Physiology of Partuition

Question 1

Partuition?

Answer 1

The process of giving birth, to be in labour.
Involved softening and effacement (dilation) of the cervix and development of uterine contractions (rupture of membranes, not essential).

Question 2

Explain the 3 stages of labour.

Answer 2

1a) Initial (latent) phase - contractions develop and cervix softens (3cm)
1b) Active phase - regular contractions and speedy dilation of the cervix (3-10cm)
2) Cervix is fully dilated (10cm), strong propulsive contractions (1-2hrs)
3) Placenta is delivered.

Question 3

Explain the role of the cervix.

Answer 3

Potent cervix maintains pregnancy - barrier to ascending infection.
Cervix - elastic tissue, some SM.
Collagen fibrils in a proteoglycan matrix
Eplithelia cell lining and mucous plug.

Question 4

Explain the preparation of the cervix (and fetal membranes) for labour.

Answer 4

<37 weeks = quiescence = membranes and cervix intact.

Activation - cervix starts ripening.
Stimulation - cervix dilates.

Membranes weaken and rupture.

Activation relies on the inflammatory response initiated by functional progesterone withdrawal, CRH, oestrogen, cervical distension and oxytocin. (Ferguson reaction).

Inflammation:
iNos, COX2
PGE2
Matrix metalloproteases (2&9), cytokines and immune cells.
Cervix softens and more likely to dilate ready for labour.

Question 5

Explain the role of the myometrium.

Answer 5

Dense smooth muscle cells embedded in connective tissue and well vascularised.
Sparsely innervated in pregnancy.

Question 6

Explain the preparation of myometrium for labour.

Answer 6

<37 weeks = quiescent = minimal uterine activity.

Activation = some uterine activity.
Stimulation - powerful effective contractions.

Contraction associated proteins, induced PG receptor, COX2, oxytocin recepto, gap junctions, Ca++ signalling proteins and ion channels = myometrium primed for contraction…

…by…CRH, oestrogen, oxytocin, uterine distension, functional progresterone withdrawal, inflammation and influx of immune cells, PGs from the fetal membranes.

Question 7

Explain what controls myometrial contractions.

Answer 7

Dependent on Ca++.
Changes in Ca__ handling at term.
Uterotonins (PG/oxytocin).
Augment contractions.

Question 8

Explain the pro-contractions pathways that are activated at labour onset.

Answer 8

VOCC open = Ca++ induced Ca++ release.
Uterotonins activate uterotonin receptors - increase IP3 = Ca++ release from SR.
Stretch.
Contractile filaments.

Question 9

Explain the pro-relaxation pathways that are suppressed at onset of labour.

Answer 9

B2 agonists to Gs GPCR = cAMP
Natriuretic peptides.
NO, CO = cGMP

K+ open - hyperpolarise.

Ca back to SR.

Na in/Ca out!

CaATP pump to extrude Ca++

Question 10

Explain the myometrial excitability and contractile activity during pregnancy.

Answer 10

Time between contractions shortens.

Resting Vm increases…K+ decreases, Ca++ increases.

Question 11

Explain the role of gap junctions.

Answer 11

Made by connexin proteins.
Cx43 and 26 are upregulated in labour = better transmission of signals between cells…increase Gjs, increase communication = increase more powerful contractions.

Question 12

Oxytocin?

Answer 12

Important uterotonin in labour.
Increases uterine sensitivity to oxytocin at term.
Increased expression of oxytocin receptor mRNA and protein towards term and peak after labour.

Question 13

Time of delivery?

Answer 13

Tightly controlled - most after 37 weeks and majority by 40.

Question 14

What affects timing of labour?

Answer 14

Mother and foetus.
Women deliver at night.
Most dominant tissue is the fetal HPA axis and the placenta.
Alterations in the balance of progesterone:oestrogen also an influence.
Multiple pregnancies - deliver earlier…2xfetal HPA axis.

Decrease progesterone.
Increase oestrogen.

Question 15

Do uterine contractions only happen when labour is immanent?

Answer 15

No, they build up to labour. Occur for several nights before labour onset - oxytocin spurts.

Question 16

Levels of oestrogen and progesterone across gestation?

Answer 16

Both steadily increase - with progesterone plateauing at term.

Question 17

Explain changes in the fetal HPA axis that are important signals in parturition.

Answer 17

Fetal hypothalamus = increase CRH.
Increases ACTH.
Increases adrenal cortisol and DHEA.
Increases placental CRH and oestrogens.
Decreases progesterone responsiveness.
Increases inflammation - increase COX2 and PGs from foetal membranes.

Question 18

Explain functional preogesterone withdrawal.

Answer 18

Increase PRA:PRB…PRA = procontraction, PRB = anti!
Altered co-repressors and activators affecting PR mediated transcription.
PR transcription blocked by NF-KB

Therefore withdraw progesterone = activate NFKB and therefore promote productions of contractile proteins.

Question 19

Role of foetal surfactant in labour?

Answer 19

Surfactant increases the immune system, increases inflammation and increase NFKB = increases contractile proteins.
And inhibit genes that mediate uterine quiescence.

Question 20

Explain the proposed mechanism for human labour.

Answer 20

see diagram!