Chronic obstructive pulmonary diseases (COPD) is a preventable and treatable disease characterized by airflow limitation that is not fully reversible, progressive, and associated with an abnormal inflammatory response of the lungs to harmful gases or particles such as cigarette smoke. COPD can also cause systemic (or extrapulmonary) adverse effects. COPD is closely related to chronic bronchitis and emphysema in the Department of Emergency Medicine, Tongji Hospital, Shanghai, China. Usually, chronic bronchitis is defined as a patient who coughs and sputters for more than 3 months per year for 2 years after excluding other known causes of chronic cough. Emphysema, on the other hand, refers to an abnormal and persistent dilatation of the distal air spaces of the terminal fine bronchi in the lungs with destruction of the alveolar walls and fine bronchi without significant pulmonary fibrosis. COPD is diagnosed in patients with chronic bronchitis and emphysema when airflow limitation is present on pulmonary function tests and is not fully reversible. The pathogenesis of COPD is not fully understood. It is generally accepted that COPD is characterized by chronic inflammation of the airways, lung parenchyma and pulmonary vasculature, with an increase in alveolar macrophages, T-lymphocytes (especially CD) and neutrophils in different parts of the lung and, in some patients, eosinophilia. Activated inflammatory cells release a variety of mediators, including leukotriene B4 (LTB4), interleukin 8 (1L-8), tumor necrosis factor alpha (TNF-α), and other mediators. These mediators can disrupt the structure of the lung and/or promote the neutrophil inflammatory response. In addition to inflammation, protease and anti-protease imbalances in the lung, oxidative and antioxidant imbalances, and autonomic nervous system dysfunction (e.g., abnormal distribution of cholinergic neuroreceptors) also play an important role in COPD pathogenesis. Inhalation of harmful particles or gases can lead to lung inflammation; smoking can induce inflammation and directly damage the lungs; and various risk factors for COPD can produce similar inflammatory processes that lead to COPD. Pathology The pathological changes characteristic of COPD are present in the central airways, peripheral airways, lung parenchyma, and the vascular system of the lung. In the central airways (trachea, bronchi, and fine bronchi with internal diameters >2-4 mm), inflammatory cells infiltrate the superficial epithelium, and mucus secretion is increased by enlarged mucus-secreting glands and increased cupped cells. In the peripheral airways (small bronchi and fine bronchi with an inner diameter <2 mm), chronic inflammation leads to a recurrent cycle of airway wall damage and repair processes. The repair process leads to structural remodeling of the airway wall, increased collagen content and scar tissue formation, and these pathological changes result in narrowing of the airspace and cause fixed airway obstruction. The typical destruction of the lung parenchyma in COPD patients manifests as lobar central emphysema, involving dilatation and destruction of the respiratory fine bronchi. In milder cases these disruptions often occur in the upper regions of the lung, but as the disease progresses, they can be diffusely distributed throughout the lung with disruption of the pulmonary capillary bed. An imbalance of endogenous pulmonary proteases and antiproteases, due to genetic factors or inflammatory cells and mediators, is the main mechanism of pulmonary destruction in emphysematous lung, with oxidation and other inflammatory consequences also playing a role. Changes in the pulmonary vasculature in COPD are characterized by thickening of the vessel wall, which begins early in the disease. The thickening of the intima is the earliest structural change, followed by an increase in smooth muscle and infiltration of inflammatory cells in the vessel wall. increased smooth muscle, proteoglycans and collagen in COPD exacerbations further thicken the vessel wall. multiple small pulmonary arteries with in situ thrombosis are seen in some patients in the late stages of COPD secondary to pulmonary heart disease. The pathophysiology of COPD is based on the pulmonary pathology of COPD, including mucus hypersecretion, ciliary dysfunction, airflow limitation, lung hyperinflation, abnormal gas exchange, pulmonary hypertension and pulmonary cardiopathy, and systemic adverse effects. Mucus hypersecretion and ciliary dysfunction lead to chronic cough and sputum, which can precede other symptoms and pathophysiologic abnormalities. Small airway inflammation, fibrosis and exudation of the lumen are associated with decreased FEV1 and FEV1/FVC. Disruption of alveolar attachments, which impairs the ability of small airways to remain open, also plays a role, but this plays a lesser role in airflow limitation. As COPD progresses, peripheral airway obstruction, lung parenchymal destruction and pulmonary vascular abnormalities reduce pulmonary gas exchange capacity, resulting in hypoxemia and later hypercapnia. Long-term chronic hypoxia can lead to extensive pulmonary vasoconstriction and pulmonary hypertension, often accompanied by intimal hyperplasia, fibrosis and occlusion of certain vessels, resulting in structural reorganization of the pulmonary circulation. pulmonary hypertension in the late stages of COPD is an important cardiovascular complication and leads to chronic pulmonary heart disease and right heart failure, suggesting a poor prognosis. COPD can lead to systemic adverse effects, including systemic inflammation and skeletal muscle dysfunction. Systemic inflammation is characterized by an abnormally high systemic oxidative load, abnormally high cytokine concentrations in circulating blood, and abnormal activation of inflammatory cells; skeletal muscle dysfunction is characterized by a gradual loss of skeletal muscle weight, etc. Systemic adverse effects of COPD are clinically important, as they can exacerbate patients' limited mobility, reduce quality of life, and worsen prognosis. Risk factors The risk factors for COPD include both individual susceptibility factors and environmental factors, both of which influence each other. Some genetic factors can increase the risk of COPD. The known genetic factor is α1-antitrypsin deficiency. Severe α1-antitrypsin deficiency is associated with emphysema formation in non-smokers. Emphysema caused by α1-antitrypsin deficiency has not been officially reported so far in China. Bronchial asthma and airway hyperresponsiveness are risk factors for COPD, and airway hyperresponsiveness may be related to certain genetic and environmental factors of the body. Second, environmental factors 1, smoking: smoking is an important factor in the development of COPD. The abnormal rate of lung function is higher in smokers, the annual rate of decline in FEV1 is faster, and more smokers die of COPD than non-smokers. Passive smoking may also contribute to respiratory symptoms and the development of COPD. Smoking in women during pregnancy may affect the growth of fetal lungs and their development in utero, and have an effect on fetal immune system function. 2, occupational dust and chemical substances: When occupational dust and chemical substances (smoke, allergens, industrial exhaust and indoor air pollution, etc.) are too concentrated or exposed for too long, they can lead to COPD that is not related to smoking. Exposure to certain specific substances, irritants, organic dust and allergens can increase airway reactivity. 3, air pollution: chemical gases such as chlorine, nitrogen oxide, sulfur dioxide, etc., have an irritating and cytotoxic effect on the bronchial mucosa. When airborne soot or sulfur dioxide increases significantly, acute COPD attacks increase significantly. Other dusts such as silica, coal dust, cotton dust, and cane dust also stimulate the bronchial mucosa, impairing airway clearance and creating conditions for bacterial invasion. The large amount of cooking fumes and soot from biofuels are associated with the development of COPD, and indoor air pollution from biofuels may have a synergistic effect with smoking. 4, Infection: Respiratory infections are another important factor in the onset and exacerbation of COPD, and Streptococcus pneumoniae and Haemophilus influenzae may be the main pathogens of acute COPD attacks. Viruses also play a role in the onset and progression of COPD. Severe lower respiratory tract infections in childhood are associated with reduced lung function and the onset of respiratory symptoms in adulthood. 5. Socioeconomic status: The onset of COPD is associated with the socioeconomic status of the patient. This may be intrinsically linked to differences in the degree of indoor and outdoor air pollution, nutritional status or other and socioeconomic status.