Hormone induction of<unk>  separation As the fetal hypothalamus matures, activation of the HPA axis (hypothalamic-pituitary-adrenal axis) initiates labour though two hormonal mechanisms. The end pathway of both mechanisms leads to contractions in the myometrium, a mechanical cause of<unk>  separation, which is due to the shear force and contractile & involution changes that occur within the uterus distorting the placentome. Fetal ACTH ACTH increases fetal cortisol, which acts by two mechanisms: * Increases Prostaglandin F2α, which both abolishes the progesterone block, and lowers the oxytocin receptor threshold; and increases expression of relaxin, stretching the pelvic ligaments * Increases expression of PTGS in the fetal trophoblast cells PTGS in turn produces prostaglandin E2, which is a catalyst for pregnenalone to C-19 steroids, such as estrogen. Estrogen increases: * Vaginal lubrication * Softening of collagen fibre structures in the cervix, vaginal, and associated tissues * Increases contraction associated proteins (i.e. connexins) *<unk>  shedding by physiological inflammation, note pathological inflammation often leads to retention of membranes (i.e. placentitis) Fetal oxytocin As the HPA axis activates, the posterior pituitary of the fetus begins to increase production of oxytocin, which stimulates the maternal myometrium to contract. Cellular changes of<unk>  separation === In the seventh month of pregnancy the MHC-I complexes increase in the interplacentomal arcade reduces the bi- and tri-nucleate cells, a source of immune suppression in pregnancy. By the ninth month the endometrial lining has thinned (due to loss of trophoblast giant cells) which exposes the endometrium directly to the fetal trophoblast epithelium. With this exposure and the increase in maternal MHC-I, T-helper 1 (Th1) cells, and macrophages induce apoptosis of trophoblast cells and endometrial epithelial cells, facilitating<unk>  release. Th1 cells attract an influx of phagocytic leukocytes into the placentome at separation, allowing further degration of the extracellular matrix. Vascular changes of<unk>  separation After delivery, loss of fetal blood return to the<unk> allows for shrinkage and collapse of the cotyledonary villi with subsequent fetal membrane separation.
Placental expulsion
Uterine inversion
Fetal movement
Retained placenta
Placental insufficiency
Rupture of membranes
Uterine septum
Vaginal contraction