Antineoplastic Agents I Flashcards

1
Q

cyclophosphamide

A

nitrogen mustard

-alkylating agent

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2
Q

ifosfamide

A

nitrogen mustard

-alkylating agent

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3
Q

busulfan

A

alkyl sulfonate

-alkylating agent

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4
Q

cisplatin

A

platinum coordinate complex

-alkylating agent

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5
Q

methotrexate

A

folic acid analog

-antimetabolite

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6
Q

fluorouracil

A

5-FU
pyrimidine analog
-antimetabolite

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7
Q

mercaptopurine

A

6-MP
purine analog
-antimetabolite

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8
Q

vinblastine

A

vinca alkaloid

-natural product

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9
Q

vincristine

A

vinca alkaloid

-natural product

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10
Q

paclitaxel

A

taxane

-natural product

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11
Q

etoposide

A

epipodophyllotoxin

-natural product

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12
Q

doxorubicin

A

antibiotic

-natural product

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13
Q

blemoycin

A

anthracenedione

-natural product

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14
Q

L-asparaginase

A

enzyme

-natural product

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15
Q

imatinib

A

protein kinase inhibitor

-misc agent

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16
Q

trastuzumab

A

monoclonal Ab

-misc agent

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17
Q

leucovorin

A

rescue agent

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18
Q

mesna

A

rescue agent

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19
Q

ondansetron

A

serotonin antagonist

-used to minimize adverse effects

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20
Q

curable by chemo

A
ALL
AML
ewing
hodgkin
non-hodgkin
DLBCL
wilms
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21
Q

causes of cancer

A

radiation
carcinogens
Hep B and C, HIV, HPV, EBV

and genetic predisposition

22
Q

primary induction treatment

A

first treatment given

23
Q

neoadjuvant therapy

A

given before primary tx
-to shrink tumor

type of induction therapy

cancer for which alternative therapy exists but less effective

24
Q

adjuvant therapy

A

given after primary treatment

-lower risk cancer will come back

25
Q

primary induction chemotherapy

A

as primary treatment

  • pt with no alternative
  • may be curative - hodgkin/NHL, AML, germ cell cancer
26
Q

G1 phase

A

synthesis of components for DNA synthesis

27
Q

S phase

A

DNA synthesis

28
Q

G2 phase

A

synthesis of components for cell division

29
Q

M phase

A

cell divides to two daughter G1 cells

activity of CDK and P16,p53 involved in transition of cell cycle

30
Q

cell cycle specific

A

cytotoxic during specific phase of cell cycle

31
Q

cell cycle nonspecific

A

cytoxic regardless of whether cell is cycling or resting (G0)

32
Q

CCS drugs

A
antimetabolites 
taxanes
vinca alkaloids
camtothecins
epipodophyllotoxins
antitumor antibiotics - blemoycin
33
Q

CCNS drugs

A
alkylating agents
anthracyclines
antitumor antibiotics
antimetabolites - cladribine
platinum analogs
34
Q

S phase CCS

A

antimetabolites and camptothecins

35
Q

S-G2 phase CCS

A

epipodophyllotoxins

-etoposide

36
Q

G2-M phase CCS

A

blemoycin

37
Q

M phase CCS

A

taxanes

vinca alkaloids

38
Q

growth fraction

A

ration of proliferating cells to cells in G0 phase

39
Q

solid tumors

A

lower growth fraction than disseminated cancers

40
Q

increase of growth fraction

A

can be induced by surgery or radiation

-make more susceptible to antineoplastic chemo agents

41
Q

burkitt lymphoma

A

100% growth fraction

-curable with chemo

42
Q

trophoblastic choriocarcinoma

A

100% growth fraction

-curable with chemo

43
Q

lung and colon cancer

A

slow growing

-10% growth fraction

44
Q

true cure

A

eradication of every cancer cell

45
Q

indications for chemo

A

tumor not amenable to surgery

-also as supplemental treatment to prevent metastasis with surgery/radiation

46
Q

log cell kill hypothesis

A

chemo kills fraction of drugs
-first-order kinetics

three-log cell kill - 10^12 to 10^9

47
Q

pharmacologic sanctuaries

A

regions where tumors cells less susceptible to antineoplastic agnents

interior of solid tumors or CNS, testes

may require localized radiation or surgical resection

48
Q

intermittent high dose therapy

A

most common

allows recovery of normal tissue

more effective with CCNS drugs

49
Q

continuous infusion therapy

A

drugs metabolized/excreted more effective

also CCS drugs more effective this way

50
Q

routes of administration for chem

A

IV and PO

51
Q

colorectal cancer

A

mets to liver - use intraarterial perfusion of chemo drugs to cathgeter in hepatic artery

lt route of admin**

52
Q

drug combo

A

benefits -
1 maximal cell killing within range of tolerated toxicity

2 effective against broader range of clones with different genetic abnormalities

3 may delay or prevent development of drug-resistant tumors