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FHB Hormone/Repro > 86 - Pregnancy > Flashcards

86 - Pregnancy Flashcards

1
Q

What is the first hormone secreted by syncytiotrophoblasts during pregnancy?

A

hCG

- Spikes at 10 weeks gestation

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2
Q

What receptors does hCG bind?
Where?
Why?

A

Binds to LH receptors on corpus luteum and keeps it viable (recall, LH is inhibited at this point by high P, E, and inhibin)

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3
Q

What hormone is responsible for nausea/morning sickness in pregnancy?

A

hCG

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4
Q

Besides binding LH receptors and keeping the fetus viable, what else does hCG do? (2)

A
  • Stimulates fetal Leydig cells and fetal adrenal cortex

- Negative feedback actions on maternal HPG axis

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5
Q

What does hPL stand for?

What’s another name for it?

A
  • Human placental lactogen
  • hCS (human chorionic somatomammotropin)

(increases throughout gestation)

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6
Q

What 2 hormones are hPL structurally similar to?

A

PRL and GH

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7
Q

*How is hPL similar to GH, besides structure? (3)

A
  • Counter-regulatory to insulin (anabolic and lipolytic)
  • Mobilizes glucose for fetal use
  • Stimulates fetal IGF-I
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8
Q

How is hPL similar to PRL, besides structure? (1)

A

Stimulates mammary gland development

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9
Q

The 1st 1/2 of pregnancy is considered an __________ state, and the 2nd 1/2 a __________ state.

A
  • Anabolic (get nutrients)

- Starvation (so fetus can grow)

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10
Q

What pregnancy-related hormones cause pregnancy to be considered an “insulin resistant state”?

A
  • hPL, E, and P4

cortisol as well

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11
Q

Where is hPL produced?

A

Placenta

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12
Q

Is hPL essential for pregnancy?

A

No

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13
Q

hPL potentiates anti-insulin actions in the mother.
Why does it increase lipolysis?
Why does it increase proteolysis?

A
  • Lipolysis: FA’s for maternal use

- Proteolysis: AA’s for fetal use

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14
Q

What is the prognosis for pts w/gestational diabetes?

A

Usually resolves with end of pregnancy, but up to 50% will go on to develop T2DM.

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15
Q

What hormones are responsible for gestational diabetes?

A

Caused by anti-insulin effects of hPL, progesterone, prolactin, and cortisol

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16
Q

What are the risk factors for gestational diabetes?

A
  • Over age 25
  • Family hx of diabetes
  • Certain ethnic groups (e.g. native americans)
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17
Q

The placenta provides a semi-protective barrier from maternal factors.
Name as many of the functions of the placenta as you can. (5)

A
  1. Supportive: provides nutrients for fetal growth
  2. Immune: prevents rejection of fetus by mom
  3. Endocrine: hormones
  4. Gas exchange (O2, CO2)
  5. Regulates fluid levels, waste disposal
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18
Q

What (2) placental cell types secrete hormones? (they act in a hypothalamo-pituitary manner)

A
  • Cytotrophoblasts

- Syncytiotrophoblasts

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19
Q

Why is the placenta considered an “imperfect endocrine organ”?

A

Lacks critical enzymes to complete many steps in steroid hormone synthesis.
- This helps protect fetus from cortisol and high gonadal hormone levels

(still makes almost all hormones we’ve talked about, but not PRL, androgens, cortisol…)

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20
Q

What provides cholesterol to the fetus?

A

The mother (NOT the placenta)

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21
Q

What adrenal enzyme does the placenta lack?

What, therefore, can it not do?

A
  • CYP17

- Can’t create androgens or cortisol

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22
Q

Because it lacks CYP17, what (fetus, mother, or placenta) converts progesterone to androgens and other steroids?

A

Fetus

fetus produces mostly androgens

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23
Q

How is E3 (estriol) formed during pregnancy?

A

Placenta cant make it, so fetus makes DHEAS precursor that goes to the placenta to be converted to E3.

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24
Q

What happens to most cortisol in the fetus?

A

Converted to cortisone (inactive) by 11beta-HSD2

- Protects fetus

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25
Q

What is fetal ACTH’s effect on placental CRH?

A

Stimulates (positive feedback loop of steroid hormone synthesis)

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26
Q

Which of the fetal adrenal zones is the biggest?

A

“Fetal zone” (future ZR)

- Makes adrenal androgens throughout gestation

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27
Q

Do we see E in the fetus?

Why or why not?

A

No, could disrupt its development.

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28
Q

What does relaxin do?

A
  • Inhibits myometrial contractions (ensure uterine quiescence in early pregnancy)
  • Relaxes pelvic bones and ligaments and softens cervix
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29
Q

Where is relaxin produced? (2)

A
  • Corpus luteum (in response to hCG)

- Placenta

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30
Q

Where is PRL produced?

A

Maternal pituitary only (NOT placenta)

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31
Q

What does PRL do, and how are its affects altered by E and P4? (read first time)

A
  • Essential for mammotrophic effects of E and P4
  • Stimulates lactogenic apparatus during gestation, but significant lactation is inhibited by high levels of P4 and E
  • E stimulates growth of the lactotrophs and increases PRL secretion
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32
Q

What are the cardiovascular changes seen during pregnancy?

A
  • ^ CO (^ HR + ^ SV)
  • MSP decreases, TPR decreases more than CO increases.
  • Catecholamines mediate chronotropic and inotropic increases
  • Some CM
  • Pulmonary pressures stays the same, off setting the increase in volume with a decrease in resistance
  • Venous pressure increases, 150% venous distension
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33
Q

What are the regional blood flow changes seen during pregnancy?
(Uterus? Skin? Kidney?)

A
  • Uterus: may receive 30% of CO (spiral aa. ^ diameter)
  • Skin blood flow increases to maintain body temperature
  • Kidney blood flow increases and GFR increases
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34
Q

What are the blood changes seen during pregnancy?

What hormone mediates the change?

A
  • Increase in blood volume: 50% increase in 2nd trimester, mediated by P4, anticipates hemorrhage. Both plasma and - RBC increase (via cortisol), with a net decrease in Hct.
35
Q

What are the respiratory changes seen during pregnancy?

A
  • Diaphragm is elevated by about 5 cm (reduction in expiratory reserve)
  • Increase in tidal volume with no change in respiratory frequency (deeper breaths)
  • Increased tidal volume results in increased alveolar ventilation
    (“functional alkalosis”)
36
Q

What are the GI changes seen during pregnancy?

A
  • An additional 30g of protein per day are required
  • Constipation
  • GERD
37
Q

What are the endocrine changes seen during pregnancy?

A
  • HPG axis is suppressed by high concentrations of placental sex steroids.
  • There is a growth of pituitary lactotrophs and an increase in PRL secretion (GnRH suppression).
38
Q

What are the metabolic changes seen during pregnancy? (summarize 1st vs. 2nd 1/2 of preg)

A

First half of pregnancy: mother is in anabolic state

  • Nl or ^ sensitivity to insulin
  • Increased fat deposition, glycogen stores
  • Promotes breast growth in mother and allows her to “stockpile”” nutrients to meet the demands of the enlarging fetus.

Second half of pregnancy: “accelerated starvation,” catabolic state characterized by insulin resistance.

  • Mediated by hPL
  • Increased plasma glucose and fatty acid levels
39
Q

What is parturition?

A

The action of giving birth

40
Q

Before labor starts, what hormone keeps the uterus inactive?

A

Progesterone

41
Q

Briefly, what are the 3 phases of labor?

A
  1. Activation of the uterus
  2. Positive feedback phase
  3. Evacuation of the uterus
42
Q

What is the Ferguson reflex?

A

Uterine stretch from mature fetus stimulates oxytocin, which stimulates more stretching, which stimulates more OXY (positive feedback loop)

43
Q

What occurs during phase 1 of labor? (activation of the uterus)
(What HPA axis hormone peaks?)

A
  • Release from inhibitory actions of P4
  • Ferguson reflex
  • Fetal HPA axis is activated – CRH levels peak
44
Q

What occurs during phase 2 of labor? (positive feedback)

A
  • Widening (dilation) and thinning (effacement) of cervix
45
Q

What occurs during phase 3 of labor? (evacuation of the uterus)

A
  1. Expulsion of fetus from uterine compartment and 2. release of placenta
46
Q

The initiation and maintenance of labor and uterine
evacuation are influenced by P4, E2, cortisol, relaxin, oxytocin, CRH, prostaglandins, catecholamines. The most dominant of these is the decrease in ______________ and increase in _______________.

A
  • Progesterone

- Estradiol

47
Q

Recall: how many AA’s is OXY?

A

9 AAs

48
Q

______________ increases the number of OT receptors in myometrial tissues in pregnancy, increasing the potency of a given concentration of OT.
(OT = oxytocin)

A

Estrogen

49
Q

When is the uterus most sensitive to OT?

A

During labor

50
Q

What is pitocin?

A

Synthetic OT used to induce labor

51
Q

Besides the Ferguson reflex, what other reflex involves OT?

A

Suckling on breast (another feedback loop)

52
Q

What does OT stimulate the release of that also causes uterine contractions?

A

Prostaglandins

53
Q

What other roles does OT have during birth besides Ferguson reflex and prostaglandins?

A
  • Promotes hemostasis of expelled placenta vessels.

- Stimulates maternal behaviors postpartum (important for maternal bonding)

54
Q

Besides OT, what else leads to increased local prostaglandins that leads to an increase in myometrial cell Ca2+, yielding more forceful myometrial cell contractions?

A

Decrease in the progesterone/E2 ratio

55
Q

What changes signal the ability for the mother to begin lactating?

A

Placenta no longer present, so decreased P4 and E2

56
Q

What hormone is high during milk secretion?

A

PRL

57
Q

What hormones does breast suckling stimulate the release of?

A

PRL, OT

58
Q

What other hormone does PRL affect?

A

Inhibits GnRH

59
Q

What other things does PRL affect besides lactation?

A

Like OT, stimulates maternal behavior during pregnancy and after parturition

60
Q

Mammary gland development is initiated at puberty through the action of __________ (hormone) and growth factors.
What hormones lead to its further differentiation during pregnancy?

A

E2

- E2, PRL, hPL

61
Q

Lactation is inhibited by high ____________ (hormone) during pregnancy.

A

P4

62
Q

What’s the name of the first breast milk produced?

How is it different from other types of milk?

A

Colostrum
- Less fat, higher protein

(cow milk very high in calcium)

63
Q

What 3 hormones are essential for continued milk production?

A

PRL, cortisol, insulin

64
Q

An infant’s cry can lead to the production of what hormone by the mother?

A

OT
- Increased contraction of myoepithelial cells, alveoli and smooth muscle of duct walls causes “milk letdown” for infant.

65
Q

What are the 2 overall effects of PRL?

A

Mammogenic effects, galactogenic effects

66
Q

What are the 3 non-endocrine and non-drug methods of contraception?

A
  1. Abstinence
  2. Coitus interruptus
  3. Barriers
67
Q

What is abstinence? (detail)

A

Natural family planning: periodic abstinence from intercourse during the fertile period surrounding the time of ovulation (”rhythm method”)

68
Q

What is coitus interruptus?

A

Withdrawal before ejaculation

69
Q

What are some barriers?

A

Condoms, diaphragms, sponge, and cervical caps in combination with spermicides

70
Q

How does BCP work? (just read)
At what levels does it work?
Why is it good for controlling heavy menstrual bleeding?

A

Multiple levels:

  • Acts on CNS and urogenital tract to inhibit reproductive function
  • Pituitary and Hypothalamus: prevents LH surge and ovulation
  • Basal gonadotropin levels are decreased
  • Ovary: follicular growth is inhibited
  • Fallopian tube motility decreased
  • *Glandular atrophy in uterine endometrium: why it is good for controlling heavy menstruation
  • Inhibits implantation of blastocyst
  • Causes thick cervical mucus: inhibits sperm motility and migration
71
Q

Progestational hormone prevents _____________ secretion.

A

LH (including blocking LH surge)

72
Q

Estrogenic hormone inhibits _____________ release.

A

FSH

- Estrogen also stabilizes endometrium and potentiates progestin action.

73
Q

What are some of the benefits of using contraceptives, besides not having a baby?

A
  • Tx of excessive menstrual bleeding
  • Protection for pelvic inflammatory disease
  • Dysmenorrhea
  • Hormone replacement therapy in postmenopausal women
74
Q

What are some of the risks and side-effects of contraceptives?

A
  • Contraindicated in heavy smokers over 35 and those with a history of estrogen-dependent breast carcinomas
  • HTN, myocardial infarction, stroke
  • Blood clots
  • Depression
  • Decreased libido
75
Q

To define female puberty, which of the “arche” occurs before which other “arche”?

A

Thelarche before menarche

- Breast buds tend to develop before periods

76
Q

Menarche (first menses) usually occurs between __ and __ years.
(What is average age in U.S.?)

A

11-14 y/o

- Avg age in U.S. is 12.5 years

77
Q

No pubertal development by age __ warrants investigation.

A

13

78
Q

In terms of Tanner stage differences, what is generally considered abnormal?

A

A greater than 2 stage difference

79
Q

What’s the first sign of pubertal development in males?

A

Increase testicular size (over 3mL)

80
Q

What’s the first sign of pubertal development in females?

A

Breast buds (thelarche)

81
Q

Puberty is considered ‘precocious’ if before age __ in males, __ in females.

A

9 (males)

6 (females, but 6-7 could be abnormal as well)

82
Q

Discuss the 5 stages of Tanner female breast development.

A
  1. Child’s typical appearance
  2. Increasing growth
  3. Increasing growth
  4. Nipple forms *secondary mound
  5. Adult (areola on plane w/rest of breast tissue)
83
Q

Discuss the 5 stages of Tanner female pubic hair development.
How is it different in the male?

A
  1. No hair
  2. Peach fuzz
  3. *Coarse hair
  4. Growth
  5. More growth
  • Basically the same for male and female stages
84
Q

Discuss the 5 stages of Tanner male testicle and penis development.

A
  1. Tiny (typical child)
  2. *Over 3mL volume (first sign of puberty in males)
  3. Growth
  4. More growth
  5. Adult size

FHB Hormone/Repro (16 decks)

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