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MCC > Wk 7 Natural Chemotherapy Agents > Flashcards

Wk 7 Natural Chemotherapy Agents Flashcards

1
Q

Name of 2 topoisomerase I inhibitor

A

Irinotecan
Topotecan

-both are Camptothecins

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2
Q

2 Topoisomerase II inhibitors

A
  1. Doxorubicin (an anthracycline)
  2. Etoposide (an epipodophyllotoxin)
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3
Q

Microtubular targeting agents

A

Vincristine - a vinca alkaloid
Paclitaxel - a taxane

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4
Q

Antibiotic chemotherapy

A

Bleomycin

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5
Q

Selective estrogen receptor modulator

A

Tamoxifen

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6
Q

LHRH agonist

A

Goserelin

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7
Q

What are the ABCDEs of melanoma?

A

A = asymmetry
B = border
C = color
D = diameter
E = evolution (melanomas change rapidly, nevi usually don’t)

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8
Q

What is a nevi?

A

a neoplasm that’s usually benign
-increase risk of melanoma
-common

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9
Q

What are tx options for malignant melanoma?

A

Immunotherapy: anti-CTLA4, anti-PD1
BRAF inhibitors

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10
Q

Melanoma Risk Factors

A

-lighter pigmentation, sunburns at young age, more UV exposure
-worse melanoma-specific survival w/ African ancestry
-p16 loss (encoded at CDKN2A)
-spontaneous melanoma w/ BRAF-activating mutations (others: NRAS, KIT, TERT promotor mutations)

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11
Q

MOA of Topoisomerase I inhibitors

A

Topoisomerase I relaxes supercoiled dsDNA
-inhibitors bind DNA and topo I together until the DNA replication fork reaches the cleavable complex and causes dsDNA breaks

-S-phase specific

-resistance can occur from mutations in topo I, decreased intracellular retention or reduced [topo I]

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12
Q

MOA Irinotecan

A

AKA SN-38
-is a prodrug
-activated by carboxylesterdase in tissues and serum
-glucuronidation = breakdown pathway
-need to check for genetic polymorphism b/c can be highly toxic w/ breakdown pathway

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13
Q

Irinotecan Tox

A

Diarrhea
-neutropenia, mucositis, N/V, alopecia

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14
Q

MOA Topo II inhibitors

A

-Topo II unwinds supercoiled dsDNA
-inhibitors bind DNA and topo II together, making transient cleavable complexes continually cleavable, preventing re-ligation

-S-phase sensitive
-Resistance due to p-glycoprotein upregulation, increase in drug degradation, or decreased [topo II]

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15
Q

Etoposide

A

AKA VP-16
IV/PO
-hepatic metabolism
-renal excretion

AE: myelosuppression, delayed secondary malignancies

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16
Q

Anthracycline (Doxorubicin) MOA

A

Intercalates w/ DNA, interferes w/ uncoiling:
-interferes w/ topo II preventing strand reconnection
-intercalation alters shape, impairing repair enzymes
-forms free radicals ->cell structure damage

-Resistance due to P-glycoprotein, alteration of topo fxn, or decreased topo II

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17
Q

Doxorubicin AE, route

A

IV
-hepatic elimination
-cardiotoxicity (acute & chronic - lifetime exposure can -> CHF)
-myelosuppression, mucositis, extravasation necrosis, alopecia, emesis
-red urine

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18
Q

What med acts as a heart protectant for anthracyclines?

A

Dexrazoxane
-chelates iron in the heart (necessary for free radical damage)
-not ideal b/c takes 1 of 3 MOAs from the anthracyclines

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19
Q

What are the 2 classes of microtubule targeting agents?

A
  1. Vinca alkaloids (know Vincristine)
  2. Taxanes (know Paclitaxel)

-both natural products from plants & trees

20
Q

MOA Vincristine

A

Bind to tubulin PREVENTING microtubule assembly

-spindle poisons, arresting cells in mitosis

21
Q

MOA Paclitaxel

A

binds to tubulin PROMOTING assembly into microtubules while simultaneously INHIBITING disassembly

-spindle poisons, arresting cells in mitosis

22
Q

When would Vincristine be fatal?

A

If given intrathecally

23
Q

Vincristine Tox

A
  1. neurotoxicity - peripheral neuropathy, autonomic neuropathy -> constipation
  2. minimal myelosuppression, SIADH, alopecia
24
Q

Paclitaxel Tox

A

Myelosuppression, peripheral sensory neuropathies
-hypersensitivity rxn
-alopecia, bradycardia, myalgias

25
Q

Natural antibiotic chemotherapy drug

A

Bleomycin

26
Q

Bleomycin MOA

A

has DNA & metal binding region, which allow it to cause DNA breaks by free radical damage in G2

27
Q

Bleomycin Tox

A

-lung fibrosis, skin marks (b/c don’t have bleomycin hydrolase in lungs or skin to break it down)
-minimal myelosuppression

28
Q

Bleomycin resistance

A

Increased DNA repair

Increases bleomycin hydrolase

29
Q

When is bleomycin used?

A

Testicular cancer
Hodgkin Lymphoma

30
Q

What are 2 drug categories under endocrine therapies?

A
  1. Antiestrogens
  2. aromatse inhibitors
31
Q

What is a SERM?

A

Selective estrogen receptor modulator
-Tamoxifen

32
Q

Tamoxifen MOA

A

=estrogen antagonist
-reversibly binds ER receptor on breast cancer cells -> RNA transcription is impaired

=pro-estrogenic (agonist) in uterus (endometrial cancer) and bone (preserves bone density)
-use in pre-menopausal

33
Q

Aromatase inhibitor MOA

A

Aromatase converts androgens to estrogen
-selective, irreversible binding to prevent production of estrogen
-structurally related to androstenedione
-use in post-menopausal

34
Q

Tamoxifen pharmacokinetics

A

oral
-a prodrug, converted to active metabolite (endoxofen) by liver via CYP2D6
-CYP2D6 interactions (SSRIs)

35
Q

Tamoxifen AEs

A

-> post-menopausal state and menopausal symptoms: hot flashes, nausea, fatigue
-endometrial carcinoma
-DVTs/PEs
-prevention of postmenopausal bone loss

36
Q

Aromatase inhibitor AEs

A

-> menopausal symptoms: sweating, fatigue, hot flashes, flu-like symptoms
-myalgia
-N/V
-decreased bone density

37
Q

What is Goserelin

A

An LHRH agonist

38
Q

Describe the hormonal regulation of androgens

A
39
Q

Goserelin (and other LHRH agonist) MOA

A

Suppresses pituitary gonadotropin release of LH and FSH by downregulating the LH receptors (a negative feedback inhibition)
-> initial surge of LH and FSH -> tumor flare from increased androgen synthesis (related to first doses and pulse dosing)
-continual dosing -> pituitary receptor down regulation and functional antagonism

40
Q

LHRH Agonist AEs

A

Hot flashes
erectile impotence
decreased libido
injection-site reactions

41
Q

LHRH Antagonist MOA

A

bind reversibly to pituitary GnRH receptors reducing release of androgens
-no tumor flare since antagonist
-Degarelix subcutaneous

42
Q

Antiandrogen MOA

A

Competitive inhibitor of androgen receptors preventing androgen receptor activation

43
Q

Antiandrogen AEs

A

-gynecomastia
-hot flashes
-diarrhea
-LFT abnormalities - monitor

44
Q

What 2 agents require monitoring with LVEF?

A
  1. Doxorubicin
  2. Trastuzumab
45
Q

Tumor Lysis Syndrome (TLS)

A

Caused by massive tumor cell ylsis and release of intracellular

-Allopurinol - decreased formation of uric acid. AEs - rash
-Rasburicase - rapid uric acid reduction by catalyzing oxidation

46
Q

LHRH Agonist Surge Effect

A

Flare (cancer SE) and intentional LH/FSH stimulations (fertility use in non-cancer) are related to first doses and pulse dosing
-continual dosing leads to pituitary receptor down regulation and functional antagonism

MCC (44 decks)

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