Embrology of the respiratory system

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Complete revision on Embryology of the Respiratory System

Complete revision on Embryology of the Respiratory System

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  • Fig 13.1A from Sadler (2006). Langman’s Medical Embryology, 10 th ed.
  • Left figure: Fig 11-4 from Schoenwolf et al. (2009). Larsen’s Human Embryology, 4 th ed. Right figure: Fig 13.3 from from Sadler (2006). Langman’s Medical Embryology, 10 th ed.
  • Left: Fig 13.6A Right: Fig 13.7
  • Schoenwolf et al: Larsen’s Human Embryology, 4 th Edition. Copyright 2008 Churchill Livingston, an imprint of Elsevier, Inc. All rights reserved
  • Carlson: Human Embryology and Developemental Biology, 4 th Edition. Copyright 2009 by Mosby, an imprint of Elsevier, Inc. All rights reserved.

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  • 1. By ORIBA DAN LANGOYA MBchB MAKcHs
  • 2. The lung buds form during the 4th week Initially appear as the respiratory diverticulum, which is a ventral outgrowth of foregut endoderm MESODERM dependent process. Langman’s Medical Embryology, 10th ed
  • 3. The respiratory tract is derived from foregut endoderm and associated mesoderm From endoderm: epithelial lining of trachea, larynx, bronchi, alveoli From splanchnic mesoderm: cartilage, muscle, and connective tissue of tract and visceral pleura.
  • 4. Splitting of foregut into esophagus and trachea Tracheo-esophageal ridges: longitudinal ridges that eventually fuse to separate trachea from esophagus.
  • 5. Tracheo-esophageal fistulas  Incomplete separation and/or atresia of trachea and esophagus (B on right shows esophageal atresia)  Defect likely in mesoderm and usually associated with other defects involving mesoderm (cardiovascular malformations, VATER / VACTERL, etc.) VATER = Vertebral anomalies, Anal atresia, Tracheoesophageal fistula, Esophageal atresia, Renal atresia VACTERL = VATER + Cardiac defects & Limb defects
  • 6. Tracheoesophageal Fistulas / Esophageal Atresia  Occur in approx 1/3000 births, most (90%) are that shown in (A) above.  Complications: PRENATAL: Polyhydramnios (due to inability to swallow amniotic fluid in utero) POSTNATAL Gastrointestinal: Infants cough and choke when swallowing because of accumulation of excessive saliva in mouth and upper respiratory tract. Milk is regurgitated immediately after feeding. Respiratory: Gastric contents may also reflux into the trachea and lungs, causing choking and often leading to pneumonitis.
  • 7. Successive stages in the development of the larynx: The epithelial lining of the larynx is of endodermal origin. The cartilages and muscles of the larynx arise from mesenchyme from the 4th and 6th pharyngeal arches 4 weeks 10 weeks 5 weeks 6 weeks
  • 8. Clinical Correlation: Laryngeal Atresia This rare anomoly results in obstruction of the upper airway - congenital high airway obstruction syndrome (CHAOS). Laryngeal Web This uncommon anomaly results from incomplete recanalization of the larynx during the 10th week. A membranous web forms at the level of the vocal cords, partially obstructing the airway
  • 9. 4 weeks 10 weeks 11 weeks 14 weeks - photomicrograph Progressive changes in the development of the laryngotracheal tube: Endodermal lining distal to the larynx differentiates into the epithelium and glands of the trachea and pulmonary epithelium. The cartilage, connective tissue and muscles of the trachea derive from splanchnic mesenchyme.
  • 10. Differentiation of pleural membranes The lung buds “punch” into the visceral mesoderm. The mesoderm, which covers the outside of the lung, develops into the visceral pleura. The somatic mesoderm, covering the body wall from the inside, becomes the parietal pleura. The space between is the pleural cavity.
  • 11. Pleuropericardial folds separate pleural and pericardial cavities. 5 weeks - pleuropericardial fold forms 8 weeks - lungs grow and expand into pleural cavity 6 weeks - pleuropericardial membrane reaches midline 7 weeks -further maturation of pericardium (expands pleural cavity
  • 12. Separating the abdominal and thoracic cavities: development of the septum transversum and diaphragm  The septum transversum stops at the gut tube, leaving two open passageways on the left and right sides, the “pericardioperitoneal canals” (shown on the left)  Closing off these canals requires growth from the dorsolateral body wall, aka the “pleuroperitoneal membranes” (shown on the right)  Defects in this process cause CDH (congenital diaphragmatic hernias): abdominal contents herniate into pleural cavities and interfere with lung development.
  • 13. First three branching events are stereotyped: After the initial bifurcation into two primary bronchi, two buds, or secondary bronchi, form on the left and three on the right predicting the five lobes of the adult human lung. Ten tertiary (segmental) bronchi form in the right lung and eight in the left lung - establishing the brochopulmonary segments of the adult human lung. Initial Patterning of the Lung:
  • 14. Stages of Maturation of the Lungs Pseudoglandular Period (5-17 weeks): By 17 weeks, all major elements have formed, except those involved with gas exchange (fetuses unable to survive if born at this stage). Canalicular Period (16-25 weeks): Bronchi, terminal bronchioles become larger, lung tissue becomes highly vascular. Alveolar ducts form by week 24. By end, some terminal sacs have formed so respiration is possible (small chance of survival at this stage). Terminal Sac Period (24 weeks to birth): Many more terminal sacs develop, their epithelium becomes very thin and capillaries bulge into the developing alveoli. Blood-air barrier becomes well-developed. (By 26-28 wks, 1000 gr fetus has a sufficient # of sacs and surfactant to survive.) Alveolar Period (late fetal period to age 8): Alveoli-like structures are present by 32 weeks. Epithelial lining of sacs attenuate to extremely thin squamous epithelia, capable of gas exchange. 95% of characteristic, mature alveoli develop after birth.
  • 15. Surfactant proteins augment function of phospholipid surfactants Four major surfactant proteins: A, B, C, and D Surfactant A: activates macrophages to elicit uterine contractions, also important in host defense Surfactant B: organizes into tubular structures that are much more efficient at reducing surface tension (specific deficiency in Surfactant B can lead to respiratory distress) Surfactant C: enhances function of surfactant phospholipids Surfactant D: important in host defense.
  • 16. Clinical Correlations: Respiratory Distress Syndrome/Hyaline Membrane Disease: This disease affects 2% of live newborn infants, with prematurely born being most susceptible. 30% of all neonatal disease results from HMD or its complications. Surfactant deficiency is the major cause of RDS or HMD. The lungs are underinflated and the alveoli contain a fluid of high protein content, probably derived from circulation substances and injured pulmonary epithelium. In addition to prematurity, prolonged intrauterine asphyxia may produce irreversible changes in Type II alveolar cells, rendering them incapable of producing surfactant. Other factors may contribute to surfactant deficiency, but the genetics of surfactant production are not well-defined. Prolonged, labored breathing damages alveolar epithelium, leading to protein deposition, or “hyaline” changes (shown in figure).
  • 17. Clinical Correlations: Congenital Lung Cysts: Cysts (filled with fluid or air) are thought to be formed by the dilation of terminal bronchi, probably due to irregularities in later development. If severe, cysts are visible on radiographs. Highly variable outcomes result from different cystic conditions. Agenesis of the Lungs: Can occur bilaterally or unilaterally. Unilateral lung agenesis is compatible with live as remaining side hyperexpands and compensates. Lung Hypoplasia: Often caused by congenital diaphragmatic hernias or congenital heart disease. Characterized by reduced lung volume. Extreme hypoplasia is inconsistent with life.
  • 18. THE END