Bronchial smooth muscle spasm

Introduction Bronchial smooth muscle spasm is a symptom caused by many diseases. It is not an independent disease. Diseases such as bronchial asthma can cause bronchial smooth muscle spasm, etc. It can also be caused by acute bronchitis. Generally, this syndrome will disappear after healing. It won't be repeated. Bronchial asthma is a chronic airway persistent inflammatory disease in which many cells play important roles, such as lymphocytes, eosinophils, mast cells, etc., accompanied by a marked increase in non-specific airway response to the airways. High reactivity (BHR) is a multifactorial disease with major clinical features.

Cause

(1) The cause of the disease is an allergic disease associated with polygenic inheritance, and environmental factors also play an important role in the pathogenesis.

1. Respiratory infections:

(1) Respiratory virus infection: In the early childhood, there are mainly respiratory syncytial virus (RSV), parainfluenza virus, influenza virus and adenovirus. Others such as measles virus, mumps virus, enterovirus and poliovirus are occasionally visible. .

(2) Mycoplasma infection: Because the immune system of infants and young children is immature, mycoplasma can cause chronic infection of infants and young children. If not treated properly, it can lead to repeated cough and wheezing.

(3) focal infection of the respiratory tract: chronic sinusitis, rhinitis, otitis media, chronic tonsillitis, is a common chronic focal lesion of the upper respiratory tract in children, which can cause repeated infection on the one hand and nerve reflex on the other hand. Repeated cough and asthma, these lesions need to be treated in a timely manner.

2. Inhalation of allergic substances: In children over 1 year old, respiratory allergies gradually form, such as indoor dust mites, cockroaches, pet fur and outdoor pollen allergens, long-term continuous low-intensity allergen inhalation, can induce Chronic airway allergic inflammation, causing body sensitization, and chronic airway atopic inflammation, promote the formation of BHR, as the time of exposure to allergen increases, airway inflammation and BHR gradually increase, often develop into childhood asthma. Short-term inhalation of high-concentration allergens can induce acute asthma; such asthma attacks are more abrupt, and most occur in the environment with high concentrations of allergens.

3. Gastroesophageal reflux: Due to anatomical structure, there are also iatrogenic factors (such as the application of aminophylline, -receptor stimulants, etc.) can cause gastroesophageal reflux, especially in infants and young children, it is caused by wheezing One of the important reasons for repeated failures. Clinically, it is characterized by severe coughing and wheezing during sleep, and there is usually milk or vomiting.

4. Genetic factors: Many survey data show that the prevalence of relatives of asthma patients is higher than the prevalence of the population, and the closer the relationship is, the higher the prevalence rate; the more serious the patient's condition, the higher the prevalence of relatives. At present, the genes related to asthma are not completely clear, but studies have shown that multiple sites of genes are associated with allergic diseases. These genes play an important role in the pathogenesis of asthma.

5. Others: Inhalation of irritating gases or strenuous exercise, crying, paint, soot, cold air inhalation can be used as non-specific irritants to induce asthma attacks, in which the gas emitted by the paint can trigger a serious and persistent cough attack, should try to avoid. Strenuous exercise, crying, rapid breathing, lowering of airway temperature or changes in fluid osmotic pressure in the respiratory tract, induce asthma attacks.

(B) pathogenesis The pathogenesis of asthma is not completely clear. Most people believe that allergies, chronic airway inflammation, airway responsiveness and autonomic dysfunction interact to participate in the pathogenesis of asthma.

1. Allergic reaction: When the allergen enters the body with allergies, it can stimulate the body's B lymphocytes to synthesize specific IgE through the transmission of macrophages and T lymphocytes, and bind to mast cells and basophils. High affinity IgE receptor (FcR1) on the cell surface. If the allergen enters the body again, it can cross-link with IgE on the surface of mast cells and basophils, thereby triggering a series of reactions in the cell, allowing the cells to synthesize and release a variety of active mediators leading to smooth muscle contraction and mucus secretion. Increased, increased vascular permeability and inflammatory cell infiltration. Inflammatory cells can secrete a variety of mediators under the action of the medium, causing aggravation of airway lesions, increased inflammatory infiltration, and clinical symptoms of asthma.

2. Airway inflammation: Chronic inflammation of the airway is considered to be the basic pathological change of asthma and the main pathophysiological mechanism of recurrent episodes. Regardless of which type of asthma, which stage of asthma, infiltration and aggregation of various inflammatory cells mainly composed of mast cells, eosinophils and T lymphocytes. These cellular interactions secrete dozens of inflammatory mediators and cytokines. These mediators, cytokines interact with inflammatory cells to form complex networks, interactions and effects that persist in airway inflammation. When the body encounters predisposing factors, these inflammatory cells can release a variety of inflammatory mediators and cytokines, causing airway smooth muscle contraction, increased mucus secretion, plasma exudation and mucosal edema. A variety of cells, including mast cells, eosinophils, neutrophils, epithelial cells, macrophages, and endothelial cells, are known to produce inflammatory mediators.

an examination

Related inspection

Chest radiograph and pleural auscultation challenge test

Auxiliary inspection

1. Pulmonary function test: Most patients with asthma control have their lung ventilation function in the normal range. In the case of asthma attacks, due to limited expiratory flow rate, the first second forced expiratory volume (FEV1), one second rate (FEV1/FVC%), maximum expiratory mid-flow velocity (MMER), exhalation 50% and 75% The maximum expiratory flow (MEF 50% vs. MEF 75%) and peak expiratory flow (PEFR) were reduced during lung capacity. The usefulness of the lungs is reduced, the amount of residual gas is increased, the amount of functional residual gas and the total amount of lungs are increased, and the percentage of residual gas accounts for the total amount of lungs. After treatment, it can gradually recover.

2, sputum eosinophils or neutrophil count: can assess airway inflammation associated with asthma.

3, exhaled NO (FeNO) concentration determination: can also be used as a non-invasive marker of airway inflammation in asthma. Sputum eosinophils and FeNo tests help to choose the best asthma treatment option.

4, allergen (ie allergen) check: allergen skin test or serum-specific IgE test can confirm the allergic state of asthma patients to help understand the risk factors that cause asthma in individuals and aggravation, can also help determine specific Sexual immunotherapy program.

5, chest x-ray examination: there is no obvious abnormality in asthma during the remission period. When the asthma attack occurs, the brightness of both lungs increases and it is over-inflated. Such as concurrent respiratory infections, increased lung texture and inflammatory infiltrates. At the same time, attention should be paid to the presence of complications such as atelectasis, pneumothorax or mediastinal emphysema.

Differential diagnosis

1. Cardiac asthma: common in left heart failure, the symptoms at the onset are similar to asthma, but cardiogenic asthma often has hypertension, acute nephritis complicated by severe circulatory congestion, coronary atherosclerotic heart disease, rheumatic heart disease And history and signs of mitral stenosis. Often coughed out with pink foam, both lungs can smell a wide range of blisters and wheezing sounds, the left heart is enlarged, the heart rate is increased, and the apex can be heard. Chest X-ray examination, visible heart enlargement, pulmonary congestion, cardiac B-ultrasound and cardiac function tests help to identify. If it is difficult to identify a nebulizable selective 2 agonist or a small dose of aminophylline to relieve symptoms after further examination, avoid epinephrine or morphine to avoid danger.

2. Tracheal endometrial lesions: Tumors of the trachea, endometrial tuberculosis, and foreign bodies, which cause obstruction of the trachea, can cause symptoms and signs similar to asthma. By raising awareness and timely performing lung flow volume curve, tracheal tomography or fiberoptic bronchoscopy, the diagnosis can usually be confirmed.

3. Tracheal foreign body: see tracheobronchial foreign body.

4. Wheezing type chronic bronchitis: In fact, chronic bronchitis with asthma, more common in middle-aged and elderly people, has a history of chronic cough, wheezing has existed for many years, there is a period of aggravation. There are signs of emphysema, and both lungs can smell blisters.

5. Bronchial lung cancer: Central lung cancer causes bronchoconstriction or infection or carcinoid syndrome, which may cause wheezing or asthma-like dyspnea, lung audible and wheezing. However, lung cancer has difficulty in breathing and wheezing symptoms, often without incentives. Cough can have blood stasis, cancer cells can be found in the sputum, chest X-ray, CT or MRI or fiberoptic bronchoscopy can often confirm the diagnosis.

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