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pcol350 final > Lui Lectures > Flashcards

Lui Lectures Flashcards

1
Q

cell cycle specific drugs

A

antimetabolites (S), vinca alkaloids(M), antibiotics, taxanes (M)
-for replicating (ex/ hematologic)

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2
Q

cell cycle non specific drugs

A

alkylating agents, antibodies, anthracyclines, antitumor antibioitcs, platinum analogs (“platin”)
replicating and non

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3
Q

log kill

A

constant fraction of cells, first order

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4
Q

may need irradiation of craniospinal axis or intrathecal drugs for

A

tumors finding sanctuaries in tissues, such as CNS

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5
Q

drugs combined at full doses

A

different toxicities, different sites of action and mechanisms

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6
Q

resistance minimized by

A

short term, intensive, intermittent therapy with drug combos

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7
Q

responsible for miltidrug resistance

A

p glycoprotein due to atp dependent pumping of drugs out of cell

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8
Q

neoplasms arising from chemo common in

A

alkylating agents

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9
Q

antimetabolite action

A

inh DNA synthesis

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10
Q

antibiotics action

A

damage or alter DNA and RNA structure

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11
Q

topoisomerase inh action

A

inhibit topoisomerase mediated religation of DNA breaks

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12
Q

alkylating agents action

A

damage or disrupt DNA and RNA structures

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13
Q

microtuble inhibitorsaction

A

disrupt mitosis

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14
Q

steroid hormones and antagonists action

A

interfere with transcription

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15
Q

monoclonal antibodies action

A

block function of targeted protein, alter function of cnacer cells and or induce cytotoxicity

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16
Q

biological response modifiers action

A

interfere with signal transduction pathways (IFN, IL)

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17
Q

tyrsine kinase inhibitors action

A

interfere with signal transduction pathways

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18
Q

proteosome inhibitors action

A

inhibit proteosome

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19
Q

angiogenesis inh action

A

disrupt tumor vasculature

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20
Q

differentiating agents action

A

allow leukemic promyelocytes to become neutropuls (all trans retinoic acid)

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21
Q

antimetabolite action

A

inh DNA synthesis; interfere with normal purine and purimidine nucleotide precursors and inhibit their synthesis and compete. S phase

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22
Q

differentiating agents action

A

allow leukemic promyelocytes to become neutropuls (all trans retinoic acid)

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23
Q

methotrexate

A

antimetabolite, related to folic acid (antagonist), inhbits dihydrofolate reductase and decreases biosynthesis of AGT and methionine and Serine
-low dose is anti inflam and immuno suppressive

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24
Q

only antimetabolite that doesn’t need conversion to become active

A

methotrexate

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25
Q

pemetrexed

A

methotrexate analog

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26
Q

antibiotics

A

doxorubicin, daunorubicin, dactinomycin, bleomycin

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27
Q

anthracycline antibiotics

A
  • doxorubicin (one of most widely used) and daunorubicin
  • used in drug combos
  • intercalate into DNA and block synthesis, generate oxygen radicals
  • cardio tox or heart failure possible
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28
Q

mixture of copper chelating glycopeptides that scize DNA oxidatively, G2

A

bleomycin

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29
Q

cardiac tox or heart failure

A

doxorubicin and daunorubicin

30
Q

pulmonary toxicity (fibrosis)

A

bleomycin

31
Q

etoposide/teniposide

A

topoisomerase inh, complex with DNA, prevent re ligation

32
Q

alkylating agents action

A

damage or disrupt DNA and RNA structures- covalent alkylation, lethal, cell cycle non specific

33
Q

microtuble inhibitors action

A

disrupt mitosis through mitotic spindle

34
Q

etoposide/teniposide

A

topoisomerase inh, complex with DNA, prevent re ligation

35
Q

can lead to secondary malignancy- mutagenic and carcinogenic

A

alkylating agents

36
Q

mechlorethamine

A

nitrogen gas in war, causes lymphocytopenia, alkylating agent, slow

37
Q

cyclophosphamide

A

most common alkylating agent, biotransformed to active compound which alkylates DNA

38
Q

alkylating agent used to treat brain cancer (cross BBB)

A

nitrosureas, temozolomide

39
Q

alkylating agents that crosslink DNA

A

cisplatin and carboplatin

40
Q

responsible for multidrug resistance

A

p glycoprotein due to atp dependent pumping of drugs out of cell

41
Q

monoclonal antibodies action

A

block function of targeted protein, alter function of cancer cells and or induce cytotoxicity

42
Q

alkylating agents that crosslink DNA

A

cisplatin and carboplatin

43
Q

vinca alkaloids

A

block mitosis in metaphase, bind tubulin (GTP dependent),

44
Q

taxanes

A

promote polymerization and stabilization of polymer rather than disassembly- favor formation of microtubulin, chromosome separation doesn’t occur
-paclitaxel, docetaxel

45
Q

taxanes

A

promote polymerization and stabilization of polymer rather than disassembly- favor formation of microtubulin, chromosome separation doesn’t occur
-paclitaxel, docetaxel

46
Q

tamoxifen

A

prevents estrogen stimulation of breast cancer cells, estrogen antagonist
-toremifene similar

47
Q

fulvestrant

A

destroys estrogen receptors

48
Q

prednisone

A

synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid.

  • for lymphoma and acute lymphocytic leukemia
  • inhibit leukocytes, antibodies, inflam and lymp stuff
49
Q

prednisone

A

synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid.

  • for lymphoma and acute lymphocytic leukemia
  • inhibit leukocytes, antibodies, inflam and lymp stuff
50
Q

prednisone

A

synthetic, potent, anti inflam, corticosteroid with less mineralcorticoid.

  • for lymphoma and acute lymphocytic leukemia
  • inhibit leukocytes, antibodies, inflam and lymp stuff
51
Q

biological therapy

A

uses human defense system, stimulate immune system for destruction of malignant cells, may risk autoimmune and other tox due to specificity
-cytokines, monoclonal antibodies, vaccines

52
Q

muro

A

murine antibodies

53
Q

zu

A

humanized antibodies

54
Q

xi

A

chimeric antibodies

55
Q

informers; ID malignancies by CDC (complement cytotoxicity) and ADCC (antibody dependent cell mediated cytotoxicity), block selected growth factors

A

monoclonal antibodies

56
Q

used as biological missiles to carry radio pharmaceutical or biological toxin to cancer cells

A

monoclonal antibodies

57
Q

targets extracellular hEGF (human epidermal growth factor) receptor protein 2 (HER2)

A

trastuzumab

58
Q

anti epidermal growth factor targetted anti-EGFR, used for 1st line metastatic colorectal cancer, head and neck cancer

A

cetuximab

59
Q

agonist against CD20

A

rituximab/ofatumumab

60
Q

anti vascular endothelial growth factor (VEGF); anti angiogenesis, 1st line metastatic colorectal cancer

A

bevacizumab

61
Q

anti vascular endothelial growth factor (VEGF); anti angiogenesis, 1st line metastatic colorectal cancer

A

bevacizumab

62
Q

biological response modifiers

A

IL2 (produced by T, growth factor, can be single agent or combo) and IFN (modulate immune responses, cell mediated cytotox, regulate differentiation and expression, *have antiviral activity
-both for many malignancies

63
Q

“tinib”

A

tyrosine kinase inhibitors

64
Q

imantinib

A

tyrosine kinase inhibitor

  • signal transduction inhibitor
  • targets *BCR-ABL (mutations in this lead to resistance)
65
Q

geftinib

A

tyrosine kinase inhibitor

  • EGFR inh; inhibits ATP binding
  • low response rate
66
Q

oral VEGF receptor 2 tyrosine kinase inhibitors

A

sunitinib, sorafenib

67
Q

proteosome inhibitor that permits cell death in neaplastic cells

A

bortezomib

68
Q

VEGF

A

best studied pro angiogenic factor; elevated elvels=prognosis and increased risk of metastasis

69
Q

bevacizumab, vandetanib, thalidomide, lenalidomide

A

disrupt tumor vasculature associated with VEGF

70
Q

all trans retinoic acid (ATRA, tretinoin)

A

drives leukemic promyelocytes to be mature neutrophils for APL treatment

pcol350 final (3 decks)

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