Early Pregnancy and Placental Functions

Early Pregnancy Hormonal Changes

• Fertilization occurs in the fallopian tubes during the luteal phase.
• Fallopian tube and uterine glands provide nutrients for early embryonic development.
• Embryo implants in the uterine endometrial layer around day 7.
• Endometrium thickens and becomes vascularized.
• Decidua is the implanted area, forming the placenta.
• Placenta is derived from fetal tissues, including the trophoblast.
• Maternal component includes the uterine wall and maternal blood vessels.
• Maternal blood surrounds placental villi for nutrient and waste exchange.
• Maternal circulation supplies fetal nutrients, not uterine wall glands.
• High estrogen levels promote endometrial and myometrial proliferation and placental blood vessel growth.
• Progesterone decreases uterine contractility, maintaining uterine quiescence.
• Trophoblast cells create a barrier and transport substances.
• hCG (human chorionic gonadotropin), structurally similar to LH and FSH, is secreted by trophoblast cells.
• hCG stimulates corpus luteum to produce estrogen and progesterone, crucial for maintaining pregnancy.
• Early pregnancy loss (miscarriage) can result from insufficient hCG, leading to hormone drops.
• Around 8-12 weeks, placenta takes over estrogen and progesterone production (placental shift).
• Corpus luteum is essential for hormones before placental shift.
• Insufficient placental hormones after 12 weeks can cause pregnancy failure.
• Placental lactogen, structurally similar to prolactin and growth hormone, plays a role in glucose metabolism and breast development.

Physiological Changes During Pregnancy

• Brain-pituitary-gonadal axis regulates to prevent ovarian cycles.
• Placental estrogen and progesterone inhibit LH and FSH, preventing follicular development.
• Progesterone increases body temperature.
• Estrogen and progesterone affect maternal behaviors.
• Increased food intake due to high metabolic demands.
• Mammary gland changes:
  • Puberty: Estrogen and growth hormone stimulate ductal growth.
  • Pregnancy: Estrogen and progesterone stimulate lobular-alveolar growth.
  • Cortisol, thyroid hormone, and prolactin contribute to breast development.
  • Placental lactogen levels rise with placental development, supporting fetal growth and alveoli structure for milk.
  • Lactogenesis requires multiple hormones including insulin and cortisol.
  • High progesterone inhibits milk production.
  • Postpartum lactation requires oxytocin stimulation.
• Cardiovascular Changes:
  • Uterine blood vessels increase to supply placenta.
  • Cardiac output increases (higher stroke volume and heart rate).
  • Blood volume increases by 40%.
  • Blood pressure decreases due to reduced total peripheral resistance.
  • Uterine and renal arteries dilate for increased blood flow.
  • Increased placental blood flow for fetal needs.
  • Gestational hypertension is abnormal pressure increase.
• Metabolic Changes:
  • High insulin levels but resistance to insulin; reduced glucose tolerance.
  • Elevated maternal glucose ensures fetal glucose supply.
  • Cortisol and placental lactogen increase insulin resistance.
  • Increased fat deposition stores for milk.
  • Shift in metabolism to supply glucose to the fetus and store fat for milk.
  • Gestational diabetes is excessive insulin resistance.

Labor and Delivery

• Estrogen stimulates labor and delivery.
• Estrogen enhances oxytocin's effect and stimulates prostaglandin secretion for myometrial contraction (PGF2 alpha).
• Estrogen increases oxytocin receptors, intensifying oxytocin's action and prostaglandin production.
• Uterine contractions stretch the cervix, stimulating oxytocin release.
• Oxytocin causes uterine contractions via prostaglandin effects.
• Positive feedback loop: Cervical stretch-oxytocin-contractions-further stretch.
• Oxytocin central to the loop, causing contractions and cervical stretch.
• Progesterone decreases estrogen/oxytocin receptors, inhibiting prostaglandin production and maintaining uterine quiescence.
• Estrogen increases receptors, increasing PGF2 alpha action. - Birth occurs when estrogen effect outweighs progesterone effect.
• Estradiol levels rise due to placental production at the end of pregnancy.
• Progesterone levels do not drop; myometrial response to progesterone decreases due to receptor changes.
• Fetus plays a role in the timing:
  • Fetal placenta produces estrogen.
  • Fetal adrenal gland produces androgens for placental estrogen production (DHEA).
  • Fetal adrenal gland maturation increases steroid production (DHEA), increasing maternal estrogen.

Lactation

• Suckling stimulates prolactin and oxytocin release.
• Prolactin from anterior pituitary increases milk protein production.
• Oxytocin from posterior pituitary causes milk ejection.
• Colostrum, early milk, is lower in protein but has glucose and antibodies.
• Milk production increases over the first few days.
• Prolactin response to suckling decreases over time.
• High prolactin levels can prevent ovulation but aren't reliable birth control.

Summary Points

• Early pregnancy maintained by corpus luteum (stimulated by hCG) followed by placental hormone production.
• Estrogen and progesterone adjust maternal physiology (mammary glands, cardiovascular).
• Estrogen needed for endometrial proliferation and placental blood flow.
• Progesterone maintains uterine quiescence; estrogen drives labor.
• Oxytocin crucial for positive feedback loop during labor.
• Prolactin and oxytocin stimulate milk production and ejection.