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Pharm 3 test 4 > Antineoplastic > Flashcards

Antineoplastic Flashcards

1
Q

List the major events happening in the cell cycle

A

G1-Cellular contents are copied-except chromosomes
S-DNA replication, chromosome duplication
G2-Grows, prepares for mitosis, checks for errors
M- Cells divide

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2
Q

Which phase is really good at proofreading and flagging cells for destruction?

A

G2

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3
Q

What are the three main ADE for chemotherapy for non targeted therapies?

A

Myelosuppression
Thrombocytopenia?
AND?

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4
Q

What phase does L-asparaginase work?

A

G1

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5
Q

What is L-asparaginases MOA?

A

deprives malignant cells of aspargine, leading to cell death

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6
Q

What cancers are L-asparaginase used in?

A

Lymphomas and leukemias

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7
Q

What is L-Asparaginases ADEs?

A

Hypersensitivity reactions common, clotting abnormalities, hyperglycemia, hypertryglyceridemia, immune suppression

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8
Q

What is the benefit of using pegaspargase? (thats L-asparaginase with a polyethylene tag

A

It causes less hypersensitivity

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9
Q

What are the S phase drugs?

A

Purine-6-mercaptopurine
Pyrimidine-5-FU, capecitabine, cytarabine, gemcitabine
Folate antagonists-Methotrexate, pemetrexed

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10
Q

What is the purine analog 6-mecaptopurines MOA?

A

Basically sneaks into the DNA synthesis because its similar to guanine, where it induces strand breaks and base mispairing. This makes it easy for the body to flag and destroy. So it inhibits de novo DNA synthesis

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11
Q

How is 6-mecaptopurine metabolized?

A

It uses the xanthine oxidase pathway for metabolism

But it must be metabolized by HGPRT to be active

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12
Q

What is 6-mecaptopurines ADEs?

A

(Mylosuppression (Bone marrow toxicity), hepatotoxic

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13
Q

What is the S phase pyrimidine, cytarabines, MOA?

A

Incorporates into DNA, inhibits DNA polymerase

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14
Q

What is cytarabines ADEs?

A

Myelosuppression, GI issues, hepatic enzyme elevation, pulmonary infiltrates

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15
Q

What is the single most effective agent in AML?

A

Cytarabine (NO ACTIVITY in solid tumors)

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16
Q

What is gemcitabines MOA?

A

Inhibits ribonucleotide reductase, inhibition of DNA polymerase, incorporated into DNA and causes it to be flagged

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17
Q

What is gemcitabines ADEs?

A

Myelosuppression, N/V, flu like symptoms

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18
Q

Can gemcitabine be used in solid tumors?

A

Yep

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19
Q

What is the MOA of 5-FU?

A

Generates FdUMP, decreases Thymidylate synthase
Generates FUTP. interferes with RNA
Generation pf FdUTP, inhibits DNA

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20
Q

What is important to know about 5-FUs phatmacokinetics?

A

It has to be activated

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21
Q

What is the other S phase Pyrimidine drug?

A

Capecitabine

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22
Q

What is the MOA of Capecitabine?

A

Prodrug of 5-FU

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23
Q

What is important to know about capectibatine?

A

It is well absorbed orally, which 5-FU is not

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24
Q

What is the MOA of folate?

A

I guess it just helps us, or the body, recognize which cells are using too much folate? Not sure on this

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25
Q

Which phase does methotrexate affect?

A

S phase

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26
Q

What is methotrexates MOA?

A

DHFR inhibitor, affects de novo synthesis
Cuz folate is required to build DNA/RNA, so it inhibits folate
Inhibits TS when polyglutamated

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27
Q

What is mtx ADEs?

A

Myelosuppression, GI problems, teratogenic, PGMTX

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28
Q

What is PGMTX? What drug is it related to?

A

Mtx, the drug is poluglutamated at high doses, leading to increase in efficacy and ADEs

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29
Q

How does lecuovorin rescue affect Mtx neurotoxicity?

A

Does not reverse it

30
Q

Explain leucovorin rescue

A

Because Mtx is unselective, it will damage normal cells. Leucovorin will come in and resuce the healthy cells because it somehow has a higher affinity for them, and it provides them with folate to continue doing its thing. It can only resuce healthy cells, not lethally damaged cells

31
Q

When should leucovorin be given?

A

Within 24-36 hours of starting HDMTX

32
Q

What do topoisomerase enzymes do?

A

Reduce stress on DNA so that regions can be replicated, repaired, and/or transcribed

33
Q

What is the MOA of Irinotecan?

A

Inhibits ability of DNA to replicate, repair, transcribe, by blocking TOPO 1

34
Q

What is the ADEs of irinotecan?

A

DIARRHEA, myelosuppression

35
Q

What are the Topo II inhibitors?

A

Etoposide, teniposide

36
Q

What is Topo II inhibitors MOA?

A

Form complexes with Topo II and DNA to prevent resealing of the breakage

37
Q

What phase do antitumor antibiotics work in?

A

G2 phase

38
Q

What is the antitumor antibiotic G2 drug?

A

Bleomycin

39
Q

What is bleomycins MOA?

A

Formation of iron complex that generates highly reactive free radical species on DNA, causing DNA breakage

40
Q

What are the ADEs for bleomycin?

A

Pulmonary and skin toxicities

41
Q

What are the two main M phase drug classes?

A

Vinca alkaloids and taxanes

42
Q

What is the MOA of vinka alkaloids?

A

Bind to beta tubulin in microtubules, inhibits polymerization into tubules
Basically microtubules dont form, causing the cells not to be able to pull apart

43
Q

What is taxanes MOA?

A

Bind to beta tubulin to stabalize the microtubule so it does not pull apart
Basically they superglue the cells together with the mictrotubules

44
Q

What is the important fact to know about vinca alkaloids administration?

A

NEVER intrathecally, will cause imminent death

45
Q

What is the vinka alkaloids metabolized by?

A

CYPs

46
Q

What is the ADE for Vincristine?

A

CNS toxicity with vinCristine, also a vesicant

47
Q

What is the ADEs for vinblastine?

A

Blood toxicity with vinBlastine, also a vesicant

48
Q

What is paclitaxels ADEs?

A

Hypersensitivity, myelosuppression, myalgia, neuropathy

49
Q

What are the nitrogen mustard drugs?

A

Bendamustine, cyclophosphamide

50
Q

What are the nitrosoureas?

A

Carmustine, lomustine

51
Q

What are the traizenes?

A

Dacarbazine, procarbazine

52
Q

What is cyclophosphamides active metabolites?

A

Activated by CYP system

Phosphamide mustard and acreolein

53
Q

What is the major ADE of cyclophosphamides?

A

Hemorrhagic cystitis

54
Q

What is bendamustines MOA?

A

Alkylating agent that cross links DNA strands; inhibits mitotic checkpoints

55
Q

What is the MOA of the nitrosoureas? Carmustine and Lomustine

A

Alkylating Agent

56
Q

Which phrase is synonymous with “alkylating agent”?

A

Cross linking

57
Q

What is the MOA of the triazenes? Dacarbazine and procarbazine

A

Methylates DNA and inhibits function/synthesis

Cross links DNA, flagging it for destruction

58
Q

What is dacarbazine have an increased risk for? 2 things

A

Potent vesicant and increased risk of secondary cancer

59
Q

What is unique about procarbazines active metabolites?

A

One is a weak MAO inhibitor

60
Q

What are the platinum drugs?

A

Cisplatin, carboplatin, and oxaliplatin

61
Q

What is the MOA of platinum drugs?

A

Specifics unknown, but same general concept as others. Flags DNA for destruction

62
Q

What do patients taking cisplatin need to do while on this drug?

A

Aggressive hydration due to its nephrotoxicity

63
Q

What is the ADE of carboplatin to know?

A

Myelosuppression

64
Q

What is the ADE of Oxaliplatin?

A

Neurotoxicity triggered by cold exposure

65
Q

Are tumors resistant to cis/carboplatin resistant to oxaliplatin?

A

NO

66
Q

What are the four MOA of anthracycline?

A

Inhibits topo II
Generates free radicals-GENERATES CARDIOTOXICITY
Intercalate DNA
After membrane fluidity and iron transport

67
Q

What are the Anthracyclines?

A

Doxorubicin, Daunorubicin, mitoxantrone

68
Q

What is the important ADE of Antracycline?

A

Cardiotoxicity

69
Q

What is anthracyclines max lifetime dose?

A

450mg/m

70
Q

What is unique about the two “D” anthracyclines color?

A

It is red. Can turn urine red

71
Q

What color is mitoxantrone?

A

Blue, can cause blue discoloration

72
Q

What color is Daunorubicin?

A

Red as well, red urine

Pharm 3 test 4 (5 decks)

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