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Systemic Pharm I > Cancer Treatment > Flashcards

Cancer Treatment Flashcards

1
Q

Antimetabolites

A

cytarabine, 5-fluorouracil, mercaptopurine, methotrexate, thioguanine

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2
Q

Antitumor Antibiotics

A

bleomycin, dactinomycin, doxorubicin

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3
Q

Alkylating Agents

A

carmustine, dacarbazine, lomustine, mechlorethamine

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4
Q

Mitotic Inhibitors

A

docetaxel, paclitaxel, vinblastine, vincristine

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5
Q

Steroid Hormones and Antagonists

A

aminoglutethimide, anastrozole, bicalutamide, exemestane, flutamide, goserelin, letrozole, leuprolide, nilutamide, prednisone, tamoxifen

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6
Q

Monoclonal antibodies

A

bevacizumab, retuximab, trastuzumab

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7
Q

Other Anticancer drugs

A

carboplatin, cisplatin, interferons, oxaliplatin

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8
Q

T/F 25 percent of the US population will face a diagnosis of cancer

A

true

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9
Q

What are three types of treatment for cancer?

A

surgery, local radiation, systemic chemotherapy

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10
Q

What is the overall 5 year survival rate for cancer patients?

A

65%

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11
Q

What is the goal of chemotherapy?

A

cause a lethal cytotoxic event or apoptosis in the caner cell, arresting the tumor progression

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12
Q

Where is the chemotherapy attack directed?

A

DNA or metabolic sites essential to cell replication

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13
Q

T/F there are steep dose-response curves for both toxic and therapeutic effects

A

true, chemo effects all kinds of proliferating cells not just malignant cells

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14
Q

What is the ultimate goal of treatment?

A

a cure, long term disease free survival, requires eradication of every neoplastic cell

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15
Q

What is the goal of cancer treatment if a cure is not attainable?

A

control of the disease, stop the cancer from enlarging and spreading and allow patient to maintain a normal existence

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16
Q

How is the neoplastic cell burden usually initially reduced?

A

surgery and or radiation, followed by chemotherapy, immunotherapy etc

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17
Q

What are indications for chemotherapy?

A

when tumor cells are not amenable to surgery, as supplemental treatment after surgery or radiation, to shrink tumor prior to surgery, or to prolong remission

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18
Q

How does the cell growth cycle relate to tumor susceptibility?

A

rapidly dividing cells are usually more susceptible, while non-proliferating cells (G0) usually survive toxic effects of therapy

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19
Q

How does the tumor growth rate work?

A

growth rate of tumors is initially rapid but slows as tumor size increases because nutrients and oxygen decrease

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20
Q

What cell cycle “stage” does surgery or radiation shift remaining cell types to?

A

active proliferation, making them more susceptible to chemotherapy

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21
Q

What is log kill?

A

destruction of cancer cells follows first-order kinetics so a given dose destroys constant fraction of cells

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22
Q

What is a pharmacologic sanctuary?

A

some tumor cells can hide in tissues where chemotherapeutic agents can not enter, like the CNS

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23
Q

What two treatments are aimed at “finding” the tumor?

A

radiation and alternative administration of drugs

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24
Q

What is a typical cancer treatment protocol?

A

combination of drugs is more successful, use agents with different toxicities and different MOAs

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25
Q

T/F if two drugs are combined for cancer therapy that have similar toxicities, you must decrease the dose of both

A

true

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26
Q

What are the advantages of combination drug treatment?

A

provide maximal killing with tolerated toxicity, effective against broad cell lines, may delay development of resistant cell lines

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27
Q

T/F some cells are inherently resistant to anticancer drugs

A

true

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28
Q

What are two mechanisms by which multidrug resistance occurs?

A

transmembrane protein (p-glycoprotein) can pump anticancer drugs out of tumor cells, high concentration of some drugs can inhibit the pump

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29
Q

Which cells are particularly susceptible to toxicity?

A

those that undergo rapid proliferation: lining of cheeks, bone marrow, GI mucosa, hair follicles

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30
Q

T/F chemotherapeutic agents have a broad therapeutic index

A

false, narrow

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31
Q

What are the most common adverse effects to cancer treatment?

A

severe vomiting, bone marrow suppression, alopecia and myelosuppression

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32
Q

What are treatment induced tumors?

A

chemotherapeutic agents are mutagens, neoplasms can arise 10 or more years after the original cancer was cured, especially with alkylating agents

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33
Q

What is the MOA of antimetabolites?

A

interefere with the availability of normal nucleotide base precursors by either inhibiting synthesis or competing with them in DNA or RNA synthesis

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34
Q

Are antimetabolites cell cycle specific or not?

A

cell cycle specific, maximal effects in S phase

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35
Q

What is dihydrofolate reductase?

A

the enzyme that converts folic acid to active form (tetrahydrofolic acid) which is essential for cell replication

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36
Q

What is the MOA of methotrexate?

A

dihydrofolate reductase antagonist, leads to decreased production of required nucleic compounds aka DNA, RNA, and protein synthesis is depressed leading to cell death

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37
Q

How can you reverse methotrexate?

A

use a thousandfold excess dihydrofolate or administer leucovorin

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38
Q

What is leucovorin?

A

it has a similar structure to folic acid and bypasses blocked enzyme and replenishes folate pool

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39
Q

Which cells are resistant to methotrexate?

A

non-proliferating cells

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40
Q

What drug in low doses can treat some inflammatory diseases as an antimetabolite?

A

methotrexate

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41
Q

What three inflammatory diseases can methotrexate treat?

A

severe psoriasis, rheumatoid arthritis, Crohn’s disease

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42
Q

How is methotrexate administered?

A

oral, IM and IV (intrathecal)

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43
Q

Does methotrexate penetrate the CNS?

A

no, requires intrathecal

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44
Q

Why must a patient on methotrexate be hydrated?

A

to prevent renal toxicity which can lead to crystalluria

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45
Q

What are the adverse effects of methotrexate?

A

GI upset, toxicities in constantly renewing tissues (rash, urticaria, alopecia, stomatitis, erythemia), renal damage, cirrhosis

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46
Q

What is the adverse effect of methotrexate in children?

A

pulmonary toxicity

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47
Q

What are the contraindications of methotrexate?

A

pregnancy

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48
Q

What is the MOA of mercaptopurine?

A

nucleotide formation, inhibition of protein synthesis, and incorporation into nucleic acids for RNA and DNA

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49
Q

What are pharmacokinetic considerations for mercaptopurine?

A

incomplete absorption orally, reduced bioavailability by first pass… still given orally though

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50
Q

What are the adverse effects of mercaptopurine?

A

bone marrow depression, anorexia + GI upset, jaundice

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51
Q

What is the MOA of thioguanine?

A

same as 6-MP, nucleotide formation, inhibition of protein synthesis and incorporation into nucleic acids for RNA and DNA

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52
Q

What are the pharmacokinetic considerations of thioguanine?

A

incomplete oral absorption w/ first pass, some people accumulate higher concentrations of metabolites leading to high myelosuppression and secondary malignancies (genotyping recommended)

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53
Q

What are the adverse effects of thioguanine?

A

dose-related bone marrow depression and risk of liver toxicity with long-term use

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54
Q

Is thioguanine used as a maintenance therapy?

A

no

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55
Q

What is the MOA of 5-fluorouracil?

A

enters cell through carrier-mediated transport system, forms a molecular complex that deprives the cell of thymidine stoping DNA synthesis

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56
Q

What is given in combination with 5-FU (fluorouracil)?

A

leucovorin which helps 5FU work longer

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57
Q

How is 5FU administered?

A

IV or topically

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58
Q

What are some reasons 5FU is given topically?

A

skin cancer, prevention of scar tissue formation in surgery, in some ocular surgeries

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59
Q

Does 5FU penetrate the CNS?

A

yes

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60
Q

How is 5FU excreted?

A

kidney and lungs

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61
Q

What are the adverse effects of 5FU?

A

GI upset, ulceration of oral and GI mucosa, bone marrow depression, anorexia

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62
Q

What is the MOA of cytarabine?

A

enters cell via carrier-mediated process and inhibits DNA polymerase and also can be incorporated into cellular DNA

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63
Q

Which cell cycle phase does cytarabine act during?

A

S phase specific

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64
Q

How is cytarabine administered?

A

IV only, new preparation allows penetration to CSF

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65
Q

How is cytarabine excreted?

A

kidney

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66
Q

What are the adverse effects of cytarabine?

A

GI upset, sever myelosuppression, hepatic dysfunction, CHEMICAL CONJUNCTIVITIS at high doses

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67
Q

What is the MOA of antitumor antibiotics?

A

cytotoxic due to interactions with DNA that prevent RNA synthesis and leads to the formation of toxic free radicals

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68
Q

Are anti-tumor antibiotics cell-cycle specific?

A

mostly no

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69
Q

What is the first antibiotic to find use in tumor chemotherapy?

A

dactinomycin

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70
Q

What is dactinomycin sometimes combined with?

A

methotrexate

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71
Q

What is the MOA of dactinomycin?

A

inserts into double helix and interferes with RNA polymerase

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72
Q

How is dactinomycin administered?

A

IV

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73
Q

Does dactinomycin penetrate the CSF?

A

no

74
Q

How is dactinomycin excreted?

A

via bile

75
Q

What are the adverse effects of dactinomycin?

A

bone marrow suppression, immunosuppression, GI upset, alopecia, stomatitis, sensitization to radiation

76
Q

What is doxorubicin?

A

one of the most widely used anticancer drugs– the red devil

77
Q

What are the analogues of doxorubicin?

A

idarubicin and epirubicin

78
Q

What is the MOA of doxorubicin?

A

induce cytotoxicity and produce free radicals that damage the cells’ DNA

79
Q

How is doxorubicin administered?

A

IV, deactivated in the GI tract

80
Q

What does extravasation of doxorubicin lead to?

A

tissue necrosis

81
Q

How is doxorubicin metabolized and excreted?

A

extensive liver metabolism and bile excretion

82
Q

Why is doxorubicin the red devil?

A

veins may appear dark red surrounding site of infusion and urine will be red

83
Q

What are the adverse effects of doxorubicin?

A

CARDIOTOXICITY (irreversible), bone marrow suppression, stomatitis, GI upset, severe alopecia

84
Q

What is the MOA of bleomycin?

A

oxidative scission of DNA

85
Q

Is bleomycin cell cycle specific?

A

yes, causes cells to accumulate in G2

86
Q

What is bleomycin used to treat?

A

testicular cancers

87
Q

How is bleomycin administered?

A

subc, IM, IC

88
Q

What is true of bleomycin absorption?

A

inactivating enzyme is present in liver and spleen, low in lungs, absent in skin

89
Q

How is bleomycin excreted?

A

kidney

90
Q

What are the adverse effects of bleomycin?

A

PULMONARY TOXICITY, alopecia, fever and chills, hypertrophic skin changes and HYPERPIGMENTATION

91
Q

What is the MOA of alkylating agents?

A

cause alkylation of DNA by addition of carbon chain to beginning of molecules which alters structure and function

92
Q

Are alkylating agents cell cycle specific?

A

no, used mainly for slow growing tumors

93
Q

T/F all alkylating agents are mutagenic and carcinogenic

A

true, can lead to secondary malignancies, especially leukemia

94
Q

What drug was developed as mustard gas during WWI?

A

meclorethamine

95
Q

What is the MOA of meclorethamine?

A

transported into cell, cross links with DNA guanine bases, cause strand breakage and occasional miscoding mutations

96
Q

What are the pharmacokinetic considerations of meclorethamine?

A

very unstable, blistering agent, only given IV, and has almost no drug excretion

97
Q

What are the adverse effects of meclorethamine?

A

severe GI, severe bone marrow depression, latent viral infections due to immunosuppression

98
Q

What is the MOA of carmustine and lomustine?

A

alkylation of DNA that inhibits replication and eventually RNA and protein synthesis

99
Q

What are carmustine and lomustine primarily used for?

A

treatment of brain tumors since they penetrate CNS

100
Q

What are closely related nitrosoureas specifically toxic to beta cells of the pancreas?

A

carmustine and lomustine

101
Q

When are carmustine and lomustine cytotoxic?

A

in actively dividing cells, alkylate DNA in all cell cycle phases

102
Q

How are carmustine and lomustine administered?

A

IV and oral respectively

103
Q

How are C and L excreted?

A

kidney

104
Q

What are adverse effects of C and L?

A

delayed hematopoietic depression (decreased formation of blood cells), development of aplastic marrow, renal toxicity and pulmonary fibrosis

105
Q

What is dacarbaxine used to treat?

A

melanoma

106
Q

What is the MOA of dacarbazine?

A

attacks nucleophilic groups in DNA and must undergo biotransformation to an active metabolite

107
Q

How is dacarbazine administered?

A

IV

108
Q

What are the adverse effects of dacarbazine?

A

GI, myelosuppression, hepatotoxicity

109
Q

What are mitotic spindles?

A

chromatin and microtubules needed for movement of DNA in cell division

110
Q

What is the MOA of vincristine and vinblastine?

A

bind to microtubular protein and prevent polumerization aka no formation of spindle

111
Q

Are vincrisitne and vinblastine cell cycle specific?

A

yes

112
Q

How are V and V administered?

A

IV

113
Q

T/F V and V are metabolized by the P450 system

A

true

114
Q

How are V and V excreted?

A

bile and feces

115
Q

What are adverse effects of V and V?

A

hyperuricemia (gout), GI, alopecia, phlebitis or cellulitis if extravasation occurs

116
Q

What is the MOA of paclitaxel and docetaxel?

A

bind to tubulin subunit and promote stabilization of microtubules (overly stable microtubules are nonfunctional)

117
Q

What are the pharmacokinetics of paclitaxel and docetaxel?

A

IV infusion, P450 metabolism and biliary excretion

118
Q

What are the adverse effects of paclitaxel and docetaxel?

A

neutropenia, peripheral neuropathy, hypersensitivity reaction

119
Q

Which typical adverse effect is uncommon with paclitaxel and docetaxel?

A

vomiting and diarrhea, instead there is fluid retention

120
Q

What is the contraindication of paclitaxel and docetaxel?

A

cardiac disease

121
Q

Steroid hormone sensitive tumors may be ___ or ____

A

hormone responsive or dependent (or both)

122
Q

What is hormone responsive?

A

tumor regresses following treatment with specific hormone

123
Q

What is hormone dependent?

A

removal of hormone results in tumor regression

124
Q

What is prednisone used for?

A

treatment of lymphomas, used to induce remission

125
Q

What is the MOA of prednisone?

A

triggers production of specific proteins that reduce cell growth and proliferation

126
Q

What are the pharmacokinetics of prednisone?

A

readily absorbed orally, liver metabolism, excreted in urine

127
Q

What are the adverse effects of prednisone?

A

predisposed patient to infection, hyperglycemia, cataract formation, increased IOP, osteoporosis, mood changes

128
Q

What adverse effects are the same for all corticosteroids and anti-inflammatory cancer tx?

A

predispose to infection, hyperglycemia, cataract formation, increased IOP, osteoporosis, mood changes

129
Q

What is tamoxifen?

A

an estrogen antagonists used for breast cancer

130
Q

T/F tamoxifen can be used prophylactically in women at high risk

A

true, but must be discontinued after 5 years or drug resistant tumors can develop

131
Q

What is the MOA of tamoxifen?

A

binds estrogen receptor as antagonist preventing RNA synthesis, results in depletion of estrogen receptors

132
Q

What is tamoxifen given with in premenopausal women?

A

an agent that lowers estrogen levels since the drug competes with estrogen

133
Q

Is tamoxifen cell cycle specific?

A

no

134
Q

How is tamoxifen administered?

A

orally

135
Q

How is tamoxifen metabolized and excreted?

A

partially metabolized in liver and excreted through bile

136
Q

T/F some metabolites of tamoxifen have agonist activity?

A

true

137
Q

What are adverse effects of tamoxifen?

A

hot flashes, GI, skin rash, potential for endometrial cancer because of decreased estrogen

138
Q

What is the retinal adverse effect of tamoxifen?

A

crystalline retinopathy and other vision problems, may see deposits in the cornea

139
Q

What is an aromatase reaction responsible for?

A

extra adrenal synthesis of estrogen, important source of estrogen in postmenopausal women

140
Q

What do aromatase inhibitors do?

A

decrease production of estrogen, treatment of breast cancer

141
Q

What was the first developed aromatase inhibitor?

A

aminoglutethimide

142
Q

What is aminoglutethimide normally taken with?

A

hydrocortisone

143
Q

What are anastrozole and letrozole?

A

nonsteroidal but more selective and potent aromatase inhibitors– does not need hydrocortisone supplementation and does not predispose to endometrial cancer

144
Q

What is exemestane?

A

steroidal inhibitor of aromatase

145
Q

What are the pharmacokinetics of aromatase inhibitors?

A

well absorbed orally, p450 metabolism, urine excretion

146
Q

What are leuprolide and goserelin?

A

analogs of gonadotrophin releasing hormone, act as agonists

147
Q

What is the MOA of leuprolide and goserelin?

A

binding to receptor causes desensitization and a decrease in FSH and LH so androgen and estrogen synthesis is reduced

148
Q

What are leuprolide and goserelin used for?

A

prostate cancer and advanced breast cancer

149
Q

What are two names for estrogens?

A

ethinyl estradiol and diethylstilbestrol

150
Q

What is estrogen used for?

A

treatment of prostate cancer

151
Q

What is the MOA of estrogen use?

A

blocks production of LH and decrease synthesis of androgens in the testis

152
Q

What are the adverse effects of estrogens?

A

thromboemboli, MI, stroke, hypercalcemia, gynecomastia and impotence

153
Q

What are flutamide, nilutamide, and bicalutamide?

A

nonsteroidal antiandrogens

154
Q

What are nonsteroidal antiandrogens (ex: flutamide) used for?

A

treatment of prostate cancer

155
Q

What is the MOA of nonsteroidal antiandrogens?

A

compete with natural hormone for androgen receptor, prevent translocation of hormone into nucleus

156
Q

What is the pharmacokinetics of nonsteroidal antiandrogens?

A

flutamide, nilutamide and bicalutamide, oral administration, kidney excretion

157
Q

What is an adverse effect of nilutamide?

A

visual problems

158
Q

What are monoclonal antibodies?

A

antibodies produced by one type of immune cell and all identical clones

159
Q

What is an advantage of monoclonal antibodies?

A

can create an antibody that can bind to any substance

160
Q

What is a good target for a monoclonal antibody?

A

cancer cell antigens

161
Q

How is the monoclonal Ab hybrid cell formed?

A

mice b lymphocytes fused with a tumor cell and then cloned to produce antibodies for a single antigen type

162
Q

How are monoclonal antibodies administered?

A

injection, cannot be oral because protein structure will break down

163
Q

What is the MOA of monoclonal antibodies?

A

bind to cancer specific antigens and induce an immunological response like apoptosis, growth inhibition, or interferes with cellular function OR cell is modified to deliver toxin or other active molecule

164
Q

What was the mAb approved to treat cancer?

A

rituximab

165
Q

What does rituximab treat?

A

lymphomas and leukemias

166
Q

What is the MOA of rituximab?

A

binds to site on B lymphocyte and recruits immune effector functions to induce cell mediated cytotoxicity

167
Q

What is the administration of rituximab?

A

IV infusion

168
Q

What does trastuzumab treat?

A

attaches to breast cancer-specific receptor and cells undergo G1 arrest and reduction of proliferation (reduces rate of relapse by 50% during first year.

169
Q

What is bevacizumab?

A

antiangiogenesis agent

170
Q

What is the MOA of bevacizumab?

A

attaches to a stops vascular endothelial growth factor from stimulating the formation of new blood vessels which decreases oxygen supply to tumor cells

171
Q

What is bevacizumab used to treat?

A

retinal neovascular diseases like diabetic ret, choroidal neo-vascularization etc (avastin)

172
Q

What is the MOA of platinum coordination complexes?

A

similar to alkylating agents, bind guanine and cross link DNA

173
Q

What are the pharmacokinetic considerations of platinum coordination complexes?

A

IV administration, little CSF penetration, renal excretion

174
Q

What are the adverse effects of cisplatin?

A

sever vomiting, nephrotoxicity, and ototoxicity

175
Q

What are the adverse effects of carboplatin and oxaliplatin?

A

mild nausea and myelosuppression

176
Q

What is interferon alpha?

A

primarily leukocytic

177
Q

What is interferon beta?

A

produced by connective tissue fibroblasts

178
Q

What is interferon gamma?

A

produced by t lymphocytes

179
Q

What interferons are used to treat neoplastic disease?

A

alpha 2a and 2b

180
Q

What is the MOA of interferons?

A

binding of interferon produces complex intracellular reactions that increase inflammation and decrease growth (enzyme synthesis, suppression of cell proliferation, activation of macrophages, increased cytotoxicity of lymphocytes)

181
Q

What are the pharmacokinetics of interferons?

A

IM or subc injection (or IV form of 2b), minimal liver metabolism, and excretion by kidneys

Systemic Pharm I (13 decks)

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