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Parturition

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Parturition process

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Parturition

  1. 1. PARTURITION MEDIANA SUTOPO LIEDAPRAJA PPDS TAHAP 1A OBSTETRI DAN GINEKOLOGI FAKULTAS KEDOKTERAN UNIVERSITAS INDONESIA – RSUPN CIPTOMANGUNKUSOMO
  2. 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. 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. 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. 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. 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.
  7. 7. COX -2
  8. 8. 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
  9. 9. Physical connection by multimer connexin 43. Connection formed by paracrine Prostaglandin F2α and local release of calcium. Depolarization Contraction
  10. 10. • 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.
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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.
  15. 15. THANK YOU

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