Labour Flashcards

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1
Q

What are the changes from an antenatal stage to a the intrapartum state

A
  1. The myometrium changes from a quiescent state to a contractile state. The smooth muscle contraction in labour of the myomertium differs from any other smooth muscle contraction as the smooth muscle does not relax, the muscle fibre progressively shortens, this is known as retraction.
  2. The cervix in the antenatal state is closed, to keep the fetus within the uterus. During the intrapartum stage, the cervix soften and thins- progressive effacement which allows for the ccervix to dilate
  3. The membrane in the antental state such as the amniotic sac are filled with amniotic fluid that provide a suitable environment for the fetus’’ growth and development. During intrapartum, these membranes rupture. This is the most effective way of starting labour.
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2
Q

what is uterine contractility dependent on

A

Uterine contractility is dependent on the interaction of actin and myosin.

This interaction occurs when intracellular calcium levels increase. These bind to calmodulin and activiate MCLK enzyme. This causes the phosphorylation of myosin so that it can interact with actin and result in muscle fibre shortening.

the interaction of actin and myosin is not constant during labour, it is cyclical in response to hormonal and mechancal signals.
eg: mechanical stretch upon the dilation of the cervix can cause actin-myosin to reorientate themselves to generate a greater strength of contraction. The hormones, oxytocin and prostaglandins can increase the force and frequency of contractions by increasing MLCK levels

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3
Q

What factors are important for the quiescent phase

A

-Progesterone:
- Prostacyclin(prostaglandin)
- Relaxin
-Nitric oxide
-Parathyroid hormone related peptide

-All of these function to increase CAMP and CGMP, these enable decreased levels of intracellular calcium for myometrial contractility

  • all of these factors favour a quiescent state where there is increased vasodilation to promote the relaxation of the myometrium and increased blood flow
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4
Q

What factors are important for the ACTIVATION phase

A

The activation phase: ensures there is the correct environment just before labour

  • Rise in estrogen and CRH

-Mechanical stretch: when there is sufficeint amount of stretch- that how we know it is time to give birth - eg. twins more stretch– birth comes early.

  • upregulation of genes required for contractions - (Prostaglandins and oxytocin receptors
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5
Q

What factors are important for the stimulation phase

A

Prostaglandins
Oxytocin- secreted by the posterior pituatary - they stimulate uterine contractions

CRH

increased synthesis of cytokines- (proinflammatory substances)

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6
Q

The functions of Progesterone during pregnancy

A

Progesterone is the dominant hormone during pregnancy as it maintains the uterine lining to sustain the pregnancy.
- Initially it is produced by the corpus luteum and then produced by the placenta.

-Progesterone decreases myometrial contractility: by inhibiting myometrial gap junction formation

  • Stimulates uterine: NO synthetase release
  • Increases CAMP and CGMP inhibits intracellular release of calcium from the sarcoplasmic reticulum
  • downregulate prostaglandin production, the development of calcium channels and oxytoxin receptors
  • Inhibits collegenolysis in cervix: TIMMP-1 tissue inhibitor
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7
Q

Changes in progestroge for the initiation of labour

A

The levels of progesterone do not change before labour.

  • There is an upregulation of PR-A the proinflammatory receptor & a decrease in the antiinflammatory receptor PRB
  • so there is a “functional” progesterone withdrawal
  • The upregulation of PR-A causes the expression of NF-KB. NF-KB increases the levels of proinflammatoey cytokines. —
    causes cervical ripening and upregulates oxytocin receptor expression in the myometrium -
    so it creates an environemnt more favorabale for substances that will contract the uterus.

There is increased bioavailabaility of oestrogen, this antagonises the effects of progesterone.

  • CRH and neuroendocrine mediators
  • Inc levels and Increased responsiveness of the myometrium to prostaglandins and oxytocin by increasing the concentration of receptors
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8
Q

What factors initiate labour

A

Estrogen- antagonise progesterone action

  • Oxytocin- initiates contraction
  • Prostaglandins - medicines to initate labour

-CRH

  • NO
  • Inflammatory cytokines
  • Relaxin
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9
Q

What are the stimulatory and inhibitory effects of progesterone

A
  • Inhibit Prostaglandin secretion
  • Red sensitivity to oxytocin
  • Inhibit CRH
  • Red oesterogen receptor expression
  • Degrade prostaglandins
  • Parathyroid hormone related protein synthesis
  • C-GRP (calcatonin gene related peptide) - vasodilation
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10
Q

Where is estrogen produced during pregnancy

A

The maternal and fetal adrenal glands synthesises oestrogen from DHEA.
- pneunmic to remeber enzymes- 3-17-AROMATSE

enzymes: 3BHSD, 17B-HSD, aromatase

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11
Q

What are the estrogen induced myometrial changes during labour

A
  • Inc Oestrogen and prostaglandin receptors in the myometrium
  • Up regulate the enzymes for muscle contraction Inc. MLCK enzymes and calmodulin
  • Inc connexin levels- increased gap junction formation in the myometrium
  • Induce collegenase and elastase - cervical ripening— cervical dilation
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12
Q

Oxytoxin

A
  • synthesied by posterior pituitary gland
  • produced by the myometrium, the decidua and the placenta
  • The myometrium becomes VERY sensitive to oxytocin
  • Its most conentrated in the fundus of the uterus
  • Oxytocin receptors increase by increasing levels of oestrogen and by mechanical stretch
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13
Q

Oxytoxin effects

A

Myometrium:
Increases intracellular calcium concentrations
Inc binding to calmodulin
Inc. MLCK enzyme
Inc. phosphorylation of mysoin
inc interaction of actin and myosin——– contraction

Decidua:
PGF2A synthesis and secretion——– contraction

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14
Q

Function of Relaxin

A

CERVICAL RIPENING

produced by the placenta and myometrium
in pregnancy- drives myometrial quiesence
myometrial vasodilation

  • Inc CAMP and CGMP which inhibits calcium release. Decreases the affinity of calmodulin for MLCK
  • Surpresses Oxytocin release.

BUTTT — for labour it induces cervical ripening

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15
Q

Inflammatory cytokines

A

Major enhancement of uterine contractility and cervical ripening

eg. TNF-A

Inflammatory cytokines stimulate prostaglandin secretion in the myometrium, fetal membranes and the placenta

inflammation can also trigger labour - surgical procedure, apendicitis

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16
Q

Nitric Oxide

A
  • Imp in myometrial quiesence.
    produced by fetoplacental vascular endothelium, decidua
  • Regulate vasular tone by the secretion of prostacyclins.
  • Inc CAMP and CGMP inhibits calcium concentrations
    levels elevated in the myomterim but not the cervix

BUTT NO levels at labour— think it may be involved in cervival ripening

17
Q

CRH & cortisol

A

EXTRA CRH is produced by the placenta and the myometrium
There are less CRH binding protiens- cant bind to all of the CRH
Unbound CRH- Inhibit Prostaglandins. Inc CAMP and CGMP which inhibit calcium release- promote quiescent state.

BUTT
at labour:(at term)
CRH enhances the contractile effects of prostaglandins and oxytocin

CRH— causes cortisol production
cortisol is converted into estrogen— foetal lung maturation.

18
Q

CRH and UCOROTINS

A

Urocortins are structurally similar to CRH
Increase at term
Inc. MMP, ACTH and prostaglandins
- act as proinflammatory agents

19
Q

Prostaglandins

A

Stimulatory Prostaglandins bind to the myocyte cell membrane and increase the force and frequency of contraction,.

PGE 2- iMP ROLE in cervical ripening

PGF 2a- increase intracellular calcium and contractility

Inhibitory prostaglandins- repress contraction

Prostaglandins are low during pregnancy and then they increase at term

NF-KB and COX-2 activation- upregulates PGS