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Endo/Repro: Week 6 > Fitzaekerly: Antineoplatic Hormonal Drugs > Flashcards

Fitzaekerly: Antineoplatic Hormonal Drugs Flashcards

1
Q

cancers depend on this for growth

A

steroids

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2
Q

benefit of steroid dependent cancer

A

predict whether cancer will respond to tx (take biopsy and see if receptors are present)

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3
Q

Drugs that inhibit LH and FSH secretion

A

GnRH analogues

GnRH antagonist

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4
Q

Goserelin

leuprolide

A

GnRH analogues

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5
Q

how do GnRH analogues cause a flare response

A

mimic release of GnRH>
increase in FSH/LH>
increase in testosterone/estrogen>
FLARE (increase in cancer growth/bone pain)

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6
Q

long term continuous administration of GnRH analogue

A 
increase in steady state concentrations>
decrease receptor expression in pituitary>
decrease in FSH/LH>
decrease in estrogen/testosterone>
decrease in GnRH expression
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7
Q

how are GnRH analogues administered

A

depot form

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8
Q

TU of Goserelin and Leuprolide

A

advanced prostate cancer

PRE-MW w/ ER + breast cancer

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9
Q

acute toxicity of GnRH analogues

A

flare response> bone pain
pain at injection site

*can lead to decreased hormone levels long term

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10
Q

Degarelix

A

GnRH antagonist

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11
Q

Why may Degarelix be preferred over a GnRH analogue?

A

NO flare response
FASTER decrease in testosterone levels

injection site rxn is only toxcitiy

EXPENSIVE

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12
Q

Dutasteride

Finasteride

A

5 alpha reductase inhibitors

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13
Q

MOA of Finasteride

A

inhibits converstion of testosterone to DHT> decreased cell growth

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14
Q

used to tx:
BPH
Male pattern baldness
prevention in prostate cancer pts w/ high PSA

A

Finasteride

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15
Q

TERATOGENCITIY

impotence

A

Finasteride

*may lessen decrease in bone density/muscle wasting!!

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16
Q

abiraterone acetate

A

17 alpha hydroxylase

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17
Q

blocks early stages of androgen syntehsis but DOES NOT INTERFERE w/ conversion of pregnenolone

A

17 alpha hydroylase

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18
Q

used to tx:

metastatic prostate cancer that is resistant to other androgen blocking regimens

A

abiraterone acetate

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19
Q

Irreversibly binds and inhibits aromatase

A

exemastane

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20
Q

first line non steroidal aromatase inhibitors

A

anastrozole

letrozole

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21
Q

3rd line non steroidal aromatase inhibiotr

A

aminoglutethimide

22
Q

why is aminoglutethimide a third line tx?

A

decreases concentrations of adrenal glucocorticoids, mineralcorticoids, sex hormones

23
Q

blocks the conversion of testosterone/adrostenedione to estradiol and estrone

A

aromatase inhibitors

24
Q

which aromatase inhibotrs REVERSIBLY block the enzyme

A

non steroidals

25
Q

1st line tx for ER+ breast cancer in POST MW

A

Aromatase inhibitors

26
Q

ADRENAL INSUFFICIENCY toxicity

F, Nausea, rash, HA

A

aminoglutethamide

> ultimately leads to increase in ACTH> increase in cortisol and bone marrow suppression

27
Q 
POLYARTHRALGIA
decreased bone density
increased hot flashes
Nausea
HA
A

Anastrazole
letrozole
exemestane

28
Q

Bicalutamide
flutamide
nilutamide

A

anti androgens

29
Q

decrease binding of Test to receptor>
increase in LH/FSH>
increased production of testosterone

A

Bicalutamide
flutamide
nilutamide

30
Q

not given ALONG or for very long because of SE and are often used w/ GnRH analogue (goserelin/leuprolide) to prevent FLARE response

A

Anti-androgens

31
Q

androgen deprivation therapy

A

main stay of prostate cancer tx

32
Q

NSSA + GnRH agonist

A

complete androgen blockade

33
Q

newer anti-androgens that have decreased toxicity

A

bicalutamide

nilutamide

34
Q

DECREASE IN SEXUAL FXN
HOT FLASHES
DECREASE IN LVIER FXN
METHENOGLOBINEAMIA

A

anti-androgens

35
Q

MOA of anti-estrogens

A

compete w/ estrogen for binding to estrogen receptor

36
Q

raloxifene
tamoxifen
toremifene

A

SERMS

partial agonists

37
Q

Fulverstrant

A

SERD

full antagonist

38
Q

these drugs will give you NO benefit after 5 yrs
are taken orally
and take 4-6 weeks to reach a steady state

A

SERM

39
Q

given IM at 1 month internvals

and take only 7 mos to reach a steady state

A

SERD

40
Q

which anti-estrogen is metabolized in the liver by CYP3A?

A

SERD

41
Q

mainstay tx for ER+ cancers in POST MW

A

Anti-estrogens

42
Q

what drugs are NOT used in PRE-MW b/c of feedback loop?

A

anti-estrogens

43
Q

Tamoxifen is most effective in what cancers

A

ER+ PR+

44
Q

affect of estrogen on tissues

A

poliferative in breast and uterus

prevents bone resorption

45
Q

decrease in estrogen can lead to hot flashes, N and V

A

anti-estrogens

46
Q

agonist in the uterus that can lead to an increase in endometrial cancer

A

tamoxifen

47
Q

anti-androgen that can cause GI problems, HA, back pain and injection site rxns

A

fulverstrant

48
Q

which mechanism of antineoplastic drugs is NOT used in bresat cancer therapy

A

differntiating agents

49
Q

Cytotoxic Drug regimens for BC

A

FAC: Fu, Doxo, cyclophosphamide
(used until reach max dose of doxo b/c of cardiotoxicity)

CMF: cyclo, MTX, 5-FU

50
Q

target ER + BC

A

tamoxifen, tormifene, fulverstrant

anastrazole, letrozole, exemestane

51
Q

used to tx her2NEU cancers

A

trastuzumab

Endo/Repro: Week 6 (8 decks)

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