Emphysema

Emphysema

Emphysema (pulmonary emphysema) is a remote terminal bronchiole (respiratory bronchiole, the alveolar, alveolar capsule and alveolar) airway flexibility may be over-inflated, inflatable and lung volume increase or accompanied by airway Wall undermine the pathological state. According to the etiology of several types of emphysema are as follows: the elderly emphysema, lung tissue due to old age and physical degeneration caused by; compensatory emphysema, the lung tissue due to some loss of respiratory function (such as lung wilt depression , Or after lobectomy, or chest deformities, etc.), resulting in a healthy lung tissue compensatory expansion occurred. Interstitial emphysema, the alveolar wall and respiratory bronchiole rupture, gas Yat Rufei mesenchymal have, strictly speaking, does not belong to areas of emphysema; focal emphysema, the inhalation of dust, especially in the coal dust calm Respiratory bronchiole wall caused by fibrous tissue proliferation and contraction, causing luminal expansion of production; next Jiange Xing emphysema, the lung lobular interval fibrous tissue near the alveolar over-expansion or rupture inflatable integration, emphysema bubble formation, After its breakdown can cause spontaneous pneumothorax; a1-anti-trypsin deficiency emphysema, because of genetic factors, congenital anti-serum a1-trypsin (a1-AT) lack, we can not prevent the WBC from lung tissue and macrophages Cell protein dissolution of the damage can be induced pulmonary emphysema, rare in the country; obstructive pulmonary emphysema, chronic bronchitis or other growing thin bronchial narrow, remote terminal bronchiole gas chamber over-inflated, and With gas wall expansion, arising from the breakdown, clinical chronic bronchitis for the more common complications. Smoking is the main cause. This chapter focuses on obstructive pulmonary emphysema.

[Etiology and pathogenesis]

The pathogenesis of emphysema has not yet been fully explained, is generally believed that a combination of factors is the formation of synergies. Arising from the various factors such as chronic bronchitis infection, smoking, air pollution, occupational dust and the long-term inhalation of harmful gases, such as allergies, can cause obstructive pulmonary emphysema. Its mechanism may be summarized as follows: ① because of chronic bronchial inflammation, the lumen stenosis, a not completely blocked, suction, easy access to alveolar gas, breath, pleural cavity pressure due to increase in tracheal occlusion; alveolar residual gas, So that over-inflated alveolar; ② chronic inflammation of bronchial wall of small cartilage damage, loss of normal bronchial stent, when Bronchodilation suction, gas was able to enter alveolar, but when the bronchial excessive depletion of breath, depression closed, impeding gas emission, alveolar Duoliang the accumulation of gas, alveolar significantly increased pressure and swelling; ③ chronic lung inflammation and the WBC macrophage release of decomposition of the increase in lung tissue damage and the alveolar walls of a number of lung alveolar integration into the foam or Emphysema; Zhiyan ingredients can still through cell toxicity and stimulate the activity of a cell而使neutrophil elastase release, macrophages in vitro and in vivo tests have confirmed that contacts Zhiyan smoke after the release of a similar elastase An enzyme; ④ alveolar walls of the capillary pressure, reduced blood supply, nutrition obstacles to lung tissue, also caused alveolar wall flexibility may be easier to promote emphysema occurred.

About elastase inhibitor imbalance and its doctrine that the human memory in the elastase and elastase inhibitor (mainly a1-anti-trypsin). Elastase to decomposition of elastic fibers, causing emphysema lesions. But in normal circumstances, elastase inhibitors can inhibit the activity of this enzyme, elastase and its inhibitory factor in the balance, avoid the occurrence of emphysema. If the flexibility of its protease inhibitor increased or reduced, a state of imbalance, can cause emphysema. Protease - the imbalance between the anti-theory can not explain all the experimental and human emphysema observed in the phenomenon. Such as experimental enzyme-induced pulmonary emphysema is the lobular type rather than lobular central, and the latter in chronic airway obstruction in the patients is the more common type. a1-AT emphysema due to the lack of congenital genetic caused by the lack of a1-AT. Age of onset lighter, faster progress. More foreign reports, and the domestic uncommon, and more from chronic inflammation caused by the release of neutrophil-relative increase, and formation of emphysema.

[Pathology]

Peng Lung excessive expansion, loss of flexibility, some of thoracotomy, emphysema can not be retracted, a gray or pale appearance, the surface can have multiple sizes of the large bubble. Examination see alveolar walls thin, swell, rupture or a big bubble, reduce the blood supply, elastic fiber network damage. There are many small bronchial wall infiltration of inflammatory cells, mucus gland wall and goblet cell proliferation, mast, ciliated epithelial damage, reduce the cilia. Some were slim lumen narrow or distorted expansion, the lumen with sputum retention. In the small blood vessels around the bronchial endometrial thickening or lumen can be occluded. Lobular lung involvement by the site, can be divided into obstructive pulmonary emphysema lobular central, and between all lobular type of hybrid between the three categories. Which is central to lobular多见. Lobular central terminal is due to bronchial or a small fine respiratory inflammation caused by bronchial lumen stenosis, a remote two respiratory bronchiole with cystic expansion, characterized by cystic expansion of the respiratory bronchiole 2 lobules of the Central District. All lobular type of respiratory bronchiole narrow lung tissue from their terminals, that is the alveolar - alveolar capsule and alveolar expansion, characterized by emphysema Nangqiang smaller, are found in the lung lobular. Sometimes two types of lung said at the same time there is a mixed emphysema. In many lobular central basis, with lobular area surrounding lung tissue expansion.

[Pathophysiology]

With emphysema, chronic bronchitis, depending on the severity of pathology can cause a series of physiological changes. Early lesions confined to a small airway, the only closed volume increase, dynamic lung compliance decreased, increased static lung compliance. Invasive airway disease, pulmonary function obvious obstacles, the biggest decrease in both ventilation. With the development of disease, lung tissues diminish the growing flexibility, alveolar continue to expand, the retraction obstacles, the residual gas volume and the residual gas volume of the lung to increase the percentage of the total. Emphysema have increased, a large number of pulmonary capillaries around the alveolar expansion of the extrusion and degradation, resulting in a significant reduction pulmonary capillaries, the pulmonary blood flow reduction, although at this time lung ventilation area, but no blood perfusion lung wall, Lead to physical void cavity volume increases also have some areas despite the lung blood perfusion, but the alveolar ventilation bad, can not participate in gas exchange. So, and pulmonary capillary substantial loss, reduce the dispersion area, a ratio of ventilation and blood disorders, the ventilation function of obstacles. Ventilation and ventilation dysfunction can cause hypoxia and carbon dioxide retention, in varying degrees of hypoxemia and hypercapnia, and eventually respiratory failure.