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Endocrinology and Reproduction > Female Reproductive Endocrinology IV > Flashcards

Female Reproductive Endocrinology IV Flashcards

1
Q

Exerts a stimulatory effect on the medullary respiratory drive center

-accounts for increased VT during pregnancy

A

Progesterone

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2
Q

During pregnancy functional residual capacity and expiratory reserve volume decrease approximately

A

20%

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3
Q

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

A

Elevated diaphragm and decrease in chest wall compliance seen in pregnancy

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4
Q

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

A

90% Saturation of Hb with O2

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5
Q

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

A

Hypoxemia

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6
Q

Fetal oxygenation will be maintained so long as maternal PaO2 remains

A

At or above 60%

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7
Q

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

-Helps drive increased minute ventilation

A

CO2 production

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8
Q

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

A

Fetal CO2

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9
Q

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

A

PAO2

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10
Q

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

A

Alveoli to blood

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11
Q

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

-facilitates maternal to fetal O2 transfer

A

106-108 mmHg

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12
Q

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

A

18-21 meq/L

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13
Q

So, the maternal acid-base condition is either

A
  1. ) Compensated chronic respiratory alkalosis

2. ) Chronic respiratory alkalosis w/ compensatory metabolic acidosis

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14
Q

During pregnancy, O2 carrying capacity is increased due to

A

Elevated Hb

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15
Q

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

A

2,3-DPG

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16
Q

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

A

Maternal Blood

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17
Q

Full term birth is considered to be delivery anywhere between

A

37 and 42 Weeks

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18
Q

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

A

70& of neonatal mortality

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19
Q

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

A

Relaxin

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20
Q

Serum concentrations of relaxin begin to rise during the

A

Third trimester

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21
Q

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

A

Initiation of labor

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22
Q

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

A

Fetal membrane activation

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23
Q

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

A

Prostaglandin production

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24
Q

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

A

Cervical ripening (softening) and myometrial contraction

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25
Q

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

A

Matrix metalloproteases

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26
Q

These metalloproteases degrade cervical

A

Collagen

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27
Q

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

A

Oxytocin

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28
Q

Steadily increases and peaks during delivery

A

CHR

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29
Q

Stimulates cortisol secretion and cortisol induces the production of surfactant

A

CRH

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30
Q

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

A

Labor

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31
Q

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

A

1 minute duration

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32
Q

Also dependent on the changing role of estrogens during pregnancy

A

Myometrial activation

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33
Q

Initially induces uterine growth, but this effect terminates toward term

A

Estrogen

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34
Q

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

A

Contraction

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35
Q

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

A

Prolactin (PRL) and oxytocin

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36
Q

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

A

Mammary ductal epithelial cells

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37
Q

At the same time, mammary alveoli growth is stimulated by

A

Progesterone

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38
Q

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

A

PRL

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39
Q

Inhibits PRL secretion via activation of D2 receptors

A

Dopamine

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40
Q

What are three positive regulators of PRL secretion

A

E2, Oxytocin, and prolactin-releasing peptide

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41
Q

Within the mammary gland, PRL upregulates

A

Milk production (lactation)

42
Q

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

A

Estrogens and Progesterone

43
Q

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

A

Milk let-down

44
Q

Suckling activated neural tracts which lead to the inhibition of

A

Dopamine Secretion

45
Q

Thus suckling prevents dopamine induced

A

Inhibition of PRL

46
Q

Suckling also induces the secretion of oxytocin from the

A

Posterior pituitary

47
Q

Maintain milk production and induce milk let-down, respectively

A

PRL and oxytocin

48
Q

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

A

GnRH production

49
Q

Therefore, suckling also disrupts the secretion of

A

FSH and LH (thus disrupting reproductive cycle)

50
Q

In addition, PRL can directly suppress

A

Gonadotropin secretion

51
Q

A pathologic condition most commonly due to a prolactinoma

A

Hyperprolactinemia

52
Q

Symptoms of hyperprolactinemia include

A

Galactorrhea and reproductive dysfunction

53
Q

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

A

Hyperprolactinemia

54
Q

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

A

Hyperprolactinemia in men

55
Q

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

A

Follicular recruitment

56
Q

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

A

3-4 Years

57
Q

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

A

Amenorrhea

58
Q

Characterized by 12 months of amenorrhea

A

Menopause

59
Q

Menopause prior to age 40 is abnormal and is classified as

A

Primary ovarian insufficiency

60
Q

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

A

FSH

61
Q

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

A

FSH and E2 levels

62
Q

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

A

2 years after LMP

63
Q

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

A

Follicles

64
Q

Evidence shows that inhibin B levels are reduced in

A

Perimenopausal women

65
Q

Recall that inhibin B is secreted by GC and suppresses

A

FSH secretion

66
Q

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

A

Selected to ovulate

67
Q

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

A

AMH

68
Q

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

A

AMH

69
Q

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

A

Follicular depletion

70
Q

Undetectable by the time a woman enters the menopausal transition

A

AMH

71
Q

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

A

AMH

72
Q

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

A

Drastically compromised

73
Q

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

A

Reproductively aged women

74
Q

With less follicular development comes a lower level of

A

E2 and testosterone production

75
Q

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

A

Prolonged follicular phase

76
Q

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

A

E2 production

77
Q

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

A

Cardiovascular risk

78
Q

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

A

Urinary incontinence, hot flashes, and night sweats

79
Q

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

A

Coronary heart disease

80
Q

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

A
  1. ) with uterus: estrogen and progesterone

2. ) Without uterus: estrogen only

81
Q

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

A

Venous thromboembolitic and CV disease risk

82
Q

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

A

Chronic disease

83
Q

How much testosterone do the ovaries produce per day?

A

approximately 300 ug

84
Q

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

A

E2

85
Q

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

A

Libido

86
Q

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

A

Reproductive system

87
Q

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

A

GnRH release

88
Q

Sustained elevation of GnRH will down-regulate the secretion of

A

FSH and LH

89
Q

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

A

Infertility in women and men

90
Q

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

A

Polycystic Ovary Syndrome (PCOS)

91
Q

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

A

PCOS

92
Q

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

A

PCOS

93
Q

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

A

PCOS

94
Q

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

A

No

95
Q

PCOS is now classified as a

A

Metabolic disease

96
Q

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

A

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

97
Q

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

A

Hyperandrogenic anovulation

98
Q

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

A

Ovulate an oocyte

99
Q

Women with PCOS are more often than not

A

Overweight w/ android distribution

100
Q

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

A

Women with PCOS

Endocrinology and Reproduction (15 decks)

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