Physiology of pregnancy Flashcards
function of hCG
rescue corpus luteum to stimulate luteal estrogen and progesterone secretion until placenta takes over (10 weeks)
hCG action
binds to LH receptors, structurally similar to LH, FSH, TSH. May cause transient gestational hyperthyroidism. In males, stimulates Leydig cells (testosterone). Stimulates adrenal fetal cortex.
progesterone function
required to maintain quiescent uterus during pregnancy. Decreases uterine contractions, increases secretory activity and fat deposition. Progesterone production independent of fetus. Can’t be used as indicator of fetal health.
estrogen production
placenta takes over luteal production of estrogens after 10 weeks. Feto-placental unit responsible for production of: estradiol-17beta, estrone, estriol (need DHEA-S from fetal adrenal gland).
estrogen function
Increase: uteroplacental blood flow, uterine smooth muscle hypertrophy, gap junctions, LDL receptor expression on syncitiotrophoblasts, prostaglandins, oxytocin receptors, mammary gland growth, prolactin secretion
hPL (hCS) production
produced by syncytiotrophoblasts (proportional to placental weight), levels rise throughout pregnancy
hPL actions
antagonizes insulin action (diabetogenicity of pregnancy). Increases glucose availability for fetus. Lypolytic action shifts maternal energy use to FFA. Stimulates mammary gland development.
functions of placenta
- regulate timing and progression of parturition
- maintain pregnant state of uterus
- stimulate growth and function of breasts
- support fetal growth
- regulate aspects of fetal development
PRL release
estrogen promotes PRL release. Lactotroph hypertrophy and hyperplasia increases pituitary size, may cause dizziness, vision problems, vascular insult, and necrosis (Sheehan’s).
ADH release
progesterone lowers osmolality threshold for ADH release (ADH is released sooner for a given osmolality)
T3/T4 release
Increase in total T3 and T4 in response to hCG (binds TSH receptors). No change in free T3/T4 b/c estrogen promotes liver production of TBG.
Cortisol release
Increase in total and free cortisol, despite estrogen-mediated release of CBG.
Aldosterone release
increased due to estrogens stimulating hepatic angiotensinogen production and renal renin production. No hypernatremia, hypokalemia, or HTN due to blunting effects of progesterone (competes for same receptors) and lower ADH threshold.
prostaglandin actions
- stimulate myometrial smooth m. contraction
- promotes gap junction formation btw. uterine smooth m. cells
- softening, dilation, and thinning of cervix
oxytocin function
maintains labor