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Etiology and Pathogenesis of Chronic Obstructive Pulmonary Disease (COPD)(1)
by kinglen on Feb 27, 2022
The exact cause is unclear. But it is thought to be related to the abnormal inflammatory response of the lungs to harmful gases or particles such as cigarette smoke. These responses involve the interaction of individual susceptibility factors and environmental factors.
1. Smoking is an important pathogenic factor. The prevalence of chronic bronchitis in smokers is 2-8 times higher than that in non-smokers. The longer the smoking age and the greater the amount of smoking, the higher the prevalence of COPD. Tobacco contains chemicals such as tar, nicotine and hydrocyanic acid. As mentioned in the first section of this chapter, cigarettes can damage the movement of airway epithelial cells and cilia, promote the proliferation and hypertrophy of bronchial mucus glands and goblet cells, increase mucus secretion, and make the airway Purification capacity decreased. It can also increase the production of oxygen free radicals, induce neutrophils to release proteases, damage lung elastic fibers, and induce the formation of emphysema.
2. Occupational dust and chemical substances:
Exposure to occupational dust and chemical substances, such as smoke, allergens, industrial waste gas and indoor air pollution, etc., may produce COPD similar to smoking when the concentration is too high or the time is too long.
3. Air pollution:
Harmful gases in the atmosphere, such as sulfur dioxide, nitrogen dioxide, chlorine, etc., can damage the airway mucosal epithelium, reduce the ciliary clearance function, increase mucus secretion, and increase conditions for bacterial infection.
Infection factors Similar to chronic bronchitis, infection is also one of the important factors in the development of COPD.
4. Protease-antiprotease imbalance:
Proteolytic enzymes can damage and destroy tissues; anti-protease has inhibitory functions on various proteases such as elastase, among which a1-antitrypsin (a1-AT) is the most active one. Increased protease or insufficient anti-protease can lead to the destruction of tissue structure and emphysema. Inhalation of harmful gases and substances can lead to increased production or enhanced activity of protease, while decreased production or accelerated inactivation of anti-protease; at the same time, risk factors such as oxidative stress and smoking can also reduce the activity of anti-protease. Congenital a1-antitrypsin deficiency, more common in individuals of Nordic ancestry, has not been officially reported in China.
1. Smoking is an important pathogenic factor. The prevalence of chronic bronchitis in smokers is 2-8 times higher than that in non-smokers. The longer the smoking age and the greater the amount of smoking, the higher the prevalence of COPD. Tobacco contains chemicals such as tar, nicotine and hydrocyanic acid. As mentioned in the first section of this chapter, cigarettes can damage the movement of airway epithelial cells and cilia, promote the proliferation and hypertrophy of bronchial mucus glands and goblet cells, increase mucus secretion, and make the airway Purification capacity decreased. It can also increase the production of oxygen free radicals, induce neutrophils to release proteases, damage lung elastic fibers, and induce the formation of emphysema.
2. Occupational dust and chemical substances:
Exposure to occupational dust and chemical substances, such as smoke, allergens, industrial waste gas and indoor air pollution, etc., may produce COPD similar to smoking when the concentration is too high or the time is too long.
3. Air pollution:
Harmful gases in the atmosphere, such as sulfur dioxide, nitrogen dioxide, chlorine, etc., can damage the airway mucosal epithelium, reduce the ciliary clearance function, increase mucus secretion, and increase conditions for bacterial infection.
Infection factors Similar to chronic bronchitis, infection is also one of the important factors in the development of COPD.
4. Protease-antiprotease imbalance:
Proteolytic enzymes can damage and destroy tissues; anti-protease has inhibitory functions on various proteases such as elastase, among which a1-antitrypsin (a1-AT) is the most active one. Increased protease or insufficient anti-protease can lead to the destruction of tissue structure and emphysema. Inhalation of harmful gases and substances can lead to increased production or enhanced activity of protease, while decreased production or accelerated inactivation of anti-protease; at the same time, risk factors such as oxidative stress and smoking can also reduce the activity of anti-protease. Congenital a1-antitrypsin deficiency, more common in individuals of Nordic ancestry, has not been officially reported in China.
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