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Endo Test 2 > Pregnancy > Flashcards

Pregnancy Flashcards

1
Q

what is timeline of fertilization/implantation?

A

Ovulation: 0 days after ovulation
fertilization: 1 day after
blastocyst enters uterine cavity: 4 days
implantation: 5 days
trophoblast forms and attaches to endometrium: 6 days
trophoblast begins to secrete hCG: 8 days
hCG rescues CL: 10 days

  • during pregnancy, duration is determined by date of last menstrual cycle: naormally 40 weeks total or 38 days after ovulation
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2
Q

whats detected in pregnancy test?

A

Beta hCG: peaks at 10 weeks of gestation

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3
Q

what is the timing of the major hormones of pregnancy?

A
  • hCG is seen first. it rescues the CL, to stimulate luteal E and P production
  • Placenta takes over hormone synthesis from CL around 8 weeks: “Luteal-placental shift”. P and E levels may decrease during transition
  • 2nd/3rd trimester: maternal P and E levels continue to rise. Maternal-placental-fetal unit takes over production
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4
Q

what is hCG produced by?

A

syncytiotrophoblasts

  • rapidly accumulates in maternal circ. within 24 hrs. of implantation
  • considered to be resp. for morning sickness
  • hCG peaks 10 weeks after implantation
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5
Q

what is hCG most similar to? what does hCG do?

A
  • most similar to LH. binds LH receptor with high affinity.
  • primary action is to stimulate LH receptors, and maintain luteal-derived progesterone production before the placenta takes over (1st ten weeks)
  • can also cross react with TSH receptors and can result in hyperthroidism. Also stimulates fetal Leydig cells to secrete testosterone. stimulates fetal adrenal cortex
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5
Q

what is hCG most similar to? what does hCG do?

A
  • most similar to LH. binds LH receptor with high affinity.
  • primary action is to stimulate LH receptors, and maintain luteal-derived progesterone production before the placenta takes over (1st ten weeks)
  • can also cross react with TSH receptors and can result in hyperthroidism. Also stimulates fetal Leydig cells to secrete testosterone. stimulates fetal adrenal cortex
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6
Q

Progesterone production

A

Luteal-placental shift is completed at about 8 weeks: where there is a switch from CL derived to placent-derived progesterone

  • there is an increase in maternal P throughout pregnancy
  • P production is indep. of fetus, can’t be used as an indicator of fetal health
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6
Q

Progesterone production

A

Luteal-placental shift is completed at about 8 weeks: where there is a switch from CL derived to placent-derived progesterone

  • there is an increase in maternal P throughout pregnancy
  • P production is indep. of fetus, can’t be used as an indicator of fetal health
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7
Q

main role of progesterone?

A

***inhibits myometrial contractions, i.e. quiesence, decreased uterine motility

  1. increased secretory activity that is necessary for nourishment, growth and implantation of embryo
  2. increased fat deposition early in pregnancy (stimulates appetite, diverts energy stores from sugar to fat)
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7
Q

main role of progesterone?

A

***inhibits myometrial contractions, i.e. quiesence, decreased uterine motility

  1. increased secretory activity that is necessary for nourishment, growth and implantation of embryo
  2. increased fat deposition early in pregnancy (stimulates appetite, diverts energy stores from sugar to fat)
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8
Q

What are the major estrogens?

A

Estradiold 17beta
Estrone
Estriol (major estrogen of pregnancy, requires health fetus)

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8
Q

What are the major estrogens?

A

Estradiold 17beta
Estrone
Estriol (major estrogen of pregnancy, requires health fetus)

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9
Q

what can be indication for fetal health?

A

estriol levels

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9
Q

what can be indication for fetal health?

A

estriol levels

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10
Q

what do estrogens do?

A

↑ Uteroplacental blood flow
↑ Uterine smooth muscle hypertrophy
↑ LDL receptor expression on syncytiotrophoblasts
↑ Prostaglandins
↑ Oxytocin receptors
↑ Mammary gland growth
↑ Prolactin secretion (maternal pituitary)
* essential for partuition
** E:P ratio shifts later in pregnancy, preparing for partuition.

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10
Q

what do estrogens do?

A

↑ Uteroplacental blood flow
↑ Uterine smooth muscle hypertrophy
↑ LDL receptor expression on syncytiotrophoblasts
↑ Prostaglandins
↑ Oxytocin receptors
↑ Mammary gland growth
↑ Prolactin secretion (maternal pituitary)
* essential for partuition
** E:P ratio shifts later in pregnancy, preparing for partuition.

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11
Q

what are maternal pituitary changes?

A
  1. increased PRL (estrogen stimulates PRL syth and secretion), lactotroph hypertrophy and hyperplasia
  2. increased pituitary size: if compressed against optic chiasm, enlarged pituitary can cause dizziness and vision problems. Can be susceptible to vascular insult and necrosis (i.e. Sheehan’s syndrome)
  3. decreased LH and FSH production: neg feedback inhibition of estrogens and progesterone
  4. ADH secretion augmentd (threshold altered by progesterone action) ADH released at lower osmolality (higher ADH levels earlier) = lower set point
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11
Q

what does decreased P allow for

A

decreased P after parturition allows for PRL action on the breast and lactation

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12
Q

what is hPL produced by?

A

syncytiotrophoblasts (made by placenta)

  • detected in maternal serum by 3 weeks
  • levels rise throughout pregnancy in direct proportion to placental weight
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12
Q

what is hPL produced by?

A

syncytiotrophoblasts (made by placenta)

  • detected in maternal serum by 3 weeks
  • levels rise throughout pregnancy in direct proportion to placental weight
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13
Q

main role of hPL?

A

ensure adequate glucose availability to fetus.

  • antagonizes insulin action –> diabetogenicity of pregnancy: inhibits maternal glucose uptake
  • causes lypolytic action: shifts maternal energy use to FFa’s
  • stimulates mammary gland development
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13
Q

main role of hPL?

A

ensure adequate glucose availability to fetus.

  • antagonizes insulin action –> diabetogenicity of pregnancy: inhibits maternal glucose uptake
  • causes lypolytic action: shifts maternal energy use to FFa’s
  • stimulates mammary gland development
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14
Q

what are key endocrine functions of placenta?

A
  1. Maintain pregnant state of the uterus: via P
  2. Stimulate lobuloalveolar growth and function of maternal breasts (PRL and hPL, E )
  3. Adapt aspects of maternal metabolism and physiology to support fetal growth (hPL)
  4. Regulate aspects of fetal development
  5. Regulate the timing and progression of parturition (E and prostaglandins)
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15
Q

what do synctiotrophoblasts produce?

A

steroid and protein hormones of the placenta

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16
Q

Placental limitations?

A
  1. can’t produce enough cholesterol for adequate steroidogenesis (mother can contribute this)
  2. lacks enzymes needed for estrone and estradiol production (fetus can produce these)
  3. lacks enzyme for estroil production (16 alpha hydroxylase)
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17
Q

what are maternal pituitary changes?

A

increased PRL (estrogen stimulates PRL syth and secretion), lactotroph hypertrophy and hyperplasia

increased pituitary size: if compressed against optic chiasm, enlarged pituitary can cause dizziness and vision problems. Can be susceptible to vascular insult and necrosis (i.e. Sheehan’s syndrome)

18
Q

change in MAP?

A

can be decreased or stay the same
- due to increased CO and decreased TPR
MAP = CO x TPR

19
Q

what are maternal adrenal changes?

A
  • increased cortisol: both total and free x2
    (increased total b/c estrogen stimulates increased production of CBG)
  • increased aldosterone : 8-10x
    (Estrogen stimulates increased liver production of ANG and Renal Renin) - does not results in hypernatremia, hypokalemia or hypertension. progesterone blunts aldosterone action by competing for mineralacorticoid receptors
20
Q

normal increase of weight gain?

A

25-35 lbs - depends on BMI

21
Q

Cardiovascular changes:

A
  1. increased Blood volume: decreased hematocrit
  2. increased CO: increased HR and SV
  3. decreased TPR: decreased hematocrit, increased vasodilation and vascularity (low-resistance placental circuit)
  4. decreased MAP (or normal): because of increased CO and decreased TPR
22
Q

change in plasma volume?

A
  • increased NaCL retention: due to increased Ang and Renin production stimulated by E. causes increased Aldo
  • increased H2O retention and intake: lower threshold for ADH and thirst during pregnancy (results in decreased overall osmolality); cause by increased sensitivity in osmoreceptors
23
Q

change in hematocrit?

A

decreased hematocrit “physiological anemia”
- b/c RBC production rate doesn’t match increased plasma expansion

  • decreased viscosity, causes decreased TPR, helps minimize maternal cardiac work as CO increases
24
Q

What are GI changes?

A

causing reflux:

  • decreased gastric emptying and LES tone (both due to P)
  • increased intrabdominal pressure

causing constipation:
- decreased gastric motility

25
Q

what can cause SV plateau or decrease?

A

can occur in late pregnancy

- IVC can be compressed, decreasing VR, decreasing EDV, decreasing SV (can also occur when woman is lying on back)

26
Q

what two things cause decreased TPR?

A
  1. additional low-resistance circuit: vasculogenesis and angiogenesis of the parallel circuit
  2. Vasodilation: E and P are antagonists to vasopressive action of ANG II. P may also promote vasodilation via smooth m. relaxant
27
Q

change in MAP?

A

can be decreased or stay the same
- due to increased CO and decreased TPR
MAP = CO x TPR

28
Q

edema?

A

due to starling forces

  1. due to increased venous pressure in LE. (compression of IVC by growing uterus as well as increase venodilation under hormonal influence)= increased hydrostatic pressure
  2. decreased capillary colloid osmotic pressure : maternal synthesis of plasma proteins does not keep pace with increased plasma volume
29
Q

3 causes of respiratory changes?

A
  1. elevation of diaphragm (due to increased intra-abdominal pressure and progesterone effect of relaxing m. and fascia) –> results in decreased RV and decreased FRC
  2. increased O2 demand and CO2 production: supports fetal metabolism
  3. increased sensitivity to CO2
    - due to progesterone effect
    - decreased medullary respiratory center set point for respiratory response to central chemoreceptor detection of CO2
    - increased TV and alveolar ventilation
    - decreased PCO2
30
Q

Labor stage 3

A

expulsion of placenta

  • uterus contracts reducing area of attachment
  • separation of placenta results in bleeding and clotting
  • averages about 15 minutes
31
Q

What do prostaglandins do?

A
  • ** thought to initiate labor:
  • levels rise before onset of labor by uterus, placenta and fetal membranes
  • results in increased smooth m. contractility: uterine responsiveness to prostaglandins can occur throughout pregnancy
  • increased synthesis of prostaglandins is stiulated by estrogen (conversion from arachidonic acid), oxytocin in uterine cells and uterine stretch
32
Q

What are the 5 renal changes?

A
  1. increased RBF and GFR (b/c of increased blood flow and CO)
  2. increased plasma renin/ang/aldo (b/c increased estrogens)
  3. increased Na+ (b/c increased Aldo)
  4. increased H20 retention and intake (b/c decreased threshold for ADH/AVP)
  5. decreased serum Na+ (b/c change in ADH setpoint and increased sodium and water)

Kidneys compensate for respiratory alkalosis by excreting more HCO3-

33
Q

What are GI changes?

A

causing reflux:

  • decreased gastric emptying and LES tone (both due to P)
  • increased intrabdominal pressure

causing constipation:
- decreased gastric motility

34
Q

what is necessary for maternal nutrition?

A
  • protein: supports fetus, placenta, uterus, breasts, blood volume
  • iron: necessary for maternal Hb, placenta and fetus
  • Folate: supports increased RBC production and protects against neural tube defects
35
Q

what establishes myometrial quiesence?

A

progesterone and relaxin

36
Q

Braxton Hicks contractions

A

periodic episodes of weak, slow rhythmic contractions during pregnancy “false labor”

  • become very strong during last hours of pregnancy
  • these will eventually become labor contractions and will aid in stretching the cervix and pushing baby through
  • if positive feedback fails then these contractions will fade away
37
Q

how is CRH produced? what does it do?

A
  • production and maternal serum levels rise quickly in late pregnancy due to decreased CRHbp
  • this sensitizes uterus to prostaglandin and oxytocin
  • stimulates fetal ACTH: increases fetal adrenal cortisol and increased fetoplacental estrogens
  • cortisol positively feeds back to increase fetal CRH production
  • CRH promotes contractions by sensitizing uterus to prostaglandins and oxytocin
38
Q

Labor Stage 2

A 
descent and expulsion
- " active labor" 
cervix fully dilated 10 cm
contractions push fetus downward
lasts 20-50 minutes
39
Q

Labor stage 3

A

expulsion of placenta

  • uterus contracts reducing area of attachment
  • separation of placenta results in bleeding and clotting
  • averages about 15 minutes
40
Q

what are fetal factors important in parturition?

A
  • fetal pituitary oxytocin
  • fetal placental membranes produce prostaglandins
  • fetal adrenals produce CRH (cortisol) which induces surfactant production
40
Q

What do prostaglandins do?

A
  • ** thought to initiate labor:
  • levels rise before onset of labor by uterus, placenta and fetal membranes
  • results in increased smooth m. contractility: uterine responsiveness to prostaglandins can occur throughout pregnancy
  • increased synthesis of prostaglandins is stiulated by estrogen (conversion from arachidonic acid), oxytocin in uterine cells and uterine stretch
41
Q

what are three prostoglandin actions?

A
  1. stimulates myometrial smooth m. contraction
  2. promotes gap junction formation between uterine smooth m. cells (estrogen also promotes this)
  3. softening, dilation and thinning of the cervix
  • can be used to induce labor in large doses
  • aspiring: inhibits labor and prolongs gestation by reducing PGF and PGE
42
Q

what is estrogen necessary for?

A

required for parturition

  • increased placental secretion throughout pregnancy
  • ratio of E:P shifts during last several months of pregnancy
43
Q

what are four ways that estrogen increases uterine contractility for parturition?

A

increase gap junctions
increase oxytocin receptor expression
increase myometrial sensitivity to oxytocin
increase prostaglandin production

44
Q

what does oxytocin do? when is it released?

A

maintains labor

  • uterine sensitivity to oxytocin only occurs at end of pregnancy
  • primary stimulus for release is distension of the cervix “ferguson reflex”: causes release of oxytocin from posterior pituitary in bursts during labor stage one, the frequency increases through labor
  • estrogen increases number of oxytocin greatly
45
Q

what are oxytocins actions?

A

maintain labor via:

  • receptor activation promotes uterine smooth m. contraction
  • in stage 3 of labor, uterine contractions are important for constriction of blood vessels after placental delivery, promoting hemostasis
  • stimulates uterine PGF2alpha production
46
Q

how is CRH produced? what does it do?

A
  • production and maternal serum levels rise quickly in late pregnancy due to decreased CRHbp
  • this sensitizes uterus to prostaglandin and oxytocin
  • stimulates fetal ACTH: increases fetal adrenal cortisol and increased fetoplacental estrogens
47
Q

where is relaxin produced

A

produced by corpus luteum and placenta

  • promotes myometrial quiescence during pregnancy
  • production increases during labor to soften cervix
48
Q

what are 5 important endocrine factors of parturition?

A
  1. prostaglandins
  2. estrogen
  3. oxytocin
  4. CRH
    5 Relaxin
49
Q

what are fetal factors important in parturition?

A
  • fetal pituitary oxytocin
  • fetal placental membranes produce prostaglandins
  • fetal adrenals produce CRH (cortisol) which induces surfactant production
50
Q

what mechanical factors increase uterine contractility?

A
  • stretch of smooth m. increases smooth m. contraction (i.e. twins normally born sooner)
  • contractions stimulates uterine prostaglandin production via positive feedback
50
Q

what mechanical factors increase uterine contractility?

A
  • stretch of smooth m. increases smooth m. contraction (i.e. twins normally born sooner)
  • contractions stimulates uterine prostaglandin production via positive feedback
51
Q

ferguson reflex?

A

uterine contraction push baby against cervix –> stretches cervix –> stimulates release of more oxytocin (+ feedback)

51
Q

ferguson reflex?

A

uterine contraction push baby against cervix –> stretches cervix –> stimulates release of more oxytocin (+ feedback)

Endo Test 2 (10 decks)

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