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Heme/Lymph II Exam II > Antineoplastic agents (Linger) > Flashcards

Antineoplastic agents (Linger) Flashcards

1
Q

what are some of the cancers that are curable by chemotherapy

A 
Acute lymphoblastic leukemia
Acute myeloid leukemia
Ewing sarcoma
Gestational trophoblastic carcinoma
Hodgkin disease
Non-Hodgkin lymphoma
Burkitt lymphoma
Diffuse large cell lymphoma
Follicular mixed lymphoma
Lymphoblastic lymphoma
Rhabdomyosarcoma
Testicular carcinoma
Wilms’ tumor
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2
Q

what are some cancers where chemotherapy has significant activity ?

A 
Acute lymphoblastic leukemia
Acute myeloid leukemia
Ewing sarcoma
Gestational trophoblastic carcinoma
Hodgkin disease
Non-Hodgkin lymphoma
Burkitt lymphoma
Diffuse large cell lymphoma
Follicular mixed lymphoma
Lymphoblastic lymphoma
Rhabdomyosarcoma
Testicular carcinoma
Wilms’ tumor
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3
Q

what are some cancers where chemotherapy has minor activity

A 
Brain tumors (astrocytoma)
Cervical carcinoma
Colorectal carcinoma
Hepatocellular carcinoma
Kaposi sarcoma
Melanoma
Pancreatic carcinoma
Prostate carcinoma
Soft tissue sarcoma
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4
Q

what are some cancers where adjuvant chemotherapy is effective

A 
Breast carcinoma
Colorectal carcinoma (stage III)
Osteogenic sarcoma
Ovarian carcinoma (stage III)
Testicular carcinoma
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5
Q

what are some chemical carcinogens that cause cancer

A

tobacco smoke, azo dyes, aflatoxins, asbestos, benzene, and radon

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6
Q

Hep B and Hep C

A

hepatocellular cancer

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7
Q

HIV

A

hodgkins and NHL’s

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8
Q

HPV

A

cervical cancer

head and neck cancer

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9
Q

EBV

A

nasopharyngeal cancer

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10
Q

what are the 3 main approaches to treating established cancer

A

surgical excision
irradiation
chemotherapy

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11
Q

what is primary induction therapy

A

The first treatment given.

It is often part of a standard set of treatments, such as surgery followed by chemotherapy and radiation.

When used by itself, induction therapy is the one accepted as the best treatment.

i) Drug therapy administered as the primary treatment in patients who present with advanced cancer for which no alternative treatment exists
ii) Goals of therapy are to palliate tumor-related symptoms, improve overall quality of life, and prolong time to tumor progression

If it doesn’t cure the disease or it causes severe side effects, other treatment(s) may be added or used instead. It is also called first-line therapy, primary therapy, and primary treatment.

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12
Q

what is neoadjuvant therapy

A

Treatment given as a first step to shrink a tumor before the primary treatment (usually surgery) is given. Can include chemotherapy, radiation therapy, and hormone therapy. It is a type of induction therapy.

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13
Q

what is adjuvant therapy

A

Additional cancer treatment given after the primary treatment to lower the risk that the cancer will come back. Can include chemotherapy, radiation therapy, hormone therapy, targeted therapy (designed to identify and attack specific types of cancer cells with less harm to normal cells), or biologic therapy (treatment that uses substances made from living organisms).

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14
Q

G1 phase

A

(1) Precedes DNA synthesis

(2) The cell synthesizes components necessary for DNA synthesis

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15
Q

S phase

A

DNA synthesis

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16
Q

G2 phase

A

synthesis of components for cell division (mitosis)

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17
Q

M phase

A

(1) The cell divides into two daughter G1 cells

2) Each daughter cell may re-enter the cell cycle or pass into a nonproliferative stage (G0

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18
Q

cyclophosphamide

A

nitrogen mustard

alkylating agent

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19
Q

ifosfamide

A

nitrogen mustard

alkylating agent

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20
Q

busulfan

A

alkyl sulfonate

alkylating agent

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21
Q

cisplatin

A

platinum coordination complex

alkylating agent

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22
Q

methotrexate

A

folic acid analog

antimetabolite

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23
Q

fluorouracil (5-fluorouracil; 5-FU)

A

pyrimidine analog

antimetabolite

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24
Q

mercaptopurine (6-mercaptopurine; 6-MP)

A

Purine analog

Antimetabolite

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25
Q

Vinblastine

A

Vinca alkaloid

Natural product

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26
Q

Vincristine

A

natural product

vinca alkaloid

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27
Q

Paclitaxel

A

Taxane

Natural product

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28
Q

Etoposide

A

Epipodophyllotoxin

Natural product

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29
Q

Doxorubicin

A

Antibiotic

Natural product

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30
Q

Bleomycin

A

anthracenedione

natural product

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31
Q

L-Asparaginase

A

Enzyme- Natural product

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32
Q

Imatinib

A

Protein tyrosine kinase inhibitor

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33
Q

trastuzumab

A

monoclonal antibody

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34
Q

leucovorin

A

antidote for methotrexate rescue

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35
Q

Mesna

A

Acrolein causes hemorrhagic cystitis (acrolein is a side product of cyclosphosphamide)

Mesna inactivates acrolein and is used for prophylaxis of chemotherapy-induced cystitis

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36
Q

Filgrastim

A

agent used to minimize adverse effects

G-CSF

stimulate production of white blood cells and shorten the length of the neutropenia

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37
Q

EPO

A

treatment of anemia - stimulate red cells production

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38
Q

Ondansetron

A

serotonin antagonist

minimize nausea and vomiting

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39
Q

what is the growth rate pattern of a typical tumor

A

initially rapid

decreases as the tumor size increases
-due to low nutrient and O2 availability

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40
Q

what is growth fraction

A

the ratio of proliferating cells to cells in the G0 stage

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41
Q

how does growth fraction compare in solid tumors versus disseminated tumors

A

iii) As a result of inadequate nutrient supply to the interior of solid tumors, solid tumors have a lower growth fraction than disseminated tumors

higher percentage of cells in solid tumors are found in G0 compared to disseminated tumors

v) As a general rule, antineoplastic drugs work best on tumors with a high growth fraction

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42
Q

how can growth fraction in slow growing solid tumors be changed with chemo?

A

vi) The growth fraction of slow-growing solid tumors can be increased by reducing the tumor burden through surgery or radiation, which promotes the recruitment of some of the remaining cells into active proliferation and increases their susceptibility to chemotherapeutic agents
vii) Examples of human tumors with growth fractions close to 100% are Burkitt lymphoma and trophoblastic choriocarcinoma, which are readily curable by single-agent chemotherapy
viii) Cancers of the lung or colon are slow-growing and have growth fractions less than 10%

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43
Q

what is the log cell kill hypothesis

A

i) Chemotherapy kills a fraction of cells rather than an absolute number per dose

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44
Q

what are pharmacologic sanctuaries

A

regions where tumor cells are less susceptible to antineoplastic agents

examplie–> interior of solid tumors or specific tissues (CNS, testes)

where transport constraints prevent certain chemotherapeutic drugs from entering and have been a major cause of treatment failure (e.g., acute lymphocytic leukemia in children)

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45
Q

this is the most common form of anticancer agent administration

A

Intermittent high dose therapy

(1) The most common form of anticancer agent administration
(2) Allows recovery of normal tissues (e.g., the patient’s immune system), also affected by antineoplastic agents, and reduces the risk of serious infection
(3) May be more effective with agents that are phase nonspecific (cell cycle nonspecific)

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46
Q

which drugs are more effective when administered by continuous infusion

A

drugs that are rapidly metabolized or excreted or both

cell cycle specific (act on only one portion of the cell cycle)

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47
Q

what are the advantages of drug combinations in chemotherapy

A

(1) Provides maximal cell killing within the range of tolerated toxicity
(2) Effective against a broader range of clones with different genetic abnormalities in a heterogeneous tumor population
(3) May delay or prevent the development of drug-resistant tumors

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48
Q

efficacy

A

Each drug used in combination therapy should have some individual therapeutic activity and, if possible, should be used at the maximally tolerated individual dose

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49
Q

principle of mechansim of interaction

A

Drugs that act by different mechanisms may have additive or synergistic therapeutic effects, thus increasing log cell kill and diminishing the probability of the emergence of drug resistant tumor cells

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50
Q

what is primary resistance of neoplastic cells

A

i) Some neoplastic cells exhibit primary resistance to currently available agents (an absence of response on the first exposure)
ii) Primary resistance is thought to be due to the genomic instability associated with the development of most cancers

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51
Q

what is acquired resistance of neoplastic cells

A

iii) Acquired resistance develops in response to exposure to a given antineoplastic agent
iv) Acquired resistance is often highly specific to a single drug, or class of drugs, and is usually based on a specific change in the genetic machinery of a given tumor cell with amplification or increase expression of one or more genes

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52
Q

what are the mechanisms of resistance to single antineoplastic agents

A

(1) Decreased drug transport into cells
(2) Reduced drug affinity due to mutations or alterations of the drug target
(3) Increased expression of an enzyme that causes drug inactivation
(4) Increased expression of DNA repair enzymes for drugs that damage DNA

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53
Q

what gene and gene product are associated with multidrug resistant phenotype in neoplastic cells

A

increased expression of the MDR1 gene, which encodes a cell surface transporter glycoprotein (P-glycoprotein)

54
Q

what does P-glycoprotein pump do….

A

it is a cell surface transporter

(2) The P-glycoprotein pump is an ATP-dependent transporter that confers resistance to anthracyclines, vinca alkaloids, etoposide, paclitaxel, dactinomycin, and others
(3) The P-glycoprotein transporter may be inhibited by calcium channel blockers such as verapamil

55
Q

what normal tissues in the body are major sites of toxicity of chemotherapy agents…

A

ii) Since antineoplastic agents target cells that are highly proliferative (high growth fraction), rapidly proliferating normal tissues are the major sites of toxicity of these agents (high growth fraction tissues include bone marrow, gastrointestinal tract, hair follicles, buccal mucosa, and sperm forming cells)

56
Q

which group of antineoplastic agents can cause treatment-induced tumors

A

alkylating agents

57
Q

which adverse effects occur with nearly all antineoplastic agents

A

vomiting, nausea, stomatitis (inflammation of mouth and lips) and alopecia

some others include:
-lower sperm count or even azoospermia

-developmental growth of children exposed to chemo may be depressed

58
Q

what are the outcomes of myelosuppression that is induced by chemotherapy

A

leukopenia
thrombocytopenia
anemia
predisposition to infection and impaired wound healing

59
Q

blood counts in chemo reach their low point around what days? when do they recover ? return to normal?

A

(a) Blood counts normally reach their nadir (low point) 10-14 days after treatment with recovery by day 21 and a return to normal by day 28
(b) Most regimens are given in cycles of 21-28 days

60
Q

how can the amount of adverse effects on pt’s be reduced?

A

route of administration–> reduce systemic exposure

local perfusion of drugs

removal of bone marrow prior to treatment and reimplanting it after

use GM-CSF agents (sargramostim) and G-CSF (filgrastim, pegfilgrastin) to stimulate production of white blood cells

use prelvekin to counteract thrombocytopenia

use erythropoietin or darbepoetin to stimulate red blood cell production

61
Q

which agents cause severe nausea and vomiting

A

cisplatin
dacarbazine
doxorubicin
mechlorethamine

62
Q

which other agents cause minimal emesis

A

methotrexate and fluorouracil

63
Q

what is an importnat anti-emetic agent that can reduce nausea and vomiting

A

(ii) Serotonin antagonists: ondansetron***

64
Q

what is stomatitis

how can it be prevented

A

inflammation of the oral mucosa

(a) Typically begins as erythema and edema and may progress to painful ulcerations that persist from several days to a week or more
(b) There is currently no means to prevent stomatitis except to modify the chemotherapeutic agent causing these symptoms
(c) Meticulous oral hygiene helps to diminish pathogenic oral flora and decreases the risk of secondary infections and treatment with topical oral anesthetics (lidocaine solution) can relieve pain and help maintain adequate oral intake

65
Q

when does alopecia occur?

A

1-2 weeks after initiating treatment

(b) Cessation of therapy typically causes hair to return to pretreatment levels, although the hair may be different in texture and/or color

66
Q

which agents cause the most profound alopecia

A

cyclophosphamide, dactinomycin, doxorubicin, paclitaxel, and vincristine

67
Q

what are bisphosphonates used for

A

(a) Metastatic disease that localizes in the bone can cause fractures and bone pain
(b) A number of agents, such as bisphosphonates, are available to inhibit osteoclast action and bone resorption and may be used to delay the time to the first skeletal complication.

68
Q

what are the 5 major types of alkylating agents

A

nitrogen mustards

methylhydrazines

alkyl sulfonates,

nitrosoureas,

triazenes

b) Although they do not alkylate DNA platinum compounds are included under alkylating agents

69
Q

MOA of alkylating agents

A

i) Alkylating agents are strong electrophiles and exert their cytotoxic effects by forming covalent linkages with DNA
ii) Alkylation of DNA leads to intra- and inter-strand cross-linking, which prevents the tumor from unwinding DNA for mRNA production or DNA replication
iii) Alkylation of DNA (particularly guanine bases) can also lead to miscoding through abnormal base pairing with thymine or in depurination by excision of guanine residues, which leads to DNA strand breakage
iv) Cross-linking of DNA is a major cause of the cytotoxic action of alkylating agents and replicating cells are most susceptible to these agents

70
Q

mechlorethamine

A

nitrogen mustard

alkylating agent

71
Q

are alkylating agents cell cycle specific or non specific

A

non specific

although cells in the G1 and S phase are most susceptible

72
Q

what occurs with IV administration of alkylating agents

A

iii) Acute toxicity (nausea and vomiting) occurs within 30-60 min of IV administration (pretreatment with a serotonin (5-HT3) receptor antagonist (e.g, ondansetron) can mediate emetogenic effects)

73
Q

what occurs with delayed toxicity of alkylating agents

A

bone marrow depression with leukopenia, thrombocytopenia, nephrotoxicity, alopecia, mucosal ulceration, and intestinal denudation

74
Q

what is essential during administration of alkylating agetns

A

v) Frequent monitoring of blood counts is essential during administration of these agents due to the possible development of severe leukopenia or thrombocytopenia (may necessitate discontinuation of therapy)

75
Q

what are the key adverse effects of alkylating agents

what are they at risk for

A

nausea,
vomiting
myelosuppression
tissue damage at site of administration

increased risk for secondary malignancies–> especially AML

76
Q

adverse effects of cyclophosphamide (alkylating agent- nitrogen mustard)

antidote?

A

hemorrhagic cystitis due to the accumulation of the metabolite acrolein

use Mesna parenterally!

mesna neutralizes the effects of acrloein in the acid environment of the urinary tract

77
Q

what are the adverse effects of cisplatin?

what are the antidotes

A

renal tubular damage
-overcome with hydration, diuresis

ototoxicity -tinnitus and hearing loss

  • unaffected by diuresis
  • worse in children

marked nausea and vomiting may occur (use ondansetron and high dose corticosteroids)

78
Q

what are the adverse effects of Busulfan (alkyl sulfonate- alkylating agent)

A

hyperpigmentation, pulmonary fibrosis, and adrenal insufficiency

79
Q

are antimetabolites cell cycle specific or non specific ?

A

cell cycle specific

S phase

80
Q

what are the main categories of antimetabolites

A

folic acid analogs
pyrimidine analogs
purine analogs

81
Q

what are the acute toxic effects of antimetabolites

A

cause little acute toxicity after an initial dose; they must be absorbed into each cell and enter into the pathway that the drug disrupts before many effects can be quantified

82
Q

MOA of methotrexate (folic acid analog- antimetabolite)

A

(1) Inhibits dihydrofolate reductase and blocks the conversion of folic acid to tetrahydrofolic acid, which serves as the key one-carbon carrier for enzymatic processes involved in the de novo synthesis of thymidylate, purine nucleotides, and the amino acids serine and methionine

83
Q

methotrexate at low doses- uses?

methotrexate at high doses-uses?

A

(2) At low doses, methotrexate is actively transported into the cell by membrane proteins and is less harmful on healthy tissues (common in the treatment of rheumatoid arthritis, colitis, psoriasis, and some cancers)
(3) High-dose methotrexate therapy, where methotrexate enters healthy cells by diffusion across the concentration gradient, causes injury to healthy tissues

84
Q

what antidote is used to rescue “healthy cells” from the toxic effects of methotrexate

A

leucovorin (folinic acid) is administered

(5) Leucovorin enters the thymidylate synthesis pathway in the healthy cells and allows thymidine synthesis to proceed, thus sparing the patient severe gastrointestinal and bone marrow toxicity

85
Q

what are the adverse effects of methotrexate

A

mucositis

diarrhea

myelosuppression- neutropenia, thrombocytopenia

nausea/vomiting

immunosuppression

hepatotoxicity

fatigue

86
Q

MOA of Fluorouracil (5-FU)

A

5-FU is a prodrug whereby the active compound FdUMP covalently binds thymidylate synthetase and blocks de novo synthesis of thymidylate;

active compounds (FdUTP and FUTP) are incorporated into both DNA and RNA, respectively, interfering with DNA synthesis, DNA function, RNA processing, and mRNA translation

87
Q

5-FU is the most widely used agent in what ?

A

colorectal cancer

88
Q

what re the adverse effects of 5-FU

A

anorexia
nausea
stomatitis
diarrhea

89
Q

what is cytarabine (Ara-C) and what are its uses>

A

pyrimidine analog

antimetabolite

used exclusively for hematologic malignancies NOT solid tumors

90
Q

Mercaptopurine MOA (6-MP)

A

inhibits de novo purine nucleotide synthesis and DNA and RNA synthesis due to triphosphate incorporation

91
Q

Mercaptopurine must be used with caution with what other drug?

A

Allopurinol

(3) Biotransformation includes metabolism to the inactive metabolite 6-thiouric acid by xanthine oxidase (first pass metabolism).

Allopurinol, a xanthine oxidase inhibitor, is often used as supportive care in the treatment of acute leukemias to prevent the development of hyperuricemia that often occurs with tumor cell lysis.

Simultaneous administration of allopurinol and oral 6-MP results in increased levels of 6-MP and increased toxicity. In this setting, the oral dose of mercaptopurine must be reduced by 50-75% (IV dose unaffected).

92
Q

what are the adverse effects of mercaptopurine

A

myelosuppression, immunosuppression, and hepatotoxicity

93
Q

what antimetabolite purine analog drug may be used in full doses with allopurinol?

A

Thioguanine

94
Q

what are the antimitotic drugs

A

Vinca alkaloids

Taxanes

95
Q

Vinblastine and Vincristine

MOA?

A

Vinca alkaloids- Natural products

bind to B-tubulin and inhibit microtuble ASSEMBLY

cell cycle specific M-phase

96
Q

drug resistance to vinblastine and vincristine ?

A

membrane efflux pump P-glycoprotein

97
Q

what are the adverse effects of the vinca alkaloids

A

hair loss
local cellulitis if extravasated

myelosuppression –> more so with vinblastine

Vincristine causes more predictable cumulative neurological toxicities (numbness and tingling of the extremities with loss of deep tendon reflexes, followed by motor weakness)

98
Q

Paclitaxel

drug type and MOA

A

Taxane

bind to β-tubulin and promote microtubule formation and stabilization***

99
Q

what are the adverse effects of Paclitaxel

A

bone marrow suppression

peripheral and sensory neuropathy

100
Q

Etoposide

drug type and MOA

A

Epipodophyllotoxins

iii) Cell cycle specific agents that block cell division in the late S-G2 phase

inhibits topoisomerase II –> leads to DNA damage through strand breakage induced by the formation of a ternary complex of drug, DNA and enzyme

101
Q

camptothecin analogs MOA

adverse effects

A

natural products

iii) MOA: inhibit the activity of topoisomerase I; results in DNA damage and blockade of DNA replication and transcription

adverse effects–> diarrhea !

102
Q

what are the classes of antitumor antibiotics

A

anthracyclines -doxorubicin, daunorubicin

anthracenediones - bleomycin

103
Q

MOA of doxorubicin and dactinomycin

where is doxorubicin metabolized

A

(a) Inhibits topoisomerase II
(b) Intercalates DNA and blocks synthesis of DNA and RNA and blocks DNA strand scission
(c) Generates semiquinone and oxygen free radicals
(d) Binds to cellular membranes to alter fluidity and ion transport

extensive liver metabolism

104
Q

are the anthracyclines cell cycle specific or non specific

A

non specific b/c they intercalate DNA

105
Q

what are the adverse effects of doxorubicin

A

nausea

red urine

alopecia

myelosuppression

stomatitis

cardiotoxicity - long term effect (due to free radicals)

106
Q

MOA of bleomycin

A

small peptide that binds to DNA resulting in single- and double-strand breaks and also inhibits DNA biosynthesis

cell cycle specific G2

107
Q

how is bleomycin eliminated from the body

A

mainly through renal excretion

108
Q

what are the adverse effects of bleomycin

A

(4) Pulmonary toxicity is dose-limiting; typically presents as pneumonitis with cough, dyspnea, dry inspiratory crackles, and infiltrates on chest x-ray;

also causes allergic reactions, fever, hypotension, skin toxicity, mucositis, and alopecia

109
Q

MOA of L-Asparaginase

how does it work against acute lymphoblastic leukemia

A

Hydrolyzes circulating L-aspargine into aspartic acid and ammonia –> inhibiting protein synthesis

iv) Acute lymphoblastic leukemia tumor cells lack the enzyme asparagine synthetase and require an exogenous source of L-asparagine, rendering them selective to and vulnerable to asparaginase and pegaspargase

110
Q

what are the main adverse effects of L-asparaginase

acute

chronic

A

v) Main adverse effect is an acute hypersensitivity reaction (fever, chills, nausea, vomiting, skin rash, urticaria);

delayed toxicities include an increased risk of clotting and bleeding

pancreatitis

CNS toxicity including lethargy, confusion, hallucinations, and coma

111
Q

how are steroid hormones used in cancer treatment

A

i) Useful as antineoplastic agents because of their antilymphocytic effects
ii) Commonly used as one component of combination chemotherapy
iii) Antitumor effects may be related to inhibition of glucose transport, phosphorylation, or induction of cell death in immature lymphocytes

112
Q

“nib” ending

A

protein tyrosine kinase inhibitors

113
Q

MOA of imatinib

A

(1) MOA: inhibits the tyrosine kinase domain of the Bcr-Abl oncoprotein and prevents phosphorylation of the kinase substrate by ATP;

also inhibits the kinases platelet-derived growth factor receptor (PDGFR), stem cell factor, and c-kit

114
Q

what is imatinib used clinically for

A

CML- characterized by the t(9;22) philidelphia chromosomal translocation resulting in Bcr -Abl fusion protein

GI stromal tumors

hypereosinophilia syndrome

115
Q

with what other drugs must you use Imatinib with caution

A

in drugs that might interact with CYP3A4 b/c imatinib is metabolized in the liver by CYP450’s

116
Q

what are the adverse effects of Imatinib

A

myelosuppression,

fluid retention with ankle and periorbital edema,

diarrhea,

myalgias

117
Q

what is Lapatinib MOA and what is it used for

A

inhibits internal kinase domain of HER2/neu epidermal growth factor receptor

breast cancer

118
Q

ending with “mab”

A

monoclonal antibodies

119
Q

Trastuzumab MOA

and clinical use

A

binds to the HER2/neu receptor (also known as ErbB-2, a member of the family of epidermal growth factor receptors) that is expressed on the surface of cells (about 25-30% of breast cancers) and inhibits intracellular signaling events and neoplastic cell proliferation

The HER2 receptor participates in receptor-receptor interactions that regulate cell differentiation, growth, and proliferation and overexpression of the HER2 receptor contributes to the process of neoplastic transformation

used in breast cancer

120
Q

what are the adverse effects of trastuzumab

A

cardiotoxicity (ventricular dysfunction and heart failure)

***evaluate ventricular function before and after therapy

iv) Discontinuance of trastuzumab should be strongly considered in patients who develop a clinically important decrease in left ventricular function.

121
Q

Rituximab

A

CD20 antigen

NHL

122
Q

alemtuzumbab

A

CD52

chronic lymphocytic leukemia

123
Q

Gemtuzumab

A

CD33

AML

124
Q

deferoxamine

A

iron toxicity

125
Q

N-acetylcystein use

A

Tylenol toxicity antidote

126
Q

What is the main reason for giving allopurinol prophylactically prior to starting a course of chemotherapy?

A

reduce the risk of hyperuricemia

127
Q

Blocks central serotonergic (5-HT₃) receptors

A

ondansetron

128
Q

A 43 y/o HIV-positive male with a 6 month history of CD20+ diffuse large B-cell lymphoma, a subtype of non-Hodgkin lymphoma, presents to the oncology clinic for infusion of a combination of chemotherapeutic agents (this is his third of six scheduled infusions). His current CD4 count is 150 cells/mm3. Which agent is contraindicated?

bleomycin
prednisone
rituximab
vinblastine
vincristine
A

vinblastine

adverse effects include myelosuppression

129
Q

A 63 y/o female is diagnosed with metastatic colon carcinoma. Biopsy is positive for overexpression of the epidermal growth factor receptor (EGFR). Which agent is most appropriate?

Alemtuzumab 
Bevacizumab 
Cetuximab
Gemtuzumab 
Rituximab
Trastuzumab
A

cetuximab

130
Q

A 63 y/o female is diagnosed with metastatic colon carcinoma. An agent is used that blocks the interaction of vascular endothelial growth factor (VEGF) with the VEGF receptor. Which agent is described?

Alemtuzumab 
Bevacizumab 
Cetuximab
Gemtuzumab 
Rituximab
Trastuzumab
A

bevacizumab

131
Q

A 39 y/o female with acute lymphoblastic leukemia has been admitted to the hospital for induction chemotherapy, which includes the following.
Cytarabine – 5 g IV Q 12 hr for 8 doses
Vincristine – 2 mg IV push weekly
Prednisone – 100 mg/day
Asparaginase – 15,000 U/day for 14 days
Allopurinol – 300 mg/day
On day 3, she is confused and has difficulty performing a finger-to-nose neurologic examination. After 3 weeks, she complains of numbness in her hands and feet. An eyelid lag and ataxia are noted. What is the most likely cause of her mental status?

Allopurinol
Asparaginase
Cytarabine
Prednisone
Vincristine
A
  • CNS toxicity - asparaginase***- confusion

- parasthesias - vincristine

Heme/Lymph II Exam II (5 decks)

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