breaks

A

Irinotecan and Topotecan

97
Q

MOA of Irinotecan and Topotecan

A

S-phase specific inhibitors of topoisomerase I

98
Q

Irinotecan and Topotecan are S-phase specific inhibitors of this

A

Topoisomerase I

99
Q

Topoisomerase inhibitor with life-threatening diarrhea as a toxicity
Responds well to atropine

A

Irinotecan

100
Q

Primary toxicity of topotecan and etoposide

A

Bone marrow depression

101
Q

Anticancer agent that is a S and G2-phase specific inhibitor of topoisomerase II

A

Etoposide

102
Q

MOA of etoposide

A

S and G2-phase specific inhibitor of topoisomerase II

103
Q

Target of Trastuzumab

A

Human epidermal growth factor receptor 2 (HER2)

104
Q

Human epidermal growth factor receptor 2 (HER2) is a target for this monoclonal antibody

A

Trastuzumab

105
Q

Cancer monoclonal antibody with increased risk of heart failure

A

Trastuzumab

106
Q

Primary toxicity of Trastuzumab

A

Increased risk of heart failure

107
Q

Target for Rituximab

A

CD20 antigen on normal and malignant B cells

108
Q

CD20 antigen on normal and malignant B cells is the target of this monoclonal antibody

A

Rituximab

109
Q

Bone marrow suppression is the primary toxicity of this monoclonal antibody

A

Rituximab

110
Q

Primary toxicity of Rituximab

A

Bone marrow suppression

111
Q

Target of Bevacizumab

A

Vascular endothelial growth factor (VEGF); inhibits angiogenesis

112
Q

Vascular endothelial growth factor (VEGF) is the target of this monoclonal antibody

A

Bevacizumab

113
Q

Target of Cetuximab

A

Blocks binding to the epidermal growth factor receptor on cancer cells

114
Q

Monoclonal antibody that blocks binding to the epidermal growth factor receptor on cancer cells

A

Cetuximab

115
Q

Acneiform-type rash is a primary toxicity of this monoclonal antibody

A

Cetuximab

116
Q

Primary toxicity of Cetuximab

A

Aceniform-type rash

117
Q

What is a positive sign of therapy of Cetuximab?

A

Aceniform-type rash

118
Q

Drug names ending in “-nib” are inhibitors of this

A

Targeted kinase inhibitors

119
Q

Drug names ending in “-nib” are toxic to this

A

Heart
(are targeted kinase inhibitors)

120
Q

Targeted kinase inhibitors are often toxic to this

A

Heart

121
Q

Targeted kinase inhibitor:
Rash is common and typically related to stronger therapeutic responses

A

Erlotinib

122
Q

Targeted kinase inhibitor where you should monitor for signs of heart failure and wound-healing complications

A

Sorafenib

123
Q

This is a common side effect of Erlotinib and is typically related to stronger therapeutic responses

A

Rash

124
Q

Primary toxicity of Erlotinib

A

Rash

125
Q

Mechlorethamine + Oncovin/Vincristine + Prednisone + Procarbazine (“MOPP”) is a combination therapy indicated for this

A

Hodgkin’s lymphoma

126
Q

Melanoma changes with this mutation

A

BRAF mutation

127
Q

Cancer that changes with BRAF mutation

A

Melanoma

128
Q

Breast cancer therapy for ER+/PR+ in premenopause

A

Tamoxifen

129
Q

ER antagonist in breast; indicated for breast cancer that expresses ER (ER+)

A

Tamoxifen

130
Q

Breast cancer therapy for ER+/PR+ in postmenopause

A

Aromatase inhibitors

131
Q

Drugs that block conversion of estrogen precursors (e.g. testosterone) to estradiol and estrone
Reduce concentration of estrogen that promotes growth of breast cancer cells

A

Aromatase inhibitors
Indicated for ER+/PR+ breast cancer postmenopause

132
Q

Breast cancer therapy for ER-/PR-/HER2+

A

Trastuzumab and/or lapatinib, +/- chemotherapy

133
Q

Breast cancer therapy for ER-/PR-/HER2-

A

Chemotherapy
Anthracycline + cyclophosphamide +/- taxane

134
Q

Tamoxifen or Aromatase inhibitors are treatment for this type of breast cancer

A

ER+/PR+

135
Q

Trastuzumab and/or lapatinib, +/- chemotherapy, is treatment for this type of breast cancer

A

ER-/PR-/HER2+

136
Q

Chemotherapy (Anthracycline + cyclophosphamide +/- taxane) is treatment for this type of breast cancer

A

ER-/PR-/HER2- (TNBC)

137
Q

Monoclonal antibody that targets HER2, so is used in HER2+ breast cancer, and is contraindicated during pregnancy

A

Trastuzumab

138
Q

Trastuzumab is contraindicated in this

A

Pregnancy

MF2 Conditions & Drugs (11 decks)

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