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LCRS RepDevAge > Labour > Flashcards

Labour Flashcards

1
Q

when does miscarriage most often occur by definition?

A

before week 22 (late)

also in first trimester (13 weeks)

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2
Q

in what weeks is term?

A

37-41 weeks gestation

by labour or caesarean

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3
Q

in what weeks is preterm (extremely to late) ?

A

23-37 weeks gestation

by pre-term labour or emergency caesarean

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4
Q

what is the definition of labour?

A

increasing fundally dominated contractions combined with increasing cervical ripening and effacement.

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5
Q

what can contribute to miscarriage?

A

the suddenly change in blood supply to the foetus

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6
Q

what processes are involved in labour (independent of the gestational age)?

A

o Cervical ripening and effacement – INCREASING.
o Co-ordinated myometrial contractions – INCREASING.
o Rupture of foetal membranes.
o Delivery of infant then delivery of placenta.
o Contraction of uterus.

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7
Q

in what stages of pregnancy is labour experienced?

A
  • she may not experience labour for all 39 weeks till term
  • she may experience labour in the “latent stage” –> 8 weeks leading up to term
  • she will eventually experience labour in term (12-48 hours)
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8
Q

how is labour split?

A
  • phase 1- many hours
  • phase 2- hours
    contractions and cervical changes -> baby delivered
  • phase 3- 30 minutes
    placenta delivered

phases get shorter
labour is quicker in the second pregnancy

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9
Q

time frames for term terms:
Term

Post-term

Pre-term

Extremely preterm

Very preterm

Moderate to late preterm

Miscarriage

Early miscarriage

Late miscarriage

A 
Term= 37-41 weeks
Post-term= 42 weeks or more
Pre-term= 22-37 weeks

Preterm:

  • Moderate to late preterm= 32-36 weeks
  • Very preterm= 28-32 weeks
  • Extremely preterm= 22-28 weeks

Miscarriage= Less than 22 weeks (non viable infant delivered).

Early miscarriage= First trimester

Late miscarriage= Second trimester less than 22 weeks.

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10
Q

how is labour initiated during term?

A

mechanism is not understood as studies are not doable

may be oestrogen: progesterone high ratio, CRH or oxytocin

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11
Q

how is labour initiated during preterm? i.e. causes

A

intrauterine infection bleeding
multiple pregnancy
stress (maternal)

these all cause CRH, inflammation to increase or uterine contractions to increase, leading to labour

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12
Q

what are the cervical changes in labour?

A

Change from rigid –> flexible structure.

Remodelling
– loss of ECM.

Recruitment
– of leucocytes such as neutrophils.

Inflammation
– Prostaglandin E2, IL-8.

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13
Q

what are the 3 main processes in labour?

A

o Cervical ripening and effacement
o Co-ordinated myometrial contractions
o Rupture of foetal membranes

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14
Q

how is co-ordinated myometrial contraction mediated?

A

A fundal dominance with increased power and coordination.

Mediators:

  • prostaglandin F2 alpha (E2) increased
  • oxytocin receptors increased
  • contraction associated proteins
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15
Q

why do the foetal membranes rupture? what is this mediated by?

A

loss of strength due to changes in amnion basement membrane (remodelled)

Inflammation and leucocyte recruitment
(exacerbated in preterm), increased MMPs

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16
Q

mediators of cervical ripening and effacement?

A

Prostaglandin E2
IL-8
MMPs.

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17
Q

mediators of myometrium contraction?

A
  • Prostaglandin F2alpha (E2)
  • oxytocin receptor upregulation
  • contraction associated proteins.
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18
Q

mediators of foetal membrane rupture?

A

Prostaglandins
ILs
MMPs
inflammatory processes.

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19
Q

what is NFkappaB?

A

pro-inflammatory transcription molecule

20
Q

how does NFkappaB have its inflammatory effects?

A 
via:
COX-2-->PGs
IL-8
IL-1beta
MMPs
oxytocin receptors
PG receptors
contraction-associated proteins.

increase cytokines which then go into a +ve FB loop

21
Q

what is the evidence for the role of NFkappaB in labour?

A

Pro-labour genes have NFKB binding domains in promotor regions.

Modification of NFKB sites in the domains lead to loss of expression of the cells.

22
Q

what is NFkappaB closely related to?

A

IL-1beta , IL-6, COX2, cPLA2, IL-8

23
Q

what candidate initiators of NFkappaB are involved in the regulation of labour?

A

1) CRH
- Corticotrophin Releasing Hormone.

2) PAF
- Platelet Activating Factor

24
Q

what are the main molecules that control labour?

A

CRH and PAF which activate other molecules and eventually up regulate MMPs, PGE2, COX-2 and oxytocin receptors and IL-1beta

PGE2 is constitutively expressed before any changes can be witnessed that are conducive to labour

25
Q

what examples of pathways for mediators to initiate the processes of labour?

A

e. g. COX-2–> PGE2–> cervical ripening
e. g. oxytocin receptor–> myometrium
e. g. IL-8–>neutrophils–> MMPs–> cervical ripening

all regulated by CRH and PAF

26
Q

where can CRH be produced?

A

pituitary gland AND human placenta

27
Q

how do CRH levels change during pregnancy and labour?

A

Levels rise at the end of pregnancy before labour whilst CRH-binding-proteins drop towards end of pregnancy (so there is more active CRH)

High CRH also correlates with high COX2 molecule expression.

28
Q

what produces PAF?

A

part of lung surfactant that is produced by maturing lungs before birth

29
Q

what happens to amniotic fluid near term?

A

rises

30
Q

what is the level of PAF indicative of?

A

level of foetal maturity (may stimulate labour)

31
Q

where is PAF produced? what is the effect of PAF?

A

directly made by the lungs which acts to create ILs which stimulate PG production.

32
Q

what is the effect of CRH produced in the placenta on the baby?

A

Parturition hypothesis:

  • stimulates the baby hypothalamus via the umbilical cord so ACTH can be released from the pituitary that go to the foetal adrenals to produce cortisol (a STRESS hormone)
  • cortisol will have a +ve FB effect on CRH production in the placenta
  • foetal adrenals also produce mediators for myometrial contractions
33
Q

what does the parturition hypothesis describe via the CRH mechanism?

A

o Anything that increases CRH may lead to labour (stress, multiple infants).
o Anything that increases muscle contraction may lead labour
(excess stretch of uterus).
o Anything that activates inflammatory cascades may lead labour.

this also applied preterm e.g. stress due to IU bleeding

34
Q

what is needed to sustain pregnancy?

A

progesterone

35
Q

when does progesterone level drop after being high during pregnancy?

A

after the delivery of the placenta

36
Q

how does progesterone have non-labour promoting effects?

A

binds to NFkappaB leading to its inhibition

37
Q

what is the effect of high NFkappaB?

A

has labour promoting effects:
it binds to progesterone receptors so progesterone can not sustain pregnancy so labour can begin

hence high levels of NFkappaB towards the end of term

38
Q

which progesterone receptor mediates the main effects of progesterone?

A

PR-B (more than PR-A)

found throughout pregnancy to maintain progesterone effects

39
Q

what are the changes in number of PR-B and PR-A towards term?

A

more PR-A: PR-B so progesterone can have less pregnancy sustaining effects so labour can be initiated

i.e. progesterone binds best to PR-B to have pregnancy maintaining effects

40
Q

what does labour resemble overall?

A

inflammation resposes to foetal membranes and cervix

41
Q

what are the main tissues active during labour?

A

myometrium and cervix

42
Q

what is the key regulator of labour?

A

NFkappaB

43
Q

how does preterm and term labour differ?

A

the initiator factors involved

44
Q

what is the role of labour in context of progesterone?

A

labour tries to disrupt the effects of progesterone by disrupting receptors

45
Q

what is functional progesterone withdrawal?

A

loss or change in progesterone level at the end of term

[maternal progesterone remains high during labour until placental delivery]

46
Q

what 3 main factors trigger labour?

A

1) increased CRH and PAF (e.g. twins,stress)
2) increased myometrial contraction (e.g. twins)
3) increased inflammation (e.g. IU infection,bleeding)

LCRS RepDevAge (9 decks)

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