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Sonali pathophysiology of pulm surfactant and moa of steroids

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Sonali Paradhi Mhatre

Pulmonary surfactant is a surface-active lipoprotein complex produced by type II alveolar cells that coats the lung alveoli. It acts to reduce the surface tension at the air-liquid interface to prevent alveolar collapse during expiration. Preterm infants have a deficiency of surfactant at birth compared to term infants. The introduction of antenatal corticosteroids stimulates lung maturation and surfactant production, helping to reduce respiratory distress syndrome in preterm newborns. Betamethasone and dexamethasone are the corticosteroids typically used, with recommended courses of two doses of betamethasone or four doses of dexamethasone.

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Pathophysiology of Pulmonary Surfactant Presented by : Dr Sonali Mhatre.
Basic Physics : Surface Tension ï‚´Attractive forces among liquid molecules are responsible for phenomena of surface tension. ï‚´Each molecule is pulled equally in the inside direction. Thus, SPHERICAL SHAPE of water molecule is seen.
Sonali pathophysiology of pulm surfactant and moa of steroids
The lung alveoli are coated with surfactant molecules. Thus, preventing collapse on expiration and reducing pressure needed for next inspiration. Hydrophobic head Hydrophillic tail
Lipids form a monolayer at the air-water interface Surface tension decreases as lipid monolayer is compressed
Before surfactant After surfactant
Pulmonary Physiology
Sonali pathophysiology of pulm surfactant and moa of steroids
ï‚´Stable alveolar volume depends on a balance between: 1) Surface tension at the liquid-gas interface. 2) Recoil of tissue elasticity.
Pulmonary Surfactant ï‚´Surface active lipoprotein complex formed by Type 2 alveolar cells. ï‚´Contains both proteins and lipids. Thus has both hydrophilic and hydrophobic regions.
Components Of Pulmonary Surfactant.
Components & Functions * Major Lipids (~90%) Saturated Phosphatidylcholine DPPC (Lecithin) 60-80% Unsaturated Phosphospholipids Phosphatidylglycerol (PG) ~10% * Proteins (~10%) SP-A Hydrophilic, Host defence. Surfactant homeostasis. SP-B Hydrophobic, Spreading,  surface tension SP-C Hydrophilic , Adsorption SP-D: ? Phagocytic function
How it works…??? Starts at the terminal sac stage of lung development the Type 2 cells. At 20wk gestation, the lamellar bodies appear in cytoplasm. Lamellar bodies are secreted by exocytosis into the surface water layer lining the alveolar airspace. Here, surfactant forms a meshwork of tubular myelin.
Basic Structure of Alveoli
Half life of alveolar surfactant is 5-10 hrs after secretion. Broken down by macrophages and/or reabsorbed into the lamellar bodies.
Functions of surfactant Decreases the surface tension. To promote lung expansion during inspiration. To prevent alveolar collapse and loss of lung volume at the end of expiration. Facilitates recruitment of collapsed alveoli.
Normal Expiration With Surfactant Abnormal Respiration Without Surfactant
Why Preterms..???? ï‚´TERM BABIES : have storage pool of approximately 100 mg/kg of surfactant at birth. ï‚´PRETERM BABIES : have a storage pool of approx. 4-5 mg/kg surfactant at birth.
Deficiency of surfactant Progressive Atelectasis. Loss of functional residual capacity. Alterations in ventilation perfusion ratios. Uneven distribution of ventilation.
Role of Antenatal Corticosteroids ï‚´ Stimulation of developmentally regulated gene expression and physiologic functions resulting in lung maturation. ï‚´ Accelerate development of Type1 & Type2 pneumocytes, leading to structural and biochemical changes that improve both lung mechanics (max lung volumes, compliance) and gas exchange. ï‚´ Induction of Type 2 pneumocytes increases surfactant production by inducing enzyme responsible for surfactant proteins and phospholipid synthesis. ï‚´ Enhances the neonatal response to postnatal surfactant administration.
Role of Antenatal Corticosteroids (cont…)  Other effects that help in lung fluid resorption : 1. Induction of pulmonary beta receptors which play a role in surfactant release and absorption of alveolar fluid. 2. Induction of fetal lung antioxidant enzyme. 3. Upregulation of gene expression for the epithelial Na+ channel , which is important for the absorbtion of lung fluid after birth.
Which steroid to use…???  The steroids used are generally Betamethasone or Dexamethasone.  They are identical biologically and readily cross the placenta.  They have little mineralocorticoid activity and are relatively weak in immune suppression.  Dosage recommended : 2 doses of Betamethasone 12mg given 24 hrs apart OR 4 doses of Dexamethasone 6mg given 12 hrs apart.
 The lung alveoli are coated with surfactant molecules which act by reducing the surface tension at the fluid-air interface.  Thus, preventing collapse on expiration and reducing pressure needed for next inspiration.  The introduction of corticosteroids for fetal lung maturity in patients at risk of preterm labor was a major milestone in reducing the neonatal morbidity and mortality from RDS.  Studies have proved that antenatal steroids do not harm the health of the mother. Take Home messages……..!!!!!
Take Home messages……..!!!!! Betamethasone and Dexamethasone are the steroids of choice.  Recommended dosages are : 2 doses of Betamethasone 12mg given 24 hrs apart OR 4 doses of Dexamethasone 6mg given 12 hrs apart.  Efforts should be made to ensure that a single course is given at the most beneficial time for the fetus rather than exposing the women and their fetuses to multiple courses.  The possibility of ongoing long term harm need further evaluation.
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Sonali pathophysiology of pulm surfactant and moa of steroids

  • 2. Basic Physics : Surface Tension ï‚´Attractive forces among liquid molecules are responsible for phenomena of surface tension. ï‚´Each molecule is pulled equally in the inside direction. Thus, SPHERICAL SHAPE of water molecule is seen.
  • 4. The lung alveoli are coated with surfactant molecules. Thus, preventing collapse on expiration and reducing pressure needed for next inspiration. Hydrophobic head Hydrophillic tail
  • 5. Lipids form a monolayer at the air-water interface Surface tension decreases as lipid monolayer is compressed
  • 9. ï‚´Stable alveolar volume depends on a balance between: 1) Surface tension at the liquid-gas interface. 2) Recoil of tissue elasticity.
  • 10. Pulmonary Surfactant ï‚´Surface active lipoprotein complex formed by Type 2 alveolar cells. ï‚´Contains both proteins and lipids. Thus has both hydrophilic and hydrophobic regions.
  • 12. Components & Functions * Major Lipids (~90%) Saturated Phosphatidylcholine DPPC (Lecithin) 60-80% Unsaturated Phosphospholipids Phosphatidylglycerol (PG) ~10% * Proteins (~10%) SP-A Hydrophilic, Host defence. Surfactant homeostasis. SP-B Hydrophobic, Spreading,  surface tension SP-C Hydrophilic , Adsorption SP-D: ? Phagocytic function
  • 13. How it works…??? Starts at the terminal sac stage of lung development the Type 2 cells. At 20wk gestation, the lamellar bodies appear in cytoplasm. Lamellar bodies are secreted by exocytosis into the surface water layer lining the alveolar airspace. Here, surfactant forms a meshwork of tubular myelin.
  • 15. Half life of alveolar surfactant is 5-10 hrs after secretion. Broken down by macrophages and/or reabsorbed into the lamellar bodies.
  • 16. Functions of surfactant Decreases the surface tension. To promote lung expansion during inspiration. To prevent alveolar collapse and loss of lung volume at the end of expiration. Facilitates recruitment of collapsed alveoli.
  • 17. Normal Expiration With Surfactant Abnormal Respiration Without Surfactant
  • 18. Why Preterms..???? ï‚´TERM BABIES : have storage pool of approximately 100 mg/kg of surfactant at birth. ï‚´PRETERM BABIES : have a storage pool of approx. 4-5 mg/kg surfactant at birth.
  • 19. Deficiency of surfactant Progressive Atelectasis. Loss of functional residual capacity. Alterations in ventilation perfusion ratios. Uneven distribution of ventilation.
  • 20. Role of Antenatal Corticosteroids ï‚´ Stimulation of developmentally regulated gene expression and physiologic functions resulting in lung maturation. ï‚´ Accelerate development of Type1 & Type2 pneumocytes, leading to structural and biochemical changes that improve both lung mechanics (max lung volumes, compliance) and gas exchange. ï‚´ Induction of Type 2 pneumocytes increases surfactant production by inducing enzyme responsible for surfactant proteins and phospholipid synthesis. ï‚´ Enhances the neonatal response to postnatal surfactant administration.
  • 21. Role of Antenatal Corticosteroids (cont…) ï‚´ Other effects that help in lung fluid resorption : 1. Induction of pulmonary beta receptors which play a role in surfactant release and absorption of alveolar fluid. 2. Induction of fetal lung antioxidant enzyme. 3. Upregulation of gene expression for the epithelial Na+ channel , which is important for the absorbtion of lung fluid after birth.
  • 22. Which steroid to use…??? ï‚´ The steroids used are generally Betamethasone or Dexamethasone. ï‚´ They are identical biologically and readily cross the placenta. ï‚´ They have little mineralocorticoid activity and are relatively weak in immune suppression. ï‚´ Dosage recommended : 2 doses of Betamethasone 12mg given 24 hrs apart OR 4 doses of Dexamethasone 6mg given 12 hrs apart.
  • 23. ï‚´ The lung alveoli are coated with surfactant molecules which act by reducing the surface tension at the fluid-air interface. ï‚´ Thus, preventing collapse on expiration and reducing pressure needed for next inspiration. ï‚´ The introduction of corticosteroids for fetal lung maturity in patients at risk of preterm labor was a major milestone in reducing the neonatal morbidity and mortality from RDS. ï‚´ Studies have proved that antenatal steroids do not harm the health of the mother. Take Home messages……..!!!!!
  • 24. Take Home messages……..!!!!! Betamethasone and Dexamethasone are the steroids of choice. ï‚´ Recommended dosages are : 2 doses of Betamethasone 12mg given 24 hrs apart OR 4 doses of Dexamethasone 6mg given 12 hrs apart. ï‚´ Efforts should be made to ensure that a single course is given at the most beneficial time for the fetus rather than exposing the women and their fetuses to multiple courses. ï‚´ The possibility of ongoing long term harm need further evaluation.