Various pathological manifestations of emphysema
Emphysema is one of the more serious secondary lung diseases, because of the different sources of disease, the pathological manifestations will be different or very different. Pathogens include inflammatory pathological reactions such as repeated infection and chronic bronchitis, as well as mechanical pathological reactions such as alveolar and capillary compression, imbalance of elastase and its inhibitors. The emphysema with general mechanical pathological reaction is mild and the prognosis is good.
of elastase
Chronic bronchitis has great damage to the bronchi of the lung respiratory tract, leading to stenosis of the lumen, incomplete obstruction, premature closure during exhalation, increased alveolar residual volume and excessive alveolar inflation; chronic bronchitis can also destroy the cartilage of the small bronchial wall, lose the function of stent, and the bronchi shrink excessively when exhalation, even collapse, excessive residual volume and rupture, resulting in large-area emphysema and pulmonary bullae.
If chronic bronchitis is combined with repeated infection, the protein decomposition of leukocytes and macrophages will increase, the damage of lung tissue and alveolar wall will be further deepened, and multiple pulmonary bullae will be synthesized into larger pulmonary bullae. Pleura, chest diaphragm, heart and other diseases, resulting in alveolar wall capillary pressure, lung tissue blood supply will be reduced, and then nutritional disorders, alveolar wall elasticity will decrease rupture, local emphysema occurs.
Pulmonary alveolar wall and capillaries
Neutrophils α1-antitrypsin and other elastases in human body are closely related to cardiovascular atherosclerosis. Similarly, the lung bronchus, alveoli and other effects are also strong, if for various reasons, resulting in protease and inhibitor imbalance, but also easy to cause emphysema. For example, direct or indirect smoking, the body will respond to the release of elastase, smoke will also reduce the activity of alpha 1-antitrypsin, leading to the breakdown of elastic fibers in lung tissue, resulting in emphysema. There are congenital inheritance, lack of alpha 1-antitrypsin, also prone to emphysema.
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