Introduction:
Chronic obstructive pulmonary diseaseReferred to as chronic obstructive pulmonary disease (COPD), it is a destructive lung disease characterized by incomplete reversible airflow limitation. Airflow limitation usually develops progressively and is abnormal with harmful particles or gases in the lungs. Inflammatory response. 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 are mainly characterized by 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. Interventional 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. On the basis of the central type of the lobule, the lung tissue in the peripheral area of the lobular swell is inflated.
[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, and the maximum expiratory 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 expansion 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.
symptom:
The main symptoms:
1. Chronic cough can develop unhealed with the course of the disease. 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 examination and palpation of the anteroposterior diameter of the thoracic cavity, the lower sternal angle of the xiphoid is widened (barrel-shaped 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 inspection] Refer to the inspection contents
[Diagnosis and severity grading] Mainly based on a 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. A small number of patients have no symptoms of cough and cough. FEV1/FVC <70% and PEV1 ≥ 80% predicted only in pulmonary function tests. After excluding other diseases, COPD can also be diagnosed.
The severity of COPD can be graded according to FEV1/FVC, FEV1% predicted values and symptoms (Table 2-6-1). Table 2-6-1 Severity of Chronic Obstructive Pulmonary Disease Grading and Grading Criteria Level 0: Risk factors for COPD in high-risk patients. Pulmonary function has chronic cough and cough in the normal range. Grade I: Mild FEV1/FVC<70 % FEV1 ≥ 80% predicted with or without chronic cough, cough symptoms II: moderate FEV1/FVC <70% 50%
How do patients judge that they may have COPD?
In the early stage of COPD, patients often have no obvious discomfort. Many patients often wait until the breathing difficulties are serious, and then the condition has progressed to moderate or above. The following patient self-test questions help early detection:
1. How many times do you cough every day?
2. How often do you have?
3. Are you more likely to feel short of breath than your peers?
4. Is your age more than 40 years old?
5. Do you smoke now, or have you ever smoked?
If there are more than three questions to answer "yes", you should consult a doctor and perform a pulmonary function test. Pulmonary function tests are an important means of diagnosis of chronic obstructive pulmonary disease, which helps early diagnosis of COPD and early treatment.
COPD is closely related to chronic bronchitis and emphysema. Chronic bronchitis refers to chronic, non-specific inflammation of the bronchial wall. Chronic bronchitis can be diagnosed if the patient has cough and cough for more than 3 months, for 2 consecutive years or longer, and can exclude other known chronic coughs. Emphysema refers to the abnormal long-term expansion of the distal air chamber of the terminal bronchioles, accompanied by destruction of the alveolar wall and bronchioles without significant pulmonary fibrosis. "Destruction" means that the respiratory air cavity is enlarged and the morphology is uneven, and the normal morphology of the alveoli and its components is destroyed and lost. COPD is diagnosed when pulmonary function tests in patients with chronic bronchitis or (and) emphysema are limited by airflow and are not fully reversible. If the patient has only chronic bronchitis or (and) emphysema, and no airflow is limited, it can not be diagnosed as COPD, and is considered a high-risk period of COPD. bronchusasthmaIt also has airflow limitation. However, bronchial asthma is a special airway inflammatory disease, and its airflow limitation is reversible. It is not a COPD.
diagnosis:
First, bronchial asthma is more common in children or adolescents, characterized by episodic wheezing. When the attack occurs, the two lungs are full of wheezing sounds, and the symptoms disappear after remission. There is often a history of family or personal allergy. The airflow limitation of asthma is mostly reversible, and its bronchodilation test is positive.
Second, bronchiectasis has repeated episodes of cough and cough, often repeated hemoptysis. There is a lot of purulent sputum in the combined infection. Physical examination often has a fixed wet voice in the lungs. Part of the chest X-ray showed a rough or curled lung texture, and high-resolution CT showed a change in bronchiectasis.
three,tuberculosis There may be symptoms of tuberculosis poisoning such as low fever, fatigue, and night sweats in the afternoon. The sputum examination can detect the presence of M. tuberculosis and chest X-ray examination.
Fourth, lung cancer has chronic cough, cough, blood can be taken in the recent sputum, and repeated, chest X-ray film and CT can be found in the lesion or obstructive atelectasis or pneumonia. Sputum cytology, fiberoptic bronchoscopy and even lung biopsy can help to confirm the diagnosis.
V. Other causes of respiratory air cavity enlargement emphysema is a pathological diagnosis. Although the respiratory air cavity is uniformly enlarged without accompanying the destruction of the alveolar wall, although it does not meet the strict definition of emphysema, it is often used in the clinic as emphysema, such as compensatory emphysema and senile lung gas. Swollen, congenital emphysema in Down syndrome. Clinical manifestations may show signs of exertional dyspnea and emphysema, but there is no airflow limitation in the lung function test, ie FEV1/FVC ≥ 70%, which is different from COPD.
complication:
First, chronic respiratory failure often occurs in the acute exacerbation of COPD, its symptoms are significantly aggravated, hypoxemia and (or) hypercapnia, may have clinical manifestations of hypoxia and carbon dioxide retention.
Second, spontaneous pneumothorax if sudden aggravation of breathing difficulties, accompanied by obvious cyanosis, the affected side of the lungs percussion for drum sound, auscultation of breath sounds weakened or disappeared, should consider spontaneous pneumothorax, X-ray examination can be diagnosed.
Third, chronic pulmonary heart disease due to COPD lung lesions caused by pulmonary vascular bed reduction and hypoxia-induced pulmonary artery spasm, vascular remodeling, leading to pulmonary hypertension, right ventricular hypertrophy, and eventually right heart dysfunction.
Fourth, gastric ulcer
Five, sleep disordered breathing
treatment:
Including early intervention, stable treatment, acute exacerbation treatment.
The most important measure in early intervention is to quit smoking. Studies have shown that patients of any age or age can effectively slow the decline in FEV1 and the progression of the disease after quitting smoking. All smokers need to get quit smoking education and treatment. Smoking-dependent treatment for smokers includes support from the family society and nicotine replacement therapy. Treatment requires a long-term process, and any failure to quit smoking requires re-education and re-treatment. Even if the drug quits, the cost is much less than the cost of treating health damage caused by smoking.
Stable treatment includes medication, oxygen therapy, respiratory rehabilitation, and lung surgery. The drug has bronchodilators, such as oral or inhaled beta agonists and M receptor blockers, theophylline oral drugs and a combination of beta agonists and glucocorticoids. The study found that hormones can act on multiple segments of COPD inflammation. In stable patients, FEV1 can be increased to a small extent, and bronchial reactivity can be improved. In patients with severe COPD, the number of acute exacerbations can be reduced, but not changed. FEV1. The combination of two or more drugs is superior to monotherapy. Arterial oxygen partial pressure <55 mmHg should be given long-term oxygen therapy, so that the patient's arterial oxygen saturation in any state (including exercise, activity and sleep) is >90%.
Rehabilitation is required for patients with dyspnea or restricted exercise, including a healthy lifestyle, respiratory muscle exercise and physical exercise. Surgical treatment is a major advance in the treatment of COPD, including alveolar resection, lung volume reduction and lung transplantation. Aggravation of cough, cough, and difficulty breathing in patients on weekdays is defined as acute exacerbation of COPD. Acute exacerbations of COPD are further classified into grades I, II, and III. Class I patients were treated with outpatient treatment, while patients with grade II were hospitalized, and patients with grade III were severely aggravated and required ICU rescue. Treatments vary according to grade 3, including oxygen therapy, antibacterial therapy, bronchodilators, hormones, noninvasive or invasive mechanical ventilation.
First, stable treatment
1. Educate and persuade patients to quit; due to occupational or environmental dust or irritating gases, they should be free from pollution.
2. Bronchodilators include short-term on-demand applications to temporarily relieve symptoms, and long-term rule applications to prevent and alleviate symptoms.
(l) β2 adrenergic receptor agonist: mainly salbutamol (salbutamol) aerosol, each time l00-2OOug (1-2 spray), aerosol inhalation, the effect lasts 4-5 hours, no more than 8 per 24 hours -12 spray. Terbutaline aerosols have the same effect.
(2) Anticholinergic drugs: It is a commonly used preparation for COPD. The main product is ipratropium (ipratropium) aerosol. It is sprayed slowly and has a slower effect than salbutamol. It lasts for 6-8 hours, 40-80ug each time. 20ug), 3-4 times a day.
(3) Theophylline: slow-release or controlled-release tablets of theophylline, 0.2 g, once in the morning and evening; aminophylline, 0.1 g, 3 times a day. In addition to the above bronchodilators, there are still salmeterols (salmeterol),Formotero(formoterol) and other long-acting β2 adrenergic receptor agonists, if necessary.
3. Peony can be applied to people who are not easy to cough. Commonly used drugs are ambroxol hydrochloride, 30mg, 3 times a day, or carbosteineine 0.5g, 3 times a day.
4, long-term family oxygen therapy (LTOT) for COPD chronic respiratory failure can improve the quality of life and survival rate. It has a beneficial effect on hemodynamics, exercise capacity, lung physiology and mental state. LTOT indication: 1 PaO2 ≤ 55 mmHg or Sa02 ≤ 88%, with or without hypercapnia. 2PaO2 55-6OmmHg, or Sa02<89%, andpulmonary hypertensionHeart failure or edemaPolycythemia(hematocrit > 0.55). Generally, the nasal cannula is used for oxygen absorption, the oxygen flow rate is l.0-2.0 L/min, and the oxygen inhalation time is >15 h/d. The goal is to achieve a PaO2 ≥ 60 mmHg and/or a Sa02 increase to 90% at sea level and at rest.
Second, acute exacerbation treatment
1. Determine the cause of the acute exacerbation period and the severity of the condition. The most common cause of acute exacerbation is bacterial or viral infection.
2. Determine outpatient or hospitalization depending on the severity of the condition.
3. Bronchodilator drugs are in stable phase. Patients with severe wheezing may be given a larger dose of aerosol inhalation therapy, such as applicationSalbutamol2500ug or ipratropium bromide 500ug, or salbutamol 1000ug plus ipratropium bromide 250-500ug inhaled by a small inhaler to relieve symptoms.
4. Controlled oxygen inhalation Oxygenemia can be performed by nasal cannula or by oxygen in a Venturi mask. When the nasal cannula is given oxygen, the concentration of oxygen inhaled is related to the flow rate of oxygen. The estimated formula is the concentration of inhaled oxygen (%) = 21 1/4 * oxygen flow (L / min). Generally, the concentration of inhaled oxygen is 28%-30%, and the excessive concentration of inhaled oxygen should be avoided to cause carbon dioxide retention.
5. Antibiotics When patients have increased difficulty in breathing, cough with increased sputum volume, and purulent sputum, antibiotics should be actively selected according to the type of common pathogens and drug sensitivity in the patient's location. Such as the administration of β-lactam/β-lactamase inhibitors; second-generation cephalosporins, macrolides or quinophthalones. For example, amoxicillin/clavulanic acid, ceftizoxime 0.25g 3 times daily, cefuroxime 0.5g twice daily, levofloxacin 0.2g twice daily, moxifloxacin or gatifloxacin 0.4g per clinic Once a day; heavier patients can apply ceftriaxone sodium 2.0g intravenously in saline, once a day. Inpatients are given more active antibiotics based on the severity of the disease and the expected pathogens, usually in multiple intravenous infusions.
6. Glucocorticoids may be considered for oral administration of prednisolone 30-40 mg/d in patients with acute exacerbation requiring hospitalization.Methylprednisolone. 5-7 days in a row. If the patient has respiratory failure, pulmonary heart disease, heart failure, the specific treatment methods can refer to the relevant section of treatment.
prevention:
The prevention of COPD is mainly to avoid the risk factors of the disease, the predisposing factors of acute exacerbation and the enhancement of immunity. Quitting smoking is an important measure to prevent COPD, and it is also the easiest measure. It is beneficial to stop smoking at any stage of the disease to prevent the occurrence and development of COPD. Control occupational and environmental pollution, reduce the inhalation of harmful gases or harmful Kerry, and reduce the abnormal inflammatory response of the airways and lungs. Active prevention of respiratory infections in infants and children may help reduce future COPD. Influenza vaccines, pneumococcal vaccines, etc. may be beneficial in preventing repeated infections in patients with COPD. Strengthening physical exercise, enhancing physical fitness, and improving the body's immunity can help improve the general condition of the body. In addition, for people with high risk factors for COPD, pulmonary function monitoring should be performed regularly to detect COPD as early as possible and to intervene in time.
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