What are the various pathological manifestations of emphysema

Emphysema is one of the more serious secondary lung diseases, and because the source of the disease differs, the pathological manifestations can also vary or differ greatly. In terms of causative factors, there are inflammatory pathological reactions such as repeated infection and chronic bronchitis, as well as mechanical pathological reactions such as compression of alveoli and capillaries and imbalance between elastase and its inhibitor. Generally, emphysema caused by mechanical pathological reactions is milder and has a good prognosis.

Elastase

Chronic bronchitis causes relatively great damage to the bronchi of the lung respiratory tract, leading to narrowing of the lumen, formation of incomplete obstruction, premature closure during exhalation, and increased residual alveolar gas volume, which causes overinflation of the alveoli; chronic bronchitis also destroys the cartilage of the small bronchial walls, causing loss of the supporting function, so that during exhalation the bronchi contract excessively or even collapse, and the residual gas volume becomes excessive and ruptures, resulting in large-area emphysema and bullae.

If chronic bronchitis is combined with repeated infection, then the proteolysis by leukocytes and macrophages increases, damage to lung tissue and alveolar walls deepens further, and multiple bullae may merge into larger bullae. Diseases of the pleura, diaphragm, heart, and others cause compression of the capillaries in the alveolar walls, so blood supply to lung tissue decreases, which then leads to nutritional disturbance, and the elasticity of the alveolar walls declines and ruptures, resulting in localized emphysema.

Alveolar walls and capillaries in cor pulmonale

In the human body, elastases such as neutrophil alpha1-antitrypsin are closely related to cardiovascular atherosclerosis. They also have a relatively strong effect on the bronchi and alveoli of the lungs. If, for various reasons, proteases and inhibitors become imbalanced, emphysema is also easily triggered. For example, with direct or indirect smoking, the human body releases elastase as a self-response, and smoke also reduces the activity of alpha1-antitrypsin, leading to decomposition of elastic fibers in lung tissue and causing emphysema. In addition, congenital inheritance and deficiency of alpha1-antitrypsin also make emphysema more likely to occur.

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