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Reproductive > Female Sex Hormones > Flashcards

Female Sex Hormones Flashcards

1
Q

3 naturally occurring steroidal estrogens

A

estrone, estradiol, estriol

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2
Q

Nonsteroidal estrogenic compound

A

flavinoids (soybeans)

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3
Q

_____ is the major product of ovarian steroidgenesis

A

Estradiol/E2

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4
Q

During first part of menstrual cycle estrogens are produced by theca and granulosa cell of _____

A

graafian follicle

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5
Q

After ovulation, estrogens are produced by the ____

A

corpus lutem

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6
Q

During pregnancy estrogens are produced by the ____

A

fetoplacental unit

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7
Q

During menopause, estrogens are produced by ____

A

adrenal and hepatic conversion of precursors

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8
Q

____ and _____ are formed in the liver from estradiol or in peripheral tissues from andostendione.

A

Estrone/E1 and Estriol/E3

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9
Q

4 main female sex hormones

A

Progesterone, E1 estrone, E2 estradiol, E3 estriol

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10
Q

Product from which all sex hormones are derived is ____

A

pregnenolone (from cholesterol)

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11
Q

Two main male sex hormones

A

androstenedione and testosterone

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12
Q

_____ converts male sex hormones to estrogens.

A

aromatase

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13
Q

Functions of estrogen

A

female maturation, endometrial proliferation during follicular phase, hematologic effect, metabolic effect

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14
Q

T/F estrogen is an important modulator of bone growth and fusion of ephiphyses

A

T

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15
Q

Hematologic effects of estrogens

A

increases coagulability of blood in extrinsic pathway (increased II, VII, IX, X and decreases antithrombin III) + increase in HDL, increased TAG –> unclear what the net effect is

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16
Q

Metabolic effects of estrogens

A

increased production of leptin, tbg, fibrinogen, transferrin, cbg, shbg

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17
Q

Estrogen is a vasodilator/vasoconstrictor

A

vasodilator

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18
Q

How does estrogen decrease resorption of bone?

A

promotes apoptosis of osteoclasts

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19
Q

In a non pregnant state, progesterone is produced by____

A

LH stimulated corpus luteum

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20
Q

In a pregnant state, progesterone is produced by the ____

A

placenta

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21
Q

Functions of progesterone

A

progestational profile of the endometrium/preparation for implantation, renders uterus refractory to oxytocin until onset of labor

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22
Q

4 types of steroid receptor ligands

A

pure agonist, mixed agonist/antagonist, pure antagonist I, pure antagonist II

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23
Q

MOA of pure agonist

A

agonist binds to receptor –> complex binds to HRE –> recruits coactivator –>gene transcription

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24
Q

MOA of mixed agonist/antagonist

A

Ligand binds to receptor –> complex binds HRE –> differential recruitment of co-activator/repressor –> abrogated gene transcription (type III-IV antagonist)

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25
Q

MOA of pure agonist II

A

ligand binds to receptor –> complex binds to HRE –> recruits co-repressor –> 0 gene transcription

26
Q

MOA of pure agonist I

A

ligand binds to receptor –> complex does not bind HRE –> no gene transcription

27
Q

T/F estrogen can have a genomic or a non-genomic resposne

A

T –> i.e. binding to blood vessels will vasodilate without a genomic response

28
Q

How do natural and synthetic estrogens/progestins affect the pathway?

A

receptor agonism

29
Q

How does antiprogesterone RU486/mifepristone affect the pathway?

A

receptor antagonism

30
Q

How does a selective ER modulator affect the pathway?

A

receptor modulation

31
Q

How do aromatase inhibitors affect the pathway?

A

synthesis inhibition

32
Q

3 indications of estrogen agonism

A

primary hypogonadism/secondary estrogen deficiency, suppression of ovulation, post-menopausal estrogen replacement

33
Q

ERT increases/decreases HDL, increases/decreases LDL and increases/decreases oxidation of HDL/LDL.

A

increases, decreases, decreases

34
Q

ERT increases/decreases the thickness of externa and media layers of the carotid but speeds up/delays intimal thickening.

A

increases, delays

35
Q

ERT increases/decreases formation of angiotensin II.

A

decreases

36
Q

ERT promotes/reverses acetylcholine induced vasoconstriction of the carotid.

A

reverses

37
Q

T/F ERT relieves hot flashes, night sweats, vaginal dryness, and vaginal atrophy.

A

T

38
Q

T/F ERT increases bone loss and hip fractures.

A

F –> reduces

39
Q

T/F ERT increases colon cancer risk.

A

F –> reduces

40
Q

T/F ERT decreases thrombotic risk.

A

F –> increases

41
Q

T/F ERT increases stroke of risk.

A

T

42
Q

T/F ERT increases incidence of ovarian/endometrial cancer.

A

T

43
Q

T/F ERT decreases risk of breast cancer.

A

F –> increases

44
Q

T/F ERT increases risk of MI.

A

T

45
Q

MOA of SERMs

A

bind to ER –> complex binds to ERE in nucleus- -> conformational state dependent recruitment of coactivator/repressor –> tissue specific agonism/antagonism

46
Q

Goal of SERM use

A

maintain good effects of ERT on bone, eliminate bad effects on endometrium and breast

47
Q

Tamoxifen MOA

A

suppresses E2 dependent growth of breast cancer (antagonist); agonist in uterus, bone

48
Q

Tamoxifen is a type ___ estrogen receptor modulator

A

IV

49
Q

Tamoxifen is tumoristatic/tumoricidal

A

tumoristatic

50
Q

Raloixifene MOA

A

suppresses E2 dependent growth of breast AND uterine tissue; agonist in bone; lowers LDL

51
Q

Raloxifene is a type ____ estrogen receptor modulator

A

III

52
Q

Raloxifene is tumoristatic/tumoricidal

A

tumoristatic

53
Q

T/F tamoxifen increases risk of endometrial hyperplasia

A

T –> but raloxifene does not

54
Q

anastrozole and exemestane MOA

A

inhibit action of aromatase–> tx of ER+ tumors

55
Q

Indications for progestin therapy

A

replacement therapy, contraception/ivf, endometriosis, dysfunctional uterine bleeding

56
Q

RU486 is a progesterone receptor type II _____

A

antagonist via a corepressor

57
Q

Tx of hypogonadism

A

estrogens –> mestranol

58
Q

Tx of ERT

A

estradiol cypionate

59
Q

Tx of osteoporosis

A

raloxifene (SERM)

60
Q

Tx of breast cancer

A

tamoxifen (SERM) and letrozole (aromatase inhibitor)

61
Q

Tx of abortion

A

RU486

Reproductive (38 decks)

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