Female Reproductive Endocrinology IV Flashcards by Joel Glotfelty

Exerts a stimulatory effect on the medullary respiratory drive center

-accounts for increased VT during pregnancy

Progesterone

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During pregnancy functional residual capacity and expiratory reserve volume decrease approximately

20%

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This 20% decrese in FRC and ERV is because of the

Elevated diaphragm and decrease in chest wall compliance seen in pregnancy

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Remember from pulmonary function that a PaO2 of 60% represents about

90% Saturation of Hb with O2

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Defined as PaO2 less than 60% or Saturation less than 90%

Hypoxemia

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Fetal oxygenation will be maintained so long as maternal PaO2 remains

At or above 60%

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Realize that the demands of a growing fetus dramatically increase maternal metabolism; this causes an increase in

-Helps drive increased minute ventilation

CO2 production

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A couple of things result from the reduced PaCO2. First, lower PaCO2 creates a pressure gradient that is favorable for the offloading of

Fetal CO2

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Second, low PaCO2 results in reduced PACO2, allowing for increased

PAO2

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Therefore, the alveolar-to-arterial O2 gradient is favorable for the diffusion of O2 from

Alveoli to blood

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During the first trimester, this increases PaO2 to as much as

-facilitates maternal to fetal O2 transfer

106-108 mmHg

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Recall that reduced PaCO2 due to increased ventilation is defined as respiratory alkalosis. This is compensated by the renal excretion of HCO3-, such that maternal HCO3- is around

18-21 meq/L

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So, the maternal acid-base condition is either

) Compensated chronic respiratory alkalosis

2. ) Chronic respiratory alkalosis w/ compensatory metabolic acidosis

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During pregnancy, O2 carrying capacity is increased due to

Elevated Hb

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The fetal Hb-O2 dissociation curve is shifted to the left due to lower levels of

2,3-DPG

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Recall that a leftward shift in the curve causes increased affinity of Hb for O2; thus enabling maximal extraction of O2 from

Maternal Blood

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Full term birth is considered to be delivery anywhere between

37 and 42 Weeks

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Approximately 5-15% of pregnancies result in preterm birth. This accounts for approximately

70& of neonatal mortality

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Secreted from the corpus luteum to soften the pelvic ligaments in preparation for parturition

Relaxin

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Serum concentrations of relaxin begin to rise during the

Third trimester

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Changes in the levels of CHR, progesterone receptor activity, and production of prostaglandins mediate

Initiation of labor

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As term nears. an inflammatory process occurs within the fetal membranes. This is known as

Fetal membrane activation

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Within the chorion and amnion this process results in the cessation of production of inhibitors of

Prostaglandin production

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Prostaglandins are involved in which two hallmark events during the onset of labor?

Cervical ripening (softening) and myometrial contraction

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Cervical softening is also promoted by the actions of an inflammatory infiltrate which results in the release of

Matrix metalloproteases

These metalloproteases degrade cervical

Collagen

In order for labor contractions to occur, there must be synergy and permissive actions between estrogens, prostaglandins, and

Oxytocin

Steadily increases and peaks during delivery

CHR

Stimulates cortisol secretion and cortisol induces the production of surfactant

CRH

In addition to its effects on fetal/neonatal pulmonary function, some surfactant is released into the amniotic fluid where it is believed to exert the inflammatory actions within the myometrium and cervix that promote

Labor

A typical myometrial contraction manifests a slow rise and fall of tension over approximately

1 minute duration

Also dependent on the changing role of estrogens during pregnancy

Myometrial activation

Initially induces uterine growth, but this effect terminates toward term

Estrogen

Although the uterus stops growing, the fetus continues a remarkable rate of growth; this results in tension against the uterine wall. Like most other smooth muscle organs, stretch stimulates

Contraction

In women who breastfeed, there is a special neuroendocrine/hormone system activated.This system is mediated by

Prolactin (PRL) and oxytocin

The processes that enable lactation are established during pregnancy when estrogen stimulates the proliferation of

Mammary ductal epithelial cells

At the same time, mammary alveoli growth is stimulated by

Progesterone

Secreted from anterior pituitary lactotrophs and is under control of numerous factors

PRL

Inhibits PRL secretion via activation of D2 receptors

Dopamine

What are three positive regulators of PRL secretion

E2, Oxytocin, and prolactin-releasing peptide

Within the mammary gland, PRL upregulates

Milk production (lactation)

Milk letdown (the secretion of milk) is prevented during pregnancy due to the combined elevation in maternal serum concentrations of

Estrogens and Progesterone

Maternal estrogen and progesterone levels fall following parturition; this frees the suckling induced neuroendocrine mechanisms which cause

Milk let-down

Suckling activated neural tracts which lead to the inhibition of

Dopamine Secretion

Thus suckling prevents dopamine induced

Inhibition of PRL

Suckling also induces the secretion of oxytocin from the

Posterior pituitary

Maintain milk production and induce milk let-down, respectively

PRL and oxytocin

Another component of the suckling reflex blocks activity within the preoptic nucleus. Recall that this is the site for

GnRH production

Therefore, suckling also disrupts the secretion of

FSH and LH (thus disrupting reproductive cycle)

In addition, PRL can directly suppress

Gonadotropin secretion

A pathologic condition most commonly due to a prolactinoma

Hyperprolactinemia

Symptoms of hyperprolactinemia include

Galactorrhea and reproductive dysfunction

In women, this condition can manifest as amenorrhea, oligomenorrhea, menorrhagia, or regular menses with infertility (attributable to a shortened luteal phase)

Hyperprolactinemia

Can result in loss of libido, erectile dysfunction, premature ejaculation, and impaired spermatogenesis

Hyperprolactinemia in men

As described above, the decline in female fertility begins around age 30-35 years due to less

Follicular recruitment

The peri-menopausal transition generally begins in the mid-late 4th decade and lasts for approximately

3-4 Years

During this transition, the menstrual cycle becomes irregular with periods of

Amenorrhea

Characterized by 12 months of amenorrhea

Menopause

Menopause prior to age 40 is abnormal and is classified as

Primary ovarian insufficiency

The onset of ovarian failure occurs in the presence of increased plasma

FSH

The menopausal transition encompasses approximately 4 years in most women, and during this time frame, we see the greatest rate of change in the pattern of plasma

FSH and E2 levels

Beginning around 2 years preceding the last menstrual period (LMP), FSH begins to rise, and plasma FSH increases steadily until about

2 years after LMP

These changes in FSH and E2 production are due to the severely depleted

Follicles

Evidence shows that inhibin B levels are reduced in

Perimenopausal women

Recall that inhibin B is secreted by GC and suppresses

FSH secretion

Therefore, without the normal influence of inhibin B, FSH secretion is relatively unimpeded. In the presence of elevated FSH, more follicular growth could occur during each cycle, but still only one follicle will be

Selected to ovulate

Secreted from the GC within small growing follicles and suppresses recruitment and reduces sensitivity of young follicles to FSH

AMH

Since the overall number of follicles is depleted, we see a decrease in the levels of

AMH

From a functional viewpoint, the loss of the counter-modulatory effect of AMH on recruitment may free-up the entry of some more of what few follicles remain into the growing cohorts, exacerbating

Follicular depletion

Undetectable by the time a woman enters the menopausal transition

AMH

Has been identified as a marker to predict the onset of Menopausal transition

AMH

Women in their 40s (and possibly early 50s) can undergo menses; however, oocyte viability is

Drastically compromised

In addition to the increased risk of fetal genetic abnormalities (e.g., aneuploidies), maternal complications during pregnancy, and fetal/neonatal death are significantly elevated in

Reproductively aged women

With less follicular development comes a lower level of

E2 and testosterone production

The disruption in ovarian steroidogenesis leads to menstrual irregularities due to a

Prolonged follicular phase

During menopause, the follicular reserve has been severely depleted and normal menstruation does not occur. The normal FSH:LH ratio is increased and we see a precipitous decline in

E2 production

Other postmenopausal occurrences can include an increase in the ratio of serum LDL:HDL, and atherosclerosis; markers of increased

Cardiovascular risk

Although not life-threatening, the loss of E2 production can also cause the psychologically disturbing problems of

Urinary incontinence, hot flashes, and night sweats

Hormone therapy can promote a favorable serum lipid profile in some women, but there are no data showing a beneficial effect of HT on reducing the risk of

Coronary heart disease

A general rule of thumb for administering hormone therapy to women who are candidates is

1. ) with uterus: estrogen and progesterone | 2. ) Without uterus: estrogen only

It has been reported that it is appropriate to recommend HT to women who are not at elevated risk for breast cancer and with normal

Venous thromboembolitic and CV disease risk

Current evidence does not support the use of estrogen + progesterone or estrogen alone for long-term prevention of

Chronic disease

How much testosterone do the ovaries produce per day?

approximately 300 ug

The overwhelming majority of testosterone secreted by the ovaries is converted to

An androgen deficiency can occur in post menopausal women, and this lack of testosterone has been associated with decreased

Libido

Anything that disrupts the normal production of FSH and LH will cause disorders of the

Reproductive system

Normally, the circadian rhythm for GnRH secretion occurs in a pulsatile manner; defined by temporal changes in the amplitude and frequency of

GnRH release

Sustained elevation of GnRH will down-regulate the secretion of

FSH and LH

Sustained use of exogenous androgens, such as anabolic androgenic steroids will impair the neuroendocrine system in a similar fashion, and cause

Infertility in women and men

Affects approximately 6-20% of reproductive age women. As such, it represents the most common endocrine disorder affecting women of reproductive age

Polycystic Ovary Syndrome (PCOS)

Clinically defined by infertility resulting from oligomenorrhea (less than 9 cycles per year) and or amenorrhea

PCOS

Diagnosed by: 1) history of irregular menses and anovulation, with onset at puberty; 2) chemically measurable hyperandrogenemia (ovarian androgens including free and total testosterone; presence of hirsutism); and 3) exclusion of other hormonal pathologies which have similar clinical features

PCOS

Was historically named due to the presence of large follicular cysts within the ovaries

PCOS

Is the presence of follicular cysts required for the diagnosis of PCOS?

PCOS is now classified as a

Metabolic disease

What are the four different sets of criteria that can be applied for diagnosing PCOS?

1) Hyperandrogenism with chronic anovulation 2) Hyperandrogenism plus polycystic ovaries with ovulation 3) Chronic anovulation plus polycystic ovaries w/out hyperandrogenism 4) Chronic anovulation plus hyperandrogenism with polycystic ovaries

For our purposes, please recognize PCOS that is (arguably) most commonly a condition of

Hyperandrogenic anovulation

When present, the cystic follicles are in some undefined arrested stage of folliculogenesis, and as such, do not

Ovulate an oocyte

Women with PCOS are more often than not

Overweight w/ android distribution

Are hyperandrogenemic (elevated serum androgens: testosterone, DHT, and/or DHEA-S) and/or present with hyperandrogenism

Women with PCOS

Female Reproductive Endocrinology IV Flashcards

(100 cards)