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File:IPLab13Hyaline9.jpg|This higher-power photomicrograph shows more clearly the hyaline membranes (arrows) and the congestion in the interstitium.
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== Study Questions ==
* <spoiler text="What causes Respiratory Distress Syndrome (RDS), or Hyaline Membrane Disease (HMD) as it is described in this case?">Most cases of respiratory distress syndrome (RDS) or hyaline membrane disease are idiopathic (the cause is unknown).
Known contributory factors include:
# over-administration of sedatives to the mother during delivery leading to respiratory depression in the infant;
# failure of the infant's central respiratory centers due to brain injury;
# reduced respiratory ability of the infant secondary to lung and skeletal muscle immaturity;
# physical obstruction of ventilation caused by the aspiration of blood clot and amniotic fluid during birth, and
# partial asphyxiation of the infant resulting from restrictive coils of umbilical cord wrapped around the infant's neck.</spoiler>
* <spoiler text="What factors play important roles in the pathogenesis of this syndrome?">Deficiency of pulmonary surfactant is the basic defect in respiratory distress syndrome.
Surfactant reduces surface tension within the alveoli so that less pressure is required to hold alveoli open. Surfactant also maintains alveolar expansion by varying surface tension with alveolar size, which helps keep the alveoli open and reduces the inspiratory effort needed to expand the lung. With a deficiency of surfactant, the lungs collapse with each successive breath, so the infant must work as hard with each successive breath as it did with the first.
The problem of STIFF atelectatic lungs is compounded by the SOFT thoracic wall that is pulled in as the diaphragm descends. Progressive atelectasis and reduced lung compliance then lead to a worsening clinical course.</spoiler>
* <spoiler text="What makes up the red hyaline material seen in HMD?">With a deficiency of surfactant, the alveoli collapse with each breath resulting in injury to the epithelial cells lining the alveolar wall. This injury causes a protein-rich, fibrin-rich exudate to be released into the alveolar spaces. This exudate forms the hyaline membranes.
The fibrin-hyaline membranes constitute a barrier to gas exchange, leading to carbon dioxide retention and hypoxemia. The hypoxemia itself further impairs surfactant synthesis leading to more lung damage.</spoiler>
{{IPLab 13}}
[[Category: IPLab:Lab 13]]
