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Endocrinology and Reproduction > Female Reproductive Endocrinology II > Flashcards

Female Reproductive Endocrinology II Flashcards

1
Q

In the selected follicle, fully differentiate into androgen producing cells, producing androstenedione and testosterone

A

Theca cells

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2
Q

Also, GC cells in the selected follicle begin to express high levels of

A

CYP19 (P450 aramotase) and 17B-HSD

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3
Q

The enzymes that convert androgens into E2

A

CYP19 (P450 aramotase) and 17B-HSD

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4
Q

During the advanced phase of antral follicle growth, a developmental switch occurs; whereby we see an increase in the production of

A

E2

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5
Q

This transient elevation in serum E2 exerts a positive feedback effect on the production and release of

A

FSH and LH from the pituitary

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6
Q

Rising FSH during the late follicular phase induces the expression of

A

LH receptors within the GC of the selected follicle

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7
Q

Therefore, the selected follicle can now respond to

A

FSH and LH

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8
Q

The rise in FSH and LH during the late follicular phase of the cycle supports further growth and differentiation of

A

Previously recruited younger follicles

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9
Q

The rise in FSH and LH during the late follicular phase of the cycle supports a robust increase in

A

Steroidogenesis by the selected follicle

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10
Q

The rise in FSH and LH during the late follicular phase of the cycle supports initial luteinization of the

A

Selected follicle

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11
Q

Inhibin B secretion drops just prior to mid-cycle; this releases its feedback inhibition on the pituitary peptide

A

Activin

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12
Q

Activin is expressed within gonadotropes, and activin stimulates

A

FSH secretion

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13
Q

The feedback dynamics between the selected follicle and the hypothalamus pituitary lead to the

A

Preovulatory gonadotropin surge

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14
Q

The combination of preovulatory levels of E2, rising progesterone, and an increase in inhibin A production by the (luteinizing) GC within the preovulatory follicle, and ultimately the corpus luteum, disrupts the patterns of

A

GnRH pulsatility

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15
Q

This results in negative feedback at the level of the hypothalamus on the secretion of both

A

FSH (E2 dependent) and LH (P4 dependent)

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16
Q

Note that the hypothalamus expresses

-mediate negative feedback on gonadotropin secretion

A

Estrogen receptor-alpha (ERa) and progesterone receptor

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17
Q

This results in a profound decline in gonadotropin secretion upon ovulation, and this continues through the

A

Luteal phase

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18
Q

During the luteal phase, we see a negative feedback on LH secretion via chronic stimulation by

A

Progesterone

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19
Q

It is this cyclical nature of E2, progesterone, and gonadotropin secretion, with inhibins and activin, that controls

A

Female Cyclicity

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20
Q

In antral follicles, theca cells are stimulated by LH to produce

A

Androstenedione and (some) testosterone

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21
Q

GC cells are then stimulated by FSH to

A

Aromatize these androgens

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22
Q

A product of GC within preantral and small antral follicles, and thus represents the number of follicles which reach somewhat advanced stages of development

A

AMH

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23
Q

Therefore, AMH is a marker of healthy growing follicles and this correlates with

A

Fertility

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24
Q

Following this peak in a woman’s mid-20s, AMH declines to undetectable levels around age

A

40-45 years

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25
Q

What this all means is that the depletion of the ovarian follicular reserve, and serum AMH levels are

A

Related

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26
Q

Indicates the greatest number of healthy growing follicles and hence, maximum fertility

A

Peak AMH

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27
Q

The decline in fertility which begins in a woman’s early 30s is reflected by the precipitous decline in

A

AMH

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28
Q

In a woman less than 38 years old with normal follicular status, serum AMH levels should be between

A

2.0-6.8 ng/mL

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29
Q

Dependent upon the gonadotropin surge, and LH is a main player

A

Ovulation

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30
Q

Can be considered the”ovulation gonadotropin”

A

LH

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31
Q

LH and FSH stimulate the terminal differentiation of GC; whereby GC switch from almost the exclusive production of E2 to the production of

A

E2 and progesterone (luteinization)

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32
Q

This change in steroidogenesis begins immediately prior to ovulation with the expression of LH receptors within the

A

GC of the dominant follicle q

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33
Q

A thermogenic hormone; this accounts for the biphasic 0.5 ˚F rise in basal body temperature that occurs upon ovulation and during the luteal phase

A

Progesterone

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34
Q

LH also stimulates the production of

A

Prostaglandins

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35
Q

Collectively, the aforementioned molecules dissociate some of the intercellular connections that join

A

GC

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36
Q

Increases in the follicular vasculature are also involved; these angiogenic effects appear to be mediated by

A

Prostaglandins, cytokines, and growth factors

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37
Q

The oocyte is ovulated with an attached surrounding layer of GC called the

A

Cumulus GC

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38
Q

Thus, the ovulated complex is referred to as the

A

Oocyte-cumulus complex

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39
Q

Upon ovulation, changes in cAMP signaling in the GC and oocyte signal the oocyte to complete the

A

First meiotic division

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40
Q

This can be identified microscopically by the extrusion of the first

A

Polar body into the ooplasm

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41
Q

A haploid product of meiosis I that contains one set of 23 paired chromosomes; this structure fragments and disappears

A

1st polar body

42
Q

The oocyte-cumulus complex is extruded into the region of the fimbrae of the

A

Oviduct (Fallopian tube)

43
Q

The remnant of what was the preovulatory follicle is just the

A

GC and theca cells

44
Q

The remnant of what was the preovulatory follicle is stimulated by LH to terminally differentiate into the

A

Corpus Luteum

45
Q

In general, in response to LH, luteal cells produce

A

E2 and progesterone

46
Q

Indicates that ovulation has occurred

A

Luteal progesterone

47
Q

A woman who has ovulated can predict a meager rise in basal body temperature through the

A

Mid-luteal phase of her cycle

48
Q

Targets the uterus, and has a quiescing effect on the myometrium (uterine muscle)

A

Progesterone

49
Q

The corpus luteum also produces

A

Inhibin A

50
Q

Like inhibin B during the early-mid follicular phase, inhibin A exerts negative feedback on

A

Gonadotropin secretion

51
Q

In the event of fertilization, elevated progesterone is absolutely required for

A

Implantation

52
Q

Has proliferative and angiogenic effects within the endometrium

-also required for implantation

A

E2

53
Q

If pregnancy does not occur, LH levels decline, and without LH, the corpus luteum undergoes

A

Degeneration (luteolysis)

54
Q

Mediated by prostaglandins and other factors

A

Luteolysis

55
Q

The fertile endometrium undergoes cycles of

A

Proliferation, differentiation, and tissue breakdown

56
Q

The endometrium has which two main layers?

A
  1. ) Functional upper layer

2. ) Deep basal layer

57
Q

During the proliferative (i.e. follicular) phase of the cycle, the endometrium is stimulated by

A

E2

58
Q

Within the functional endometrium, E2 induces the expression of

A

ERa, progesterone receptors (PR), and growth factors

59
Q

This enables regeneration (due to shedding from the previous cycle) and proliferation of the

A

Endometrium

60
Q

Recall that the secretory (i.e. luteal) phase of the cycle begins following

A

Ovulation

61
Q

During the early secretory phase, the endometrium is targeted by

A

E2 and progesterone

62
Q

Results in the development of a rich blood supply that supports the endocrine and paracrine mechanisms required for implantation of the blastocyst

A

E2 and Progesterone’s effects on the endometrium in early secretory phase

63
Q

With rising progesterone levels during the mid secretory phase, we see a down-regulation of

A

PR and ERa

64
Q

During the mid-phase, also causes changes in gene expression within the endometrium that induce decidualization

-prepares endometrium for implantation

A

Progesterone

65
Q

Consider that optimal conditions for implantation exist for approximately

A

6-10 days post LH surge

66
Q

During the late secretory phase, the uterus is essentially a refractory tissue; it briefly assumes the properties of a

A

Pregnant Uterus

67
Q

Should implantation occur, a complex cascade of events is initiated through interactions between the embryo and the decidua which maintain the

A

Pregnant Uterus

68
Q

Results from the precipitous drop in progesterone and E2 that occurs during the late\ luteal phase

A

Menstruation

69
Q

The processes which enable the endometrial breakdown in fact begin due to progesterone-stimulated changes in gene expression during the

A

Early secretory phase

70
Q

Primes the endometrium to shed

A

Progesterone

71
Q

In the absence of progesterone and E2 support, the upper 2/3 of the functional layer sheds off, the uterus again assumes the

A

Steroid-responsive phenotype

72
Q

Diagnosed as the inability of a couple to conceive after one year of unprotected intercourse

A

Infertility

73
Q

Indicates that a woman has never conceived

A

Primary infertility

74
Q

Type of infertility where a woman has conceived previously

A

Secondary infertility

75
Q

The incidence of diagnosed female infertility is approximately

A

13%

76
Q

The absence of menses by age 13 without normal growth or secondary sexual development; or no menses by age 15 with normal growth and secondary sexual development

A

Primary amenorrhea

77
Q

Having had one or more consecutive cycles with the absence of 3 consecutive cycles for 6 consecutive months

A

Secondary Amenorrhea

78
Q

Defects in the mechanisms leading to ovulation and/or the luteal phase are classified as

A

Functional causes of infertility

79
Q

Pelvic and cervical anomalies are classified as

A

Structural causes of infertility

80
Q

The basic premise for treating infertility is to support enhanced follicular growth so that several preovulatory follicles develop for

A

Retrieval or Ovulation

81
Q

The basic idea is to exogenously manipulate the hormonal regulation of the

A

Menstrual Cycle

82
Q

First,neuroendocrine function is controlled by the use of either a

A

GnRH agonist or antagonist

83
Q

A so-called selective estrogen receptor modulator (ER antagonist within the hypothalamus) which releases GnRH from feedback inhibition by E2

A

Clomiphene

84
Q

Therefore, the short term effect of Clomiphene is that of a

A

GnRH antagonist

85
Q

Can be given on days 3-5 of the cycle for 5 days, and this results in spikes of GnRH secretion

A

Clomiphene

86
Q

These GnRH spikes subsequently drive FSH secretion leading to enhanced follicular growth and the formation of several

A

Preovulatory follicles

87
Q

These follicles functionally differentiate as would occur naturally, and thus produce

A

E2 and inhibins

88
Q

In the event of a GnRH suppression protocol, a GnRH pulsatility is disrupted using either an antagonist (e.g., clomiphene) or agonist such as

A

Leuprolide

89
Q

Recall that the chronic loss of GnRH pulsatility, as occurs with GnRH antagonists or agonists, attenuates

A

FSH secretion

90
Q

This causes the down-regulation of the

A

Pituitary drive

91
Q

Once down-regulation has been established (as determined by a serum E2 < 50 pg/ml), we administer

A

Recombinant FSH (rFSH)

92
Q

After a few days of rFSH treatment, follicle growth is assessed by

A

Transvaginal ultrasound

93
Q

So long as ≥ 3 follicles with a diameter of ≥ 17 mm are detected, the processes leading to ovulation are induced by giving

A

hCG

94
Q

Oocytes are aspirated from the large follicles guided by transvaginal ultrasound at around

A

36 hours post hCG

95
Q

Keep in mind that with the development of several preovulatory follicles, and the exposure of these follicles to a hefty dose of LH (i.e. hCG), comes the normal pattern of increased

A

E2 secretion, luteinization (P4 secretion), and endometrial priming

96
Q

Under normal circumstances, fertilization occurs within the

A

Oviduct

97
Q

The oocyte can be fertilized up to approximately

A

24 hours post ovulation

98
Q

During the fertilization process, a single sperm burrows through the outer cumulus GC and binds to the

A

Zona pellucida of the oocyte

99
Q

The cortical reaction within the oocyte occurs as follows: sperm binding stimulates its incorporation into the ooplasm, and this is followed by which three things?

A
  1. ) Oocyte membrane hyperpolarization
  2. ) Increased intracellular [Ca2+]
  3. ) Cortical granule hardening
100
Q

These cellular changes prevent additional sperm-oocyte interactions, known as

A

Polyspermia

Endocrinology and Reproduction (15 decks)

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