Parturition process

1. PARTURITION
MEDIANA SUTOPO LIEDAPRAJA
PPDS TAHAP 1A
OBSTETRI DAN GINEKOLOGI FAKULTAS KEDOKTERAN
UNIVERSITAS INDONESIA – RSUPN CIPTOMANGUNKUSOMO

2. • The timing of birth development of placenta
 gene expression of CRH (corticotropin releasing
hormone)
• Maternal plasma CRH increase as pregnancy advances
 peak at time of delivery
• Human produce CRHBP for CRH  end of pregnancy 
CRHBP falls  CRH rise.
Birth Placenta CRH

3. CRH RECEPTORS
CRH secreted from placenta
into maternal blood and fetal
circulation
CRH bind to CRH type 1 R
(G Protein couple receptor).
Mother CRH-R 
Pituitary, myometrium,
adrenal glands
Fetus CRH-R 
Pituitary, Adrenal Glands, Lungs.
MOTHER + FETUS  initiate
the changes of parturition.

4. stimulate placenta release CRH
Glucocorticoids stimulate CRH gene and
production CRH  CRH stimulate pituitary 
produce corticotropin
Adrenal cortex to release cortisol +DHEAS
Estrogen synthesis.
“CRH level has a relatively specific association with risk of preterm
birth  Maternal CRH levels is the most accurate predictor.”

5. CRH IN THE FETUS
Synthesis cortisol
by adrenal glands
and maturation of
fetal lungs
Lung maturation 
increased of
Surfactant protein A
and phospholipids
Pro-
inflammatory
action +
stimulate
contraction 
increase
prostaglandins
CRH stimulation of
fetal adrenal 
placental formation
of DHEA 
Precursor of
estrogen 
inducing
contraction.

6. IN CONCLUSION
as gestation advances Systems in mother and fetus
increase in placental CRH
 change in fetal cortisol concentration, fetal lung
maturations, amniotic fluid protein, phospholipids and
myometrial receptor expression.

8. COX -2

9. ACTIVATION OF THE MYOMETRIUM AT TERM
Important event  “ Contraction associated proteins” 
Relax ?? Or contraction ??
3 types:
1. Interaction between actin and myosin proteins
2. Excitability of myometrial cells
3. Intercellular connectivity

10. Physical connection by
multimer connexin 43.
Connection formed by
paracrine Prostaglandin
F2α and local release of
calcium.
Depolarization
Contraction

11. • Action and Myosin interaction =
Contraction
• Actin converted  Globular to
Filamentous
• Actin partner  Myosin  activated by
M-light chain kinase  activated by
Calmodulin and Intracellular Calcium.
• Myocyte depolarizes  Influx
extracellular Ca2+  contraction.
Example :
Nifedipine  Tocolytic  block voltage-
regulated Ca2+ channel.

13. 1
• Stretching of myometrium (fetal growth)mitogen
activated protein kinase
2
• increase intracellular CAMP
• activating protein kinase A.
3
• inactivate myosin light chain
4
•Contraction

14. FETAL MEMBRANE ACTIVATION
Production of surfactant proteins,
phospholipids and inflammatory
cytokines in amniotic fluid
Increase as COX-2 activity
and PGE2 in amnion.
Mediators of
inflammation in the
amnion

15. Chorion underlies the amnion 
Produce PDGH (prostaglandin
dehydrogenase)
As Potent “Inactivator”
of Prostaglandins.
Release of
Metalloproteases
Weaken placental
membrane
CRH
MMP-9
Degradate
Collagen
Cervix
Structure

17. A Better Understanding of the pathway to normal birth should
provide a pathological process.
The goal is to predict which pregnancies carry a risk of preterm,
Reduce the incidences of cerebral palsy and cognitive
impairment associated with preterm birth.

18. THANK YOU