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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
Which phase does methotrexate affect?
S phase
26
What is methotrexates MOA?
DHFR inhibitor, affects de novo synthesis Cuz folate is required to build DNA/RNA, so it inhibits folate Inhibits TS when polyglutamated
27
What is mtx ADEs?
Myelosuppression, GI problems, teratogenic, PGMTX
28
What is PGMTX? What drug is it related to?
Mtx, the drug is poluglutamated at high doses, leading to increase in efficacy and ADEs
29
How does lecuovorin rescue affect Mtx neurotoxicity?
Does not reverse it
30
Explain leucovorin rescue
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
When should leucovorin be given?
Within 24-36 hours of starting HDMTX
32
What do topoisomerase enzymes do?
Reduce stress on DNA so that regions can be replicated, repaired, and/or transcribed
33
What is the MOA of Irinotecan?
Inhibits ability of DNA to replicate, repair, transcribe, by blocking TOPO 1
34
What is the ADEs of irinotecan?
DIARRHEA, myelosuppression
35
What are the Topo II inhibitors?
Etoposide, teniposide
36
What is Topo II inhibitors MOA?
Form complexes with Topo II and DNA to prevent resealing of the breakage
37
What phase do antitumor antibiotics work in?
G2 phase
38
What is the antitumor antibiotic G2 drug?
Bleomycin
39
What is bleomycins MOA?
Formation of iron complex that generates highly reactive free radical species on DNA, causing DNA breakage
40
What are the ADEs for bleomycin?
Pulmonary and skin toxicities
41
What are the two main M phase drug classes?
Vinca alkaloids and taxanes
42
What is the MOA of vinka alkaloids?
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
What is taxanes MOA?
Bind to beta tubulin to stabalize the microtubule so it does not pull apart Basically they superglue the cells together with the mictrotubules
44
What is the important fact to know about vinca alkaloids administration?
NEVER intrathecally, will cause imminent death
45
What is the vinka alkaloids metabolized by?
CYPs
46
What is the ADE for Vincristine?
CNS toxicity with vinCristine, also a vesicant
47
What is the ADEs for vinblastine?
Blood toxicity with vinBlastine, also a vesicant
48
What is paclitaxels ADEs?
Hypersensitivity, myelosuppression, myalgia, neuropathy
49
What are the nitrogen mustard drugs?
Bendamustine, cyclophosphamide
50
What are the nitrosoureas?
Carmustine, lomustine
51
What are the traizenes?
Dacarbazine, procarbazine
52
What is cyclophosphamides active metabolites?
Activated by CYP system | Phosphamide mustard and acreolein
53
What is the major ADE of cyclophosphamides?
Hemorrhagic cystitis
54
What is bendamustines MOA?
Alkylating agent that cross links DNA strands; inhibits mitotic checkpoints
55
What is the MOA of the nitrosoureas? Carmustine and Lomustine
Alkylating Agent
56
Which phrase is synonymous with "alkylating agent"?
Cross linking
57
What is the MOA of the triazenes? Dacarbazine and procarbazine
Methylates DNA and inhibits function/synthesis | Cross links DNA, flagging it for destruction
58
What is dacarbazine have an increased risk for? 2 things
Potent vesicant and increased risk of secondary cancer
59
What is unique about procarbazines active metabolites?
One is a weak MAO inhibitor
60
What are the platinum drugs?
Cisplatin, carboplatin, and oxaliplatin
61
What is the MOA of platinum drugs?
Specifics unknown, but same general concept as others. Flags DNA for destruction
62
What do patients taking cisplatin need to do while on this drug?
Aggressive hydration due to its nephrotoxicity
63
What is the ADE of carboplatin to know?
Myelosuppression
64
What is the ADE of Oxaliplatin?
Neurotoxicity triggered by cold exposure
65
Are tumors resistant to cis/carboplatin resistant to oxaliplatin?
NO
66
What are the four MOA of anthracycline?
Inhibits topo II Generates free radicals-GENERATES CARDIOTOXICITY Intercalate DNA After membrane fluidity and iron transport
67
What are the Anthracyclines?
Doxorubicin, Daunorubicin, mitoxantrone
68
What is the important ADE of Antracycline?
Cardiotoxicity
69
What is anthracyclines max lifetime dose?
450mg/m
70
What is unique about the two "D" anthracyclines color?
It is red. Can turn urine red
71
What color is mitoxantrone?
Blue, can cause blue discoloration
72
What color is Daunorubicin?
Red as well, red urine

Pharm 3 test 4 (5 decks)

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