PARTURITION

MEDIANA SUTOPO LIEDAPRAJA

PPDS TAHAP 1A

OBSTETRI DAN GINEKOLOGI FAKULTAS KEDOKTERANUNIVERSITAS INDONESIA – RSUPN CIPTOMANGUNKUSOMO

• 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

CRH RECEPTORS

CRH secreted from placentainto 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.

stimulate placenta release CRH

Glucocorticoids stimulate CRH gene and production CRH CRH stimulate pituitary

produce corticotropinAdrenal 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.”

CRH IN THE FETUS

Synthesis cortisolby 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.

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.

COX -2

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

Physical connection by multimer connexin 43.

Connection formed by paracrine Prostaglandin F2α and local release of calcium.

Depolarization

Contraction

• 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.

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

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

Chorion underlies the amnion

Produce PDGH (prostaglandin dehydrogenase)

As Potent “Inactivator” of Prostaglandins.

Release of Metalloproteases

Weaken placental membrane

CRH

MMP-9

DegradateCollagen

Cervix Structure

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.

THANK YOU