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Endo: Exam 2 > Pregnancy > Flashcards

Pregnancy Flashcards

1
Q

1st tri

A

hCG rescues CL to stimulate luteal E2 and progesterone production

placenta takes over hormone synth from CL by 8 wks
P and E2 may decrease at this point

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2
Q

2nd and 3rd trimester

A

maternal P and E2 continue to rise

maternal placental fetal unit takes over

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3
Q

hCG

A

first hormone produced by SCBs
detected by preg tests
rapidly accums in maternal circ within 24h of implantation- rescues CL
considered to be responsible for morning sickness

peaks 10wks after implantation (doubles every 2 days during first 6 wks)

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4
Q

hCG actions

A

binds with high affinity to LH receptor
stimulate Lh receptor on CL to prevent luteolysis, maintains progesterone production from CL for the first 10 wks

weak binding of TSH—>hyperthyroid
simulates fetal Testosterone

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5
Q

progesterone

A

luteal-placental shift at 8wks

  • *must be adequate to maintain pregnancy (inhibits uterine contractions)
  • -independent of fetus ( can tell you about placental health, but does not tell out about fetal health)

*need available CYP11A1, 3B HSD and maternal cholesterol

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6
Q

progesterone actions

A

dec uterine motility
increased secretory activity for feeding embryo
increased fat deposition early in pregnancy, stimulates appetite, and diverts energy stores from sugar to fat

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7
Q

Estrogen synth

A

DO require contribution from the fetus (DHEAS from fetal adrenal glands)

E3 is unique to pregnancy (rises steadily and can be used as a marker for health of fetus)

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8
Q

Estrogens functions

A 
inc uteroplacental blood flow 
increased uterine smooth muscle hypertrophy (mitogentic)
increased LDL-R on SCBs 
increase PGs
inc oxytocin receptors 
promoting mammary gland growth 
increase Prl secretion
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9
Q

ratio of E2:P

A

both steadily increase during pregnancy, but shifts toward E2 later in pregnancy to promote parturition

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10
Q

Human placental lactogen

A

aka hCS
from SCBs

detected in serum by 3 wks
rise thru pregnancy in proportion to placental weight

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11
Q

functions of hPL

A

maintain adequate glucose for the fetus
similar to GH and Prl, diabetogenicity during pregnancy (gestational diabetes)

inhibits insulin and increases lipolysis in mother

stimulates mammary gland development

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12
Q

functions of the placenta

A

1) maintain pregnant status of uterus (P)
2) stimulate breast growth and development (E2)
3) adapt maternal metabolism to support fetal growth (hCL)
4) regulate aspects of fetal devo
5) regulate timing of parturition

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13
Q

placental limitations

A

1) cannot make adequate cholesterol (from mother)
2) lacks enzymes for estrone and E2
3) lacks enzymes for E3 production (mother)

must be supplemented from the mother

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14
Q

maternal pituitary changes during pregnancy

A

increased PRL from lactotroph hypertrophy
increased in pituitary size (think sheehan’s)
decreased LH and FSH
ADH augmented (threshold altered, ADH released at a lower osm-lower setpoint)

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15
Q

thyroid changes during pregnancy

A

increased thyroid size
hCG binds TSH receptors causing transiation hyperthyroidism
E2 increasesT4 and T3 with increased TGB

no change in free T3 and T3

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16
Q

adrenal gland changes in pregnancy

A

increased total cort and CGB
increased free cort (2x by partiuation)

estrogens increase ANG II and renin—.increased ald

**does not cause hypernatremia or hypokalemia or THN bc progesterone blunts ald action

17
Q

physical changes in pregnancy

A

normally there is an increase in 25-35lb change

18
Q

CV changes

A

increased blood volume (low hc)

increased CO

Decreased TPR

decrease or nc in MAP (due to inc CO and dec TPR)

19
Q

changes in blood volume

A

increased by 45%

facilitates fetal perfusion and protect mother from exs blood loss from delivery

**major contributor is the increase in plasma volume (NaCl retention and increased water retention and intake)

increase in RBC does not match plasma volume

20
Q

physiological anemia

A

there is an inc in RBC production, but it does not match the increase in blood volume so Hct drops

causes a decrease in TPR

21
Q

changes in CO

A

increases by 50% by the end of pregnancy

inc HR and SV (major contributor- due to increased volume)

22
Q

SV plateau

A

occurs later in pregnancy
may periodically decrease due to compression of the IVC—> dec VR—>decreased EDV—> decreased SV

*Left lateral decubitus is best position

23
Q

changes in TPR

A

decreases due a addition of another vascular bed in parallel (vasculogenesis and angiogenesis)

also due to vasodilation due to E and P via ANG II and vasodilation

24
Q

pregnancy and edema

A

increased venous pressure on the IVC from fetus (increased vasodilation under hormonal control, promotes edema)

decreased capillary colloid osmotic pressure ( due to dramatic increase in plasma volume)

25
Q

changes to the respiratory system

A

overall increase in alveolar ventilation

1) elevation of diaphragm
2) increased O2 demand and CO2 produciton
3) sensitivity to CO2

decreased PCo2—>resp alkalosis—>increased bicarb excretion

26
Q

renal changes during pregnancy

A

increased RBF, and Inc GFR (due to inc CO and blood volume

2) increased Renin, angII, ald (E2 dependnet)
3) increased Na retention (inc ald)
4) increased H2O retention (due to inc ADH)
5) decreased serum Na (due to inc water retention)
6) increased bicarb excretion

27
Q

GI changes

A

decreased gastric emptying rate (P)
decreased LES tone (P)

inc intra-abdominal pressure
decreased gastric motility

net= reflux and constipation

28
Q

parturition

A

onset initiated at 38 wks (fetal age) or 40 wks after LMP

positive feedback sustains

29
Q

Braxton hicks contractions

A

periodic epidsodes of weak, slow contractions during pregnancy, become stronger later

eventually become labor contractions

30
Q

Labor stage 1

A

initiation of laber
contractions from 30min to 10 min
7-12 h

31
Q

stage 2

A

active labor
cervix dilated fully to 10 cm
contractions push fetus down ward

baby is delivered

20-50 min

32
Q

stage 3

A

uterus contracts reducing area of attachment
separation of placenta results in bleeding and clotting

bleeding limited by uterine contractions that compress vessels supplying placenta

avg 15 min, placenta expelled

33
Q

prostaglandin action

A

1) stimulate uterine contraction
2) increased gap junction expression b/w smooth muscle cells
3) softening, dilation, thinning of the cervix

**dont take aspirin

34
Q

estrogens and partuition

A 
sharp increase in estrogen prior to parturition 
increases gap juncitons 
increase oxytocin receptor 
increase myometrial sensitivity to oxy 
increased PG produciton
35
Q

oxytocin and partuition

A

1) promotes uterine smooth muscle contraction (PLC—>Ca–> modulates MLC kinase)
2) constriction of blood vessels in stage 3
3) stimulates PGF production

36
Q

placental CRH

A

sensitizes urterus to PGs and oxytocin

increases fetal ACTH and cortisol which increases fetal estrogens

initiates a positive feedback loop that increases DHEAS and estrogens to help induce partuition

37
Q

relaxin

A

from the CL and then the placenta
thought to be involved in myometrial quiescence during pregnancy

increases during labor

may soften cervix during labor

38
Q

Estriol

A

used as a marker for placental and fetal health

39
Q

mechanical factors for uterine contractility

A

increased stretch of smooth m.—>increased smooth m. contraction

fetal movement can elicit smooth muscle contraction, twins are typically born earlier

contractions and positive feedback stimulate positive feedback to increase PGE and Oxy production

Endo: Exam 2 (11 decks)

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