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Endocrine And Reproduction Exam #2 > Pregnancy, Parturition and Lactation > Flashcards

Pregnancy, Parturition and Lactation Flashcards

1
Q

What is the intervillous space?

A

Where blood exchange occurs. The “capillaries” of the placenta.

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2
Q

What is the functional unit of the placenta?

Why?

A

Chorionic villi.

It has extensive branches and increased SA to allow for exchange.

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3
Q

Which arteries (from mom) empty into the intervillous space?

A

Spiral as.

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4
Q

Maternal BF

A
  1. Blood enters via pulsitile spurts from uterus.
  2. Enters intervillous space toward chorionic plate.
  3. Blood bathes the chorionic villi and then moves to the basal plate.
  4. Enters larger maternal veins –> pelvic vs. –> circulation.
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5
Q

3 principal factors that regulate maternal BF

A

Maternal arterial BF
Intra-uterine pressure
Uterine contractions

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6
Q

What do uterine contractions do to BF?

What is the result?

A

They slow arterial inflow and cease venous drainage.

The volume in the inervillous space increases to provide continual (but reduced) exchange.

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7
Q

Where does oxygenated/nutrient-rich and deoxy blood come from?

A

OXY - umbilical v. (1 vein)

DEOXY - umbilical as. (2 arteries)

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8
Q

2 functions of amniotic fluid

A
  1. Mechanical buffer (protection)

2. Excretion of waste products from fetus

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9
Q

What is the effect of diffusion of O2 from mom into the chorionic villi?

A

Causes the PO2 of blood in the intervillous space to drop

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10
Q

How does the fetus compensate for the low PO2 of maternal blood in the intervillous space?

A

Mainly because FHb has a higher affinity for O2.

-also, there is generally increased CO and increased O2 carrying capacity (Hb) levels are high in pregnancy.

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11
Q 
Excretion of products across placenta
Urea/creatinine
Lipid-sol Hs
Glc
AAs
Vits/minerals
LDL/transferrin/Abs
A

Urea/creatinine: passive movement (F–>M)
Lipid-sol Hs: simple diffusion (both ways)
Glc: facilitated diffusion (M–>F)
AAs: secondary AT
Vits/minerals: AT
LDL/transferrin/Abs: receptor-mediated endocytosis

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12
Q

What cells of the placenta produce steroid/protein Hs?

A

Syncytiotrophoblasts

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13
Q 
hCG
Produced by:
Composed of:
Binding affinity:
Half-life:
A

Produced by syncytiotrophoblasts.
Composed of aGSU and B-hCG
BInds to high affinity to LH R
Long half-life

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14
Q

hCG and uptake into maternal circulation

A

Rapidly accumulate in circulation.
Detectable within 24 hrs.
Double every 2 days for first 6 wks until wk 10 (peak), then they fall to constant level.

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15
Q

Primary action of hCG

A

+ LH Rs of CL to maintain progesterone production for first 10 wks

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16
Q

hPL (human placental lactogen) is structurally similar to:

A

GH and PRL

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17
Q

What happens to levels of hPL during pregnancy?

A

Maternal levels rise progressively throughout pregnancy.

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18
Q

Function of hPL

A

Antagonistic effect to insulin –> diabetogenicity of pregnancy.
Causes lipolysis and leads to use of FFAs for energy by mom.
Increases Glc by inhibiting maternal Glc uptake.

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19
Q

Progesterone is needed to maintain what?

A

Inactivity of myometrium and a pregnant uterus

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20
Q

Regulation of progesterone and its concentrations during pregnancy

A

Mostly unregulated and increases throughout pregnancy

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21
Q

Major estrogen of pregnancy

A

Estriol

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22
Q

Estriol levels can be used to assess:

A

Fetal well-being

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23
Q

Functions of estrogen in pregnancy

A
  1. increase uteroplacental BF.
  2. enhance LDL receptor expression in syncytiotrophoblasts.
  3. increase PGs and oxytocin Rs –> parturition.
  4. increase growth and development of mammary glands.
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24
Q

What 2 things (in the menstrual cycle) does progesterone inhibit?

A

Inhibits myometrial contractions and inhibits menstruation.

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25
Q

What is the “window of receptivity”? What induces it? When is it?

A

Induced by progesterone.
It is the increased adhesivity of endometrium.
Day 20-24 of menstrual cycle.

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26
Q

How are elevated levels of progesterone and estrogens achieved in pregnancy?

A

hCG rescuing CL (1st trimester).

Placenta (by 8 wks it becomes major source of P and E).

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27
Q

Why is the placenta an “imperfect” endocrine organ?

A

Poor at making enough cholesterol.
No 17a and desmolase.
No 16a (needed for estriol synthesis).

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28
Q

How does the maternal-placenta-fetal unit overcome its imperfection? (2 ways)

A
  1. Mom supplies most cholesterol as LDL.

2. Fetal adrenals and liver supply the lacking enzymes of the placenta (17a, desmolase, 16a).

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29
Q

Why can’t the fetus make estrogens on its own?

A

No 3B-HSD or aromatase.

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30
Q

Why should the fetus NOT make estrogens on its own?

A

Because the mother needs the estrogens mainly, not the fetus.

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31
Q

The placenta is a sink for “weak androgens”. Why is that helpful?

A

It prevents the masculinization of a female

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32
Q

How does the fetus “weaken” steroid hormones?

A

Conjugates them to sulfate and lowers their activity.

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33
Q

Maternal BV during pregnancy

A

Begins to increase during 1st trimester, rises steeply 2nd trimester, rises slower 3rd trimester and plateaus last few wks of pregnancy.
Increases 40-50%.

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34
Q

What mediates the increase in BV during pregnancy?

A

Mainly mediated increased aldosterone

35
Q

MAP and BV during pregnancy

A

Surprisingly, BV increases and MAP decreases mid-pregnancy and rises in 3rd trimester, but is lower than normal.

36
Q

What is the reason for the low MAP initially?

A

Due to decreased PVR (because progesterone and estriol cause vasodilation).

37
Q

When does CO increase most in pregnancy?

A

Mostly in 1st trimester

38
Q

What does increased progesterone due to alveolar ventilation?

A

Increases alveolar ventilation –> increased tidal vol.

39
Q

GI changes during pregnancy

A

Prolonged gastric emptying
Increased GERD.
Decreased motility of colon –> constipation.

40
Q

Pregnancy causes increased demand for (3):

A

Protein
Iron
Folic acid

41
Q

What hormones cause the uterus to be “quiet” in pregnancy?

A

Progesteron and relaxin

42
Q

Birth ages (2)

A

Fetal age: 38 wks post fertilization

40 wks post LMP

43
Q

Obstetric definition of labor

A

Series of regular, rhythmic and forceful contractions that leads to thinning and dilation of cervix

44
Q

Presenting part

A

Part of baby that leads the way thru birth canal

45
Q

What is 0 station?

A

When baby’s head is even w/ ischial spines

46
Q

When is baby “engaged”?

A

When largest part of head has entered pelvis

47
Q

If presenting part lies above ischial spines, what is the station reported as?

A

A negative number: -1 to -5

Below would be positive number.

48
Q

What is the activity of the uterus toward the end of pregnancy? Why?

A

More excitable, due to hormonal changes and mechanical changes.

49
Q

Estrogen’r role in parturition

A

Increases uterine contractility.
From 7th mo gestation, estrogen increases and progesterone decreases.
Stimulates synthesis of oxytocin Rs.
Stimulates synthesis of PG.

50
Q

PGs (PGF2a ans PGE2) role in parturition

A

Initiate labor.
Increases motility of SM.
Can be used to induce labor.
Stimulated by uterine stretch.

51
Q

What H increases OT Rs in myometrium and decidual tissues? Why is OT not produced throughout pregnancy then?

A

Estrogen

Uterus is sensitive to OT only at end of pregnancy.

52
Q

Function of OT:

What stimulates its release?

A

+ powerful contractions to sustain labor.

+ by stretch of cervix.

53
Q

Who initiates labor: OT or PGs?

A

PGs initiate, OT does NOT initiate the contractions of uterus.

54
Q

OT can bind Rs on _______ and stimulate _______ production.

A

Decidual cells to + PGF2a production

55
Q

What is the purpose of OT immediately after baby is expelled?

A

TO limit blood loss and blood flow

56
Q 
Relaxin functions (2-3)
Where is it produced?
A

Keep uterus inactive during pregnancy and soften/dilate cervix during labor.
Produced by CL, placenta and decidua.

57
Q

Cortisol effect on uterus

A

Uterine stimulant

58
Q

Fetal placental membranes’ effect on uterus (2)

A

Release PGs during labor.

Increase intensity of uterine contractions.

59
Q

Why might twins be born earlier?

A

Because increased fetal movement can elicit SM contractions.

60
Q

Braxton Hicks contractions are?

What do they become?

A

Weak and slow rhythmic contractions that become stronger (known as labor contractions).

61
Q

Positive feedback during parturition

A

Fetus drops in uterus –> cervix stretches –> (+) uterine contractions and (+) OT release –> (+) PGs (which activate everything else)

62
Q

Ferguson reflex

A

Stretch of cervix –> uterine contraction

63
Q

Dilation and effacement:

What are contractions and frequency?

A

1st phase of delivery. The cervix preps for delivery.

Contractions < 10 min apart and avg 7-12 hrs duration.

64
Q

Descent and expulsion:

Duration of contractions:

A

2nd phase of delivery. Cervix is fully dilated (10 cm).

Avg 20-50 min duration

65
Q

Expulsion of the placenta:

Duration of contractions:

A

3rd phase of delivery. Uterus contracts. Separation of placenta –> bleeding/clotting.
Avg 15 min.

66
Q 
Prolonged labor is:
Main causes (3):
A

Labor longer than 18-24 hrs.

Poor uterine contractions, abnormal positioning of baby, pelvical/birth canal problems.

67
Q

Labor dystocia

A 
Obstructed labor.
Can cause prolonged labor.
Baby may not get enough oxygen.
Increased rick for mom.
May require C-section.
68
Q

Preterm labor

A

Labor before 37th wk.

69
Q

Preeclampsia occurs when?
What is it characterized by?
What is the cause?

A

Occurs after wk 20.
Characterized by HBP and signs of damage to another organ system (usually kidneys).
No known cause, but maybe due to disease of placenta.

70
Q

Anatomy of the breast

A

Alveoli –> Lobules (15-20) –> duct –> lactiferous duct.

71
Q

Hs leading to development of breasts in pregnancy (4)

A

PRL
hPL
Estrogens
Progesterone

72
Q 
Effects of Hs:
Mammogenic
Lactogenic
Galactokinetic
Galactpoietic
A

Mammogenic: + proliferation.
Lactogenic: + initiation of milk production.
Galactokinetic: + milk ejection.
Galactpoietic: maintain milk production after it is established.

73
Q

Secretory pathway of lactation (4)

A

Lactoalbumin and casein made in ER and sorted to golgi.
Alveolar cells add Ca2+ and phosphate to lumen.
Lactose synthetase made.
Exocytosis.

74
Q

How are Igs taken up thru the basolateral membrane?

A

Endocytosis and transported to apical membrane and secreted by exocytosis.

75
Q

Lipid pathway pf lactation

A

FA form lipid droplets that move to apical membrane and are pinched off and secreted in a membrane bound sac.

76
Q

Transcellular salt and water transport

A

Salt goes across many different ways.

Water follows osmosis laws.

77
Q

What can move paracellularly in the secretory epithelial cell of the breast?

A

Salt, water, Leukocytes

78
Q

What inhibits PRL?

A

High estrogen and progesterone

79
Q

Colostrum

A

Thin, yellowisk milk-like substance secreted first few days of parturition.
Has lots of Igs.

80
Q

Initiation of lactation

A

PRL up, Estrogen/Progesterone down.

Suckling**

81
Q

PRL and OT effect at the breast:

A

PRL - milk synthesis.

OT - contraction of myoepithelial cells –> ejection

82
Q

4 effects of suckling on H release

A
  1. Suckling stimulus (sight/sound of child)
  2. DA is inhibited
  3. Production and release of OT
  4. Decreased GnRH –> inhibits ovarian cycle
83
Q

Immuno factors in breast milk (3)

A

IgA
WBCs
Growth factors

Endocrine And Reproduction Exam #2 (6 decks)

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