During pregnancy blood flows through remodelled spiral arteries into placenta and pools in intervillus space where gasexchange takes place
Until 8 weeks the corpus luteum secretes progesterone. After the luteal-placental shift the placenta is the predominant secretor of progesterone.
Progesterone decreases uterine contractions and motility to prevent labour and rejection of foetus
Oestriol is produced by foetal adrenal glands and the trophoblasts covert it to oestrogen to promote organ development
Relaxin is produced by the placenta to relax the uterus for embryoimplantation and increase blood supply to maternal heart and kidneys.
Relaxin in partuition ruptures membranes and relaxes pelvicligaments
At labour initiation- myometrial cells awaken and increase expression of CAPS to increase contractility of uterus
Oestrogen in labour promotes uterine contraction and cervical dilation through CAP genes
At the end of pregnancy- uterus becomes desensitised to progesterone and disinhibits oestrogen actions so it is prepared for labour
Prostaglandins increase towards the end of term
Prostaglandin F2A and E2 are produced by uterine decimal cells and increase contractions via positive feedback
Oxytocin sustains labour- uterus becomes sensitised at 20 weeks and oestrogen increased oxytocin receptor quantities
Oxytocin acts on myometrial cells to increase intracellular Ca to promote muscle contraction. Facilitated through PGF2A
Oxytocin also acts on decimal cells to increase expression of COX enzymes to increase prostaglandin production and clamp spiralarteries after delivery
Ferguson reflex = oxytocin released from posterior pituitary is stimulated by cervicaldistension
Maternal blood volume increases by 1-2 L in pregnancy
Oestrogen acts on hypothalamus and brainstem to increase renal sympathetic nerve activity and increase RAAS leading to increased thirst
To compensate for increased blood vol, bone marrow increased erythrocyte production but this is not enough so there is a decrease in Hb and Red cell count
Oestradiol increases NO production to decrease bloodpressure. Mixed with resistance to AngII there is increase in orthostatichypotension
Cardiac output, HR and stroke volume increases due to increased leftventricular mass
Increase in Factors VIII, IX and X and fibrinogen to cause an increase in clotting
Increase in GFR causes increased urinaryfrequency and glucosuria
Pregnancy causes a hypervolaemichyponatraemic state due to increased water retention and tempered effects of aldosterone
Increased metabolic rate In pregnancy increases oxygen demand. Means there is a slight alkalosis compensated by more urinary excretion of bicarbonate
Total lung capacity decreases due to growing foetus but is compensated by increase in subcostalangle
Progesterone causes smooth muscle relaxation so an increase in constipation, bloating and nausea is seen