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IBI Test 3 > B3.042 - Antineoplastic Drugs > Flashcards

B3.042 - Antineoplastic Drugs Flashcards

1
Q

what are purine analogs

A

6-mercaptopurine, 6 - thioguanine

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2
Q

what is the base of cis platin

A

platinum

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3
Q

what diseases are associated with diminished or no UGT1A1

A

crigler najjar
gilbert
hyperbilirubinemia

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4
Q

how is bortezomib given

A

IV half life of 5.5 hours

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5
Q

AEs of tamoxifen

A

nausea hot flushes vaginal bleeding

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6
Q

what are adverse effects of cyclophosphamide

A

nausea and vomiting
bone marrow depression
alopecia
sterile hemorrhagic cystitis

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7
Q

primary use of mechlorethamine

A

hodgkins disease

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8
Q

if theres no hprt how does that affect purine analogs

A

the drugs wont work

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9
Q

bevacizumab is single drug therapy for what

A

glioblstoma

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10
Q

what is secondary resistance

A

tumor cells develop resistance during therapy

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11
Q

how is myelosuppression treated

A

GM-CSF or platelet transfusions

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12
Q

what do aromatase inhibitors

A

block conversions of androgens to estrogens

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13
Q

what is neoadjuvant chemo

A

chemo before surgery or radiation

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14
Q

when are hydrocortisone and prednisone used

A

leukemias and lymphomas

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15
Q

what does Bcr Abl do

A

kinase that drives cell proliferation in CML

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16
Q

what is adjuvant chemo

A

chemo following surgery or radiation

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17
Q

how is etoposide admiinistered

A

oral and IV

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18
Q

how are taxanes administered

A

IV

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19
Q

DNA damage requires what, to die

A

P53

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20
Q

what are AEs of hydrocortisone and prednisone

A

fluid retention
immunosuppression
diabetes

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21
Q

what is Interferon alpha used for

A

alters gene expression, antiviral and immunomodulatory

used against hematologic malignancies, metastatic melanoma, renal cell carcinoma

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22
Q

what does UGT1A1 deficiency cause with irinotecan

A

hematological toxicity

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23
Q

what are AEs of taxanes

A

acute hypersensitivity, nausea

delated bone marrow suppression, some neuropathy

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24
Q

how do secondary malignancies arise

A

carcinogens act by covalently modifying nuclear DNA leading to altered structure and function, so do alkylating agents

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25
Q

what is bortezomib

A

inhibits 26s proteosome

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26
Q

what is mechlorethamine

A

a nigrogen mustard, first alkylating agent

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27
Q

what is acrolein

A

side product of metabolism of cyclophosphamide

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28
Q

how do taxanes differ from vincas

A

they affect microtubules but by stabilization, you build the spindles but cant contract (prevent depolarization)

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29
Q

what is imatinib

A

TKI

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30
Q

most alkylating agents are bifunctional meaning what

A

they bite DNA twice

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31
Q

how is SN-38 inactvated

A

glucuronidation by UGT1A1

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32
Q

what do you give when you give 5-FU and why

A

folinic acid to ensure folic acid will bind to it, required that all 3 are there to enhance its efficacy

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33
Q

what are AEs of mechlorethamine

A

acute - nausea, vomiting

Delayed - decreased blood counts, moderate iwth most doses

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34
Q

what does alkaline phosphatase do

A

chops off phosphatases blocking active form of drug (triphosphate form)

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35
Q

what are AEs of imatinab

A

myelosuppressive
edema and fluid retention
hepatotoxicirty

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36
Q

how is methotrexate excreted

A

urine

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37
Q

what is bevacizumab

A

inhibitor of angiogenesis

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38
Q

what are the taxane drugs

A

paclitaxel

docetaxel

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39
Q

What are general delayed effects of chemotherapy

A

myelosuppression

usully leukopenia and thronbocytopenia

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40
Q

what is etoposide

A

topoisomerase inhibitor

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41
Q

what drugs target M phase

A

microtubule poisons

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42
Q

if no TMPT is there genetically then

A

theres no way to clear purine synthesis

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43
Q

what does gemcitabine do

A

cytosine analogue, inhibits polymerase and chain terminator

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44
Q

what is the signature adverse effect of athracyclines

A

cardiotoxicity, fuction of cumulative dose

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45
Q

resistance to methotrexate causes what

A

decreased drug accumulation, amplified DHFR, altered DHFR

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46
Q

how is cis platin administered and cleared

A

IV, cleared in urine

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47
Q

what is the administration and half life of sirolimus

A

oral

60 years

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48
Q

what is tamoxifen

A

ER antagonist in breast

ER agonist in edometrium

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49
Q

about what percentage of cancers can be cured using multi modality therapy?

A

50%

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50
Q

Antitumor antibiotics are produced by what

A

microbes

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51
Q

are alkylating agents cidal or static

A

static but work better in dividing cells

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52
Q

what are AEs of gefitinib

A

fever

dyspnea

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53
Q

what does nivolumabd do

A

Human Mab against PD-1

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54
Q

adverse effects of anthracyclines

A

bone marrow suppression
GI
sever alopecia

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55
Q

how is gefitinib administered

A

orally

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56
Q

how is tamoxifen given

A

orally

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57
Q

what is sirolimus

A

inhibits mTORC1 downstream component of PI3K signaling pathway that drives proliferation

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58
Q

what makes imatinib and dasatinib so specific

A

it blocks Bcr Abl which is only in tumor cells

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59
Q

what are two current targets of immune checkpoint inhibitors

A

CTLA-4

PD-1/Ligand

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60
Q

How is selective toxicity achieved?

A
  1. unique target present on pathogen and not host
  2. target structurally different in pathogen than host
  3. target more essential in pathogen than in host
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61
Q

what cardiac effects do anthracyclines cause

A

arrhythmias, cardiomyopathy, CHF

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62
Q

what does dexrazoxane do

A

given with anthracyclines offers protection from free radicals causing cardiotoxicity

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63
Q

what are AEs of Nivolumab

A

rash, fatigue, dyspnea

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64
Q

what does cremophor do

A

helps taxanes efficacy, cause a lot of AEs

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65
Q

What are the two anthracycline antitumor antibiotics

A

Doxorubicine daunorubicin

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66
Q

how is mechlorethamine administered

A

IV only

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67
Q

What are the types of cell cycle non specific drugs

A

Alkylating agents

Antitumor antibiotics

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68
Q

how are hydrocortisone and presdnisone administered

A

orally

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69
Q

how doe satezolimumab work

A

blocks interaction of PD-L1 with PD-1 promote T cell antitumor response

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70
Q

how do alkylating agents block access to DNA

A

crosslinking

71
Q

what are general characteristics of tumor cells

A
  1. excessive/inappropriate growth
  2. diminished apoptosis
  3. loss of differentiation
  4. invasive
  5. metastatic
72
Q

does trastuzamab cross the blood brain barrier

A

no

73
Q

how do antimetabolites work

A

enter normal met pathway and blocks that pathway

74
Q

how does bevacizumab work

A

humanized Ab against VEGF-A

75
Q

what does bevacizumab do

A

decreases vascularization and increases capillary permeability

76
Q

what is a secondary malignancy

A

malignancy due to drug for cancer

77
Q

Is toxicity to pathogen v host relative or absolute?

A

Relative

78
Q

what drugs are S cell specific

A

antimetabolites

79
Q

how do taxanes work

A

block progress through mitosis

80
Q

what are adverse effects of alkylating agents

A

targets bone marrow, GI tract, spermatogenesiis

81
Q

what is ipilimumab

A

human Mab against CTLA-4

82
Q

what does gefitinib do

A

inhibits EGF-R TK

83
Q

Cure requires what

A

“total kill”

84
Q

what is bortezomib approved to treat

A

multiple myeloma mantle cell lymphoma

85
Q

What norma cell populations have high proliferative potentila

A

Bone marrow
Epithelial cells
immune system
hair follicles

86
Q

how is atezolimumab given

A

IV q21 days

87
Q

what are AEs of vinblastin

A

nasea vomiting
bone marrow depression
alopecia

88
Q

what do hydrocortisone and prednisone do

A

suppress proliferation of immune cells

89
Q

how are antitumor antibiotics given

A

IV

90
Q

what is trastuzumab used for

A

breast cancer

monocllonal antibody agaisnt HER2neu oncogene product

91
Q

what does cytarabine do

A

cytosine analogue, chain terminator

92
Q

how does imatinab work

A

blocks grwoth factor signaling in chronic myelogenous leukemia
also blocks kit kinase in GI stromal tumors

93
Q

what is the t1/2 of mechlorethamine

A

several minutes

94
Q

what are AEs of interferon alpha

A

fever chills anorexia weakness

95
Q

how is sterile hemorrhagic cystitis pervented

A

give lots of fluids and/or give Mensa

96
Q

what are general acute adverse effects of chemotherapy and how is it treated

A

Nausea and vomiting treated with antiemetics

97
Q

what are AEs of aromatase inhibitors

A

mild nausea, headaceh, fatigue, hot flushes

98
Q

acute adverse effects of cis platin

A

severe nausea, vomiting

renal toxicity

99
Q

how many cancer cells is incompatible with like

A

10x12

100
Q

how is trastuzumab administered and what are AEs

A

IV
hypersensitivity
cardiomyopathy

101
Q

how are purine analogs cleared

A

TPMT chops methyl group and makes them not useful as dugs

102
Q

what are AEs of bortezomib

A

thormbocyopenia
fatigue
peripheral neuropathy

103
Q

What is hand and foot syndrome

A

neuropathy in hands and feet

104
Q

what is folinic acid rescue

A

high dose given of methotrexate and then given folinic acid is supplied to save normal cells

105
Q

what are antiemetics

A

5-HT3 antagonists

Phenothiazines

106
Q

how is vinca administered/excreted

A

IV, biliary

107
Q

how are purine analogs administered

A

orally

108
Q

what is cis platin

A

bifucntional platinating agent

109
Q

what is hprt

A

enzyme that adds sugar back onto purine to make a nucleoside, only functional when drugs are in active form

110
Q

what are adverse effects of sirolimus

A

rash
mucositis
anemia
fatigue

111
Q

what are the cell cycle specific drug types

A

Antimetabolites
Topoisomerase inhibitors
microtubule poisons

112
Q

which is more toxic pyrimidine or purine analogs

A

pyrimidine

113
Q

what is the rule to preventing drug resistance

A

combination chemo

114
Q

what drug has antifolate effects and what does that mean

A

Methotrexate, bone marrow and GI get affected

115
Q

how do purine analogs work

A

block DNA and RNA synthesis

116
Q

how does 6-TG work

A

incorporated into RNA and DNA altering fucntion

117
Q

what are AEs of vincristine

A

less toxic to bone marrow, no nausea and vomiting

peripheral neuropathy so used in limited duration

118
Q

chronic use of methotrexate can cause what AE

A

hepatotoxicity

119
Q

why can cyclophosphamide be given orally?

A

itself it isnt reactive it has to be metabolized to active form

120
Q

what do the microtubule poisons like vinca do and when in the cell cycle

A

inhibit/reverse tubulin polymerization, disrupt mitotic spindles causing metaphase arrest

121
Q

what is dasatinib

A

Bcr-Abl inhibitor

122
Q

when is bleomycin active in the cell cycle

A

G2

123
Q

how does methotrexate work

A

DHFR substrate and inhibitor

Blocks production of DNA synthesis

124
Q

all of the antitumor antibiotics are what except bleomycin

A

CCNS, bleomycin is CCS (G2)

125
Q

what is cyclophosphamide

A

alkylating agent

126
Q

resistance to purine analogs is caused by what

A

hprt activity, or increase in alkaline phosphatase

127
Q

how is bevacizumab given and whats half life

A

IV, 4 weeks

128
Q

what does cis platin do

A

its an alkylating agent that crosslinks DNA

129
Q

which alkylating agent is relatively non toxic to bone

A

cis platin

130
Q

how is ipilimumab given

A

IV usually q21 days x 4

131
Q

how are purine analogs tolerated

A

well, bone marrow depression only at high doses

132
Q

how does nivolumab work

A

blocks interaction with PD-1 ligands restore or maintain . T cell antitumor response

133
Q

what are 2 uses of folinic acid in chemo drugs

A
  1. methotrexate used for salvage therapy

2. 5-FU used to enhance drug efficacy

134
Q

what are AEs of irinotecan

A

nausea vomiting diarrhea

bone marrow suppression nausea dose limiting diarrhea

135
Q

the most effective anticancer drugs do what

A

activate apoptosis

136
Q

how does 6-MP work

A

inhibits AMP and GMP synthesis

137
Q

when are CCNS agents most effective

A

rapidly cycling cells

138
Q

what are adverse effects of bleomycin

A

hypersensitivity, cutaneous rxns

pulmonary toxicity, fibrosis

139
Q

concern for alkylating agents inducing second malignancy is inversely proportional to what

A

age

140
Q

what are AEs of etoposide

A

nausea, vomiting, alopecia, bone marrow suppression

141
Q

Are all chemo drugs toxic?

A

yes

142
Q

what are taxanes

A

microtubule poisons

143
Q

what proteins can export multiple classes of anticancer drugs out of the cell

A

P glycoprotein Pgp, MDR1

144
Q

what does flutamide do

A

orally given used to block androgen receptors

145
Q

What do alkylating agents do

A

covalently bind to/modify biological molecules

DNA is the key target

146
Q

what does bleomycin do

A

binds DNA, generates radicals

causes strand breaks

147
Q

how do antitumor antibiotics work

A

block access to/function of DNA or RNA

148
Q

TPMT is polymorphic meaning

A

genotype is needed pre treatment

149
Q

what does 5-FU do

A

inhibits thymidylate synthase, you can make DNA without thymidine so it causes a thymineless death

150
Q

what are signature delayed adverse effects of chemo other than myelosuppression

A

GI effects
Alopecia
neuropathies
Hand and foot syndrome

151
Q

how do doxorubicin and daunorubicin work

A

intercalate DNA and RNA
block topoisomerase II
Inhibit DNA and RNA synthesis and cause strand breaks
generate free radicals

152
Q

If you give alkylating agents and a patients CBC remains normal what does that mean

A

dose is too low and something needs to be adjusted

153
Q

why are anticancer drugs more effective in replication phase

A

theres less time to repair

154
Q

what is atezolimumab

A

human Mab against PD-:1

155
Q

whats the difference between alkylating agents and antitumor antibiotics

A

AAs interact with DNA and/or RNA but most do not alkylate

156
Q

how are doxorubicin and daunorubicin metabolized

A

in the liver

157
Q

what is primary resistance

A

tumor cells initially not sensitive to a given drug

158
Q

alkylating agents must be

A

reactive, inherent or generated by metabolism

159
Q

resistance mechanisms for alkylating agents

A

impermeable to drug, pump drug out
alternate targets
increased DNA repair
no apoptosis

160
Q

what do CTLA-4 and PD-1 do

A

associated with T cell response to antigens

161
Q

what does vinca come from

A

perriwinkle

162
Q

when does etoposide work

A

arrests cells in S-G2 stage

163
Q

what are anastrazole and letrozole used for

A

treatment for ER+ primary and metastatic breast cancer

164
Q

how is methotrexate administered

A

orally, IV, intrathecally

165
Q

how does irinotecan work

A

gest converted to SN-38 by esterase, inhibits topoisomerase I

166
Q

what is total kill

A

must kill all cells with proliferative potential

167
Q

how is cyclophosphamide administered/activated

A

oral or IV

168
Q

how does ipilimumab work

A

blocks interaction with B7 enhancing T cell activation

169
Q

what are AEs of ipilimumab

A

skin and GI tract

immune inflammatory adverse effects

170
Q

how does etoposide work

A

causes double strand breaks, DNA degradation

171
Q

what is bleomycin

A

mixture of glycopeptides used as an antitumor antibiotic

172
Q

what is irinotecan

A

a topoisomerase inhibitor

173
Q

what are AEs of bevacizumab

A

risk of blood vessel injury and bleeding
hypertension proteinuria
arterial thromboembolic events

IBI Test 3 (16 decks)

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