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Heme and Lymph Midterm > Fitzy 3 and 4: Antimitotic and G/M phase drugs > Flashcards

Fitzy 3 and 4: Antimitotic and G/M phase drugs Flashcards

1
Q

What are the 2 classes of antimitotic drugs?

A

vina alkaloids

taxanes

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2
Q

3 members of vinca alkaloid family?

A

Vinblastine
Vincristine
Vinorelbine

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3
Q

2 members of the Taxanes family

A

Taxol and Taxotere

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4
Q

What do the Vinca alkaloids do?

A

inhibit tubulin polymerization

-block assembly of microtubules

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5
Q

What do the taxanes do?

A

Enhance tubulin polymerization

-stabilize microtubules

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6
Q

Therepeutic (TU) use of Vinblastine?

A

Testicular cancer, lymphomas, neuroblastoma

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7
Q

TU of Vincristine?

A

ALL, lymphoma, neuroblastoma, Wilms tumor, Ewings sarcoma

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8
Q

TU of vinorelbine

A

Advanced NSCL cancer

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9
Q

TU of Paclitaxel?

A

advanced breast and ovarian

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10
Q

Docetaxel

A

Advanced breast, ovarian recurrence

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11
Q

What are taxanes effective against?

A

solid tumors (this was in bold red soo watch out

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12
Q

Vinblastine toxicity

A

Bone marrow suppression; vesicant-blisters

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13
Q

Vincristine toxicity

A

NEurotoxitcity; peripheral neuropathy (these two bolded in red
-paralytic ileus; vesicant-blisters

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14
Q

Vinorelbine toxicity

A

Bone marrow suppression; vesicant-blisters

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15
Q

Paclitaxel toxicity

A

neutropenia; Thrombocytopenia; peripheral neuropathy; sever hypersensitivity during infusion- requires anti-histamine and coricosteroid pretreatment

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16
Q

Docetaxel toxicity

A

Neutropenia; peripheral neuropathy`

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17
Q

Antimitotic drugs MOA?

A

disruption of microtubule stability

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18
Q

Vinca Alkaloids MOA?

A

inhibit tubulin polymerization

  • they just stop what’s happening at the positive forming end of the microtubule
  • meanwhile, the negative end keeps fraying off
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19
Q

MOA of Taxanes?

A

bind to Btubulin at the forming end of microtubules…

  • the taxane-tubulin complexes migrate to the negative end… inhibit depolymerization
  • they stop the negative end from fraying off
  • enhances tubulin polymerization and stabilizes microtubules
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20
Q

So, since Vinca alkaloids and taxane drugs impair spindle integrity, what phase of the cell cycle do they act at?

A

the M phase!

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21
Q

What were the S phase antimetabolites again?

A 
5FU
Capecitabine
AraC
Gemcitabine
MTX and pemetrexed
Thiopurines- 6MP, 6TG
Cladribine, fludarabine
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22
Q

What are the M-Phase antimitotics again?

A

Taxanes: Paclitaxel and docetaxel

Vinca alkaloids: vinblastine, vincristine, vinorelbine

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23
Q

What do we replace vincristine with when it starts giving us neuropathy?

A

Vinblastine

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24
Q

What does treatment with these drugs lead to ?

A

Multi drug resistance

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25
Q

Why does MDR occur here?

A

due to incrased expression of P-glycoprotein and its enhanced extrusion of drugs from the tumor cell

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26
Q

How are the Vinca Alkaloids and taxanes administered?

A

IV

  • metabolized by liver,
  • so, impaired hepatic function warrants dose adjustment
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27
Q

What happens with ppl being treated for metastatic cancer 90% of the time when we use these drugs?

A

MDR :(

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28
Q

What does the p glycoprotein do exactly?

A

pumpes the drugs out of the cell

-efflux pump

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29
Q

What drugs are not prone to P-glycoprotein drug resistance?

A

drugs that work outside the cell

-monoclonal antibodies

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30
Q

What are the drugs that cause DNA strand breaks?

A

Topoisomerase inhibitors

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31
Q

What are the 2 classes of Topoisomerase inhibitors

A

Epipodophyllotoxins

camptothecins

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32
Q

Epipodophyllotoxins class members?

A

Etoposide and teniposide

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33
Q

Camptothecins class members?

A

Irinotecan and topotecan

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34
Q

Active metabolite of irinotecan?

A

SN38

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35
Q

What do the epipodophyllotoxins do?

A

Inhibit topoisomerase 2

-leads to DOUBLE strand breaks which is nice

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36
Q

What do the camptothecins do?

A

Inhibit topoisomerase 1

-causes DNA single strand breaks

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37
Q

TU of etoposide?

A

OAT cell carcinoma of lung; testicular cancer

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38
Q

TU of teniposide

A

glioma and neuroblastoma

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39
Q

TU of irinotecan

A

Metastatic colorectal cancer

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40
Q

TU of topotecan

A

2nd line various-failed prior 1st line (bolded in red)….

41
Q

Etoposide toxicity?

A

leukopenia; secondary cancer

42
Q

Teniposide toxicity?

A

leukopenia

43
Q

Irinotecan toxicity

A

Severe diarrhea; myelosuppression

44
Q

Topotecan toxicit

A

neutropenia; mucositis

45
Q

How are these topoisomerase inhibitors administered?

A

IV

46
Q

How is Etoposide and teniposide cleared?

A

CYP450 in liver

47
Q

how is irinotecan and topotecan cleared?

A

Renal clearance

48
Q

MOA of topoisomerase inhibitors?

A

Bind to DNA-enyme complex and created a persistently cleavable complex

49
Q

What phase of cell cycle do the TI 1 inhibitors work at?

A

S phase

50
Q

Cell cycle phase for TI 2 inhibitors?

A

mixed?

51
Q

What are the 2 classes of drugs that cause DNA strand breaks by intercalation of oxidative scission?

A

Antibiotics

Anthracyclines

52
Q

Antibiotics?

A
  • Bleomycin (bolded)

- Dactinomycin

53
Q

Anthracyclines?

A 
Doxorubicin
Daunorubicin
Epirubicin
Idarubicin
Mistoxantrone
54
Q

What does bleomycin do?

A

Fe mediated free radical generation

-dna strand breaks

55
Q

What does dactinomycin do?

A

DNA intercalation

56
Q

What does Doxo, dauno, epi, and idarubicin do?

A
  • inhibit TI2
  • DNA intrecalating
  • Free radical generation
  • DNA strand breaks
57
Q

What does Mitoxantrone do?

A

inhibit TI2

58
Q

TU of Bleomycin

A

testicular cancer

59
Q

TU of doxorubicin and epirubicin

A

wide spectrum-breast, ovarian, lung, thyroid, lymphoma, sarcoma

60
Q

TU of daunorubicin

A

Leukemia (AML, ALL)

61
Q

TU of Idarubicin

A

Leukemia (AML, ALL, CML in blast crisis)

62
Q

TU of MItoxantrone?

A

breast, prostate, non-hodgkin lymphoma

63
Q

Bleomycin toxicity (you better fucking get this one right)

A

Pulmonary fibrosis!!!!*****

64
Q

The “rubicin” toxicity

A

Cardiotoxicity, dilated cardiomyopathy, congestiv heart failure

65
Q

Mitoxantrone toxicity

A

Similar to rubicins

66
Q

Doxorubicin MOA?

A

intercalating agent
-it’s really flat, inserts into DNA… creates distortions
-inhihbits RNA synth and replication as well
it also make superoxides out of O2

67
Q

What does Bleomycin cause damage to?

A

skin and lung because those tissues do not have the enzyme required to metabolize bleomycin

68
Q

What bleomycin cause siginificant myelosuppression?

A

NO!

69
Q

What element does bleomycin use to make radicals?

A

Fe

70
Q

What does Bleomycin give us again as a nasty side effect?

A

fibrosis

71
Q

What toxicity does doxorubicin give us again?

A

dilated cardiomyopathy

72
Q

What phase of the cell cycle do the anthracyclines (doxorubicin) and bleomycin act?

A

G2 phase

73
Q

What do we want to keep in mind when choosing a chemotherapy regimen?

A

use drug combos that distribute toxicity among different organs

74
Q

What is the ABVD regimen for Hodgkin lymphoma?

A

Adriamycin (doxorubicin)
Bleomycin
Vinblastine
Dacarbazine

75
Q

What is the toxicities with each of the ABVD drugs?

A

Adriamycin (doxorubicin): dilated cardiomyopathy
Bleomycin: pulmonary fibrosis
Vinblastine: peripheral neuropathy
Dacarbazine: Nausea/vomiting and myelosuppression

76
Q

Activity, clearance, and toxicity of Doxorubicin (A)

A
  • DNA damage and intercalating agent
  • Hepatic metabolism
  • cardiomyopathy
77
Q

Activity, clearance, and toxicity of Bleomycin (B)

A
  • anti tumor antibiotic
  • renal
  • pulmonary fibrosis
78
Q

Activity, clearance, and toxicity of Vinblastine (V)

A
  • Antimitotic, destabilizes microtubules
  • CYP3A4/5 metabolism
  • Neuropathy
79
Q

Activity, clearance, and toxicity of Dacarbazine (D)

A
  • DNA damage alkylating agent
  • Hepatic metabolism
  • Marrow suppression
80
Q

What is the CHOP regimen used for?

A

Non-hodgkin lymphoma

81
Q

What is the CHOP regimen?

A
  • Cyclophosphamide
  • Hydroxydaunorubicin (Doxorubicin)
  • Oncovin (Vincristine)
  • Prednisone
82
Q

What are the toxicities of the CHOP regimen?

A

Cyclophosphamide: hemorrhagic cystitis
Hydroxydaunorubicin: cardiotoxicity
Oncovin: peripheral neuropathy
Prednisone: Hyperglycemia, osteopenia

83
Q

Activity, clearance, and toxicity of Cyclophosphamide?

A
  • alkylating agent
  • CYP3A4/5 CYP2D6 pro-drug
  • Acrolein…. leads to hemorrhagic cysts
84
Q

Activity, clearance, and toxicity of Doxorubicin (H)

A
  • DNA damage, intercalating agent
  • Hepatic metabolism
  • Cardiomyopathy
85
Q

Activity, clearance, and toxicity of Vincristine (O)

A
  • Anti-mitotic, destabilizes microtubules
  • CYP3A4/5
  • NEuropathy, constipation
86
Q

Activity, clearance, and toxicity of prednisone (P)

A
  • corticosteroid
  • 100% bioavailable
  • Hyperglycemia, osteopenia
87
Q

What does allopurinol and febuxostat do?

A

inhibit Xanthine oxidase

  • this way, Uric acid can’t be made and won’t build up
  • this is a treatment for gout
88
Q

What’s wrong with inhibiting XO?

A

XO metabolizes drugs use din cancer chemotherapy

-confers risk of overexposure and requirs dose adjustments

89
Q

What drugs are metabolized by XO tha will build up?

A
  • 6Mercaptopurine
  • Azathioprine
  • theophylline
90
Q

What happens when we kill a shit ton of cells using chemotherapy?

A

those cells release their contents into our body

-hyperuricemia, electrolyte complications

91
Q

How is acute nephrotoxicity produced by excessive uric acid managed?

A

administration of allopurinol, and xanthine oxidase inhibitor

92
Q

Where does all that uric acid come from anyways?

A

break down of purines from dead cells

93
Q

What all gets released when cells get killed like that?

A
  • K+
  • Phosphate: leads to hypocalcemia
  • Uric acid
94
Q

If we give a patient Allopurinol and 6-mercaptopurine, what will happen?

A

can result in excessive exposure to 6-MP because that is metabolized by XO which is being inhibited by Allopurinol
-just reduce the dose of 6-MP

95
Q

What does Pegloticase do?

A

turns uric acid into Allantoin

96
Q

What does chemotherapy make people do a lot?

A

throw up: nausea and vomiting

97
Q

How does chemotherapy induce nausea and vomiting?

A
  • direct activation of medullary CTZ

- Cell damage of the GI tract: 5HT3 receptors get activated on enterochromaffin cells

98
Q

What will we do to help with the nausea and vomiting?

A

give them a setron… 5-HT3 receptor antagonist

Heme and Lymph Midterm (11 decks)

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