Female Reproductive Endocrinology III Flashcards by Joel Glotfelty

Once the sperm fertilizes the oocyte, we see the

Second meiotic division of the oocyte

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

-contains haploid chromosomes

Pronucleus

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The female and male pronuclei fuse and form the

Diploid conceptus (Zygote)

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

X or Y chromosome

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

Pregnancy

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

Mitotic divisions

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

) Outer cell layer (trophoblast)

2. ) Inner cell mass (embryo)

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This differentiated structure is identified as the

Blastocyst

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

Zona Pellucida

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Required for the implantation of the embry into the uterine wall

The so-called zona hatching process

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Generally occurs somewhere around 4-6 days following fertilization

Implantation

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About 1 in 5 pregnancies result in

Spontaneous abortion

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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

Pregnancy

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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

Effector T cells

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The maternal placenta is comprised of

Endometrial tissue

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The fetal placenta differentiates from the

Trophoblast cells

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

Chorion

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

Umbilical arteries and veins

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

Passive diffusion

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Undergo facilitated diffusion between the mother and fetus

Glucose and lactate

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

) Transport
) Immune
) Endocrine

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Forms during the first 5 weeks of embryonic growth

Amniotic cavity

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

Amniotic fluid

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The fetal stage of pregnancy begins at

Week 10

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

Fetal growth

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

Hyperplasia

After approximately 32 weeks, fetal growth is due to

Hypertrophy

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

40%

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

25%

The trophoblast chorionic cells secrete the protein hormone

hCG

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

7-14 days post ovulation

A good clinical marker of pregnancy

hCG doubling time

Binds to the LH receptor and stimulates the corpus luteum to continue producing progesterone -has LH like bioactivity

hCG

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

Progesterone

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

Progesterone replacement

The loss of corpus luteum does not affect pregnancy after around

46 days

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

Early first trimester

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

Terminated

Remember, folliculogenesis and ovulation can not occur without

FSH and LH

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

Urine of pregnant women

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

Progesterone and E2 production

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

Maternal recognition of pregnancy

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

Placental steroidogenesis

Placental progesterone production is driven by an abundant supply of

LDLs and VLDLs

Unlike gonadal and adrenal steroidogenesis, placental steroidogenesis is not

Acutely regulated

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

Hypothalamic/pituitary production of gonadotropins

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

Arrested

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

Oral contraceptives

Serves as the substrate for fetal estrogen production

DHEA

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

Pregnancy

Ensure that numerous fetal tissues/structures develop properly

Mitosis and apoptosis

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

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

After the first trimester, we see a decline in

hCG

Serum progesterone, estrogens, and CRH all peak during the

Third trimester

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

Estrogen Receptor (ER)

This is in order to prevent estrogenic actions such as

Uterine myometrial contraction

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

Gene transcription

This results in the expression of myometrial

Contractile proteins

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

CRH

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

E3 production

This raises the ratio of E3:E2 to approximately

10:1

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

Uterine contraction

What happens in the event of fetal death?

E3 plummets and E2 dominates

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

Progesterone

Important fetal anabolic hormones

IGF-I and IGF-2

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

Placental GH and Human placental lactogen

Maternal serum concentrations of IGF-I peak during the

Third trimester

Recall that glucocorticoid synthesis is under the control of

ACTH (corticotropin)

ACTH secretion is stimulated by

CRH

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

Delivery

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

Organogenesis and maturation

Recall that CRH stimulates the anterior pituitary corticotropes to secrete

ACTH

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

Glucocorticoids (Cortisol) and DHEAS

Upregulates the placental expression of CHR

Cortisol

A precursor for the formation of estrogens

DHEAS

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

11B-HSD2

Catalyzes the conversion of cortisol into the relatively inert metabolite cortisone

11B-HSD2

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

Cortisol

During a healthy pregnancy, intravascular volume increases as much as

50%

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

Week 30

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

Progesterone, E2, and RAS

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

Progesterone

Activates the RAS causing secretion of aldosterone

Placental E2

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

AVP

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

GFR

Elevated GFR can saturate

SGLT2

This SGLT2 saturation results in the non-pathologic -seen in 50% of women during pregnancy

Glucosuria

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

Local vasodilators

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

Pulse pressure (due to lower Diastolic pressure)

BP increases to prepregnancy levels at around week

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

Weeks 12-24

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

Weeks 25 on

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

Increased HR

During pregnancy, Hb content is

Elevated

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

Plasma volume

We call this condition

Dilutional Anemia

However, O2 delivery is mintained by the increase in

Cardiac Output

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

Pregnancy

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

High flow/low pressure environment

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

Tidal volume