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Chemotherapy Viruses > Chemotherapy III > Flashcards

Chemotherapy III Flashcards

1
Q

Class of Doxorubicin

A

Anthracycline Antitumor antibiotic

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2
Q

Cycle specificity of Doxorubicin

A

CCNS

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3
Q

Macromolecular target of Doxorubicin

A

DNA

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4
Q

MOA of Doxorubicin

A

Intercalation between base pairs of DNA leading to strand breaks due to inhibition of topoisomerase II

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5
Q

Topoisomerase II inhibiting drugs that are intercalators

A

Daunomycin
Doxorubicin
Mitoxanthrone
Dactinomycin

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6
Q

Topoisomerase II inhibiting drugs that are non-intercalators

A

Etoposide

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7
Q

Tomoisomerase I inhibiting drugs

A

Topotecan

Irinotecan

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8
Q

Role of topoisomerase I

A

Single strand DNA breaks, relaxation of the strand and re-anneal the strands
Inhibiting agents arrest in the replication fork

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9
Q

Role of topoisomerase II

A

Double strand breaks in the DNA, relaxation and re-anneal the strands of DNA
Inhibiting agents inhibit chromosome replication

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10
Q

Metabolism of Doxorubicin

A

Liver

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11
Q

Excretion of Doxorubicin

A

Excreted as a thiol adduct into the bile

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12
Q

Define multidrug resistance

A

Intercalting and non-intercalating topoisomerase II inhibitors and the tubulin inhibitors (vinca alkaloids) are all cross resistant due to the P-glycoprotein membrane bound efflux pump
Exports big bulky hydrophobic groups

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13
Q

How is the glycoprotein downregulated (reverse resistance)

A

Giving drug as continuous infusion

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14
Q

What drugs may block the efflux pump and reverse resistance

A

Quinine
Verapamil
Cyclosporine

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15
Q

SEs of Doxorubicin

A

Nausea and vomiting
Hair loss
Stomatitis
Myelosuppression (dose limiting toxicity)
Cardiac toxicity- congestive cardiomyopathy (cumulative and schedule dependent )
Vesicant

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16
Q

Dose limiting SE of Doxorubicin

A

Myelosuppression

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17
Q

What tests must be done before administration of Doxorubicin

A 
Determine EF (ECHO or MUGA scan)
Bilirubin level
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18
Q

Dose reduction for Doxorubicin

A

Presence of jaundice

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19
Q

How can cardiac toxicity of Doxorubicin be avoided

A

-Lifetime dose lower than 400mg/M^2
-Longer length of infusion (96 hours) of the dose of the drug
-Pretreatment with an iron chelator may be helpful- dexrazoxane
Prevent cumulative toxicity and schedule dependent toxicity

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20
Q

How can we describe the cardiac toxicity of doxorubicin

A

Cumulative toxicity

Schedule dependent toxicity

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21
Q

Which drug is red?

A

Doxorubicin (good for screening patients for prior treatment)

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22
Q

Schedule dependence of Doxorubicin

A

Schedule dependent cardiac toxicity

Schedule independent cytotoxicity

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23
Q

Presumed mechanism of Doxorubicin cardiac toxicity

A

Free radical damage due to high plasma concentrations
Due to complexes of iron with Doxorubicin

DIFFERENT THAN MOA OF CYTOTOXICITY

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24
Q

Cardiopreotective agent for patients taking Doxorubicin

A

Dexazoxane (iron chelator)

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25
Q

Contraindications of Doxorubicin

A

Prior mediastinal irradiation and long standing uncontrolled HTN (increased risk of cardiotoxicity)

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26
Q

Uses of Doxorubicin

A

Breast cancer
Leukemia
Sarcoma
Hodgkin’s and non Hodgkin’s lymphomas

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27
Q

Compounds in the anthracycline antibiotic class

A 
Doxorubicin
Daunomycin
Idarubicin
Epirubicin
Mitoxantrone
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28
Q

Differences between Daunomycin and Doxorubicin

A

Less cardiac toxic

Less effective against solid tumors

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29
Q

Use of Daunomycin

A

Treatment of some leukemias

NOT solid tumrs

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30
Q

Use of Idarubicin and epirubicin

A

Exclusively leukemia

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31
Q

SEs of all anthracycline antibiotics

A

Dose limiting myelosuppression

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32
Q

Class of Irinotecan

A

Camptothecin
Topoisomerase I inhibitor
Plant alkaloid

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33
Q

Macromolecular target of Irinotecan

A

DNA

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34
Q

Cycle specificity of Irinotecan

A

CCNS

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35
Q

Bioactivation of Irinotecan

A

Prodrug

Converted by carboxylesterase to 7-ethyl-10-hydroxycamptothecin (SN-38)

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36
Q

MOA of Irinotecan

A

Topoisomerase I inhibition leading to single strand breaks in the DNA

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37
Q

Metabolism of Irinotecan

A

Hepatic metabolism

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38
Q

Dose reduction of Irinotecan

A

Jaundice

39
Q

Metbolism of Irinotecan

A

UGTIAI is responsible for clearance by glucuronidation of drug and bilirubin

40
Q

Gilbert’s Syndrome and Irinotecan use

A

Gilbert’s syndrome: genetic polymorphism (7/7 genotype) in the UGT1A1 promoter (UGT1A1*28) results in enzyme underexpression and decreased bilirubin and irinotecan metabolism
Decreased glucoronidation
No guidelines of what to do however

41
Q

SEs of Irinotecan

A 
Nausea
Vomiting
Myelosupression (dose limiting)
Stomatitis 
Hair loss 
Early cholinergic diarrhea
Late secretory diarrhea (7-10 days later)
Death
42
Q

Treatment of cholinergic diarrhea from Irinotecan

A

Atropine (pre-medicate)

43
Q

Treatment of secretory diarrhea from Irinotecan

A

Imodium

44
Q

Uses of Irinotecan

A

GI tract malignancies (Colon cancer)

45
Q

Use of Topotecan

A

Ovarian cancer patients who have become resistant to carboplatin and paclitaxel

46
Q

Class of Bleomycin

A

Antitumor antibiotic

47
Q

Cycle specificity of Bleomycin

A

CCS (G2-M phase)

48
Q

Macromolecular target of Bleomycin

A

DNA

49
Q

MOA of Bleomycin

A

Binds to DNA, free radical production leading to single and double strand DNA breaks

50
Q

Active species of Bleomycin

A

Bleomycin- iron form

51
Q

Excretion of Bleomycin

A

50% in urine

52
Q

Inactivation of Bleomycin

A

Liver and kidneys rapidly inactivate the drug via bleomycin hydrolase
Lung and skin have low levels of bleomycin hydrolase= toxicities

53
Q

SEs of Bleomycin

A

Pulmonary toxicity is dose limiting - cumulative toxicity (dec. in pulmonary diffusion capacity)
Hyperpigmented skin- hyperkeratosis of the palms
Stomatitis and hair loss
NOT myelosuppressive
Anaphylactoid reactions (following first dose in lymphoma)
Fever and chills are common

54
Q

Dose limiting toxicity of Bleomycin

A

Pulmonary toxicity

55
Q

Dosing of Bleomycin

A

30 units per dose X ~13 doses

No more than 400 units total dose

56
Q

Testing before use of Bleomycin

A

Test dose to monitor for severe reactions

Test pulmonary function

57
Q

Monitoring of Bleomycin

A

Diffusion capacity of carbon monoxide- PFTs

58
Q

Routes of administration of Bleomycin

A

IV, IM, subcutaneous, intracavitary (pleural space for palliation of a pleural effusion)

59
Q

Caution of O2 administration in patients treated with Bleomycin

A

If given high inspired oxygen concentrations, these is a risk of pulmonary damage and death (ARDS)
Give lowest FiO2 to maintain O2 saturation >90%

60
Q

Dose reduction of Bleomycin

A

Renal insufficiency

61
Q

Uses of Bleomycin

A 
Testicular cancer (30 units IV weekly for 12 weeks)
Hodgkin's disease
62
Q

What is the BEP regimen for testicular cancer

A

Bleomycin, etoposide, cisplatin

63
Q

Drug class of Prednisone

A

Steroid

64
Q

Macromolecular target of Prednisone

A

Steroid receptor

65
Q

SEs of Prednisone

A 
Euphoria
Weight gain
Increased appetitite
Mania
Hypertension
Sodium and fluid retention
Aggrevation of diabetes
Hypokalemia
Alteration of the sleep-wake cycle
Peptic ulceration of the stomach
Spontaneous colon performation
Cataracts
Osteoporosis
Cushingoid appearance
Suppression of the pituitary adrenal axis
66
Q

Use of Prednisone

A

100 mg/ day or more
Hodgkin’s disease and non-Hodgkin’s lymphoma
Multiple myeloma
Some leukemias

67
Q

Use of dexamethasone

A

Reduce cerebral edema in patients with brain metastases

Potentiates effect of 5HT3 receptor antagonists (ondansetron)- used to control emesis and nausea

68
Q

Class of Tamoxifen

A

SERM

69
Q

Macromolecular target of Tamoxifen

A

Estrogen receptor

70
Q

Bioactivation of Tamoxifen

A

Prodrug and is metabolized in the liver to 4-hydroxytamoxifen

71
Q

MOA of Tamoxifen

A

Ant of breast cancer ER

Agonist of endometrial and bone ER

72
Q

Metabolism of Tamoxifen

A

Metabolized by the liver

73
Q

SEs of Tamoxifen

A 
Weight gain
Hot flashes
Endometrial cancer
Thrombosis
*Dec. bone loss
74
Q

Use of Tamoxifen

A 
Breast cancer (20 mg daily)
Chemoprevention of breast cancer (5 years) - can develop ER - breast CA
75
Q

Use of Raloxifene

A

Breast cancer chemoprevention

76
Q

Class of Anastrozole

A

Selective Aromatase inhibitor

77
Q

Effect of Anastrozole

A

Reduce estradiol 70% after 24 hours

80% reducton after 2 weeks

78
Q

Metabolism of Anastrozole

A

Liver

79
Q

SEs of Anastrozole

A 
Hot flashes
Mood disturbance
Arthritis
Arthralgias
Bone pain
Bone loss
Osteoporosis
80
Q

Route of administration of Anastrozole

A

Oral

81
Q

Use of Anastrozole

A

Hormone receptor + breast cancer

82
Q

Aromatase inhibitors

A

Anastrozole, Letrozole, Exemestane

83
Q

MOA of Flutamide

A

Inhibits the uptake and binding of the testosterone to specific receptors in hormonally sensitive prostate cancer cells

84
Q

SEs of Flutamide

A

Well-tolerated
Diarrhea (20% of patients)
Elevated LFTs

85
Q

Use of Flutamide

A

Androgen deprivation treatment therapy of metastatic prostate cancer

86
Q

Testosterone receptor antagonists

A

Flutamide, Bicalutamide, Nilutamide

87
Q

Benefit of Bicalutamide and Nilutamide

A

Less diarrhea

88
Q

Class of Leuprolide acetate

A

GnRH receptor agonist

89
Q

MOA of Leuprolide acetate

A

Binds to the pituitary GnRH receptors and initially produces an increase in LH and FSH leading to an increase in T and thus initially can stimulate tumor growth
By interrupting the normal pulsatile stimulation of the GnRH receptors, leuprolide down regulates the secretion of LH and FSH, leading to a reduction in T levels

90
Q

SES of Leuprolide

A

Tumor flare reaction (pretreat with flutamide or bicalutamide)
Hot flashes
Androgen deprivation therapy (ADT): weakness, decreased libido, loss of muscle mass, ED, change in body fat distribution, gynecomastia

91
Q

Coadministration of Leuprolide with:

A

Flutamide or bicalutamide for 2-4 weeks before institutation of leuprolide acetate treatment (depot injections)

92
Q

Route of administration of Leuprolide

A

IM

Depot injections

93
Q

GnRH receptor agonists

A

Leuprolide

Goserelin (agonist of LHRH)

Chemotherapy Viruses (5 decks)

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