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Summary Cases for Turning Blue

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A snapshot of the summary - Cases for Turning Blue

  • 3 Turning Blue

  • Where is there less blood flow on the lung?
    There is less perfusion at the top of the lung= ventilation is greater. 
    Therefore, the pulmonary blood flow is less at the apices of the lung compared to the base.
  • What causes the difference in pulmonary blood flow?
    After quiet expiration, the alveoli pressure=atmospheric pressure. However, gravity creates a blood pressure gradient of around 20mmHg, in where there is a greater pressure at the bottom of the lung.
  • What is normal pulmonary blood pressure?
    10-25mmHg
  • 3.1 Respiratory disease

  • Characteristic features of chest pain
    1. localised, intermittent, constant
    2. associated tenderness- muscle
    3. pleuretic pain- respiration- usually worse during inspiration
  • 3.1.1.1 Pathogenesis

  • What is the characterising factor of COPD?
    Inflammation of the airway, parenchyma and pulmonary vasculature. Rise in inflammatory cells, which release their mediators and cause damage to the lung structures.
  • What accounts for the irreversibility?
    Fibroblasts make fibronin which causes the scarring. The scarred tissue accounts for the irreversibility.
  • What is the protease-antiprotease imbalance hypothesis?
    - patients with a genetic deficiency of the alpha1-antitrypsin antiprotease have a significantly increased chance of developing pulmonary emphysema.
  • What is alpha1-antitrypsin?
    an inhibitor which prevents the actions of the protease enzymes which are capable of destroying the wall of the alveoli. 
    An example is neutrophil elastase, which is released by neutrophils following an inflammatory response.  

    Neutrophils are recruited during an inflammatory response-> a few may enter the airspaces-> release their mediators-> alpha1-antitrypsin would inhibit damage, therefore a deficiency may lead to emphysema.
  • How does smoking contribute to the development of emphysema?
    Smoking triggers an inflammatory response and so recruits neutrophils. 
    Smoking may be responsible for triggering the release of macrophage elastases- which are not affected by alpha1-antitrypsin, however also appear to cause damage to the connective tissue.
    Smoking also releases oxidative radicals, which cannot be defended against by the natural antioxidative properties of the lungs- these can cause damage to native antiproteases= cause functional alpha1-antitrypsin antiproteases. 
  • What are the consequences of the loss of the elastic connective tissue of the walls of the alveoli?
    Alveoli are found at the end of the respiratory bronchioles. The loss of the elastic connective tissue results in a reduction in radial traction and may cause the respiratory bronchioles to collapse following expiration= functional airflow obstruction.
    Collapses because the airway tube is supported by the connective tissue of the lung- withstands the pressure of the chest wall- should there be damage to the connective tissue, the tube cannot be supported and so upon expiration will collapse- air becomes trapped and the chest appears hyperexpanded.
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