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Female Sex Hormones Flashcards

1
Q

What are the three naturally occurring steroidal estrogens?

A

Estrone, estrodiol, estriol

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2
Q

Where and how is estradiol (E2) produced?

A

Follicular phase: theca and granulosa cell of graafian follicle After ovulation: corpus luteum During pregnancy: fetoplacental unit During menopause: adrenal and hepatic conversion of precursors

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3
Q

Where are estrone and estriol formed and from what?

A

Liver from estradiol or in peripheral tissues from androstenedione

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4
Q

What converts androgens to estrogens?

A

Aromatase

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5
Q

What is the physiological role of estrogen during female maturation?

A

-Dev of vagina, uterus, fallopian tubes -2ndary sex characteristics -Closure of epiphyses of long bones -Areolar and genital skin pigmentation -Fat redistribution

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6
Q

What are the endometrial effects of estrogen?

A

-Proliferation of endometrial lining in follicular phase -Endometrial hyperplasia

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7
Q

What are the cardiovascular-hematologic effects of estrogen?

A

-Enhances coagulability of blood -Increase HDL and TGs -Contributes to normal vascular structure and function -vasodilation?/??

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8
Q

What are the metabolic effects of estrogen?

A

-Increase production of leptin -Increased biosynthesis of binding globulins like TBG, fibrinogen, transferrin etc

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9
Q

What are the bone effects of estrogen?

A

Promotes apoptosis of osteoclasts, dec resorption of bone

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10
Q

Where and how is progesterone produced?

A

-Non pregnant: corpus luteum -Pregnant: placenta

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11
Q

What is progesterone a precursor to?

A

Estrogens, androgens, corticosteroid hormones

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12
Q

What does progesterone do to the endometrium?

A

Promotes proliferation and prepares it for implantation

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13
Q

What does progesterone do to uterus?

A

Renders it refractory (reduces response) to oxytocin until onset of labor

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14
Q

List the 4 types of steroid receptor ligands

A
  1. Pure agonist (full agonist, amplified gene transcrip) 2. Mixed agonist/antagonist (Type 3/4 antagonist, tissue specific recruits co-repressor or activator, altered gene transc) 3. Pure antagonist (Type II antagonist, requires co-repressor, no gene transcription) 4. Pure antagonist (Type I, no gene transcription)
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15
Q

Why use estrogen agonists?

A

-Treats primary hypogonadism -Secondary estrogen deficiency -Suppresses ovulation -Post-menopausal estrogen replacement (HRT)

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16
Q

What are the benefits to HRT?

A

-Relieves hot flashes and night sweats -Relieves vaginal dryness and atrophy -Reduces bone loss and hip fractures -Reduces risk of colon cancer (EPT)

17
Q

What are the risks to HRT?

A

-Increases risk of thrombosis -Inc risk of stroke -Inc incidence ovarian and endometrial cancer (ET) -Inc in breast cancer (EPT) -Inc risk of MI (EPT)

18
Q

Why use estrogen receptor modulators?

A

We want an antagonist at female reproductive tissues and an agonist for bone

19
Q

What is SERM?

A

Selective estrogen receptor modulators (SERM) -Type III-IV Antagonist -Requires tissue-specific co-activator or co-repressor be recruited to work and alter gene transcription

20
Q

Why do we use SERM?

A

Treatment of ER+ breast cancers

21
Q

Name two SERMs

A

Tamoxifen and Raloxifene

22
Q

Who do we give tamoxifen to?

A

Post-menopausal women or women without a uterus because it is an agonist for uterus, bone and maybe CVS

23
Q

What is temoxifen?

A

Type IV estrogen receptor modulator -Suppresses E2 dependent growth of breast cancer (antagonist) -Tumoristatic and not tumoricidal

24
Q

Who do we give raloxifene to?

A

Safe for women of any age/menopausal status

25
Q

What is raloxifene and how does it work?

A

-Type III estrogen receptor modulator -Suppresses E2 dep growth of breast AND uterine tissue -Agonist in bone and CVS -Changes bone density for the better -Lowers LDL cholesterol -Tumeristatic and not tumoricidal (ie not chemotherapeutic)

26
Q

How do estrogen synthesis inhibitors work? What do we use them for?

A

Inhibit aromatase enzyme (inhibit final step in estrogen biosynth) -Treat ER+ tumors

27
Q

What do we use progestin therapy for?

A

-Replacement therapy -Contraceptives and IVF -Endometriosis -Dysfunctional uterine bleeding

28
Q

What is RU486?

A

Progesterone type II antagonist (ie req co-repressor)

29
Q

Summary Slide

A

Reproduction (23 decks)

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