Chronic obstructive pulmonary disease (COPD)

Introduction: Chronic obstructive pulmonary disease (COPD) is a destructive lung disease characterized by incomplete reversible airflow limitation. Airflow limitation usually develops progressively with the lungs. It is related to abnormal inflammatory reactions of harmful particles or gases. COPD is a chronic airway inflammatory disease that can be prevented and treated. Although COPD is a disease of the airway, the systemic impact on the whole body cannot be ignored. Cause: [Etiology and pathogenesis] The exact cause is unclear. It is related to the following factors that cause chronic bronchitis. 1. Smoking is an important disease factor. Tobacco contains tar, nicotine and hydrocyanic acid, which can damage airway epithelial cells, reduce ciliary movement and reduce macrophage phagocytosis; bronchial mucin gland hypertrophy, goblet cells Hyperplasia, increased mucus secretion, decreased airway purification ability; bronchial mucosa congestion and edema, mucus accumulation, easy secondary infection, chronic inflammation and smoking stimulate submucosal receptors, causing parasympathetic hyperfunction, causing bronchial smooth muscle contraction, airflow limitation. Tobacco and smoke can also increase the production of oxygen free radicals, induce neutrophils to release proteases, inhibit the anti-protease system, destroy lung elastic fibers, and induce emphysema formation. The prevalence of chronic bronchitis in smokers is 2-8 times higher than that of non-smokers. The longer the age of smoking, the greater the smoking, the higher the prevalence of COPD. Second, occupational dust and chemical substances Occupational dust and chemical substances, such as smoke, allergens, industrial waste gas and indoor air pollution, excessive concentration or contact time is too long, may produce COPD unrelated to smoking. Third, air pollution The harmful gases in the atmosphere such as sulfur dioxide, nitrogen dioxide, chlorine and other damage to the airway mucosa and its cytotoxic effects, so that the cilia clearance function decreased, mucus secretion increased, increasing conditions for bacterial infection. Fourth, infection is one of the important factors in the development of COPD. Viruses, bacteria and mycoplasma are important factors in the acute exacerbation of this disease. The viruses are mainly influenza virus, rhinovirus, adenovirus and respiratory syncytial virus; bacterial infections are more common with Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus. 5. Protease-antiprotease imbalance Proteolytic enzyme has damage and destruction to tissues; anti-protease has inhibitory function on various proteases such as elastase. Among them, α1-antitrypsin (α1-AT) is the most active one. Maintaining a balance between protease and anti-protease is a major factor in ensuring normal structure of lung tissue from damage and destruction. Increased proteases or insufficient protease resistance can lead to the destruction of tissue structure to produce emphysema. Sixth, other factors such as the internal factors of the body, autonomic dysfunction, nutrition, temperature changes, etc. may participate in the occurrence and development of CDPD. [Pathological changes] The pathological changes of CDPD mainly manifested as pathological changes of chronic bronchitis and emphysema. Degeneration, necrosis and ulceration of bronchial epithelial cells. The cilia are lodging, shortening, ignoring, sticking, and partially falling off. Mucosal epithelial repair, hyperplasia, squamous metaplasia and granuloma formation during remission. The number of goblet cells is increased, hypersecretion, and secretions in the lumen. The basement membrane thickens and necrosis. The bronchial gland hyperplasia hypertrophy, the ratio of glandular hypertrophy to bronchial wall thickness is often greater than 0.55-0.79 (normally less than 0.4). There are various types of inflammatory cell infiltration in the bronchial wall at all levels, mainly plasma cells and lymphocytes. A large number of neutrophils can be seen in the acute attack period. Severe cases are suppurative inflammation, mucosal congestion, edema, degeneration and necrosis and ulcer formation. Basal granulation tissue and mechanized fibrous tissue hyperplasia lead to stenosis. Inflammation leads to repeated cycles of damage and repair of the airway wall. The repair process leads to structural remodeling of the airway wall, increased collagen content and scar formation. These pathological changes are one of the main pathological basis of COPD airflow limitation. Pathological changes in emphysema showed excessive lung expansion and decreased elasticity. The appearance is gray or pale, and many large bubbles of different sizes can be seen on the surface. Microscopic examination showed that the alveolar wall became thinner, the alveolar cavity expanded, ruptured or formed a large bubble, the blood supply was reduced, and the elastic fiber web was destroyed. There are inflammatory cell infiltration in the bronchiole wall, mucosal gland and goblet cell hyperplasia, hypertrophy, ciliated epithelial damage, and cilia reduction. Some lumens are slender or distorted, and sputum remains in the lumen. The endothelium of the bronchioles may be thickened or occluded. Obstructive emphysema can be divided into small leaflet type (Fig. 2-6-1), full small leaf type (Fig. 2-6-2) and mixed type between the two. class. Among them, the central type of leaflet is more common. The central lobules are caused by end-stage bronchioles or first-grade respiratory bronchiol inflammation leading to stenosis, and the distal secondary respiratory bronchioles are cystic dilatation, which is characterized by cystic dilated respiratory bronchioles. The central area of the leaflet. The whole lobular type is the end-stage lung tissue caused by respiratory bronchiole stenosis, that is, the expansion of the alveolar duct-alveolar sac and alveoli, which is characterized by a small cystic cavity and spread throughout the lobules of the lung. Sometimes there is a type of mixed emphysema in the lungs. Mostly on the base of the small leaflet, the lung tissue in the peripheral area of the small leaflet expands. [Pathophysiology] In the early stage, it is generally normal to check the function of the airway such as the first-second forced expiratory volume (FEV1), the maximum ventilation volume, and the maximum expiratory mid-flow rate. However, some patients have abnormalities in small airway function (airway less than 2 mm in diameter). As the condition worsens, the airway narrows, the resistance increases, and the conventional ventilation function test may have different degrees of abnormality. Most of the remission period returned to normal. As the disease progresses, airway resistance increases and airflow limitation becomes irreversible. Chronic bronchitis complicated with emphysema, depending on its severity can cause a series of pathophysiological changes. Early lesions were confined to the small airways, and only the closed volume increased, reflecting the dynamic resistance of the lung tissue and the dynamic lung compliance of the small airway resistance decreased. When the lesion invades the airway, the pulmonary ventilation function is significantly impaired, and the maximum ventilation is reduced. With the development of the disease, the elasticity of the lung tissue is declining, the alveoli continue to expand, and the retraction disorder, the percentage of residual gas and residual gas to the total lung volume increases. Emphysema is increasing, and a large number of capillaries around the alveoli are degraded by the swelling of the alveoli, resulting in a decrease in pulmonary capillaries and a decrease in blood flow between the alveoli. At this time, although the alveoli are ventilated, there is no blood perfusion in the alveolar wall, resulting in The physiological ineffective cavity volume is increased; although some of the lung regions have blood perfusion, the alveolar ventilation is poor and cannot participate in gas exchange. In this way, the alveolar and capillaries are largely lost, the area of diffusion is reduced, and the ratio of ventilation to blood flow is imbalanced, which causes an obstacle to the ventilation function. Ventilation and ventilation dysfunction can cause hypoxia and carbon dioxide retention, varying degrees of hypoxemia and hypercapnia, and eventually respiratory failure. Symptoms: Main symptoms: 1. Chronic cough can be unhealed for life. Coughing is obvious in the morning, and there is a cough or sputum at night. 2. Cough is generally white mucus or serous foamy sputum, even with bloodshot, more sputum in the morning. Increased sputum during acute attacks may have purulent sputum. 3. Shortness of breath or difficulty in breathing occurs early in labor, and then gradually increases, so that you feel short of breath during daily activities or even rest. It is a hallmark symptom of COPD. 4. Wheezing and chest tightness Some patients have wheezing especially in severe patients or acute exacerbations. 5. Other advanced patients have weight loss, loss of appetite, etc. Second, the early signs of the signs can be no abnormalities, with the following signs of disease progression: 1. Visual and palpation of the thoracic anteroposterior diameter, sternal lower sternal angle widened (barrel chest). Some patients have shallower breathing and increased frequency. In severe cases, they may have lip-reducing breathing; tactile tremor is weakened. 2. The percussion of the lungs was over-voiced, the heart-cloudy sounds narrowed, and the lower lung and liver dullness decreased. 3. The auscultation of the two lungs is weakened by breath sounds, and the exhalation is prolonged. Some patients may smell dry voices and/or wet voices. [Laboratory and special examinations] The contents of the reference examination [diagnosis and severity classification] are mainly determined based on comprehensive analysis of the history of high-risk factors such as smoking, clinical symptoms, signs and pulmonary function tests. Incomplete reversible airflow limitation is a prerequisite for COPD diagnosis. FEV1/FVC <70% and FEV1 <80% predicted after inhalation of bronchodilator can be determined as incomplete reversible airflow limitation. Read more...