Chronic obstructive pulmonary disease

Introduction to chronic obstructive pulmonary disease Chronic obstructive pulmonary disease (COPD) is a destructive lung disease characterized by incomplete reversible airflow limitation. Airflow limitation is usually progressive and harmful to the lungs. An abnormal inflammatory response to particles or gases. COPD is a chronic airway inflammatory disease that can be prevented and treated. Although COPD is an airway disease, the systemic effects on the whole body cannot be ignored. Infection is one of the important factors in the development of COPD. Virus, bacteria and mycoplasma are important factors for the acute exacerbation of this disease. The viruses are mainly influenza virus, rhinovirus, adenovirus and respiratory syncytial virus; bacterial infection is caused by Streptococcus pneumoniae. Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus are common. Occupational dust and chemicals, such as smoke, allergens, industrial waste gas and indoor air pollution, excessive concentration or prolonged exposure may result in COPD unrelated to smoking. Harmful gases in the atmosphere, such as sulfur dioxide, nitrogen dioxide, chlorine, etc., damage the airway mucosa and its cytotoxic effects, causing a decrease in cilia clearance and an increase in mucus secretion, which increases conditions for bacterial infection. basic knowledge The proportion of illness: 0.21% Susceptible people: no special people Mode of infection: non-infectious Complications: Chronic respiratory failure Spontaneous pneumothorax Chronic pulmonary heart disease Pulmonary hypertension Secondary erythrocytosis Emphysema

Causes of chronic obstructive pulmonary disease

Smoking (25%)

As 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 mucosa hypertrophy, goblet cell hyperplasia, mucus Increased secretion, decreased airway purification ability; bronchial mucosa congestion and edema, accumulation of mucus, easy secondary infection, chronic inflammation and smoking stimulate submucosal receptors, hyperparathyroidism, bronchial smooth muscle contraction, airflow limitation, tobacco, smoke It can also increase the production of oxygen free radicals, induce neutrophils to release proteases, inhibit the anti-protease system, destroy the lung elastic fibers, and induce the formation of emphysema. The prevalence of chronic bronchitis in smokers is 2-8 higher than that of non-smokers. Times, the longer the age of smoking, the greater the amount of smoking, the higher the prevalence of COPD.

Infection (35%)

Infection is one of the important factors in the development of COPD. Virus, bacteria and mycoplasma are important factors for the acute exacerbation of this disease. The viruses are mainly influenza virus, rhinovirus, adenovirus and respiratory syncytial virus; bacterial infection is caused by Streptococcus pneumoniae. Haemophilus influenzae, Moraxella catarrhalis and Staphylococcus are common.

Environmental factors (15%)

Occupational dust and chemicals, such as smoke, allergens, industrial waste gas and indoor air pollution, excessive concentration or prolonged exposure may result in COPD unrelated to smoking. Harmful gases in the atmosphere, such as sulfur dioxide, nitrogen dioxide, chlorine, etc., damage the airway mucosa and its cytotoxic effects, causing a decrease in cilia clearance and an increase in mucus secretion, which increases conditions for bacterial infection.

Protease-antiprotease imbalance (15%)

Proteolytic enzymes have damage and destruction to tissues; anti-protease has inhibitory functions on various proteases such as elastase, among which 1-antitrypsin (1-AT) is the most active one, and protease and anti-protease maintain balance. The main factors that ensure the normal structure of lung tissue from damage and destruction, increased protease or insufficient protease can lead to the destruction of tissue structure and emphysema.

Other factors (5%)

Such as the internal factors of the body, autonomic dysfunction, nutrition, sudden changes in temperature, 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 of bronchial epithelial cells, necrosis, ulcer formation, cilia lodging, shortening, irregularity, adhesion, partial shedding, mucosal epithelial repair, hyperplasia, squamous metaplasia and granuloma formation, increased number of goblet cells, Hypersecretion, retention of endocrine secretions, thickening and necrosis of basement membrane, hypertrophy of bronchial glands, ratio of glandular hypertrophy to bronchial wall thickness is often greater than 0.55-0.79 (normally less than 0.4), and inflammatory cells infiltrate in various bronchial walls. Plasma cells, lymphocytes, mainly in the acute attack period can be seen a large number of neutrophils, severe cases of suppurative inflammation, mucosal congestion, edema, degeneration and necrosis and ulcer formation, basal granulation tissue and mechanical fiber tissue proliferation leading to the tube The stenosis of the cavity leads to repeated damage to the airway wall and the repair process. 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 of emphysema can show excessive lung expansion, decreased elasticity, gray or pale appearance, visible surface Large bubbles of different sizes, microscopic examination showed alveolar wall thinning, alveolar cavity enlargement, rupture or formation of large bubbles, reduced blood supply, destruction of elastic fiber web, inflammatory cell infiltration in the bronchiole wall, mucous gland and cup-shaped wall Cell hyperplasia, hypertrophy, cilia epithelial damage, cilia reduction, some tubules are slender or stenotic, and there is sputum retention in the lumen. The endobronchial membrane of the bronchiole can be thickened or occluded, depending on the location of the pulmonary lobules Obstructive emphysema can be divided into small leaf central type, full small leaf type and mixed type between the two, among which the central type of small leaf is more common, the central type of small leaf is due to terminal bronchiole or one Grade respiratory bronchiolitis leads to luminal stenosis, and the distal secondary respiratory bronchioles are cystic dilatation, characterized by a cystic dilated respiratory bronchiole located in the central region of the secondary lobule, and the whole lobular type is breathing Sexual bronchiole stenosis causes end-stage lung tissue, ie alveolar duct-alveolar sac and alveolar dilatation, characterized by small emphysema cysts, distributed throughout the lobules of the lungs, and sometimes a type of lung Said hybrid emphysema, mostly in the centrilobular based on concurrent lobular area surrounding lung tissue expansion.

[pathophysiology]

In the early stage, the examination of atmospheric function is generally reflected, such as the first second forced expiratory volume (FEV1), the maximum ventilation, and the maximum mid-expiratory flow rate are normal, but some patients have small airway function (airway less than 2 mm in diameter). Abnormalities occur, as the condition worsens, the airway narrows, the resistance increases, the conventional ventilation function test may have different degrees of abnormality, most of the remission period returns to normal, with the development of the disease, the airway resistance increases, the airflow limitation becomes irreversible, and the chronic bronchitis is concurrent When emphysema, depending on its severity, it can cause a series of pathophysiological changes. Early lesions are limited to small airways, and only the closed volume increases, which reflects the dynamic resistance of lung tissue and the dynamic lung compliance of small airway resistance. The lesions invade the atmosphere. At the time of the road, the pulmonary ventilation function is obviously disordered, and the maximum ventilation is reduced. With the development of the disease, the elasticity of the lung tissue is decreasing, the alveoli continues to expand, and the retraction disorder, the residual air volume and the residual gas volume account for the percentage of the total lung volume, lung The emphysema is getting worse, and a large number of capillaries around the alveoli are degenerated by the swelling of the expanding alveoli, resulting in large pulmonary capillaries. Decreased, the blood flow between the alveoli decreased, although the alveoli were ventilated, but there was no blood perfusion in the alveolar wall, resulting in an increase in physiological ineffective cavity volume; although some lung areas had blood perfusion, alveolar ventilation was poor and could not participate in gas exchange. In this way, the alveolar and capillaries are largely lost, the area of diffusion is reduced, the ratio of ventilation and blood flow is imbalanced, and the ventilation function is impaired. Ventilation and ventilation dysfunction can cause hypoxia and carbon dioxide retention, and different degrees of hypoxemia occur. And hypercapnia, eventually respiratory failure.

Chronic obstructive pulmonary disease 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. Smoking cessation is an important measure to prevent COPD, and it is also the easiest and most easy measure. Quitting smoking at any stage of the disease is beneficial to prevent COPD. Occurrence and development, control of occupational and environmental pollution, reduction of harmful gases or harmful Kerry inhalation, can reduce abnormal inflammation of the airway and lungs, and actively prevent respiratory infections in infants and children, may help reduce COPD in the future The occurrence of influenza vaccine, pneumococcal vaccine, etc. may be beneficial to prevent repeated infections in patients with COPD. Strengthening physical exercise, enhancing physical fitness, and improving immunity may help improve the general condition of the body. In addition, for people with high risk factors for COPD, Pulmonary function monitoring is performed regularly to detect COPD as early as possible and to intervene in a timely manner.

Chronic obstructive pulmonary disease complications Complications chronic respiratory failure spontaneous pneumothorax chronic pulmonary heart disease pulmonary hypertension secondary polycythemia emphysema emphysema

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, stomach ulcers.

Fifth, sleep and breathing disorders.

Sixth, secondary polycythemia.

Chronic obstructive pulmonary disease symptoms Common symptoms Breathing difficulty, wheezing, chest tightness, breath sounds, loss of appetite, shortness of breath, chronic sputum, chronic cough, barrel chest, pulmonary fibrosis

The main symptoms

l. Chronic cough can develop unhealed with the course of the disease, often coughing in the morning, coughing or sputuming at night.

2. Cough is generally white mucus or serous foamy sputum, even with bloodshot, more convulsions in the morning, increased sputum during acute attack, may have purulent sputum.

3. Shortness of breath or difficulty in breathing Early in labor, and gradually worsened, so that shortness of breath during daily activities and even rest is a 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.

Sign

Early signs can be abnormal, and the following signs appear as the disease progresses:

l. Visual examination and palpation of the anterior and posterior diameter of the thoracic cage, the lower sternal angle of the xiphoid is widened (barrel-shaped chest), some patients have shallower breathing, the frequency increases, and severe cases 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.

Examination of chronic obstructive pulmonary disease

First, lung function test

It is the main objective indicator for determining airflow limitation, and is of great significance for the diagnosis of COPD, severity assessment, disease progression, prognosis and treatment response.

1. The first second forced expiratory volume occupancy Percentage of vital capacity (FEV1/FVC) is a sensitive indicator for assessing airflow limitation. The first second forced expiratory volume accounts for the predicted percentage (FEV1% predicted value), which is the assessment of COPD. A good indicator of severity, its variability is small, easy to operate, FEV1/FVC <70% and FEV1 <80% predicted after inhalation of bronchodilator, can be determined to be completely irreversible airflow limitation.

2. Total lung volume (TLC), functional residual capacity (FRC) and residual gas volume (RV) increased, lung capacity (VC) decreased, indicating lung hyperinflation, with reference value, because the increase in TLC is less than the increase in RV, so RV / Increased TLC, from carbon monoxide diffusion (DLCO) and DLCO to alveolar ventilation (VA) ratio (DLCO / VA), this indicator for diagnostic reference.

Second, chest X-ray examination

There is no change in the early chest X-ray of COPD. Later, there may be non-specific changes such as thickening of the lung texture, disorder, and emphysema. X-ray chest radiograph changes are not specific for the diagnosis of COPD, mainly for determining pulmonary complications. And for identification of other lung diseases.

Third, chest CT examination

CT examination should not be used as a routine examination of COPD, high-resolution CT, and it has certain significance for the differential diagnosis of suspected cases.

Fourth, blood gas examination is of great value in determining the occurrence of hypoxemia, hypercapnia, acid-base balance disorders and the type of respiratory failure.

5. When other COPD combined with bacterial infection, the white blood cells are increased, the nucleus is shifted to the left, and the pathogenic bacteria may be detected in the sputum culture; the common pathogens are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Klebsiella pneumoniae and the like.

Significance of COPD pulmonary function tests:

Spirometry is necessary to determine the diagnosis. Anyone who is considered to have COPD should perform this test. After applying inhaled bronchodilator, the ratio of forced expiratory volume to forced expiratory volume in one second. (FEV1/FVC) < 0.7 can establish the diagnosis of COPD, and this test can also evaluate the severity of COPD: FEV1/FVC > 0.7, FEV1 80% have a risk of developing COPD; FEV1/FVC 0.7, FEV180% are mild COPD; FEV1/FVC0.7, FEV1 is moderate COPD in 50%~80%; FEV1/FVC0.7, FEV1 is severe COPD in 30%~50%; FEV1/FVC 0.7, FEV1 <30% for severe COPD, chronic obstructive pulmonary disease is a progressive exacerbation of the disease, patients should regularly monitor lung function, monitor the progress of the disease, timely adjustment of medication and other treatment options to maintain optimal lungs for a long time Function and improve quality of life.

Diagnosis and diagnosis of chronic obstructive pulmonary disease

diagnosis

Mainly based on the history of high-risk factors such as smoking, clinical symptoms, signs and lung function tests and other comprehensive analysis.

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, and a few patients do not have cough , cough symptoms, FEV1/FVC <70% only in the pulmonary function test, and FEV1 80% predicted value, after the exclusion of other diseases, can also be diagnosed as COPD.

According to FEV1/FVC, FEV1% predicted values and symptoms can be used to grade the severity of COPD. The severity of chronic obstructive pulmonary disease is graded and graded. Grade 0: High risk of risk factors for COPD. Pulmonary function is chronic in the normal range. Cough, cough symptoms Grade I: mild FEV1/FVC <70% FEV1 80% predicted with or without chronic cough, cough symptoms II: moderate FEV1/FVC <70% 50%.

Differential diagnosis

First, bronchial asthma

Most of the onset in children or adolescents, characterized by episodic wheezing, the two lungs are full of wheezing during the attack, the symptoms disappear after remission, often have family or personal allergies, and the airflow limitation of asthma is mostly reversible. The bronchodilation test was positive.

Second, bronchiectasis

There are repeated episodes of cough, cough, often repeated hemoptysis, there are a lot of purulent sputum in the infection, the body often has a fixed wet voice of the lungs, some chest X-ray shows rough texture or curly hair, high resolution CT shows a change in bronchiectasis.

Third, tuberculosis

There may be symptoms of tuberculosis poisoning such as low fever, fatigue, night sweats, etc., and M. tuberculosis can be found in the sputum examination. The chest X-ray film can detect the lesion.

Fourth, lung cancer

Chronic cough, cough, blood in the recent sputum, and repeated, chest X-ray and CT can find space-occupying lesions or obstructive atelectasis or pneumonia, sputum cytology, fiberoptic bronchoscopy and even lung biopsy Can help to confirm the diagnosis.

5. Other causes of respiratory air cavity enlargement

Emphysema is a pathological diagnosis term. When the respiratory 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 compensation. Pulmonary emphysema, senile emphysema, congenital emphysema in Down syndrome, clinical manifestations of labor dyspnea and emphysema signs, but lung function determination without airflow limitation, ie FEV1 /FVC 70%, which is different from COPD.

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