onset and management of parturition Flashcards
what is parturition ?
the process of giving birth
what are the 4 stages of parturition are?
0 (latent phase) - irregular contraction, effacement (thinning of the cervix) and dilatation of the cervix)
1 - onset of regular uterine contractions, accompanied by effacement of the cervix and dilation of the cervical os to full dilatation.
2- full dilation of the is, uteri to birth of the baby. when at full dilatation the contractions last longer and fewer.
3- birth of baby to expulsion of the placenta and membranes - can be done it two ways - left to do it on own and skin to skin contact helps, or can have active stage 3, aided by medicine.
what is the definition of labour?
4cm dilated plus regular painful contractions
what makes labour happen ?
The molecular mechanisms that drive the onset and maintenance of labour remain uncertain
despite this there are several key pathways that have been identified.
- the activation of the myometrium (maternal/fetal HPA axis, and proliferation of stretch and oxytocin receptors)
- the actions of placental steroids
- the action of prostaglandins/ inflammatory
- the action of oxytocin
- the positive biofeedback mechanism (ferguson reflex)
what is myometrial quiescence?
relaxed uterus
throughout pregnancy what happens to the smooth muscle of the uterus?
Throughout pregnancy – significant proliferation and hypertrophy in smooth muscle of uterus
how is the capacity for contractility of the uterus decreased?
hCG (inhibits formation of myometrial gap junctions (MGJ))
Progesterone (inhibits circulating oestrogen – MGJ)
Corticotrophin- releasing hormone (CRH)
Relaxin (smooth muscle)
Oxytocin (stimulate synthesis of relaxatory prostaglandins until hCG levels decr at onset of labour
Melatonin (suppresses myometrial oxytocin receptors)
at term myometrial contractility is enhanced by a series of molecular processes involving:
uterine stretch and activation
substantial increase in oxytocin receptors in endometrium and myometrium (MGJ)
endocrine pathway involving the fetal-hypothalamic-pituitary adrenal (HPA) axis and increased output of cortisol
what is associated with uterine stretch and activation?
Rapid fetal growth at term – accelerated uterine distension with associated incr in oxytocin receptors
During late pregnancy there is a 50 fold incr in such receptors before the onset of labour.
Maximum myometrial receptor concentrations have been found in early labour
stretch and activation factors are found Highest in the fundus and corpus
when do myometrial gap junctions form?
what are they?
how do they work?
From approx 32 weeks gestation
Composed of symmetrical portions of plasma membrane from adjacent cells
they form intracellular channels - rapid propagation of action potentials between cells.
the formation is stimulated by oestrogen, prostaglandin and melatonin
Inhibited by progesterone, hCG and relaxin
where do you get high concentrations of myometrial gap junction?
At term, higher concentrations occur in fundus compared with lower segment
what do myometrial gap junctions do?
Creates fundal dominance – progressive conductance of electrical activity from fundus to cervix
Synchronise myometrial responsiveness to neuroendocrine and intrauterine oxytocin systems
Corticotropin releasing hormone in pregnancy?
Synthesised by placental tissues and secreted intro maternal circulation during pregnancy – incr exponentially throughout.
Precise function unknown although it is known that a series of molecular events mediated by the autocrine, endocrine and paracrine action of CRH is activated at term.
Duration of pregnancy strongly related to circulating levels of CRH
high levels of CRH = labour
what are the hypothesis of the effect of CRH on pregnancy?
CRH – direct quiescent / contractile effect on myometrial muscle
May affect contractility indirectly by stimulating prostaglandin production by the fetal membranes and the placenta
May augment the myometrial contractile response to PGE2 and oxytocin
Fetal Input to the Process of Parturition??
Activation of Fetal HPA Function
Fetus triggered the onset of parturition through activation of the fetal HPA axis, with increased output of cortisol from the fetal adrenal gland
Fetal cortisol acts on the placenta -results in a decrease in placental output of progesterone and increased output of oestrogen.
Result - increase in the output of stimulatory prostaglandins (PG) from the uterus, between layers of the fetal membranes