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A, Diagram of normal structures within the acinus, the fundamental unit of the lung. A terminal bronchiole (not shown) is immediately proximal to the respiratory.

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Presentation on theme: "A, Diagram of normal structures within the acinus, the fundamental unit of the lung. A terminal bronchiole (not shown) is immediately proximal to the respiratory."— Presentation transcript:

1 A, Diagram of normal structures within the acinus, the fundamental unit of the lung. A terminal bronchiole (not shown) is immediately proximal to the respiratory bronchiole. B, Centrilobular emphysema with dilation that initially affects the respiratory bronchioles. C, Panacinar emphysema with initial distention of the peripheral structures (i.e., the alveolus and alveolar duct); the disease later extends to affect the respiratory bronchioles. Emphysema Centriacinar Vs Panacinar

2 Centrilobular emphysema occurs with loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli. This pattern is most typical for

3 The respiratory bronchioles and some of the alveolar ducts in the middle of the pulmonary lobules are destroyed. This results in holes being formed – emphysematous spaces. These areas are black because of the accumulation of carbon pigment in the peribronchial lymphatics. Centrilobular emphysema

4 There is severe diffuse involvement of the acini; the whole acinus is markedly dilated. Panacinar emphysema

5 The 'substance' of the lung has been almost completely lost. When such lungs are removed from the body they are soft and can often be squeezed into a small ball. The pathology can be demonstrated by inflating the intact lung by running formalin into the main bronchus, allowing it to float in formalin for 48 hours for fixation, then slicing it with a long, sharp knife. As the lung is cut, the formalin runs out of the emphysematous spaces but the holey organ can be examined by immersing the slices in water, as was done for this photograph. Pan-acinar destructive emphysema – severe emphysema.

6 The protease-antiprotease imbalance and oxidant-antioxidant imbalance are additive in their effects and contribute to tissue damage. α1-Antitrypsin (α1AT) deficiency can be either congenital or "functional" as a result of oxidative inactivation. See text for details. IL-8, interleukin 8; LTB4, leukotriene B4; TNF, tumor necrosis factor. Pathogenesis of emphysema

7 The chest cavity is opened at autopsy to reveal numerous large bullae apparent on the surface of the lungs in a patient dying with emphysema. Bullae are large dilated airspaces that bulge out from beneath the pleura. Emphysema is characterized by a loss of lung parenchyma by destruction of alveoli so that there is permanent dilation of airspaces. Advanced emphysema

8 There is marked enlargement of airspaces, with thinning and destruction of alveolar septa. ( Pulmonary emphysema

9 There are large apical and subpleural bullae Bullous emphysema


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