Clinical meaning
Preeclampsia originates from abnormal placental implantation with deficient trophoblastic invasion of spiral arteries, leading to placental ischemia and release of antiangiogenic factors such as soluble fms-like tyrosine kinase-1 that cause widespread endothelial dysfunction, hypertension, proteinuria, and multiorgan damage. Gestational diabetes mellitus results from progressive insulin resistance driven by placental hormones including human placental lactogen, cortisol, and progesterone, which overwhelm pancreatic beta-cell compensation in susceptible individuals, producing maternal hyperglycemia that crosses the placenta and causes fetal macrosomia and hyperinsulinemia. Reproductive endocrinology governing contraception and fertility depends on the hypothalamic-pituitary-ovarian axis, where gonadotropin-releasing hormone pulses regulate FSH and LH secretion to control folliculogenesis, ovulation, and corpus luteum function. Anti-Mullerian hormone produced by granulosa cells of small antral follicles serves as a reliable marker of ovarian reserve and is used in infertility evaluation alongside day-3 FSH and estradiol levels.