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Endocrinology > Reproductive Lecture 3 > Flashcards

Reproductive Lecture 3 Flashcards

1
Q

What inhibits GnRH?

A

dopamine, endorphins, CRH

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2
Q

What stimulates GnRH?

A

norep

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3
Q

Where is oxytocin made

A

magnocellular neurons in hypothalamus - released from posterior pituitary

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4
Q

What does GnRH do?

A

stimulate calcium release (high GnRH, high Ca++)

release FSH and LH

high GnRH all the time, high Ca++

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5
Q

Two main functions of FSH?

A

1) follicular development

2) estradiol secretion

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6
Q

Two main functions of LH?

A

1) promotes ovulation

2) leutinization

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7
Q

What produces estrogen in the ovary? What produces progesterone?

A

Follicle: estrogens

corpus luteum: progesterone

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8
Q

True or false: the ovary also produces small amounts of androgens?

A

true

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9
Q

What binds to activin in the blood? and serves to reduce its effective concentration

A

follistatin (net effect: inhibitory)

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10
Q

What is clomiphene?

A

estrogen receptor antagonist

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11
Q

How does clomiphene work?

A

decreased estrogen binding to hypothalamus —> decreased negative feedback —-> increased GnRH —–> increased FSH/LH —> ovulation

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12
Q

What are SERMs?

A

selective estrogen receptor modulator

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13
Q

What are the 3 phases of menstruation?

A

1) follicular
2) ovulatory
3) luteal

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14
Q

Describe the follicular phase

A

1) hyp secretes GnRH
2) GnRH stimulates FSH/LH release
3) developing follicle makes E2 which promotes follicular development
4) E2 and inhibin decrease sensitivity of FSH-secreting cells
5) FSH decreases slightly but LH/E2 continues to rise

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15
Q

What is the feedback during the follicular phase?

A

estrogen and inhibin decrease sensitivity of FSH-secreting cells/inhibit

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16
Q

Why is it important to note that negative feedback is not a complete shutdown?

A

because it just keeps the volume down as capacity builds

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17
Q

Inhibin B comes from:

Inhibin A comes from:

A

B –> dominant follicle

A –> corpus luteum

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18
Q

how does inhibin B influence androgen production by theca cells?

A

AUGMENTS it (paracrine effect is positive and opposite of etymology)

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19
Q

What is the trigger for switching from the follicular stage to the ovulatory one?

A

surge of estradiol (once E2 reaches a certain threshold)

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20
Q

What occurs during ovulation?

A

1) LH surge
2) rupture of follicle causes decrease in E2 (leads to positive feedback —> decrease in LH to new plateau)
3) follicle reorganizes into corpus luteum, begins making E2 and progesterone

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21
Q

What does the LH surge follow?

A

estradiol crossing the threshold

22
Q

What causes the rupture of the follicle?

A

LH surge

why home ovulation tests look for LH in the urine

23
Q

What are the 2 dominant hormones during the luteal phase?

A

1) estradiol

2) progesterone

24
Q

True or false: estradiol and progesterone both have potent negative feedback

A

TRUE

25
Q

What does corpus luteum need to sustain itself?

A

LH or the equivalent hormone, hCG (secreted by implanted egg) and E2

26
Q

Plasma testosterone is ____ fold lower in women than men (and surges a bit at the end of follicular stage to increase libido)

A

20

27
Q

What are estradiol and progesterone levels like during menses?

A

LOW because of regression of corpus luteum and new immature follicles

(leads to sudden sloughing off of functional endometrial layer)

28
Q

Is the surge mode of hormone release found in males?

A

NO; exclusively tonic mode

29
Q

What are FSH and LH levels like post menopause

A

HIGH with high pulse frequency (lack of negative feedback, non functioning ovaries)

30
Q

What is required for development from primordial –> primary follicles?

A

gonadotropins (ovarian receptors for LH/FSH)

if estrogen levels are too low (17a hydroxylase deficiency), primordial follicles do not develop into primary ones

31
Q

To make secondary follicles, what cells proliferate and develop LH receptors?

A

theca

32
Q

What type of cells acquire receptors for FSH, androgens, and estrogens?

A

granulosa

33
Q

What hormone drives proliferation of granulosa cells and increases FSH and LH receptors on them?

A

FSH

34
Q

What are 5 main functions of E2?

A

1) inhibit growth of other follicles
2) prime GnRH action on LH secretion to evoke ovulatory surge of LH
3) prepare uterine endometrium for progesterone to evoke secretory response
4) affect fallopian tube to favor transport of ovum and zygote
5) alter cervical mucus

35
Q

What cells make aromatase?

A

granulosa (in response to FSH) but estradiol production depends on androgens provided by theca cells

36
Q

Which cells are vascularized?

A

Theca! (why they have androgens and granulosa cells do not)

37
Q

Which cells convert cholesterol to steroid hormones

A

both but theca does most of it

38
Q

What is the 2 compartment theory for follicular estradiol production?

A

theca cells

granulosa cells

39
Q

Which hormone is produced faster, progesterone or estradiol?

A

progesterone

40
Q

What is the life span of corpus luteum?

A

9-10 days

41
Q

When is the proliferative phase of the endometrium?

A

mid-late follicular phase

stromal and endothelial layers thicken, vascularization occurs, increase in progesterone and estrogen receptors

42
Q

Proliferative phase of endometrium is dominated by which hormone?

A

estradiol

43
Q

secretory phase of endometrium is dominated by which hormone?

A

progesterone

44
Q

When does the secretory phase take over?

A

day one of ovulation to late luteal phase

45
Q

Describe the secretory phase

A

endometrial glands secrete large amounts of carb rich mucus

46
Q

What happens to progesterone as menstruation occurs (ischemic)

A

declines

47
Q

What is the change in cervical mucus characterized by?

A

Spinnbarkeit (stretchable mucus)

48
Q

In the mid-late follicular phase, vagina is dominated by _______

A

estrogens

49
Q

inth eluteal phase, vagina is dominated by _________

A

progesterones

50
Q

Describe the hormonal changes that occur precipitating menopause?

A

ovaries stop producing estradiol and inhibin so there is no negative feedback on FSH/LH (makes FSH>LH)

51
Q

What are some consequences of menopause?

A

1) osteoporosis
2) CV disease (increased cholesterol)
3) hot flashes

52
Q

What is the timing hypothesis?

A

refers to the optimal timing to administer hormone therapy for peri-menopausal women

Endocrinology (16 decks)

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