pregnancy and parturition Flashcards
fertilization
1 day
blastocyst enters uterine cavity
4 days
implantation
5 days
trophoblast froms and attaches to endometrium
6 days
trophoblast begins to secrete HCG
8 days
HCG rescues corpus luteum
10 days
HCG
from syncytiotrophoblasts
pregnancy test detect beta subunit
responsible for nausea
peaks 10 weeks after implantation
actions of HCG
stimulates LH receptors on corpus luteum
weakly binds TSH receptors (transient gestational hyperthyroidism)
stimulates fetal leydig cells -> T
stimulates fetal adrenal Cx
progesterone production requires
CYP11A1 and 3beta HSD and cholesterol
progesterone actions in pregnancy
decrease uterine motility/contractions
increase secretory activity necessary for nourishment, growth, and implantation of embryo
increase fat deposition early in pregnancy (drives appetite)
E production during preg
comes from placenta, but needs DHEA-S from fetal adrenal gland, therefore E3 levels can indicate fetal health
E actions while prego
increase uteroplacental blood flow increase uterine smooth m hypertrophy increase LDL receptor expression on synctiotrophoblasts increase prostoglandins increase oxytocin receptors increase mammary gland growth increase prolactin needed for parturition
E:P
P higher early
around wk24 switches and E higher
P drops after parturition for PRL to have effect
hPL
aka hCS
produced by synctiotrophoblasts
detected in maternal serum by wk 3
directly proportional to placental growth
hPL actions
antagonizes insulin (diabetogenicity of pregnancy)
increase glucose of fetus
lypolytic action
stimulates mammary gland development
mom->fetus
O2 water, electrolytes carbs, lipids, aa, vitamins hormones antibodies drugs viruses
fetus -> mom
CO2
water, urea
waste
hormones
fnx of placenta
synctiotrophoblasts produce steroids and peptide hormones
maintain pregnant state
stimulate luboloalveolar growth and fnx of breasts
adapt aspects of maternal meta and phys to support fetus
regulate aspects of fetal development
regulate timing and progression of parturition
placental limtations
cannot make adequate cholesterol
lacks enzymes for estrone and estradiol production
lacks enzyme for estriol production
LH and FSH prego
down, due to high levels of estrogen and progesterone
ASH prego
secretion augmented
threshold altered by P
ADH released at lower osmolality
thyroid prego
increases in size b/c stimulated by hCG
increase in total T4 and T3 due to hCG
no change in free
cortisol prego
high, due to E stimulated liver production of CBG
increase free cortisol late in pregnancy
inactivated by placental 11beta dehydrogenase type II to protect fetus
aldosterone prego
increased b/c E stimulate liver production of angiotensisogen and renal renin
does not result in hypernatremia, hypokalemia, of HTN, b/c P blunts action of aldosterone by competing for receptor
cardio prego
increased volume (decreased hematocrit)
increased CO
decreased TPR (decreased hematocrit, increased vasodilation, increased vascularity)
decreased to normal MAP