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Renal Pharmacology > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

15.21

1
Q

Cisplatin; Carboplatin - Tx

A

Chemo for advanced metastatic bladder cancer (use MVAC)

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2
Q

Cisplatin; Carboplatin - MOA

A

Displacement of Cl by water activates –> crosslinks DNA by binding guanines to prevent replication; drug-DNA complex attracts HMG-1 (high mobility group-1) repair proteins which become irreversibly bound –> prevents effective repair and leads to apoptosis

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3
Q

Does activation occur more slowly in cisplatin or carboplatin?

A

Carboplatin

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4
Q

Cisplatin; Carboplatin - MOR (2)

A

1) . Increased nucleotide excision repair protein;

2) . loss of function of mismatch repair (HMG-1)

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5
Q

Cisplatin; Carboplatin - Tox and how to minimize them (4)

A
  1. Nephrotoxicity (minimized w/ hydration/saline diuresis)
  2. Ototoxicity
  3. Marked nausea/vomiting (given w/ anti-emetic)
  4. Myelosuppression (Carboplatin only)
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6
Q

What is MVAC combo?

A

Methotrexate, vinblastine, doxorubicin, cisplatin

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7
Q

Which is generally less toxic: carboplatin or cisplatin?

A

Carboplatin

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8
Q

Which is used for pts w/renal dysfunction: carboplatin or cisplatin? (+1 more drug)

A

Carboplatin in combo w/paclitaxel

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9
Q

What is used w/cisplatin to minimize renal damage?

A

Hydration/saline diuresis

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10
Q

Doxorubicin; Mitoxantrone - Tx

A

Chemotherapy - Hormone Refractory/metastatic prostate cancer

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11
Q

Doxorubicin; Mitoxantrone - MOA

A

Intercalates DNA

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12
Q

Mitoxantrone - Class; used w/

A

Doxorubicin analog (sometimes used w/prednisone)

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13
Q

Doxorubicin; Mitoxantrone - SE (3)

A

Myelosuppression, cardiac toxicity, mucositis

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14
Q

Doxorubicin; Mitoxantrone - C/I

A

Cardiac disease

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15
Q

Which has less cardiotoxicity: doxorubicin or mitoxantrone?

A

Mitoxantrone

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16
Q

Paclitaxel; Docetaxel - Tx; used w/

A

Chemotherapy - Hormone refractory prostate cancer; docetaxel used in combo w/estramustine

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17
Q

Paclitaxel; Docetaxel - MOA

A

Antagonizes/blocks microtubule spindle disassembly by inhibiting mitosis by binding to beta-tubulin

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18
Q

Paclitaxel; Docetaxel - MOR (2)

A
  1. Multidrug resistance pumps

2. Beta-tubulin mutations

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19
Q

Paclitaxel; Docetaxel - Tox (3)

A

(1) Neutropenia, (2) peripheral neuropathy, (3) hypersensitivity (can use w/ dexamethasone)

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20
Q

Flutamide, Bicalutamide, Nilutamide - Tx

A

Chemotherapy; hormonal tx of prostate cancer

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21
Q

Flutamide, Bicalutamide, Nilutamide - Class

A

Nonsteroidal Androgen Receptor Antagonists

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22
Q

Flutamide, Bicalutamide, Nilutamide - MOA

A

Inhibit ligand binding of receptor and translocation of the androgen receptor-ligand complex to the nucleus

***Rarely used alone; used in combo w/ GnRH agonist during first few weeks of treatment to prevent excess androgen production

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23
Q

Flutamide, Bicalutamide, Nilutamide - SE (2)

A
  1. Gynecomastia

2. Mild hepatic toxicity

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24
Q

Which is more potent of the nonsteroidal androgen receptor antagonists?

A

Bicalutamide/Nilutamide –> orally active, more potent w/ fewer side effects compared to Flutamide

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25
Q

Cyproterone - Class

A

Steroidal androgen receptor antagonist

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26
Q

Cyproterone - Tx

A

Chemo - prostate cancer

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27
Q

Cyproterone - MOA

A

Steroidal androgen receptor antagonist/partial agonist

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28
Q

Cyproterone - Used w/

A

Rarely used alone
Used in combo w/ GnRH agonist (Leuprolide, Goserelin) during first few weeks of treatment to prevent excess androgen production

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29
Q

Leuprolide, Goserelin - Tx

A

Chemo- prostate cancer

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30
Q

Leuprolide, Goserelin - Class and MOA

A

GnRH agonist –> 1st 2-4 wks causes agonism at receptor to exacerbate symptoms via promotion of testosterone production=> eventually downregulate GnRH receptors to decrease LH production and thus androgen production => pharmacological castration ; Altered amino acid sequence-> less degradation and greater affinity for GnRH receptor compared to GnRH

31
Q

Leuprolide, Goserelin - SE (5)

A

Headache, lightheadedness, nausea, injection site reactions; hypogonadism (pharmacological castration)

32
Q

Degarelix - Tx

A

Hormonal tx of prostate cancer

33
Q

Degarelix - Class/MOA

A

GnRH antagonist

34
Q

Advantage of Degarelix

A

Avoids flare phenomenon of GnRH agonists and is not associated w/systemic allergic rxns

35
Q

Abiraterone - Class

A

Irreversible inhibitor of 17-hydroxylase and C-17,20-lyase CYP17 activity that blocks testosterone biosynthesis (so inhibitor of steroidogenesis)

36
Q

Abiraterone used w/

A

Glucocorticoid prednisone b/c abiraterone increases ACTH levels, resulting in mineralocorticoid excess

37
Q

Which has greater potency: abiraterone or ketoconazole?

A

Abiraterone

38
Q

Abiraterone - Tx

A

Castration-resistant prostate cancer (as secondary hormone therapy)

39
Q

Finasteride - Tx

A

Hormonal tx- benign prostatic hypertrophy (BPH) (as used for male pattern baldness)

40
Q

Finasteride - MOA

A

Inhibits 5a-reductase-> prevents conversion of testosterone to dihydrotestosterone

41
Q

Finasteride - SE (2)

A

Impotence, gynecomastia

42
Q

Ketoconazole - Tx

A

Chemo- prostate cancer (2nd hormone therapy to reduce adrenal androgen synthesis in castration-resistant prostate cancer)

43
Q

Ketoconazole - MOA

A

Decreases CYP17 (17-hydroxylase) production and inhibits sex steroid synthesis (by both testicular and adrenal steroidogenesis)

44
Q

Ketoconazole - SE

A

Diarrhea and hepatic enzyme elevations

45
Q

Thiotepa - Tx

A

Chemo- bladder cancer

46
Q

Thiotepa - MOA

A

Intravesicular agent; Activated by CytP450 to an alkylator –> crosslinks DNA;

47
Q

Thiotepa - SE

A

Mild myelosuppression due to some systemic absorption

48
Q

Mitomycin - Tx

A

Chemo- bladder cancer

49
Q

Mitomycin - MOA

A

Intravesicular agent

Dual alkylator-> crosslinks DNA @ G and A=> prevents DNA synthesis and repair attempts lead to strand breaks

Requires activation for alkylation

50
Q

Mitomycin - MOR (2)

A

Decreased activation, efflux pump

51
Q

Mitomycin - SE (2)

A

Myelosuppression, nephrotoxicity

52
Q

Bacillus Calmette-Guerin - Tx

A

Chemo- bladder cancer

53
Q

Bacillus Calmette-Guerin - MOA

A

Intravesicular agent (given intravesicularly)

Live, attenuated Mycobacterium bovis –> induces granulomatous rxn in bladder wall

54
Q

Bacillus Calmette-Guerin - SE (6)

A

Hypersensitivity, shock, chills, fever, malaise, immune complex disease

55
Q

Interleukin-2 (IL-2) - Tx

A

Chemo - renal cell carcinoma and melanoma; used in cancers that are refractory to conventional treatment

56
Q

Interleukin-2 (IL-2) - MOA

A

Stimulate proliferation and activation of lymphokine-activated killer (LAK) cells

57
Q

Interleukin-2 (IL-2) - SE (12)

A

Hypotension, arrhythmia, peripheral edema, azotemia, increased liver enzymes, anemia, thrombocytopenia, nausea, vomiting, diarrhea, confusion, fever

58
Q

Sunitinib, Sorafenib - Tx

A

Renal cell carcinoma

59
Q

Sunitinib - MOA

A

Inhibitor of receptor tyrosine kinases (VEGF-R2, PDGF-R, others) to reduce proliferation and angiogenesis

60
Q

Sorafenib - MOA

A

Oral inhibitor of VEGF-R1,2,3 tyrosine kinases within tumor cells to reduce proliferation and angiogenesis

61
Q

Sunitinib, Sorafenib - SE (6)

A

bleeding, HTN, proteinuria, thromboemboli, intestinal perforation, myelosuppression

62
Q

Bevacizumab (Avastatin) - Tx

A

Renal cell carcinoma

63
Q

Bevacizumab (Avastatin) - MOA

A

Humanized monoclonal Ab against VEGF –> inhibits interaction with VEGF receptors (VEGF-Trap) => inhibits angiogenesis in tumors

64
Q

Bevacizumab (Avastatin) - SE/Toxicity (7)

A

Severe HTN, proteinuria, CHF, hemorrhage, stroke, MI, gastric perforation

65
Q

Pazopanib - Tx

A

Renal cell carcinoma

66
Q

Pazopanib - MOA

A

Inhibits the tyrosine kinase activity of VEGFR-2; inhibitor of angiogenesis

67
Q

Which 3 drugs inhibit tyrosine kinase activity of VEGFR-2?

A

Pazopanib, sorafenib and sunitinib

68
Q

Temsirolimus (metabolized to sirolimus), Everolimus (Rapamycin) - MOA

A

Normally: mTOR forms the mTORC1 complex with a member of the FK506-binding protein family, FKBP12. Among other actions, mTORC1 phosphorylates S6 kinase and also relieves the inhibitory effect of 4EBP on initiation factor elf-4E, thereby promoting protein synthesis and metabolism.

MOA: The antitumor actions of the Rapamycins result from their binding to FKBP12 and inhibition of mTORC1.

69
Q

Temsirolimus (metabolized to sirolimus), Everolimus (Rapamycin) - Effects

A

Sirolimus, temsirolimus (metabolized to sirolimus) or everolimus (Rapamycins) have immunosuppressive effects, inhibit cell-cycle progression and angiogenesis, and promote apoptosis.

70
Q

Temsirolimus (metabolized to sirolimus), Everolimus (Rapamycin) - Class/Tx

A

mTOR Inhibitors: Rapamycin Analogs

Post-transplant immunosuppression; renal cancer (including intermediate, advanced, and poor prognosis)

71
Q

mTOR stands for?

A

Mammalian target of rapamycin, or mTOR, an effector PI3 kinase signaling

72
Q

What is rapamycin?

A

Sirolimus; a fungal fermentation product that inhibits the proper functioning of a serine/threonine protein kinase in mammalian cells

73
Q

Temsirolimus (metabolized to sirolimus), Everolimus (Rapamycin) - SE (8)

A

Mild maculopapular rash, mucositis, anemia, and fatigue, leukopenia or thrombocytopenia (reversed w/discontinuation of drug), hyperglycemia, and hypertriglyceridemia

Renal Pharmacology (17 decks)

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