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Oncology > Antineoplastics Natural Products > Flashcards

Antineoplastics Natural Products Flashcards

1
Q

What are your Microtubule-damaging agents(microtubule inhibitors)?

A

Vinca alkaloids and Taxanes, Estramustine, Epothilones

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1
Q

Vinca Alkaloids?

A

Vinblastine, Vincristine, Virnorelbine, Eribulin

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2
Q

Taxanes?

A

Paclitaxel, Docetaxel

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3
Q

Camptothecin Analogues

A

Topetecan, Irinotecan

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4
Q

Epipodophyllotoxins

A

Etoposide, Teniposide

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5
Q

Nature-derived?

A

L-Asparaginase, Hydroxyurea, Retinoids, Arsenic Trioxide, Mitotane

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6
Q

Plant derived drugs?

A

Microtubule damaging agents, Camptothecins, epipdophyllotoxins

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7
Q

In the M phase?

A

cell growth and protein production stops
Division of two daughter cells (chromosome seperation)

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8
Q

What do mitotic inhibitors do?

A

interfere with assembly and disassembly of tubulin into microtubule polymers-> inhibits mitosis->Apoptosis

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9
Q

Which drug class disrupts microtubule polymerization?

A

Vinca alkaloids

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10
Q

Which drug class stabilizes microtubule formation (inhibiting microtubule de-polymerization)

A

Taxanes

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11
Q

Vinca Alkaloids work in which phase of cell cycle?

A

Cell cycle specific for M Phase

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12
Q

Vinca Alkaloids MOA?

A

binds to B-tubulin and blocks polymerization with a-tubulin into microtubules–> prevents mitotic spindle formation –>interrupts chromosome aligning and cell division arrests–>apoptosis

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13
Q

Where are microtubules highest at?

A

The Brain

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14
Q

AE of Vinca alkaloids?

A

Neurotoxicity
Constipation

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15
Q

Increased Pgp?

A

Cancer drug resistance

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16
Q

PgP (P-glycoprotein) known as?

A

MDR1, ABCB1, CD243
-ATP dependent efflux pump: provides cellular defense mechanism against potentially harmful substances

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17
Q

Vinca alkaloids are metabolized?

A

Hepatically
Reduce dose in hepatic dysfunction or elevated billirubin

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18
Q

Vinblastine is part of curative treatment for?

A

Hodgkin disease

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19
Q

Curative treatment for metastatic testicular cancer?

A

Vinblastine with Bleomycin and Cisplatin

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20
Q

For childhood leukemia?

A

Vincristine with glucocorticoids (better tolerated in kids)

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21
Q

What is the CHOP regimen?

A

Cyclophosphamide, Hydroxyrubocin, Oncovin, Prednisolone
-Used in Non-Hodgkin lymphoma

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22
Q

For Wilms tumor, Neuroblatoma, Rhabdomyosarcoma?

A

Vincristine -standard for leukemis and lymphomas especially in pediatrics

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23
Q

Vincristine and Neuro?

A

mostly neurological manifestations that can be reversed once stopped, reduced, or suspended

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24
Q

Vinorelbine AE

A

Granulocytopenia
less neurotoxicity

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25
Q

Eribulin is a poor substrate of _____ and is effective in?

A

Pgp efflux pump and effective in drug resistant tumors that overexpress Pgp

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26
Q

Eribulin used in?

A

drug resistant metastatic breast cancer and liposarcoma

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27
Q

Taxanes MOA?

A

bind to a different site on B-tubulin and promote microtubule formation—>stabalizes tubulin-GDP

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28
Q

Paclitaxel MOA?

A

binds to B-tubulin subunit on the inner surface of microtubules and antagonizes their disassembly–>bundles of microtubules appear–>arrest in mitosis–>cell death

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29
Q

Drugs that block cell-cycle progression prior to Mitosis _____ the toxic effects of taxanes

A

antagonize
(Like Cisplatin given before)

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30
Q

Increased membrane bound efflux proteins such as MRP1 and Pgp

A

decrease cellular drug accumulation

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31
Q

Cabazitaxel is a

A

poor substrate for Pgp—->useful for treating multidrug resistant tumors like hormone refractory metastatic prostate cancer previously treated with docetaxel

32
Q

Resistance: increase in a-aurora kinase

A

promotes completion of mitosis

33
Q

upregulation of BIII-isoform of tubulin lacks

A

taxane binding capacity or direct alteration of the drug target by mutation

34
Q

Antiapoptotic factor (increases surviving) thus _____

A

downregulates taxanes

35
Q

Paclitaxel clearance is delayed by drugs that ____

A

inhibit Pgp (cyclosporine A)

36
Q

Taxanes use in cancers?

A

metastatic ovarian, breast, lung, GI, Genitourinary, and head and neck cancers

37
Q

Paclitaxel exerts its toxic effects where?

A

Bone marrow

38
Q

Taxanes AE?

A

Neutropenia (Docetaxel), peripheral neuropathy, hypersensitivity reactions

39
Q

Etramustine MOA

A

Binds to B tubulin and microtubule proteins causing dissasembly and antimitotic actions

40
Q

Estramustine use?

A

Metastatic advanced hormone refractory prostate cancer

41
Q

Estramustine active drug form accumulates where?

A

prostate

42
Q

Estramustine _____the clearance of taxanes

A

inhibits

43
Q

Epothilones MOA

A

bind to a B tubulin site distinct from taxanes__>trigger microtubule nucleation —>dysfunctional microtubule stabilization—>cell-cycle arrest at G2-M interface and apoptosis

44
Q

Cremophor what to give before?

A

premedicate with H1 and H2 antagonists

45
Q

Camptothecin targets?

A

Nuclear enzyme topoisomerase I by inhibiting

46
Q

what are Camptothecins?

A

Irinotecan and topotecan

47
Q

Irnotecan is a _____

A

Prodrug

48
Q

DNA topoisomerases do what?

A

reduce torsional stress in supercoiled DNA
-allowing to untagle to replicate, repair and transcribe

49
Q

Camptothecins are cell cycle specific where?

A

S-phase

50
Q

low-dose protracted camptothecins

A

have less toxicity and greater antitumor activity than short courses

51
Q

Toptecan is a substrate for?

A

Pgp but poor substrate

52
Q

ABCG2/BCRP overexpression in cancer makes it

A

resistant to irinotecan

53
Q

Irinotecan –>_____—–>

A

converted by carboxylesterase to active metabolite SN-38

54
Q

if you have decreased carboxylesterase activity then you have ____ to Irinotecan

A

resistance

55
Q

what organs have sufficient carboxylesterase activity?

A

liver and red blood cells

56
Q

Topotecan not for

A

Renal impairment

57
Q

Irinotecan SN38G is a

A

Inactive metabolite by glucuronidated UGT1A1

58
Q

SN38G Inversely correlates with risk of

A

diarrhea

59
Q

Irinotecan use first line?

A

advanced colorectal cancer

60
Q

Bacterial glucuronidase contributes to GI toxicity by

A

releasing unconjugated SN38

61
Q

What are Epipdophylltoxins

A

Etoposide and Teniposide

62
Q

Etoposide and Teniposide MOA?

A

form ternary complexes with topoisomerase II and DNA–>prevents resealing of break –>accumulation of DNA breaks leads to cell death

63
Q

Which cell cycle are most sensitive to Etopside and teniposide?

A

S and G2 phase

64
Q

Resistance to Etoposide and Teniposide occur when?

A

Mutations of p53
Mutation or decreased topoisomerase II
Amplification of MDR1 gene –>Pgp drug efflux

65
Q

Curative therapy for testicular cancer?

A

bleomycin and cisplatin

66
Q

pts with decreased albumin in etoposide and Teniposide have

A

greater risk of toxicity

67
Q

AE of Teniposide and Etoposide?

A

development of unusual form of acute nonlymphocytic leukemia

68
Q

Monocytic leukemia in infants?

A

Teniposide

69
Q

L-ASP MOA?

A

catalyzes hydrolysis of asparagine to aspartic acid and ammonia–>depriving malignant cells of asparagine—>cell death

70
Q

L-ASP 1st line treatment for?

A

ALL (Acute lymphocytci leukemia)

71
Q

L-ASP AE?

A

Hypersensitivity reactions
lowers serum albumin
terminates antitumor activity of MTX

72
Q

Hydroxyurea normal levels?

A

30-200

73
Q

Hydroxyurea MOA?

A

inhibits ribonucleotide reductase

74
Q

Hydroxyurea is specific to which cell cycle?

A

S phase

75
Q

Hyrdoxyurea produces arrest at G1/S phase which

A

prevents cells from leaving and radiosensitizing activity by maintaining cells in radiation sensitive G1 phase and interfering with DNA repair

76
Q

Hydroxyurea BBW

A

not to be used in women of childbearing potential

77
Q

hydroxyurea aka

A

radiosensitizer –>used for CML

Oncology (10 decks)

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