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fhb exam 4: endocrinology and reproduction > Reproduction II/III/IV: Female Reproduction > Flashcards

Reproduction II/III/IV: Female Reproduction Flashcards

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1
Q

What is the fundamental reproductive unit of the ovary?

A

follicle

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2
Q

RnRH is activated at puberty by ______ in the _______.

A

kisspeptin; hypothalamus

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3
Q

HPG axis feedback mechanisms are responsible for generation of what?

A

cyclical monthly pattern of hormone secretion called the “menstrual rhythm”

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4
Q

The menstrual cycle consists of which 2 cycles?

A

ovarian cycle and uterine cycle, due to physiological changes in these two organs

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5
Q

___ levels are much higher than ____ levels during periods of reproductive quiescence.

A

FSH; LH

This maintains a lower level of estradiol synthesis during these life stages.

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6
Q

What do increased LH levels stimulate during puberty and reproductive years?

A

stimulate steroidogenesis in the ovary, causing elevated E2 levels and the ultimate generation of (+) feedback loops that promote ovulation

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7
Q

What are the functions of LH and FSH in the female reproductive system?

A
  • LH: stimulates biosynthesis of estrogens (steroidogenesis) and induces ovulation and luteinization
  • FSH: stimulates follicular development and conversion of androgen precursors to estradiol
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8
Q

What are the features of theca vs. granulosa cells?

A
  • theca: produce androgens and progestins; only have LH receptors
  • granulosa: produce estrogens, progestins, inhibins, and activins; have both LH and FSH receptors
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9
Q

What are the 3 phases of the ovarian vs. endometrial (uterine) cycle?

A
  • ovarian: follicular, ovulatory, and luteal phase

- endometrial: menstrual, proliferative, and secretory phase

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10
Q

What is required for development from primordial follicle to primary follicle?

A

FSH stimulation; this can happen in utero

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11
Q

What is the dominant follicle based on?

A

sensitivity to FSH and local paracrine actions of AMH

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12
Q

For how long is the primary oocyte arrested in the diplotene stage?

A

until the LH surge

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13
Q

In the Graafian (“dominant”) follicle, what are the characteristic features?

A 
Granulosa cells stratify into:
1) Mural cells
2) Cumulus cells
3) Antral cells
Characterized by enlargement of antrum and appearance of cumulus oophorous. Exponential growth continues with large amounts of antral fluid.
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14
Q

Why is FSH high at the end of the ovarian cycle?

A

High FSH is important for recruiting a new cohort of follicles to enter the follicular phase.

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15
Q

What is the difference b/t inhibin B and inhibin A?

A
  • inhibin B: produced by follicles, positive paracrine effect in thecal cells to augment steroidogenesis, negative feedback on FSH
  • inhibin A: produced by corpus luteum, does not contribute to negative feedback on FSH during luteal phase
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16
Q

The LH surge requires a sustained exposure to __________.

A

critical concentrations of estradiol

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17
Q

The corpus luteum is the new ___________ formed from a ruptured follicle.

A

endocrine unit

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18
Q

What does the corpus luteum secrete/provide?

A

It secretes large amounts of progesterone and provides gonadal steroids that optimize implantation and maintain the zygote.

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19
Q

What happens to the corpus luteum if there is no fertilization?

A

regresses, undergoes “luteolysis,” and becomes necrotic; fibrous scar tissue is formed (corpus albicans)

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20
Q

Loss of LH at the end of the luteal phase will cause the corpus luteum to degrade unless what happens?

A

it is “rescued” by the equivalent hormone secreted by implantation of a fertilized embryo– HCG

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21
Q

What are the 3 layers of the uterus?

A

from innermost to outermost- endometrium, myometrium, perimetrium
(the cervix does NOT have an endometrial layer)

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22
Q

Explain hormone levels during menses.

A

Estradiol and progesterone levels are low due to regression of corpus luteum (and because new follicles are immature). Plasma FSH rises due to lack of negative feedback. Sudden withdrawal of steroids leads to sloughing of the endometrial layer.

23
Q

What stimulates proliferation of the endometrium?

A

Increased levels of E2 from the growing follicle.

24
Q

What happens during the secretory phase of the uterine cycle?

A

Uterine glands begin secreting large amounts of carbohydrate-rich mucous. The endometrium becomes engorged and the stroma because edematous. Vascularization continues to increase and stromal cells undergo process of predecidualization (impt. for development of placenta should pregnancy occur)/

25
Q

What happens to the uterine lining during menses?

A

There is reduced blood flow to spiral arteries, resulting in ischemia in the endometrium. The tissue becomes necrotic and proteolytic enzymes increase to digest the necrotic tissue. The endometrium then sloughs off.

26
Q

Why does menstrual blood not usually clot?

A

due to high levels of fibrolysins released from necrotic tissue

27
Q

How does cervical mucous change throughout the ovarian cycle?

A
  • follicular phase: mucous increases, becoming more alkaline and less viscous
  • ovulatory phase: characterized by Spinnbarkeit (stretchable mucous) and Ferning pattern (characteristic pattern when dried on glass slide); these changes promote survival and transport of sperm
28
Q

What are some changes that occur in the vagina throughout the ovarian cycle?

A
  • dominated by estrogens in mid to late follicular phase; vaginal epithelial cells become large, squamous, and cornified with small or absent nuclei
  • dominated by progesterone in luteal phase; small basophilic cells with many leukocytes
29
Q

What are some of the main actions of estradiol during the ovarian and endometrial cycles?

A
  • inhibits growth of cohort follicles to promote growth of dominant follicle
  • alters cervical mucous to enhance sperm transport
  • affects fallopian tubes to favor transport of ovum and zygote
  • prepares uterine endometrium for progesterone to evoke secretory response
  • primes GnRH action on LH secretion to evoke ovulatory surge of LH
30
Q

What is the primary form of estradiol during the reproductive period of a woman’s lifespan?

A

17β-estradiol (E2)

31
Q

The actions of estrogens are mediated through 2 high-affinity nuclear receptors:

A

ERα and ERβ

32
Q

The placenta is formed by the ___________ cells surrounding the blastocyst.

A

syncytiotrophoblast

33
Q

What is the basic concept behind pre-eclampsia/eclampsia?

A

failure of the maternal uterine arteries to adapt to the development placenta; this is potential fatal for both mother and fetus

34
Q

What are the most common causes of secondary amenorrhea?

A

pregnancy, lactation, menopause (prolactinomas and panhypopituitarism can also be causes)

35
Q

What is the most common cause of oligomenorrhea?

A

changes due to functional abnormalities in CNS mechanisms that regulate GnRH release, including stress and illness

36
Q

What was the first drug used to treat oligomenorrhea, and how does it work?

A

clomiphene– blocks estrogen receptors in the brain, leading to increased activation of the HPG axis due to lack of negative feedback from estrogen

37
Q

What is released during menses that contributes to dysmenorrhea?

A

prostaglandins, which cause uterine contraction (may be severe enough to cause ischemia and pain)

38
Q

What is the common treatment for dysmenorrhea?

A

prostaglandin synthesis inhibitors and oral contraceptives

39
Q

True or false: progesterone replacement can be used to significantly alleviate the symptoms of PMS

A

false– there is no clear link of PMS to progesterone (progesterone replacement has NOT been found to alleviate PMS symptoms or postpartum depression)

40
Q

What is the first-line treatment of PMS when socioeconomic dysfunction is present?

A

SSRIs and oral contraceptives to suppress ovulation

41
Q

What is the single most common cause of female work and school absenteeism?

A

dysmenorrhea

42
Q

What is hirsutism?

A

inappropriately heavy hair growth in androgen-sensitive areas

43
Q

What are the main causes of hirsutism?

A
  • intake of exogenous androgens
  • excessive androgen production by adrenals
  • idiopathic increases in sensitivity to androgens
44
Q

What is a leading cause of infertility in women?

A

PCOS

45
Q

What are the root causes of PCOS?

A

Insulin resistance and obesity. High insulin stimulates androgen production (causing infertility) and increased conversion to estrogens (causing weight gain).

46
Q

What are the treatments for PCOS?

A

weight loss, smoking cessation, metformin

metformin and clomiphene effective in restoring fertility

47
Q

What allows for high local concentrations of estrogens?

A

high conversion by aromatase in target tissues

48
Q

How are estrogens transported in the blood?

A

60% bound to albumin, 38% bound to SHBG, 2-3% free

49
Q

When are E1 and E3 primarily produced?

A

E1 (estrone) produced in higher amounts after menopause; E3 (estriol) produced by placenta (and also converted from estrone in the liver)

50
Q

Excessive estrogens can increase the risk of what?

A

breast and uterine cancer

51
Q

What is the difference between ERα and ERβ?

A

ERα mediates most reproductive effects of estrogens and ERβ mediates non-reproductive effects (cardioprotection, neuroprotection, mood)

52
Q

What are SERMs and what are they used for?

A

Selective Estrogen Receptor Modulators - bind to estrogen receptors and cause recruitment of a co-repressor that represses estrogen genes; used for breast cancer patients (ex: tamoxifen)

53
Q

How is progesterone transported in the blood?

A

mostly bound to albumin, low affinity for SHBG

54
Q

What are the main actions of progesterone?

A
  • prepares endometrium for implantation of embryo
  • inhibits myometrial contractions (maintains pregnancy)
  • stimulates mammary gland development
  • antagonizes actions of estrogen

fhb exam 4: endocrinology and reproduction (14 decks)

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