onset and management of parturition Flashcards

1
Q

what is parturition ?

A

the process of giving birth

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2
Q

what are the 4 stages of parturition are?

A

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.

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3
Q

what is the definition of labour?

A

4cm dilated plus regular painful contractions

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4
Q

what makes labour happen ?

A

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)
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5
Q

what is myometrial quiescence?

A

relaxed uterus

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6
Q

throughout pregnancy what happens to the smooth muscle of the uterus?

A

Throughout pregnancy – significant proliferation and hypertrophy in smooth muscle of uterus

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7
Q

how is the capacity for contractility of the uterus decreased?

A

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)

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8
Q

at term myometrial contractility is enhanced by a series of molecular processes involving:

A

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

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9
Q

what is associated with uterine stretch and activation?

A

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

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10
Q

when do myometrial gap junctions form?
what are they?
how do they work?

A

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

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11
Q

where do you get high concentrations of myometrial gap junction?

A

At term, higher concentrations occur in fundus compared with lower segment

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12
Q

what do myometrial gap junctions do?

A

Creates fundal dominance – progressive conductance of electrical activity from fundus to cervix

Synchronise myometrial responsiveness to neuroendocrine and intrauterine oxytocin systems

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13
Q

Corticotropin releasing hormone in pregnancy?

A

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

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14
Q

what are the hypothesis of the effect of CRH on pregnancy?

A

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

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15
Q

Fetal Input to the Process of Parturition??

Activation of Fetal HPA Function

A

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

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16
Q

Prostaglandins role in parturition?

A

It seems likely that prostaglandins play a significant part in the mechanisms of parturition both at term and preterm.

Concentrations of prostaglandins are increased in the blood, urine and amniotic fluid during labour

Prostaglandins are synthesized by uterine tissues / fetal membranes and increased rates of production occur during labour.

Administration of prostaglandins will induce labour and delivery, whereas inhibition of prostaglandin biosynthesis will delay labour and delivery

Prostaglandin concentrations increase in amniotic fluid prior to myometrial contractions, and the activity of prostaglandin increases in the chorion and amnion at labour.

17
Q

what is the inflammatory uterocervical processes?

A

Towards latter part of pregnancy
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

18
Q

what is cervical ripening and dilatation associated with?

A

Cervical ripening and dilatation are associated with major alterations of the extracellular matrix and the cellular composition of cervical tissue

19
Q

what is cervical ripening?

A

the change in the cervix in preparation for pregnancy - stretchy cervix

20
Q

where is oxytocin produced?

A

Maternal oxytocin produced by the supraoptic nucleus and paraventricular nucleus.

21
Q

what is the paraventricular nucleus?

A

Theparaventricular nucleus(PVN, PVA, or PVH) is a neuronal nucleus in thehypothalamus. It contains groups ofneuronsthat can be activated bystressfuland/orphsiologicalchanges.

The PVN containsmagnocellular neurosecretory cells that project directly to the posteriorpituitary where they releaseoxytocin orvasopressin into the general circulation

22
Q

oxytocin in pregnancy?

A

Oxytocin : Powerful uterotonic – significant part to play in parturition

Modulated by progesterone and under certain circumstances, indirectly inhibits release ofadrenocorticotrophic releasing hormoneandcortisoland, in those situations, may be considered an antagonist of vasopressin

Strong link to emotional well being and bonding (partic. with lactation and let down reflex)

From 32 weeks – incr in nocturnal release of oxytocin

Coincides with decrease in plasma progesterone/ oestrogen ratio and rise of oxytocin receptor density in uterus.

23
Q

when is oxytocin released and what is it regulated by?

A

Released in labour as a result of feedback to brainstem from uterus, cervix and vagina

Regulated by oxytocinase – enzyme that rapidly degrades oxytocin. Prevents receptor desensitisation during prolonged oxytocin release.

24
Q

how may oxytocin stimulate uterine contractions?

A

by acting both directly on the myometrium and indirectly on decidual prostaglandin production.

25
Q

how does oxytocin prepare neurones for delivery?

A

Crossing the placenta, maternal oxytocin reaches the fetal brain and induces a switch in the action of neurotransmitter GABA from excitatory to inhibitory on fetal cortical neurons. This silences the fetal brain for the period of delivery and reduces its vulnerability to hypoxic damage.

26
Q

what is the positive feedback mechanism of the stretch pathway?

A

stretching pathway –> sensory afferent nerve

–>transmit signals via spinal cord and brainstem

–>oxytocin neurones in hypothalamus

–>release of oxytocin via hypothalamo-hypophyseal tract

–>maternal circulation

–> sensory afferent nerve

27
Q

what are secondary powers?

A

Expulsion of fetus aided by voluntary muscles of diaphragm and abdominal wall.

Presenting part exerts pressure on pelvic floor – overwhelming sensation to bear down.

Chest and abdominal wall react reflexively – diaphragm lowered and abdominal muscles contract.

28
Q

what is the ferguson reflex?

A

Irritation / stretching of the cervix causes a neurogenic reflex through the paraventriculr and supraoptic nuclei of the hypothalamus.

This causes the posterior pituitary gland to increase the secretion of oxytocin

Increased contractions pressure on cervix from presenting part

positive feedback mechanism

29
Q

what are pushing techniques? should they be done??

A

Valsalva manoeuvre – closed glottis (holding breath) pushing.

Increases intra thoracic pressure and reduces venous return to the heart.

Result – fall in cardiac output, drop in BP, reduction in utero-placental blood flow.

even though babies will be born quicker, they are much more likely to be hypoxic.