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Human Reproduction > Week 4: Reproductive Pharmacology Prework > Flashcards

Week 4: Reproductive Pharmacology Prework Flashcards

1
Q

What is the mechanism of control of ovarian secretion?

A

Hypothalamus - anterior pituitary - ovarian axis

GnRH from hypothalamus

FSH & LH from anterior pituitary

Estradiol & inhibin

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2
Q

What does the ovary produce in the follicular phase?

A

mainly estrogens

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3
Q

What does the ovary produce in the luteal phase?

A

estrogens and progesterone

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4
Q

Where is GnRH produced?

A

produced by neurons in the hypothalamic arcuate nucleus

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5
Q

What are the name of the cells that produce GnRH?

A

Arcuate nucleus in the hypothalamus

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6
Q

Explain the hypothalamic-ant pit-ovarian axis

A
  • Pulsatile GnRH secretion is required to stimulate the gonadotrophs to produce and release LH and FSH
  • Sustained nonpulsatile administration of GnRH (or by GnRH analogs) inhibits the release of FSH and LH by the pituitary in both women and men resulting in hypogonadotropic hypogonadism
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7
Q

Effect of continuous administration of estrogen

A

Continuous administration of estrogen, especially with progestin inhibits the secretion of gonadotropins from the anterior pituitary

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8
Q

What are the forms of estrogen produced by women

A

The major estrogens produced by women are estradiol (estradiol-17β, E2), estrone (E1) and estriol (E3)

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9
Q

E2 AKA

A

Estradiol-17β

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10
Q

E1 AKA

A

Estrone

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11
Q

E3 AKA

A

Estriol

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12
Q

What is the major secretory product of the ovary?

A

Estradiol

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13
Q

Where is estrone and estiol produced?

A

although some estrone is produced in the ovary, most estrone and estriol are formed in the liver from estradiol or in peripheral tissues from androstenedione and other androgens

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14
Q

Describe the biosynthesis pathway of the various forms of estrogen

A
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15
Q

What is responsible for the development of the genital structures and secondary sexual characteristics in females?

A

Estrogens

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16
Q

What are some of the systemic effects of estrogens?

A
  • Modify serum protein levels
  • reduce bone resorption
  • enhance coagulability of blood
  • Increase plasma triglyceride levels; decrease LDL cholesterol and increase HDL cholesterol
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17
Q

How do estrogens travel around the body?

A

In the blood, boun to Sex Hormone-Binding Globulin (SHBG; also called Sex steroid-binding protein)

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18
Q

SHBG AKA

A

Sex-Hormone Binding Globulin

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19
Q

Estrogen receptor types

A

two genes code for two estrogen receptor isoforms

α and β

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20
Q

Where are estrogen receptors found?

A

Estrogen receptors are found predominantly in the nucleus bound to heat shock proteins

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21
Q

What does activation of Estrogen receptors do?

A
  • The receptor-hormone complex regulates gene transcription via binding to estrogen response elements (EREs) in the regulatory regions of various genes and interactions with various coregulators and transcription factors
  • The relative concentrations and types of receptors, receptor coregulators and transcription factors confer the cell specificity of estrogens’ action.
  • Estrogens also exert rapid nongenomic effects
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22
Q

How do different types of cells respond to estrogens differently?

A

The relative concentrations and types of receptors, receptor coregulators and transcription factors confer the cell specificity of estrogens’ action.

23
Q

Estrogen toxicity and considerations

A
  • In hypogonadal girls, dosage must be adjusted carefully to prevent premature closure of the epiphyses of the long bones and short stature
  • When used as Hormone replacement therapy (HRT), estrogen increases the risk of endometrial cancer; this effect is prevented by combining the estrogen with a progestin
  • Dose-dependent toxicity includes nausea, breast-tenderness, increased risk of migraine headache, thromboembolic events (eg deep vein thrombosis), gallbladder disease, hypertriglyceridemia and hypertension
24
Q

Considerations of Estrogen use in hypogonadal girls

A

In hypogonadal girls, dosage must be adjusted carefully to prevent premature closure of the epiphyses of the long bones causing short stature

25
Q

Considerations of Estrogen use as HRT in menopausal women

A

When used as Hormone replacement therapy (HRT), estrogen increases the risk of endometrial cancer; this effect is prevented by combining the estrogen with a progestin

26
Q

Features of estrogen toxicity

A

A Dose-dependent toxicity that can present as:

  • nausea
  • breast-tenderness
  • increased risk of migraine headache
  • thromboembolic events (eg deep vein thrombosis)
  • gallbladder disease
  • hypertriglyceridemia
  • hypertension
27
Q

Forms of Progestins

A
  • Progesterone is the major progestin in humans
28
Q

Effects of Progestins

A
  • Progesterone induces secretory changes in the endometrium and is required for the maintenance of pregnancy
  • Other progestins also stabilize the endometrium but do not support pregnancy
  • Affect carbohydrate metabolism and stimulate fat depostion
29
Q

Where are androgens produced?

A

Testosterone and the related androgens are produced in the testis, the adrenal and to a small extent the ovary

30
Q

How is testosterone synthesized?

A

Testosterone is synthesized from progesterone and dehydroepiandrosterone (DHEA)

31
Q

How does testosterone travel through the body?

A

In the plasma, testosterone is partly bound to sex-hormone-binding globulin (SHBG), a transport protein

32
Q

SHBG AKA

A

sex-hormone-binding globulin

33
Q

Testosterone conversion

A

Testosterone is converted in several organs (eg prostate) to dihydrotestosterone (DHT), which is the active hormone in those tissues

34
Q

What are the function of androgens?

A
  • induce virilization
  • responsible for forming the male external genitalia in the fetus (absence results in a female phenotype despite the presence of 46 XY karyotype) (eg androgen insensitivity syndrome)
  • responsible for the development of the secondary sexual organs and ducts (seminal vesicles and the prostate)
35
Q

Describe Testosterone biosynthesis

A
36
Q

Describe the metabolism of testosterone

A

Active metabolites

  • Testosterone is converted to 5α-dihydrotestosterone (DHT) by 5α-reductase
  • Testosterone is converted to estradiol by aromatase

Inactive metabolites

  • Androsterone and Etiocholanone by 17β-hydroxy dehydrogenase
37
Q

Active metabolites of testosterone metabolism and enzymes responsible

A
  • 5α-dihydrotestosterone (DHT)
    • by 5α-reductase
  • estradio
    • l by aromatase
38
Q

Describe the inactive metabolites of testosterone metabolism and the enzymes responsible

A

Androsterone and Etiocholanone by 17β-hydroxy dehydrogenase

39
Q

Testosterone -17β-hydroxy dehydrogenase->

A
  • Androsterone
  • Etiocholanolone
40
Q

Testosterone -5α-reductase->

A

Dihydrotestosterone (DHT)

41
Q

Testosterone -Aromatase->

A

Estradiol

42
Q

How are androgen levels controlled?

A
  • Compeitive inhibition of GnRH receptors
  • stimulation (+, pulsatile administration) or inhibition (-, continuous administration)
  • decreased synthesis of testosterone in the testis
  • decreased synthesis of dihydrotestosterone by inhibition of 5α-reductase
  • Competition for binding to cytosol androgen receptors
43
Q

Describe the hypothalamic-pituitary-gonadal axis

A
44
Q

Adipose and androgens

A
  • In obese patients, increased aromatase activity (aromatase is also found in adipose tissue) is thought to result in increased estradiol production
  • The increased estradiol level inhibits FSH and LH secretion from the pituitary, which result in reduced FSH and LH stimulation of the Sertoli and Leydig cells in the testes and a reduction in testosterone synthesis and sperm production
45
Q

Considerations of exogenous testosterone in obese patients for fertility

A
  • If Fertility is the goal, administration of testosterone in counterproductive because it provides negative feedback to the pituitary and causes further inhibition of LH and FSH secretion
  • Decreased LH and FSH of the testes further inhibits spermatogenesis
46
Q

Describe the hypothalamic-pituitary-gonadal axis in men

A
47
Q

Describe Testosterone MOA

A

Testosterone and dihydrotestosterone bind to the intracellular androgen receptor leading to growth, differentiation and synthesis of a variety of proteins

48
Q

What tissues predominantly use DHT as the dominant androgen?

A
  • Skin
  • Prostate
  • Seminal vesicles
  • Epididymis
49
Q

Dominant androgen in the skin

A

DHT (5α-dihydrotestosterone)

50
Q

Dominant androgen in the prostate

A

DHT (5α-dihydrotestosterone)

51
Q

Dominant androgen in the seminal vesicles

A

DHT (5α-dihydrotestosterone)

52
Q

Dominant androgen in the epididymis

A

DHT (5α-dihydrotestosterone)

53
Q

Describe the role of androgens in development

A
  • Testosterone is necessary for the normal development of the male fetus and infant and is responsible for the major changes in the male at puberty (growth of penis, larynx, skeleton; development of facial, pubic and axillary hair; darkening of skin, enlargement of muscle mass)
  • After puberty testosterone acts to maintain secondary sex characteristics, fertility and libido
54
Q

Androgen effects outside of development

A

the major effect of androgenic hormones outside of development and maintenance are:

  • anabolic action for increased muscle mass and strength
  • increased red blood cell production
  • Excretion of urea nitrogen is reduced and the nitrogen balance becomes more positive
  • Testosterone also helps maintain normal bone density

Human Reproduction (40 decks)

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