normal labour Flashcards
what are the 4 stages of labour?
0 - latent phase = irregular contractions, effacement and dilation of the cervix 0 -4cm
1 - active phase - onset of regular uterine contractions, accompanied by effacement of the cervix and dilation of the cervial os to full dilation 4-10cm
2 - full dilation of the os uteri to birth of the baby
3 - birth of baby to expulsion of placenta and membranes
what key pathways have been identified that drives the onset and maintenance of labour?
activation of the myometrium
action of oxytocin
positive feedback mechanisms = Ferguson reflex
action of placental steroids
action of prostaglandins/inflammatory uterocervical processes
what causes myometrial quiescence?
hCG = inhibits formation of myometrial gap junctions
progesterone = inhibits circulating oestrogen
corticotrophin releasing hormone
relaxin
oxytocin = stimulates synthesis of relaxatory prostaglandins until hCG levels decrease at onset of labour
melatonin = suppresses myometrial oxytocin receptors
at term myometrial contractility is enhanced by a series of molecular processes involving what?
uterine stretch and activation
substantial increase in oxytocin receptors in endometrium and myometrium
endocrine pathway involving the fetal-hypothalamic-pituitary adrenal axis and increased output of cortisol
how does uterine stretch and activation cause contraction?
rapid fetal growth at term = accelerated uterine distension with associated increase in oxytocin receptors
during late pregnancy there is 50x increase in oxytocin receptors before the onset of labour
max. myometrial receptor concentrations have been found in early Labour
highest in fundus and corpus
how do myometrial gap junctions cause contraction?
MGJ appear from 32 weeks gestation
composed of symmetrical portions of plasma membrane from adjacent cells
form intracellular channels - rapid propagation of action potentials between cells
formation stimulated by oestrogen, prostaglandin and melatonin
inhibited by progesterone, hCG and relaxin
where are higher concentrations of myometrial gap junctions found? and what does it create?
at term higher conc in fundus compared with lower segment
creates fundal dominance = progressive conductance of electrical activity from fundus to cervix
synchronise myometrial responsiveness to neuroendocrine and intrauterine oxytocin systems
how does the hypothalamic-pituitary adrenal axis increase myometrial contraction?
control response to stress
produces corticotrophin releasing hormone = synthesised by placental tissue and secreted into maternal circulation during pregnancy - increases exponentially throughout
precise function unknown although CRH is known to be activated at term
what are the hypotheses for corticotrophin releasing hormone action?
CRH = direct quiescent/contractile effect on myometrial muscle
may affect contractility indirectly by stimulating prostaglandin production by fetal membranes and placenta
may augment the myometrial contractile response to PGE2 and oxytocin
how does activation of fetal HPA function cause parturition?
fetus triggers onset of parturition through activation of fetal HPA axis with increased output of cortisol from fetal adrenals
fetal cortisol acts on placenta = decrease in placental output of progesterone and increased output of oestrogen
results = increase in output of stimulatory prostaglandins from uterus, between layers of fetal membranes
what role to prostaglandins plat in parturition?
concentrations of prostaglandins increase in blood, urine and amniotic fluid during labour
synthesised by uterine tissues/fetal membranes and increased rates of production occur during labour
we known that administration of prostaglandins will induce labour and delivery whereas inhibition of prostaglandin biosynthesis will delay labour and delivery
prostaglandin conc increases in amniotic fluid prior to myometrial contractions and the activity of prostaglandin increases in the chorion and amnion at labour
how does the inflammatory uterocervical process cause parturition?
progressive release of inflammatory mediators:
cytokines = stimulates synthesis of prostaglandins
interleukins = increases collagenolytic activity of cervix
nitric oxide = stimulates release of PGE2 from fetal membranes
cervical ripening and dilation are associated with major alterations of extracellular matrix and the cellular composition of cervical tissue
what is oxytocin role in parturition?
produced by supraoptic nucleus and paraventricular nucleus in hypothalamus - posterior pituitary release oxytocin and vasopressin into general circulation
= powerful uterotonic
modulated by progesterone
indirectly inhibits release of adrenocorticotrophic releasing hormone and cortisol = antagonist of vasopressin
strong link to emotional well being and bonding
increases nocturnal release from 32 weeks (coincides with decrease in plasma progesterone/oestrogen ratio and rise in oxytocin receptor density in uterus
released in labour as result of feedback to brainstem from uterus, cervix and vagina
regulated by oxytocinase = enzyme that rapidly degrades oxytocin and prevents receptor desensitisation during prolonged oxytocin release
oxytocin may therefore stimulate uterine contractions by acting both directly on myometrium and indirectly on decimal prostagladin production
how does oxytocin prepare the fetal neutrons for delivery?
crossing placenta, maternal oxytocin reaches the fetal brain and induces a switch in the action of neurotransmitter GABA from excitatory to inhibitory on fetal cortical neutrons , this silences the fetal brain for the period of delivery and reduces it vulnerability to hypoxic damage
what is labour characterised by?
involuntary
intermittent and reglar
painful contractions
fundal dominance
contraction and retraction of uterine muscle fibres - fetal axis pressure
