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Human Reproduction > Week 3: Ovarian and Menstrual Cycle > Flashcards

Week 3: Ovarian and Menstrual Cycle Flashcards

1
Q

Identify

A
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2
Q

When does oogenesis begin?

A

~week 4 of embryo

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3
Q

When does follicle formulation begin?

A

~week 18

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4
Q

How many oogonia do you have at birth

A

somewhere between 400,000 and 600,000 for your entire reproductive life

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5
Q

Describe the meitotic arrest of oocytes

A

All eggs are arrested at an early stage (prophase I) of the first meiotic division as a primary oocyte (primordial follicle). Following purberty, during each menstrual cycle, pituitary gonadotrophin stimulates completion of meiosis 1 the day before ovulation

Meiosis I proceeds until birth and then picks up again after puberty

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6
Q

Describe the process of the menstrual cycle

A
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7
Q

Portion of the ovary where the vasculature comes in

A
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8
Q

What is the final fate of corpus luteum

A

Corpora albicans (scars throughout every menstrual period of lifetime)

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9
Q

of Primordial follicles

A

about 400,000 - 600,000

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10
Q

What are the possible fates of primordial follicles?

A

Each primordial follicle has four possible fates:

  • remain quiescent
  • die by attrition
  • begin development but later be lost by atresia
  • or begin development and ultimately release an oocyte followed by formation of a short-lived corpus luteum
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11
Q

Describe the process of growth of Primordial follicles

A

they undergo cycles of growth and atresia

For the beggining growth after puberty, they grow independent of hormonal stimulation

If they are not rescued by gonadotropins they go into a cycle of atresia (85 days)

Growth is promoted by FSH

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12
Q

Follicle activation reversibility

A

follicle activation is irreversible

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13
Q

Describe the process of recruitment of primordial follciles

A
  • Early growth is independent of hormonal stimulation and eventually cells reach a stage where they need to be rescued by FSH or will become atretic (atresia)
  • follicles continue over several cycles of growth and rescued by gonadotropins (FSH) to grow each time
  • The follicle destined to ovulate is recruited (along with a cohort of other follicles which managed to achieve adequate hormonal stimulation
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14
Q

Identify the features of primordial follicles

A
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15
Q

Describe the signalling pathway for primordial follicles

A

Endocrine cycle of hypothalamus ant pit amd ovary

hypothalamus -GnRH-> Ant. Pit -FSH & LH-> Ovary primordial follicle growth by FSH

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16
Q

What is the effect of FSH on primordial follicles

A

FSH induces aromatization of androgen and results in the production of estrogen in granulosa cells

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17
Q

Estrogen synthesis in granulosa cells

A

FSH -> granulosa cell FSH receptor activates aromatase

Androstendione/testosterone -Aromatase-> Estrone/Estradiol

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18
Q

How is a primordial follicle chosen for ovulation?

A

The follicle which produces the most estrogen from:

FSH stimulation and the conversion of Androstendione/Testosterone -aromatase-> Estrone/Estradiol

The production of E2 actually further stimulates the granulosa cell to convert more androstendione to Estradiol by increasing the number of FSH receptors on the surface of the granulosa cell

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19
Q

E2 AKA

A

Estradiol

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20
Q

What is Estradiol?

A

A very potent form of estrogen produced by granulosa cells in response to FSH activation of aromatase

Estradiold is also the most common estrogen component of birth control pills

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21
Q

Most common estrogen component of birth control pills

A

Estradiol

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22
Q

FSH receptor signals for upregulation

A

FSH and E2

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23
Q

Where are FSH receptors first detected on primordial follicles?

A

FSH receptors are first detected on the pre-antral follicle

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24
Q

Primordial follicle Estrogen production is limited by?

A

The number of FSH receptors

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25
Q

Ways to upregulate FSH receptors

A
  • FSH raises the concentration of its own receptor on granulosa cells
  • Estrogen increases the concentration as well
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26
Q

The success of pre-antral folicles to ovulate depends upon?

A

its ability to convert an androgen-dominated microenvironment to an estrogen-dominated microenvironment

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27
Q

What happens to a follicle/granulosa cells that are dominated by androgens?

A

wont become the dominant follicle

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28
Q

Identify features of secondary (pre-antral) follicles

A
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29
Q

Where are LH receptors in respect to the mestrual cycle during the secondary follicle stage

A
  • LH receptors are present only on the Theca cells
  • FSH receptors are only on the granulosa cells
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30
Q

What receptors do Theca cells have

A

During the secondary follicle stage Theca cells have LH receptors

*FSH receptors are only on the granulosa cells*

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31
Q

What receptors do granulosa cells have during the secondary follicle stage?

A

During the secondary follicle stage Granulosa cells have FSH receptors

*LH receptors are only on Theca cells*

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32
Q

Aromatase activity in Granulosa cells and Theca cells

A

The aromatase activity of granulosa cells far exceeds

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33
Q

Theca cells and granulosa cells function in making estrogen

A

LH receptor on theca cells causes conversion of cholesterol to androstendione

Granulosa cells also convert cholesterol to androstendione but not as much as theca cells

the androstendione then is converted by aromatase which is activated by FSH receptors

Theca cells produce more substrate (androstendione) for the aromatase in granulosa cells to produce more E2

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34
Q

Features of a tertiary follicle

A

Antrum which is filled with an estrogen rich fluid

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35
Q

How many follicles are still in the race in the tertiary follicle stage?

A

still a bunch

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36
Q

So how is a dominant follicle chosen?

A
  • Estrogen acts as a negative feedback inhibitor of the hupothalamus (GnRH) which results in reduced pulsatile GnRH secretion and reduced FSH secretion
  • Less FSH to the ovary leads to less help from FSH of the follicles
  • The follicles that really upregulated the FSH receptors are able to continue to grow leading to a dominant follicle
  • The fall of FSH leads to limited estrogen production of the less mature follicles
  • The dominant follicle overcomes the decline of FSH by
    • having more FSH receptors due to increased rate granulosa cell development and enhanced FSH action because of its high intrafollicular Estrogen concentration
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37
Q

Describe features of graffian follicle

A

increased vascularity brings more nutrients and FSH for more estrogen production

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38
Q

menstrual cycle day 9 events

A

On cycle day 9, the vascularity in the dominant follicle is twice that of other antral follicles allowing preferrential delivery of gonadotropins to the follicle

This is important for both the emerging dominant follicle as well as the early corpus luteum

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39
Q

dominat follicle and increasing negative feedback

A

The dominant follicle optimizes its own environment to the detriment of the lesser follicles

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40
Q

Graffian follicle progression

A
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41
Q

FSH focus change

A
  • Mid-cycle, with increasing estrogen in the follicle, FSH changes its focus from up-regulating its own receptor to generation of LH receptors on the granulosa cells
  • LH can also induce the formation of its own receptors in FSH-primed granulosa cells
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42
Q

What is the functional change of LH receptors appearing on the granulosa cells

A

This increase in LH receptors on the granulosa cells helps to prepare the follicle to become the corpus luteum

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43
Q

Describe the dual role of estrogen in the menstrual cycle

A
  • Estrogen can have both negative and positive feedback on LH
  • At low levels estrogen has a negative feedback on LH
  • As estrogen levels increase it exerts a positive stimulatory feedback on LH
  • This level of estrogen is generally not reached until the dominant follicle reaches ~15mm in diameter
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44
Q

Function of inhibin in the menstrual cycle

A

Important inhibitor of FSH secretion

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45
Q

Function of activin in the menstrual cycle

A

Stimulates FSH release in the pituitary and augments FSH activity in the ovary

46
Q

Function of follistatin in the menstrual cycle

A

Suppresses FSH activity (likely by bindind activin)

47
Q

Types of inhibin

A

Inhibin A

Inhibin B

48
Q

When is inhibin A secreted and by what?

A
  • secreted in the follicular phase by granulosa cells
49
Q

When is inhibin B secreted and by what?

A

Secreted in the luteal phase

50
Q

What stimulates the secretion of inhibin A?

A

Stimulated by FSH

51
Q

What is the function of inhibin A?

A

suppresses FSH secretion

This withdrawal of FSH caused by inhibin further amplifies the effects on smaller follicles, helping to secure growth of the emerging dominant follicle

52
Q

Graffian follicle and ovulation

A

LH helps synthesize proteases and cell membrane enzymes to cleave the follicle

bursts open releasing the oocyte

53
Q

Describe corpus luteum formation

A
  • upon ovulation, the membrane between granulosa cells and theca cells of the empty follicle breaks down and blood vessels invade
  • granulosa cells hemorrhage into follicle and hypertrophy to form large yellow lutein cells
  • Theca cells form the small lutein cells
  • Both make progesterone due to LH stimulation
54
Q

Describe the features of the luteal phase

A
  • Progesteron produced by luteal cells
  • Corpus luteum makes inhibin which inhibits FSH secretion
  • Progesterone rises - negative feedback to hypothalamus and pituitary
  • LH decreases from the negative feedback so progesterone decreases
55
Q

Possible fates of the corpus luteum

A

sperm fertilizes egg process of pregnancy (corpus albicans)

or

process of menstruation

56
Q

Identify hormones at specific time periods in the menstrual cycle

A

1 = FSH

2 = Estrogen

3 = LH

4 = Progesterone

57
Q

Ovulation and meiosis

A
  • Stimulation to ovulate (rising LH) induces the egg to continue through meisosis
  • The first meiotic division is completed and the first polar body is formed prior to release of the egg from the ovary
  • The second meiotic division begins immediately but stops at metaphase, where the oocyte remains arrested until fertilization
  • Penetration by the sperm triggers completion of the final meiotic division and the formation of the second polar body
58
Q

Abnormal menses Mnemonic

A

PALM-COEIN

Polyp

Adenomyosis

Leiomyoma (submucosal or other)

Malignancy & hyperplasia

Coagulopathy

Ovulatory dysfunction

Eendometrial

Iatrogenic

Not yet classified

or

POLICEMAN

59
Q

menorhhaga amount of blood

A

~>80cc

60
Q

Question 1

A

E. Progesterone

61
Q

Histology of endometrium

A
62
Q

What phase is this endometrium in?

A

Early proliferative

63
Q

What phase is this endometrium in?

A

Late proliferative

64
Q

What phase is this endometrium in?

A

Secretory

65
Q

What phase is this endometrium in?

A

Menstrual

66
Q

Day 1 of the menstrual cycle is?

A

Menses

67
Q

When is progesterone in the menstrual cycle

A

only in the second half of the menstrual cycle

68
Q

What does estrogen do to the endometrium

A

growth and proliferation

69
Q

What does progesterone do to the estrogen

A

causes a little bit of growth but to create a 1:1 gland to stroma ratio and caps the growth for a stable structure for the possibility of implantation

70
Q

Describe an endometrial biopsy

A
71
Q

Simplified menstrual cycle for clinical purposes

A
72
Q

What is the most common cause of irregular menstruation

A

anovulation

73
Q

Endometrial cycle

A

estrogen first

progesterone after arrow (ovulation)

74
Q

Question 2

A

A. Adenomyosis

nonfocal thickening and myometrium and pelvic pain are the clues

75
Q

what kind of Symptoms from endometrial polyps

A

abnormal bleeding

76
Q

what kind of Symptoms from endometritis

A

signs of infection

77
Q

what kind of Symptoms from Leiomyoma

A

Heavy bleeding

78
Q

what kind of Symptoms from Mittelschmerz?

A

pain of ovulation (middle cycle pain)

79
Q

Adenomyosis vs Leiomyomata

A

Adenomyosis - endometrial glands and stroma in the myometrium (a form of endometriosus)

Leimyomata - polyp or fibroids

80
Q

Question 3

A

C. Elevated LH

81
Q

PCOS AKA

A

Polycystic Ovarian Syndrome

82
Q

Polycystic Ovarian Syndrome clinical presentation

A
  • Hyperandrogenism
  • Anovulation
  • Obesity/infertility
83
Q

Polycystic Ovarian Syndrome epidemiology

A

5-10% of women

84
Q

Polycystic Ovarian Syndrome diagnostic criteria

A
  • Irregular menses caused by anovulation or irregular ovulation
  • Evidence of elevated androgen levels
    • signs (excess hair growth, acne or male-pattern balding)
    • Blood tests (high androgen levels)
  • Polycystic ovaries on pelvic ultrasound
85
Q

Etiology of PCOS

A
  • Insulin resistance
    • leads to increased insulin
    • high levels of insulin lead to increased production of ovarian androgens
    • Interferes with ovulation, leading to infertility
    • 50% risk of Type 2 diabetes by age 40
  • High levels of LH and androgens interfere with menstrual cycle
  • Classically, LH/FSH ratio is high
86
Q

Question 4

A

B. Complex hyperplasia

87
Q

Anovulation and the endometrium

A

unopposed estrogen

88
Q

Pathophysiology of complex hyperplasia

A

Unopposed estrogen

89
Q

Histology of complex hyperplasia

A
90
Q

Endometrial cancer pathophysiology

A

More unopposed estrogen

91
Q

Histology of Endometrial cancer

A
92
Q

Question 5

A

D. 21 days

because 35 - 14 = 21 days

the luteal phase of the menstrual cycle is very regular while the follicular phase can be highly variable in length

93
Q

Menstrual cycle length

A

majority of women 28 days

94
Q

What determines the menstrual cycle length?

A

The duration of the follicular phase determines the menstrual cycle length (12-16 days)

The luteal phase is constant at 14 days

95
Q

Length of the menstrual period closer to menopause

A

The follicular phase shortens the closer to menopause resulting in a shorter mentrual cycle length

96
Q

Question 6

A

C. Granulosa cells begin to express LH Receptors

97
Q

Describe the 2-cell gonadotropin model

A

occurs around mid-cycle

before mid-cycle the granulosa cells only have FSH receptors

98
Q

Wrong answers to question 6

A
99
Q

Important concepts of the 2-cell gonadotropin model

A
100
Q

Question 7

A

A. Anovulatory cycles

clues:

  • *proliferative*
  • disorganized endometrial glands
  • on day 20 she should be in the secretory phase
  • since shes not must be anovulatory
  • straight glands (progesterone causes 1:1 gland to stroma and they tend to be more tortuous)
101
Q

Question 8

A

B. Complex hyperplasia

clues:

  • 4 months of continuous bleeding throughout her cycle (think anovulation)
  • anovulation is a risk factor for hyperplasia
  • small crowded glands with atypia (atypia is concerning for endometrial cancer)
102
Q

Question 9

A

E. Low progesterone

luteal phase defect should be debunked but the idea is that there is not a long-enough luteal phase, however, the luteal phase is thought to be constant so it doesn’t make a lot of sense

but the thought is that;

not enough LH receptors leading to insufficient progesterone leading to inadequate luteal phase

103
Q

Describe the Luteal phase defect

A

luteal phase defect should be debunked but the idea is that there is not a long-enough luteal phase, however, the luteal phase is thought to be constant so it doesn’t make a lot of sense

but the thought is that;

not enough LH receptors leading to insufficient progesterone leading to inadequate luteal phase

104
Q

Question 10

A

E. Progesterone

105
Q

Question 11

A

E. Ovarian follicle

106
Q

Question 12

A
107
Q

Whats likely and whats bad?

A
108
Q

Describe anovulation

A
109
Q

Additional considerations

A
110
Q

Endometrium on COCs

A

Human Reproduction (40 decks)

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