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Rob's RDA > Labour > Flashcards

Labour Flashcards

1
Q

What is usually considered miscarriage vs preterm

A

Miscarriage (<23 weeks of gestation)

Preterm: 23-37 weeks of gestation

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2
Q

Define labour

A

The process of expulsion of the fetus and the placenta from the uterus.

In stages

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3
Q

What are the stages of labour

A
  1. Onset of uterine contractions through the period of dilation of the os uteri
  2. period of expulsive effort, beginning with complete dilation of the cervix and ending with expulsion of the infant
  3. Placental stage, delivery of infant and then expulsion of placenta and membranes
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4
Q

Main tissues involved in labour

A

uterus and cervix

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5
Q

Main events in human labour

A

Cervical ripening and effacement

Co-ordinated myometrial contractions, Preceded by “Braxton Hicks contractions” or ‘contractures’

Rupture of fetal membranes

Delivery of infant

Delivery of placenta

Contraction of uterus to limit maternal blood loss (from spiral arteries)

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6
Q

More detail on stage 1 of labour

A
  • Changes in cervix and myometrium

- Rupture of the fetal membranes also normally occurs during the first stage

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7
Q

How long is each stage of labour

A

1- 8hrs
2 &3- 30 mins each

stage 1 and 2 can get shorter in subsequent pregnancies

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8
Q

What is involution

A

Very powerful contractions of the uterus, leading to a rapid decrease in overall size

Associated with stage 3 (placental delivery)

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9
Q

Why is involution necessary

A

Once the placenta has been delivered, this involution of the uterus is very important, as this is the primary process through which blood flow through the spiral arteries is stopped.

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10
Q

If involution does not occur what can be given

A

his process is linked to increased maternal levels of oxytocin – if it does not occur spontaneously, an injection of oxytocin (or similar muscle contracting agent) can be given to accelerate the process.

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11
Q

Outline the process of cervical remodelling and dilation

A
  • remodelling of ECM of cervix over many hours
  • change from rigid to rlexible
  • also due to increasing pressure of foetal head on cervix caused by increasing strength and frequency of myometrial contraction
  • recruitment of leukocytes
  • inflammatory (see mediators)
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12
Q

Which factors are most important in regulating changes in the cervix in labour

A

I.e. in stage 1 (cervical ripening and effacement)

PGE2

IL8

MMPs

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13
Q

Which factors are most important in regulating changes in the myometrium in labour

A

PGF2a (lesser E2) increases from foetal membranes

Oxytocin receptor increases

Contraction associated proteins increase

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14
Q

Which factors that are most important in regulating the changes in foetal membrane

A

INFLAMMATORY

Prostaglandins, interleukins, MMPs

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15
Q

T/f labour differs depending on gestational age

A

F: it seems that similar mechanisms are involved in labour at all gestational ages, so the changes summarised above will be present during preterm labour at 28 weeks, and during term labour at 40 weeks of gestational age.

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16
Q

Outline the coordinated myometrial contractions in stage 1 of labour

A

Fundal dominance
Increased co-ordination of contractions
Increased power of contractions

look at the key mediators

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17
Q

Outline rupture of foetal membranes occurring in stage 1 of labour

A
  • lose strength due to changes in amnion basement membrane component
  • Inflammatory changes, leukocyte recruitment (not much in normal labour but exacerbated in preterm)
  • Increased levels and activity of MMPs
  • Inflammatory process in fetal membranes

(CHECK MEDIATORS)

18
Q

Key transcription factor in inflammation

What does it do

A

NFkB

Molecules like COX2, cytokines (IL8, IL6, IL1b), MMPs are upregulated by NFkB in any tissue

19
Q

Role of NFkB in labour

A

Many initiators activate NFkB

Leads to upregulation of many genes especially inflammatory ones that lead to labour.

COX-2 (prostaglandins - PGs),

IL-8, IL-1b,

MMPs,

Oxytocin receptor,

PG receptors;

contraction-associated proteins

Tissues involved in labour (cervix, uterus, foetal membranes) etc. have NFkB biding domains in promoter regions of their genes, and will upregulate their production of these inflammatory molecules in response to the many initiators which are binding to the NFkB

Coordinated, family of genes all switched on

Hard to stop labour once it has started

20
Q

Why is IL1b important in labour

A

Many initiators result in NFkB activation and production of LOTS of genes making inflammatory molecules in the labour tissues

IL1b can causes further activation of NFkB so it is a feedforward loop that goes on until you get delivery

21
Q

What is linked with preterm labour

A

So we said that the production of all these inflammatory molecules due to NFkB by many initiators results in labour.

Well, those inflammatory molecules are also produced in infection, stress etc.

INFECTION LINKED TO PRETERM LABOUR

(INTRAUTERINE INFECTION)

22
Q

T/f biochemical changes occur in advance of clinical presentation of labour

A

T…….

before any clinical signs of labour such as uterine contraction or cervix dilation,

slide 52

On left, the tissue from foetal membrane was given an initator, and prostaglandin increased

On the right, the tissue from the foetal membrane was given an initiator, but prostaglandin could not increase any more because it was already so high

The woman on the right was biochemically already in labour because the rate of prostaglandin synthesis and release was sky high but without clinical presentation yet

23
Q

2 drivers of normal term labour

A

PAF and CRH

Not just produced in one tissue

24
Q

What hormone changes in run up to delivery.

What is the effect

A

CRH increases in the few weeks before delivery

As well as CRH increasing, there was found to be increased COX 2 expression (and thus prostaglandins).

So the initiatory CRH might be increasing expression of PGs in the tissues involved in labour (one of which is the foetal embrane here)

25
Q

Where is platelet activating factor found

A

Part of lung surfactant

Surfactant proteins and complexes

LUNGS ARE LAST STRUCTURE TO MATURE BEFORE BIRTH (so late in development in early stages of pregnancy but also late to mature)

PAF produced by maturing lung before birth

Levels in amniotic fluid increase near term

Fetal signal of maturity

I.e. as the lungs are last structure to mature, could be that when they have enough surfactant (meaning they could breathe air well now) this driver labour (it increases the prostaglandin levels in the labour related tissue!!!)

26
Q

T/F PAF increases inflammatory molecule synthesis as does CRH. Endotoxin can too

A

T

(PAF and CRH bothincrease prostaglandin (PGE2) synthesis……. endotoxin is a bacterial antigen. Remember that infections preterm can drive labour, and endotoxin, CRH and PAF all increase IL1b production too, another inflammatory molecule involved in labour and which is responsible for the fast forward feedback loop to increase NFkB promoter activation)

27
Q

Where is CRH produced

A

So we said that PAF is produced as part of lung surfactant

CRH produced in the placenta

28
Q

Outline a possible hypothesis for the interaction between PAF and CRH in parturition

A

Baby is producing PAF from lung surfactant which is acting as an initiator to increase NFkB to increase the levels of the inflammatory molecules responsible for labour.

CRH produced in placenta and is also acting as an initator.

IN ADDITION, CRH acts on baby’s pituitary gland to increase ACTH.

ACTH acts on the adrenal gland to produce cortisol.

Cortisol increases lung maturation (which will then cause more PAF release)

AND

cortisol can go back to the placenta and can go back via the umbilical cord to the placenta,

and bind to GC receptors in the placenta

AND STIMULATE MORE CRH PRODUCTION (NOTE THIS IS POSTIVE FEEDBACK)

***CRH from placenta ALSO increases the DHEAS from baby adrenal glands, producting oestrogen in the placenta which also is involved in labour

29
Q

What is the difference between the action of cortisol in the placenta vs hypothalamus

A

normally in hypothalamus would negatively feedback on CRH production

in placenta, feedsforward. cortisol binding to GC in the placenta increases cortisol release

30
Q

What can lead to pre-term labour then

A

Anything that increases CRH may predispose to labour (stress, multiple infants)

Anything that increases muscle contraction may predispose to labour (excess stretch of uterus)

Anything that activates inflammatory cascades may predispose to labour

The above apply to preterm labour (intrauterine infection, bleeding, twins)

31
Q

What is required to sustain pregnany

A

PROGESTERONE (Progesterone receptor blockade: pregnancy loss)

32
Q

What happens to progesterone levels in human labour

A

DOESNT REDUCE AS YOU’D EXPECT IT TO (as pregnancy is ending)

INSTEAD

EFFECT of progesterone LOST in normal term labour

33
Q

What does progesterone do in pregnancy vs in labour

A

Progesterone binds to its progesterone receptor

This binds to NFkB to stop it releasing inflammatory molecules.

This is good because inflammatory molecules initiate labour and you don’t want this in pregnancy

At end of pregnancy:

progesterone receptor levels fall, despite progesterone still being high, progesterone has reduced effect so NFkB goes up and can now switch on genes for production of inflammatory molecules and cause labour

=FUNCTIONAL PROGESTERONE WITHDRAWAL

34
Q

How do progesterone receptor levels change near term

A

PR-B mediates the main effects of progesterone via gene expression

PR-A is less able to mediate these effects

Ratio of PR-A : PR-B increases at term

LEADS TO FUNCTIONAL PROGESTERONE WITHDRAWAL

35
Q

t/f PROGESTERONE affects the genes for PGF2a, COX-2 and IL-8

A

yes because of its effect on NFkB….

36
Q

When might pregnancy cause risk to mother becfore labour

A

If the mother is in poor health at the beginning of pregnancy (e.g. due to socio-economic factors such a poor nutrition), then the additional strain on her system caused by pregnancy may have considerable impact.

Pre-eclampsia can affect maternal vascular system and pose risks to maternal health

37
Q

T/f preterm labour and delivery poses additional risk to mother

A

F

38
Q

Why is mother at risk in labour

A

Necessity for uterine involution after delivery of the placenta. Due to the remodelling of the spiral arteries (see Session 3), they cannot vasoconstrict in the normal way to decrease blood flow, and hence blood loss into the uterine lumen.

The powerful uterine contractions of involution effectively close the spiral arteries, and limit blood loss

39
Q

Foetal risks during labour

A

Delivery at term normally has few specific risks for the infant, but delivery at gestations less than 32 weeks are much more likely to cause infant morbidities or mortality.

40
Q

Why is the incidence and severity ofbrain damage in preterm infants very high

A

The fetal brain is particularly sensitive to inflammatory mediators.

As labour is an inflammatory process, and one clear cause of preterm labour is intrauterine infection, the incidence and severity of brain damage is particularly high in these extremely preterm infants.

41
Q

Other than brain damage due to inflammatory mediators, what is the other risk for the baby with early deliveyr

A

incomplete development of lungs, brain, digestive or immune systems,

Rob's RDA (10 decks)

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