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Flashcards in test 1 Deck (94):
1

pyrimidine analogs

fluoruracil, floxuridine, capecitabine, cytarabine, gemcitabine

2

5-FU use

treatment for GI, pancreas, head & neck, colon, rectum, breast and ovarian cancers

3

5-FU toxicity

bone marrow suppression, mucosal damage, N/V, cardiac, hand and foot syndrome, alopecia, hyperpigmentation, neurologic deficits

4

arabinose nucleotides cannot form

phosphodiester bonds bc of the -OH at C2. -> DNA fragmentation

5

cytarabine (AraC) indication

acute leukemia

6

most specific antimetabolite for the S phase

cytarabine

7

cytarabine (AraC) MOA

activated by kinases to AraCTP which acts as an inhibitor of DNA polymerase

8

side effect of cytarabine

hand and foot syndrome. severe myelosuppression, mucosal membrane inflammation, etc

9

xeloda generic

capecitabine.

10

capecitabine indication

breast cancer. prodrug of 5-FU

11

gemcitabine is used to treat

locally advanced or metastatic pancreatic cancer

12

triphosphate-gemcitabine inhibits

DNA polymerases (termination of DNA chain elongation)

13

diphosphate- gemcitabine inhibits

ribonucleotide reductase

14

nucleotide analogue of the antiviral agent vidarabine

fludaraine

15

fludarabine MOA

- phosphorylated (inhibition of DNA polymerases)
- incorporation into the DNA strands (chain termination)

16

purine analogs

6-MP, thioguanine, cladribine, pentostatin

17

6-mercaptopurine indication

childhood leukemia

18

both 6-MP and thioguanine are activated by

HGPRT to toxic nucleotides that inhibit several enzymes involved in purine metabolism

19

reistance to 6-MP and thioguanine

due to cancer cells have decreased HGPRT activity

20

6-MP is metabolized in the liver by

xanthine oxidase

21

drug interaction with 6-MP and

allopurinol. if used together, dose of 6-MP should be reduced by at least 75%

22

ribonucleotide reductase

catalyzes conversion of ribonucleotide diphosphates to deoxyribonucleotide diphosphates

23

hydroxyurea specifically inhibits

ribonucleotide reductase. inhibits DNA synthesis without affecting RNA synthesis. limited use in cancer

24

3 antimitotic agents

taxols, vinca alkaloids, colchicine

25

vinca alkaloid MOA

bind with the already grown microtubule and help to depolymerize it-> break down microtubule

26

taxol MOA

binds to the microtubule and helps stabilize it, making it more rigid

27

vinca alkaloid drugs

vincristine, vinblastine, ajmalicine, vindesine

28

vinca alkaloids are

cell cycle specific. act in late G2 & M phases

29

vinblastine, vinorelbine and vincristine are both

vesicants

30

vincristine cannot be given

intrathecally- neurotoxicity

31

less neurotoxicity than all other vincas

vinorelbine

32

major mechanism of resistance

MDR-P glycoprotein efflux pump

33

taxols are

cell cycle specific. active in G2 and M phases

34

what is a requirement for biological activity of taxanes?

C13 side chain

35

taxol drugs are always administered after

premedication with antihistamines, corticosteroids, etc bc the vehicle can degrade tubing and cause histamine release. dexamethasone 20mg PO 12 and 6 hours prior, pepcid or tagamet, benedryl plus anti-emetic

36

when given with other chemo drugs, give taxol

first

37

is taxol an irritant?

yes

38

premedication with docetaxel

examethasone 8mg PO BID starting 1 day prior & continuing 4 days after

39

what is abraxane?

albumin-bound, cremophor- free formulation of paclitaxel (solvent free)

40

taxanes promote

microtubule formation!

41

adriyamycin

doxorubicin

42

type 1 topos

introduces a break in ONE strand to remove a supercoil

43

type 2 topos

introduce breaks in both chains

44

type 1 functions to remove

positive supercoils during transcription

45

type 2 performs a similar function during

DNA replication & decatanates & separates daughter chromosomes in mitosis

46

MOA of topo agents

cause accumulation of DNA cleavable complexes composed to protein-linked DNA strand breaks

47

epipodophyllotoxins

etoposide & teniposide
topo II inhibitors. cause DS breaks

48

etoposide/ teniposide toxicities

neutropenia, myelosuppression & secondary leukemias

49

topo I inhibitor drugs

camptothecin, irinotecan, topotecan

50

SN-38 aka

irinotecan

51

major side effect of irinotecan

major diarrhea

52

antitumor antibiotics- anthracyclines

daunorubicin, doxorubicin, idarubicin

53

antitumor antibiotics- others

bleomycin, dactinomycin, mitomycin, mitoxantrone

54

anthracycline structure

tetracycline ring with a daunasamine sugar. quinone moieties that allow electron-accepting & donating functions

55

anthracyclines act as

intercalators

56

doxorubicin can also bind

iron and produce free radicals

57

is doxorubicin cell cycle specific?

no- active in all phases, most cytotoxic in S phase

58

barbituattes & dox

dox metabolism increased

59

CCBs & dox

additive cardiotoxicity

60

what is the most cardiotoxic drug?

doxorubicin

61

most intercalating antitumor antibiotics mediate their effects through

topo II inhibition

62

cummulative anthracycline dose associated with 48% risk

700mg/m^2

63

at what dose must therapy be stopped

500mg/m^2

64

semiquinone an hydroxyquionone are

free radicals

65

dexrazoxane

cardioprotective chelating agent. EDTA- derivative that can be given before dox to prevent iron-mediated free radical damage

66

liposomal products prolong

plasma concentration time and result in increased tumor concentration

67

dactinomycin MOA

intercalates between G-C. inhibits RNA polymerase & mRNA production

68

is dactinomycin and mitoxantrone vesicants?

yes

69

mitoxantrone structure

3 rings

70

mitroxantrone lacks the ability to

produce free radicals (less cardiotoxic)

71

mitomycin

bifunctional alkylating antitunor antibiotic. cell cycle non-specific

72

bleomycin can associate with

iron like dox & cause free radicals and DNA strand breaks

73

what is the most pulmonary toxic drug?

bleomycin

74

what drug has meolytic uremic syndrome?

mitomycin

75

what can be used to determine cardiotoxicity risk with dox?

BNP levels

76

is non-hodgkin;s lymphoma curable?

yes

77

aromatase converts

androgens to estrogens

78

where does most estrogen come from in premenopausal?

ovary

79

where does most estrogen come from in postmenopausal

adrenal glands

80

estrogen deprivation in premenopausal women

tamoxifen +/- ovariectomy

81

estrogen deprivation in postmenopausal women

aromatase inhibitors

82

SERMs

tamoxifen, toremifene

83

steroidal aromatase inhibitors

exemestane, testolactone

84

pure anti-estrogens

fulvestrant

85

Non-steroidl aromatase inhibitors

anastrazole, letrozole,

86

LHRH agonists

leuprolide, gpserelin, buserelin, and nafarelin

87

chronic administration of LHRH agonists leads to

receptor desensitization and their loss in the pituitary

88

LHRH agonists initially

make more LH and testosterone and then depletes it
"Tumor flares"

89

anti-androgens

flutamide, icalutamide, nilutamide, enzalutamide

90

what drug has a disulfiram-like reaction with alcohol?

nilutamide

91

LHRH MOA

bind to GnRH receptors & decrease LH & FSH production through receptor desensitization

92

corticosteroid MOA

induce marked lymphopenia & are cytotoxic to leukemic lymphoblasts by binding to glucocorticoid receptors in the nucleus

93

solu-medrol generic

methylprednisolone

94

DOC for pancreatic cancer

gemcetabine