Reproduction - pregnancy Flashcards
Endocrine function of syncytiotrophoblasts
hCG and hPL
hCG
- human chorionic gonadotropin (binds to LH receptors on corpus luteum; keeps it viable)
- what pregnancy tests detect in urine
- rapid rise in HCG causes morning sickness
- hCG stimulates leydig cells and adrenal cortex in fetus
- has negative fxn on HPG axis
hPL
Human placental lactogen
Similar to GH and prolactin
GH-like : counterregulatory to insulin (lipolytic), mobilizes glucose for fetal use, stimulates IGF-I in fetus
Prolactin-like
Stimulates mammary gland development in mother
Pregnancy is a (hormone) resistant state?
Insulin
hPL effects on maternal glucose handling
hPL can be found in higher levels in maternal than fetal circulation; not essential for maintaining pregnancy so it is more important in mother than fetus. It is anti-insulin and helps mobilize glucose and other nutrients from mother to fetus
What two steroid hormones produced by the placenta help reduce insulin sensitivity in mother
Estrogen and progesterone
Gestational diabetes
Caused by anti-insulin effects of hPL, progesterone, prolactin, and cortisol
Usually resolves at end of pregnancy, but seems to be a risk factor for T2DM
At risk most: Women >25, family history of diabetes, and T2DM
When fully formed, what are the functions of the placenta (4)
Gut (supplies nutrients ; occurs by diffusion/facilitated diffusion)
Lung (gas exchange – helped by fetal hemoglobin)
kidney (regulating fluid volume and waste disposal)
endocrine gland (hPL, estrogen, progesterone, hCG)
Functions to remove waste products such as urea, creatinine, and co2.
Provides a semi-protective barrier
Why is the placenta an imperfect endocrine gland
it lacks critical enzymes to complete many steps in steroid hormone biosythesis; protects fetus from steroids from mother like cortisol and high gonadal steroid hormone levels.
What can the placenta NOT do?
Synthesize cholesterol (relies on maternal LDL, does NOT use StAR to get cholesterol)
Convert progesterone into other steroids (no CYP17) –> progesterone is made into androgens and other steroids by fetus
Cannot make estriol - fetal LIVER makes an enzyme (CYP3A7) to convert DHEAS which can be downstream converted into estriol, which is the main circulating estrogen during pregnancy
What part of the fetus makes estriol
fetal liver - uses CP3A7 converts DHEAS to 16-hydroxyl DHEAS - this is downstream converted into estriol by placenta (E3) which is the main circulating estrogen in pregnancy
What “hypothalamic” releasing hormone is released by placenta
CRH – this release will increase with gestational age and has been inked to gestational length
Does fetal pituitary secrete ACTH?
Yes – but it does NOT have a negative feedback effect – instead it stimulates more CRH release in a positive feedback amplification release.
What are the 3 zones of the fetal adrenal gland?
Definitive zone, transitional zone, and fetal zone
definitive zone of fetal medulla
becomes zona glomerulosa, begins making aldosterone near birth
transitional zone in fetal adrenal gland
becomes zona fasiculata and begins making cortisol at about 6 months gestation
Fetal zone of fetal adrenal
Largest zone- becomes zona reticularis, makes androgens throughout gestation
Through the MAJORITY of pregnancy, what generates the estrogen and progesterone needed to maintain the pregnancy?
The placenta, because the corpus luteum cannot keep up with the high levels required to do this – takes over after ~8weeks
However – estrogen cannot be synthesized independently by the placenta because it lacks CYP17 ability to convert progesterone –> androgens
Relaxin
Produced by corpus luteum due to hCG and by placenta
Inhibits myometrial contractions (ensures uterine quiescence in early pregnancy)
Relaxes pelvic bone ligaments and soften cervix to prepare in parturition
Prolctin
Made from MATERNAL pituitary (not placenta)
Essential for mammotrophic effects of E2 and p4
prepares boobies for lactation
E2 stimulates growth of lactotrophs and increases PRL secretion
Changes in Cardiovascular system in pregnancy (effect of MAP, pulmonary pressures, venous pressure increases, TPR)
MAP decreases, TPR decreases more than CO increases
Pulmonary pressure stays the same, off setting increase in volume with a decrease in resistance
venous pressure increases by 150% due to venous distention
Regional blood flow in pregnancy
uterus receives 30% of cardiac output; skin flow increases to maintain body temperature, kidney blood flow increases and GFR increases
Blood in pregnancy
increase blood volume (primarily in 2nd trimester), body anticipates hemorrhage; both plasma and RBC increase with net decrease in hematocrit
Respiratory changes in pregnancy
Diaphram elevation (5in) Tidal volume increase, increases alveolar ventilation
GI changes in pregnancy
Decrease GI motility to absorm more nutrients, LES tone is decreased (greater reflux)
Endocrine Fxn in maternal body during pregnancy
Changed with suppression of maternal HPG axis is suppressed due to the placental sex steroids and there is significant growth of the lactrophs and net increase in PRL, which inhibits the GnRH even more
Metabolic changes in pregnancy
1st half of pregnancy- mother is in anabolic state with normal or increased sensitivity to insulin and increased fat deposition and glycogen storage; promotes breast growth in mother and allows stockpiling of nutrients to meet demands of enlarging fetus
2nd half - you get insulin resistance, accelerated starvation due to catabolic state characterized by insulin resistance; increase in plasma glucose and FA levels mediated by hPL (why pregnant ladies can develop gestational diabeties)
Parturition – what hormones mediate this
Progesterone, E2, cortisol, relaxin, oxytocin, CRH, prostaglandins, catecholamines.
And, most importantly:
Decreased ratio of progesterone : Estrogen
Stages of labor
Phase 0 - quiescent uterus kept inactive by progesterone
Phase 1 - Actiation of uterus - release of inhibitory mechanism and activation of factors that increase uterine activity; increased activation of fetal HPA axis and peak in fetal CRH levels
Phase 2- Active uterine contractions faciliated by icnreased PGs, oxy, and CRH respond in positive feedback loop.
Phase 3- expulsion of fetus from uterine compartment and expulsion of placenta
Ferguson reflex
pressure exerted from fetus on cervix that stimulates oxytocin and leads to the positive feedback cycle on uterine contractions
Phase 2 changes in hormones
Decreased P4:E2 ratio; releases PGs
E2 inreases oxytocin receptors in uterus
CRH increases fetal HPA axis, which also increases E2
Uterine contractions stimulate oxytocin which stimulates more uterine contractions
Oxytocin stimulates more prostaglandin release from uterus
Lactation is initatied after delivery by what?
Decrease in P4 and E2 because placenta is no longer present
What sustains milk secretion
repeated transient hyperprolactinemia - suckling stimulates prolactin release
Prolactin does what to reproductive function
decreases by inhibiting GnRH
Behaviorally, what does prolactin also do to the mother?
stimulate maternal behavior during pregnancy and after parturition
What is the first milk produced called
colostrum, and it’s low fat milk (it’s the great value 1%)
what hormones are essential for continued milk production
prolactin, cortisol, and insulin
What is the reflex that oxytocin induces for breastfeeding
milk let down via contraction of myoepithelial cells and alveoli and smooth muscle leads to this – can be caused by infant crying
What inhibits lactation DURING pregnancy
high progesterone
Hormonal birth control:
What does the progestational part of the hormone pill does what to hormone secretion?
What does the estrogenic hormone in the pill inhibit?
Progestational hormone Prevents LH secretion (estrogenic hormone)
Estrogenic hormone inhibits FSH release, stabilizes endometrium, pogentiates progestin action
