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Pharm 8 > chemo drugs > Flashcards

chemo drugs Flashcards

1
Q

advantages of combination therapy

A
  • suppresses development of resistance
  • increased killing of cells
  • decreased toxicity
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2
Q

cyclophosphamide MOA and uses

A

alkylating agent; converted by CYP to phosphoramide mustard
alkylates N-7 guanine causing cross-linking and DNA strand breakage
use: NHL, breast ca, ovarian ca, neuroblastoma

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3
Q

cyclophosphamide ADR

A

hemorrhagic cystitis d/t acrolein

rare: SIADH, pulmonary toxicity

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4
Q

prevention of cyclophosphamide hemorrhagic cystitis

A

MESNA - a sulfhydryl donor that neutralizes acrolein

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5
Q

cisplatin MOA and uses

A

alkylating agent

use: testicular carcinoma, bladder ca, lung ca, ovarian ca

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6
Q

cisplatin ADR

A

nephrotoxicity, ototoxicity, peripheral neuritis, n/v (worst drug)

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7
Q

prevention of cisplatin nephrotoxicity

A

amifostine

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8
Q

carboplatin

A

alkylating like cisplatin but fewer ADRs

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9
Q

procarbazine MOA and use

A

alkylating agent, forms H2O2 causing DNA damage

use: Hodgkin’s disease

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10
Q

procarbazine ADR

A

disulfiram-like reaction, leukemia

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11
Q

thiotepa

A

alkylating agent used in ovarian ca

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12
Q

busulfan

A

alkylating agent used in CML; can cause pulmonary fibrosis

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13
Q

nitrosoureas

A

alkylating agents used in CSF and brain tumors d/t lipid solubility

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14
Q

carmustine

A

a nitrosourea (alkylating agent for CNS)

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15
Q

lomustine

A

a nitrosourea (alkylating agent for CNS)

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16
Q

streptozocin

A

alkylating agent used in insulin-secreting islet cell tumors

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17
Q

mechlorethamine

A

alkylating agent; a prodrug
used in Hodgkin’s disease
ADR: extravasation during IV infusion -> irritation

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18
Q

chlorambucil

A

alkylating agent
DOC for CLL
*least toxic of nitrogen mustards b/c slow acting

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19
Q

cell-cycle specificity of alkylating agents

A

nonspecific

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20
Q

mechanisms of resistance against alkylating agents

A
  • increased repair mechanisms
  • increased expression of Pgp and MDR (efflux) or decreased permeability
  • “trapping” by chemical production
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21
Q

cell-cycle specificity of anti-metabolites

A

S phase specific

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22
Q

methotrexate MOA

A

antimetabolite

folic acid analog inhibiting DHFR, preventing THF synthesis (dec thymidylate, purine, serine, methionine synthesis)

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23
Q

MTX resistance mechanisms

A
  • decreased transport into cell
  • altered DHFR
  • decreased polyglutamate formation
  • increased levels of DHFR
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24
Q

MTX ADR

A

BMS, mucositis, folic acid deficiency

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25
Q

how to correct MTX-induced folic acid deficiency

A

leucovorin

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26
Q

leucovorin uses and MOA

A

folinic acid analog used to prevent/correct MTX folic acid deficiency and to increase effect of 5-FU in low folate state (reduced folate required for 5-FU MOA)

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27
Q

6-MP MOA

A

antimetabolite activated by HGPRT -> toxic metabolites -> inhibit purine synthesis

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28
Q

thioguanine

A

antimetabolite activated by HGPRT -> toxic metabolites -> inhibit purine synthesis

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29
Q

resistance to 6-MP and thioguanine

A
  • decreased HGPRT

- increased alkaline phosphatase activity to inactivate drugs

30
Q

cytarabine MOA

A

antimetabolite: pyrimidine analog activated to AraCTP by kinases -> inhibit DNA polymerase
* most S-phase specific

31
Q

cytarabine ADR

A

neurotoxicity (cerebellar dysfunction, peripheral neuritis)

hand-foot syndrome

32
Q

hand-foot syndrome cause

A

leakage of chemo drugs from capillaries in high heat or friction areas (extremities) causes redness, tenderness, peeling, numbness/tingling

33
Q

5-FU MOA

A

antimetabolite converted to 5-FdUMP, competes with dUMP for thymidylate synthetase, preventing formation of dTMP for DNA synthesis and growth
“thymidineless death”

34
Q

5-FU resistance

A
  • decreased activation of 5-FU

- decreased thymidylate synthetase activity

35
Q

5-FU uses

A

metastases of breast ca, GI ca, hepatoma

carcinoma of ovary, cervix, bladder, prostate, pancreas, oropharynx, colon cancer (+ levamisole)

36
Q

5-FU ADR

A

nausea, mucositis, diarrhea, hand-foot syndrome, alopecia, hyperpigmentation neurologic deficits, BMS

37
Q

cell cycle specificity of vinca alkaloids

A

M phase specific

38
Q

vinca alkaloid MOA

A

prevent assembly of tubulin dimers into microtubules

39
Q

vinca alkaloid resistance

A

increased efflux (Pgp and MDR)

40
Q

vinca alkaloid ADRs

A

severe neurotoxicity: paresthesias, loss of reflexes, foot drop, ataxia

41
Q

vinblastine specific ADR

A

BMS, alopecia, anorexia, n/v/d

42
Q

vinblastine uses

A

Hodgkin’s disease, breast ca, testicular ca

43
Q

vincristine uses

A

childhood leukemias, childhood tumors (Hodgkin’s, Wilm’s, neuroblastoma)

44
Q

vincristine specific ADR

A

peripheral neuritis, paresthesias, weakness

*spares bone marrow

45
Q

cell cycle specificity of topoisomerase inhibitors

A

late S - early G2 specific

46
Q

uses of etoposide and teniposide

A

small cell lung ca, prostate ca, testicular ca

47
Q

etoposide and teniposide MOA

A

topoisomerase 2 inhibitors -> double strand DNA breaks

48
Q

topotecan and irinotecan MOA

A

topoisomerase 1 inhibitors -> prevents single strand break necessary in supercoiling -> DNA breakage

49
Q

paclitaxel and docetaxel MOA and ADR

A

taxanes: prevent microtubule disassembly
ADR: neutropenia, peripheral neuropathy

50
Q

cell cycle specificity of taxanes

A

M phase specific

51
Q

doxorubicin and daunorubicin MOA

A

anthracycline antibiotics: intercalate DNA, inhibit topo2, generate free radicals
block DNA and RNA synthesis and cause strand scission

52
Q

anthracycline ADR

A

cardiac toxicity d/t free radicals: acute (arrhythmia, ECG changes, pericarditis, myocarditis) and chronic (DCM, HF)
BMS, alopecia, radiation recall reaction

53
Q

dexrazoxane

A

inhibits Fe-mediated free radical generation

used to prevent cardiotoxicity from anthracyclines

54
Q

bleomycin MOA

A

G2 phase specific antibiotic
binds DNA and generates free radicals (DNA-bleomycin-Fe(II) -> chromosome aberrations, SSB, DSB) and inhibits DNA synthesis

55
Q

bleomycin use and ADR

A

use: Hodgkin’s disease; sclerosing agent for breast and ovarian cavitary lesions
ADR: pulmonary fibrosis

56
Q

L-asparaginase MOA

A

catalyzes deamination of asparagine into aspartic acid and ammonia, depriving tumor of nutrient
*asparagine required for growth and function of cells, but cancer cells have decreased level of asparagine synthetase

57
Q

L-asparaginase use and ADR

A

use: childhood ALL
ADR: acute pancreatitis

58
Q

imatinib

A

targets BCR-ABL in CML

competitive inhibitor of kinase activity

59
Q

interferon alpha-2a use

A

HCL, CML, AIDS-related Kaposi sarcoma

60
Q

interferon alpha-2b use

A

HCL, melanoma, AIDS-related Kaposi sarcoma, follicular lymphoma

61
Q

trastuzumab

A

anti-Her2 for breast cancer

ADR: cardiotoxicity

62
Q

cetuximab

A

used in colon and head/neck cancers

63
Q

panitumumab

A

used in colon cancer

64
Q

bevacizumab

A

used in colon, lung, brain cancer

ADR: HTN, GI bleeding or perforation, thromboembolic events

65
Q

erlotinib

A

for lung, pancreas ca

ADR: rash, diarrhea

66
Q

sunitinib/ sorafenib

A

for renal cell ca

ADR: rash, BMS

67
Q

lapatinib

A

used post-trastuzumab failure for breast ca

ADR: rash, diarrhea

68
Q

everolimus

A

used in renal cell ca metastases and with anti-estrogens in breast ca

69
Q

treatment of chemo-induced n/v

A

ondansetron (5HT3 antagonist)

70
Q

treatment of chemo-induced BMS

A

filgrastim and sargromastim

Pharm 8 (2 decks)

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