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Endocrinology and Reproduction > Female Reproductive Endocrinology III > Flashcards

Female Reproductive Endocrinology III Flashcards

1
Q

Once the sperm fertilizes the oocyte, we see the

A

Second meiotic division of the oocyte

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2
Q

This is identified by the extrusion of the second polar body, and the appearance of the female

-contains haploid chromosomes

A

Pronucleus

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3
Q

The female and male pronuclei fuse and form the

A

Diploid conceptus (Zygote)

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4
Q

Gender of the coneptus is determined by the male contribution of either an

A

X or Y chromosome

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5
Q

It is not until after the first several weeks following fertilization that the maternal neuroendocrine system recognizes

A

Pregnancy

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6
Q

As the zygote migrates downward through the oviduct and toward the uterus, it undergoes several

A

Mitotic divisions

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7
Q

Following the formation of the morula, then blastula, the embryonic cells begin to differentiate into the

A
  1. ) Outer cell layer (trophoblast)

2. ) Inner cell mass (embryo)

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8
Q

This differentiated structure is identified as the

A

Blastocyst

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9
Q

Within the uterus, the blastocyst undergoes compaction, and then hatches from the outer layer of remaining

A

Zona Pellucida

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10
Q

Required for the implantation of the embry into the uterine wall

A

The so-called zona hatching process

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11
Q

Generally occurs somewhere around 4-6 days following fertilization

A

Implantation

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12
Q

About 1 in 5 pregnancies result in

A

Spontaneous abortion

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13
Q

Experimental evidence indicates that suppression of the maternal immune system within the uteroplacental unit and lymph nodes proximal to this region is an important mechanism that enables

A

Pregnancy

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14
Q

Moreover, the presence of paternal alloantigens have actually been shown to induce an increase in extrathymic regulatory T cells which in turn suppress the activity of

A

Effector T cells

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15
Q

The maternal placenta is comprised of

A

Endometrial tissue

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16
Q

The fetal placenta differentiates from the

A

Trophoblast cells

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17
Q

The fetal placenta differentiates from the trophoblast cells and is known as the

A

Chorion

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18
Q

The chorion is required for the formation of the highly vascularized chorionic villi, as well as the eventual formation of the

A

Umbilical arteries and veins

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19
Q

Blood gases and urea are exchanged between the mother and fetus via

A

Passive diffusion

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20
Q

Undergo facilitated diffusion between the mother and fetus

A

Glucose and lactate

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21
Q

The placenta serves three equally important functions throughout pregnancy. What are they?

A
  1. ) Transport
  2. ) Immune
  3. ) Endocrine
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22
Q

Forms during the first 5 weeks of embryonic growth

A

Amniotic cavity

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23
Q

Important for the proper development of the embryonic, renal, and respiratory systemms

A

Amniotic fluid

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24
Q

The fetal stage of pregnancy begins at

A

Week 10

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25
Q

Is in essence controlled by the maternal genome, maternal nutrition, and maternal environment

A

Fetal growth

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26
Q

During the earlier embryonic stages, fetal growth is predominantly due to

A

Hyperplasia

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27
Q

After approximately 32 weeks, fetal growth is due to

A

Hypertrophy

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28
Q

During a healthy pregnancy, maternal blood volume and cardiac output rise by approximately

A

40%

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29
Q

What percentage of cardiac output is devoted to uteroplacental blood flow?

A

25%

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30
Q

The trophoblast chorionic cells secrete the protein hormone

A

hCG

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31
Q

A placental isoform of GnRH drives hCG production, and a rise in hCG can be detected beginning approximately

A

7-14 days post ovulation

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32
Q

A good clinical marker of pregnancy

A

hCG doubling time

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33
Q

Binds to the LH receptor and stimulates the corpus luteum to continue producing progesterone

-has LH like bioactivity

A

hCG

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34
Q

hCG takes over the function of pituitary LH by stimulating the corpus luteum to secrete high levels of

A

Progesterone

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35
Q

Interestingly, loss of the corpus luteum (pathologic or surgical) within the first 35 days or so of pregnancy will result in abortion without

A

Progesterone replacement

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36
Q

The loss of corpus luteum does not affect pregnancy after around

A

46 days

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37
Q

This underscores the shift in dependence from luteal to placental progesterone secretion which occurs during the

A

Early first trimester

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38
Q

In response to elevated progesterone, the hypothalamic GnRH pulse generator is disrupted, and the release of pituitary gonadotropins is

A

Terminated

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39
Q

Remember, folliculogenesis and ovulation can not occur without

A

FSH and LH

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40
Q

A clinical marker for identifying pregnancy because it can be easily detected in the

A

Urine of pregnant women

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41
Q

By the end of the third month (the end of the first trimester), the trophoblast cells of the placenta assume the majority of

A

Progesterone and E2 production

42
Q

This switch from luteal to placental control of the hormonal regulation of pregnancy is described as the

A

Maternal recognition of pregnancy

43
Q

As the trophoblast mass increases during gestation, we see a rise in

A

Placental steroidogenesis

44
Q

Placental progesterone production is driven by an abundant supply of

A

LDLs and VLDLs

45
Q

Unlike gonadal and adrenal steroidogenesis, placental steroidogenesis is not

A

Acutely regulated

46
Q

The sustained production of progesterone and estrogens by the placenta maintains a negative feedback effect on the

A

Hypothalamic/pituitary production of gonadotropins

47
Q

Since no appreciable FSH is present, folliculogenesis beyond early antral development is

A

Arrested

48
Q

Contain a ratio of progesterone:estrogen that is sufficient to block LH secretion and thus prevent menstrual cycles

A

Oral contraceptives

49
Q

Serves as the substrate for fetal estrogen production

A

DHEA

50
Q

Maternal and fetal tissues work in concert to produce the steroid hormones (progesterone and estriol, E3) that support

A

Pregnancy

51
Q

Ensure that numerous fetal tissues/structures develop properly

A

Mitosis and apoptosis

52
Q

Beginning early within the first trimester, we see and increase in the production of which 4 things?

A
  1. ) The estrogens
    a. ) E2
    b. ) Estriol (E3)
    c. ) Estrone (E1)
  2. ) Corticotropin-releasing hormone (CRH)
53
Q

After the first trimester, we see a decline in

A

hCG

54
Q

Serum progesterone, estrogens, and CRH all peak during the

A

Third trimester

55
Q

When present in approximately equal amounts, E2 and E3 actually antagonize activation of the

A

Estrogen Receptor (ER)

56
Q

This is in order to prevent estrogenic actions such as

A

Uterine myometrial contraction

57
Q

However, whenever E2 or E3 rises, we see ER dependent changes in

A

Gene transcription

58
Q

This results in the expression of myometrial

A

Contractile proteins

59
Q

During the terminal stage of gestation, fetal adrenal DHEAS levels rise in response to increasing

A

CRH

60
Q

DHEAS is hydroxilated by 16a-hydroxylase. The metabolism of 16a-DHEA leads to a preferential increase in placental

A

E3 production

61
Q

This raises the ratio of E3:E2 to approximately

A

10:1

62
Q

This leads to the sequential activation of the ER and estrogen responsive genes which promote

A

Uterine contraction

63
Q

What happens in the event of fetal death?

A

E3 plummets and E2 dominates

64
Q

Another key component of parturition (birth) involves a slight drop in

A

Progesterone

65
Q

Important fetal anabolic hormones

A

IGF-I and IGF-2

66
Q

Stimulate maternal IGF-1 production and concomitantly upregulate the expression of IGFs in fetal tissues

A

Placental GH and Human placental lactogen

67
Q

Maternal serum concentrations of IGF-I peak during the

A

Third trimester

68
Q

Recall that glucocorticoid synthesis is under the control of

A

ACTH (corticotropin)

69
Q

ACTH secretion is stimulated by

A

CRH

70
Q

The placenta produces CRH; maternal CRH levels rise throughout pregnancy and peak at

A

Delivery

71
Q

Placental CRH is key in a feed-forward system that is vital for governing the production of glucocorticoids which are critical for fetal

A

Organogenesis and maturation

72
Q

Recall that CRH stimulates the anterior pituitary corticotropes to secrete

A

ACTH

73
Q

Within the adrenal cortex (fasciculata and reticularis), ACTH promotes the secretion of

A

Glucocorticoids (Cortisol) and DHEAS

74
Q

Upregulates the placental expression of CHR

A

Cortisol

75
Q

A precursor for the formation of estrogens

A

DHEAS

76
Q

This system induces a level of maternal serum cortisol, which would be detrimental to fetal health. The placenta affords a protective function against this by the expression of

A

11B-HSD2

77
Q

Catalyzes the conversion of cortisol into the relatively inert metabolite cortisone

A

11B-HSD2

78
Q

Exerts effects in fetal organs such as lung maturation and production of surfactant

A

Cortisol

79
Q

During a healthy pregnancy, intravascular volume increases as much as

A

50%

80
Q

This begins during the first trimester, with a rapid rise during the 2nd trimester, and plateaus around

A

Week 30

81
Q

The increase in intravascular volume is controlled by several factors; noteworthy for our purposes are the effects of

A

Progesterone, E2, and RAS

82
Q

Stimulates erythropoesis, resulting in an approximately 30% increase in RBC volume

A

Progesterone

83
Q

Activates the RAS causing secretion of aldosterone

A

Placental E2

84
Q

During pregnancy, there is a profound increase in H2O reabsorption and thus a decrease in serum [Na+]. This is the result of

A

AVP

85
Q

Creatinine production remains essentially unchanged during a healthy pregnancy; however we do see an increase in

A

GFR

86
Q

Elevated GFR can saturate

A

SGLT2

87
Q

This SGLT2 saturation results in the non-pathologic

-seen in 50% of women during pregnancy

A

Glucosuria

88
Q

Interestingly, the vasopresser effect of An-II is not manifested due to the counter regulatory effects of

A

Local vasodilators

89
Q

In fact during pregnancy, we see a slight reduction in BP and a widening of

A

Pulse pressure (due to lower Diastolic pressure)

90
Q

BP increases to prepregnancy levels at around week

A

36

91
Q

During pregnancy, cardiac output increases by about 40% with 25-30% of this rise due to an increase in SV during

A

Weeks 12-24

92
Q

Additionally there is around a 24% SV increase that occurs from

A

Weeks 25 on

93
Q

Accounts for the majority of upregulation of CO that occurs during pregnancy

A

Increased HR

94
Q

During pregnancy, Hb content is

A

Elevated

95
Q

However, we still see a condition of physiologic anemia due to the great increase in

A

Plasma volume

96
Q

We call this condition

A

Dilutional Anemia

97
Q

However, O2 delivery is mintained by the increase in

A

Cardiac Output

98
Q

Also, relative to a non pregnant woman, a vasodilatory state occurs during

A

Pregnancy

99
Q

This aids in systemic blood flow and is also important for facilitating perfusion of the placenta which depends upon a

A

High flow/low pressure environment

100
Q

During pregnancy, minute ventilation increases by about 30-50%, mainly due to an increase in

A

Tidal volume

Endocrinology and Reproduction (15 decks)

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