Physiologic/Endocrine Changes during Pregnancy and Parturition Flashcards

1
Q

ovulation

A

regularly around day 15

increasing P and E from corpus luteum

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2
Q

if fertilization occurs

A

blastocyst hatches from zona pellucida and inplantation begins day 22-23

release of hCG

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3
Q

hCG

A

rescues corpus luteum

secreted from trophoblast after it attaches to endometrium

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4
Q

receptive period

A

day 20-24 approx

decreased antiadhesion protein and increased adhesion protein uterine endometrium

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5
Q

pregnancy duration

A

determined by date of last menstrual cycle

nornally aound 40 weeks
-38 weeks from ovulation

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6
Q

hormone pregnancy test

A

beta-hCG

can be detected 24 hours after implantation in urine

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7
Q

major hormones of pregnancy

A

hCG
progesterone
estrogens
hPL / hCS

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8
Q

estrogens

A

estradiol
estrone
estriol

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9
Q

hPL

A

human placental lactogen

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10
Q

hCG

A

important first trimester

-rescue corpus luteum

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11
Q

luteal placental shift

A

production of progesterone and estrogen from corpus luteum to placenta

8 weeks

very important
if doesnt occur - no pregnancy

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12
Q

2nd and 3rd trimester

A

progesterone and estrogen levels continue to rise

release by placenta

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13
Q

hCG

A

produced by syncytiotrophoblasts
half-life 30 hours

detected by pregnancy tests

may be responsible for morning system

peaks 10 weeks after implantation

double every 2 days during first 6 weeks

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14
Q

hCG structure

A

similar to LH, FSH, TSH - mostly LH
binds to receptors with high affinity
-maintain corpus luteum

can also bind TSH receptors
-transitional gestational hyperthyroidism

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15
Q

transitional gestational hyperthyroidism

A

hCG weakly binds TSH

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16
Q

other hCG actions

A

stimulates leydig cells > testosterone (mimics LH)

stimulates adrenal cortex

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17
Q

progesterone

A

increases rapidly when production switches to placenta

around 8 weeks

required to maintain a uterus - quiescent myometrium**

cannot be indicator of fetal healthy
-just placental function

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18
Q

high levels of progesterone need

A

CYP11A1, 3-beta hydroxysteroid DH, and maternal cholesterol

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19
Q

actions of progesterone

A

decreased uterus motility/contractions

increased secretions of uterus
-nourishment, growth, implantation of embryo

increased fat deposition early in pregnancy
-appetite, sugar to fat

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20
Q

estrogens

A

placenta takes over production around week 8

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21
Q

estrogen synthesis

A

require products from fetus
-19 carbon androgen (DHEA-S) from adrenal gland

can indicate fetal status

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22
Q

estriol

A

major estrogen of pregnancy

levels used as indicator of fetal health

23
Q

actions of estrogen

A

initiation parturition
-important end of term

increased blood flow
increased smooth muscle hypertrophy
increased prostaglandins
increased oxytocin
increased mammary gland growth
increased prolactin secretion
increased LDL receptors on syncytiotropoblasts
24
Q

estrogen:progesterone ratio

A

shifts later in pregnancy

-preparing for parturition

25
Q

after parturition

A

decreased progesterone - allows for PRL action on breast and lactation

26
Q

hPL

A

aka hCS

produced by syncytiotrophoblasts

  • detected in maternal serum by 3 weeks
  • rise throughout pregnancy
  • proportional to placental growth
27
Q

rises in proportion to placenta growth

A

hPL (hCS)

28
Q

actions of hPL

A

increased glucose availability to fetus **

antagonizes insulin action

  • inhibits maternal glucose uptake
  • lipolytic
  • stimulates mammary gland development
29
Q

maternal-placental-fetal unit

A

distinct but work together

fetal health can decline with functioning placenta

non-functioning placenta always detrimental to fetus

30
Q

placenta

A

site of exchange

gas, nutrients, exchange, hormones, antibodies, drugs, viruses

31
Q

function of placenta

A

maintain pregnant state of uterus (progesterone)
stimulate lobuloaveolar growth of breasts
support fetal growth
regulate fetal development
regulate timing of parturition

32
Q

P and E normal cycle vs. pregnancy

A

much much higher levels in pregnancy

because placenta can produce so much

33
Q

limitations of placental

A

cannot make cholesterol

lacks enzymes for estrone and estradiol, estriol production

34
Q

contribution of mother

A

LDL cholesterol

35
Q

fetus contribution

A

3 main enzymes to produce estrogens

17 alpha hydroxylase
17,20 desmolase
16 alpha hydroxylase

36
Q

DHEA-S

A

produced in fetus
-first product of the 3 enzymes of estrogens

-goes back to placenta where its converted to estrogens

37
Q

prolactin

A

estrogens increases PRL release from anterior pituitary

lactotrophs hypertrophy and hyperplasia
-can increase pituitary size

38
Q

increased pituitary size

A

can cause dizziness and vision problems
-optic chiasm

can be susceptible to insult and necrosis
-sheehans syndrome

39
Q

sheehans syndrome

A

vascular insult and necrosis due to increased pituitary size during pregnancy

40
Q

decreased LH and FSH

A

negative feedback on estrogens and progesterone

41
Q

ADH secretion augmentation

A

lower set point for release
-released at lower osmolarity

threshold altered by progesterone action

42
Q

thyroid size

A

increased

  • stimulated by hCG
  • weakly binds TSH receptors

increased total T4 and total T3**

estrogen promotes increased liver production of thyroxine-binding globulin

no change in free T4 and T3**

43
Q

cortisol levels

A

increase total cortisol
-estrogen stimulate increased liver production of cortisol-binding protein

increased free cortisol

  • later in pregnancy
  • increased 2x by parturition
44
Q

cortisol inactivation

A

to protect fetus

by placental 11-beta DH type II

45
Q

aldosterone levels

A

increases dramatically

estrogen stimulates angiotensinogen and renal renin production
-ANG II and aldosterone increase

progesterone blunts aldosterone action

doesnt cause hypernatremia, hypokalemia, HTN

46
Q

woman with normal BMI

A

25-35 lb increase with pregnancy

30 lbs, 10 lbs fat, 1.5 lb uterus, 4.5 lb breasts, 1.5 lb placenta, 2.2 lb amniotic fluid, 2 lb maternal blood, 7 lbs fetus

47
Q

cardiovascular changes during pregnancy

A

increased blood volume

increased CO

decreased TPR

decreased MAP (or remains same )
-balance between CO and TPR
48
Q

MAP = ?

A

CO x TPR

49
Q

hematocrit

A

increased during pregnancy

50
Q

increased blood volume

A

increased 45% near end of pregnancy

adequate fetal perfusion and exchange
protects mother blood loss during delivery

51
Q

cause of increased blood volume

A

increased plasma volume

  • increased NaCl retention
  • stimulated by estrogen

increased water retention and intake

  • lower threshold for ADH/AVP and thirst during pregnancy
  • increased sensitivity to osmoreceptors
52
Q

hematocrit changes

A

decreased
-physiological anemia

RBC production can’t keep up with plasma increase

decreased viscosity, decreased TPR
-helps minimize maternal cardiac work

53
Q

hematocrit effect

A

decreased viscosity of blood