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Reproduction Week 2 > Lecture 15: Female Sex Hormones > Flashcards

Lecture 15: Female Sex Hormones Flashcards

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1
Q

What are the types of estrogens?

A
  1. naturally occurring steroidal estrogens
    Example: Estrone, Estradiol and Estriol (E1, E2 and E2)
  2. naturally occurring nonsteroidal estrogenic compounds
    Example: Flavonoids
  3. Synthetic compounds used in manufacture of plastics
    Example: bisphenols, alkylphenols, phthalate phenols
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2
Q

What is E1?

A

Estrone (1 –OH group)

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3
Q

What is E2?

A

Estradiol (2 –OH groups)

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4
Q

What is E3?

A

Estriol (3 –OH groups)

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5
Q

What are the main female sex hormones?

A
  1. Progesterone
  2. Estrone (E1)
  3. 17 beta Estradiol (E2)
  4. Estriol (E3)
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6
Q

What is the physiological function of estrogens?

A
  1. Female maturation
  2. Endometrial effects
    • proliferation of endometrial lining in follicular phase
    • endometrial hyperplasia
  3. Cardiovascular – hematologic effects
    • we don’t understand the CV effect of estrogen (can enhance coagulability, increase HDL as well as triglyceride)
    • vasodilation
  4. Metabolic effects
    • increases leptin
    • increases production of TBG, fibrinogen, transferrin, CBG, SHBG
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7
Q

What is TBG?

A

Thyroxine binding globulin

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8
Q

What is CBG?

A

Corticosteroid binding globulin

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9
Q

What is SHBG?

A

Sex Hormone binding globulin

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10
Q

What is the physiological role of progesterone?

A
  1. Produced in non pregnant state by LH stimulated corpus luteum
    • pregnant state by placenta
  2. PRECURSOR of estrogens, androgens and corticosteroid hormones
  3. Promotes progestational proliferation (secretory phase) of the endometrium and prepares it for implantation
  4. Renders uterus refractory to oxytocin until onset of labor
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11
Q

Where is Estradiol (E2) made?

A

Ovary

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12
Q

Where are Estrone (E1) and Estriol (E3) made?

A

Liver from estradiol

Peripheral tissues from androstenedione

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13
Q

What is the function of aromatase?

A

Converts Androstenedione to Estrone (E1)

Converts Testosterone to Estradiol (E2)

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14
Q

What do all sex hormones derive from?

A

Pregnenolone

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15
Q

How is progesterone synthesized?

A

Cholesterol to pregnenolone to progesterone

Final step is catalyzed by 3beta-HSD

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16
Q

Why is exogenous hormone use for a patient complicated?

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A

We don’t know how much of that hormone is being used as an inhibitor and how much of it is used as an agonist at the receptor

17
Q

What are the different types of steroid receptor ligands?

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A
  1. Pure agonist
  2. Mixed agonist/antagonist
  3. Pure antagonist Type I (complex doesn’t bind to DNA)
  4. Pure antagonist Type II (presence of corepressor)
18
Q

What determines response to sex hormones?

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A
  1. Amount of hormone
  2. Receptor density
  3. the type of receptors and the cosuppressor/activators
  4. The transcription factors
  5. paracrine and autocrine in nature
19
Q

How do we manipulate the pathway?

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A 
1. receptor agonists
Example: natural and synthetic estrogens and progestins
2. receptor antagonists
Example: antiprogesterone (RU 486) = MIFEPRISTONE
3. receptor modulators
Example: Selective ER modulator (SERM)
4. synthesis inhibitors
Example: aromatase inhibitors
20
Q

Where do we want estrogen agonist effects?

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A

Impact on bone (because estrogen inhibits osteoclasts)

21
Q

Where do we want estrogen antagonist effects?

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A

Impact on breast and uterus

You want to INHIBIT estrogens effect on breast and uterus

22
Q

What is the MoA of mifepristone?

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A

Antagonist of estrogen receptor

aka RU 486

23
Q

Where are natural estrogens derived from?

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A

Pregnant mare

24
Q

What are the indications for using estrogen as a therapy?

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A
  1. Primary hypogonadism or secondary estrogen deficiency
  2. suppression of ovulation
  3. post-menopausal estrogen replacement
  4. Breast cancer therapy
25
What is ERT?
Estrogen replacement therapy
26
What are the benefits of estrogen replacement therapy?
1. relieves hot flashes and night sweats 2. relieves vaginal dryness and atrophy 3. reduces bone loss and hip fractures 4. reduces risk of colon cancer (EPT = estrogen + progesterone)
27
What are the risk of estrogen replacement therapy?
1. Increases risk of thrombosis 2. increases risk of stroke 3. Increases incidence of ovarian and endometrial cancer 4. Increase in breast cancer 5. Increase in MI
28
What are the key characteristics of of SERM?
Selective estrogen receptor modulator “anti-estrogens” Goal is to maintain the good effects of ERT on bone and to ELIMINATE the bad effects on increase cancer risk Antagonist and agonist based on tissue and drug Good effect = bones Bad effect = breast and uterus
29
What is the MoA of SERM?
Binds to estrogen receptor (ER) ER-SERM complex binds to ERE (binding site) in nucleus Conformation of the complex determines which co-activator or co-repressor will be recruited to the transcription complex Menu of co-activators or co-repressors available is tissue specific Alters gene transcription
30
What is the key characteristic of Tamoxifen?
Suppresses E2 dependent growth of breast cancer (antagonist) An agonist in the uterus, bone and maybe CVS Agonist effects in uterus limit clinical utility in ERT Type IV estrogen receptor modulator (mixed agonist/antagonist) TumoriSTATIC and NOT tumoricidal
31
What is the key characteristic of Raloxifene?
Antagonists in breast AND uterine tissue Suppresses E2 dependent growth of breast and uterine tissue Agonist in bone and CVS Changes bone density by +2.4% a year Lowers LDL-cholesterol Type III estrogen receptor modulator (agonist/antagonist) Tumoristatic and NOT tumoricidal
32
What is the MoA of estrogen synthesis inhibitor?
Inhibits the action of AROMATASE Example: Anastrozole (arimidex), exemestane (aromasin) Thereby inhibits formation of estrone (from androstendione) and estradiol (from testosterone)
33
When do you use of progestin therapy?
1. replacement therapy 2. contraception and IVF 3. endometriosis 4. dysfunctional uterine bleeding
34
What causes phocomelia?
Non-steroidal synthetic estrogens | E.g. Thalidomide, diethylstilbestrol, dinestrol, methestrol
35
What is an example of a progesterone antagonist?
RU 486 | Mifeprostone
36
What are examples of SERM?
1. Tamoxifen (breast cancer) | 2. Raloxifene (osteoporosis)
37
What is an example of aromatase inhibitors?
Letrozole (breast cancer)
38
When do you want to use aromatase inhibitors and SERMs?
Breast cancer

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