Pregnancy Flashcards
1st tri
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
2nd and 3rd trimester
maternal P and E2 continue to rise
maternal placental fetal unit takes over
hCG
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)
hCG actions
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
progesterone
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
progesterone actions
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
Estrogen synth
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)
Estrogens functions
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
ratio of E2:P
both steadily increase during pregnancy, but shifts toward E2 later in pregnancy to promote parturition
Human placental lactogen
aka hCS
from SCBs
detected in serum by 3 wks
rise thru pregnancy in proportion to placental weight
functions of hPL
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
functions of the placenta
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
placental limitations
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
maternal pituitary changes during pregnancy
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)
thyroid changes during pregnancy
increased thyroid size
hCG binds TSH receptors causing transiation hyperthyroidism
E2 increasesT4 and T3 with increased TGB
no change in free T3 and T3
adrenal gland changes in pregnancy
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
physical changes in pregnancy
normally there is an increase in 25-35lb change
CV changes
increased blood volume (low hc)
increased CO
Decreased TPR
decrease or nc in MAP (due to inc CO and dec TPR)
changes in blood volume
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
physiological anemia
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
changes in CO
increases by 50% by the end of pregnancy
inc HR and SV (major contributor- due to increased volume)
SV plateau
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
changes in TPR
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
pregnancy and edema
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)
changes to the respiratory system
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
renal changes during pregnancy
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
GI changes
decreased gastric emptying rate (P)
decreased LES tone (P)
inc intra-abdominal pressure
decreased gastric motility
net= reflux and constipation
parturition
onset initiated at 38 wks (fetal age) or 40 wks after LMP
positive feedback sustains
Braxton hicks contractions
periodic epidsodes of weak, slow contractions during pregnancy, become stronger later
eventually become labor contractions
Labor stage 1
initiation of laber
contractions from 30min to 10 min
7-12 h
stage 2
active labor
cervix dilated fully to 10 cm
contractions push fetus down ward
baby is delivered
20-50 min
stage 3
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
prostaglandin action
1) stimulate uterine contraction
2) increased gap junction expression b/w smooth muscle cells
3) softening, dilation, thinning of the cervix
**dont take aspirin
estrogens and partuition
sharp increase in estrogen prior to parturition increases gap juncitons increase oxytocin receptor increase myometrial sensitivity to oxy increased PG produciton
oxytocin and partuition
1) promotes uterine smooth muscle contraction (PLC—>Ca–> modulates MLC kinase)
2) constriction of blood vessels in stage 3
3) stimulates PGF production
placental CRH
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
relaxin
from the CL and then the placenta
thought to be involved in myometrial quiescence during pregnancy
increases during labor
may soften cervix during labor
Estriol
used as a marker for placental and fetal health
mechanical factors for uterine contractility
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
