Introduction to asthma

Introduction:

bronchusasthma(bronchial asthma, asthma) is a chronic airway inflammation involving a variety of cells, especially mast cells, eosinophils and T lymphocytes. In susceptible people, this inflammation can cause recurrent wheezing, shortness of breath, chest tightness. Symptoms such as and/or cough occur more frequently at night and/or in the early hours of the morning, and the airway is more reactive toward multiple stimuli. However, the symptoms can be relieved by themselves or by treatment. In the past ten years, the prevalence and mortality of asthma in the United States, Britain, Australia, New Zealand and other countries have increased. About 100 million asthma patients in the world have become a major chronic disease that seriously threatens public health. The prevalence of asthma in China is about 1%, and children can reach 3%. It is estimated that there are more than 10 million asthma patients in the country.

Cause:

The etiology of this disease is more complicated, and most of them are considered to be a polygenic genetic disease, which is affected by both genetic factors and environmental factors.

(1) Genetic factors The relationship between asthma and heredity has received increasing attention. According to family data, most of the early studies considered that asthma is a monogenic genetic disease. Some scholars believe that it is an autosomal dominant inheritance disease, and it is also considered to be autosomal recessive inheritance.

At present, asthma is considered to be a polygenic genetic disease with a heritability of about 70% to 80%. Polygenic genetic diseases are caused by multiple pairs of pathogenic genes on different chromosomes. There is no obvious difference between these genes. Each has a weak effect on phenotype, but it has an additive effect. The incidence is affected by the environment. The influence of factors is large. Therefore, bronchial asthma is composed of several genetic factors that have a small but cumulative effect, and the genetic risk determines the risk of an individual's illness as susceptibility. The possibility that genetic factors and environmental factors work together to determine whether an individual is susceptible to asthma is called susceptibility.

The degree of heritability can measure the role of genetic factors in its pathogenesis. The higher the heritability, the greater the role of genetic factors in its pathogenesis. The higher the heritability, the greater the role of genetic factors in the pathogenesis. 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, the higher the prevalence rate; in a family, the more patients, the higher the prevalence of relatives; patients The more serious the condition, the higher the prevalence of relatives.

Wang Mingang et al investigated the prevalence of asthma in children with grade I and II in asthma, and compared with the control group, the prevalence of asthma in class I relatives in the asthma group was 8.2%, and the prevalence of class II relatives was 2.9%. The prevalence is significantly higher than the latter. The prevalence of asthma in the control group's I and II relatives was 0.9% and 0.4%, respectively, and the prevalence was lower than that of the asthmatic group I and II relatives.

An important feature of asthma is the presence of airway hyperresponsiveness. Studies in humans and animals have shown that some genetic factors control the response of the airways to environmental stimuli. Zhang Xiaodong et al used tissue inhalation method to measure the airway responsiveness of 40 parents of asthmatic children and 34 normal children. Most of the parents of asthma had different degrees of airway responsiveness, and PC20 averaged 11.6 mg/ml, while normal children. The PC20 of both parents is greater than 32mg/ml, indicating that there is a basis for airway hyperresponsiveness in the family of asthma patients, so the inheritance of airway hyperresponsiveness plays an important role in the inheritance of asthma.

At present, the genes related to asthma are not completely clear, but studies have shown that there may be asthma specific genes, IgE regulatory genes and specific immune response genes. Autosomal 11q12q13 contains an asthma gene that controls the reactivity of IgE. In recent years, foreign studies on serum total IgE genetics suggest that the gene that regulates total IgE is located on chromosome 5; the specific immune response is not the IgE regulatory gene. Controlled by the immune response gene, the immune response gene has a high recognition capacity of the antigen molecule, and it is confirmed in the mouse experiment that the immune response gene is located in the MHC region on chromosome 17.

Studies have shown that there are also immune response genes in the DR site of the HLA region on human chromosome 6, which controls the immune response to a specific antigen. Therefore, the interaction between IgE regulatory genes and immune response genes is involved in the pathogenesis of asthma. In addition, different sensitive states of cellular receptors in the nervous system and respiratory system, and the congenital deficiency of certain enzymes may also be affected by genetic factors. In short, the relationship between asthma and heredity needs to be further studied to facilitate early diagnosis, early prevention and treatment.

(B) the stimulating factors The formation of asthma and repeated onset, often the result of a combination of many complex factors.

1. Inhaled inhalants are classified into specific and non-specific. The former such as dust mites, pollen, fungi, animal dander, etc.; non-specific inhalants such as sulfuric acid, sulfur dioxide, chloramine and the like. Specific inhalation of occupational asthma such as toluene diisocyanate, phthalic anhydride, ethylenediamine, penicillin, protease, amylase, silk, animal dander or excrement, in addition, non-specific formaldehyde, formic acid Wait.

2. The formation and onset of infection with asthma are associated with repeated respiratory infections. In asthma patients, specific IgE may be present in bacteria, viruses, mycoplasmas, etc., and asthma may be stimulated if the corresponding antigen is inhaled. After the virus is infected, the airway epithelium can be directly damaged, resulting in increased respiratory responsiveness. Some scholars believe that interferon and IL-1 produced by viral infection increase the amount of histamine released by basophils. In the early childhood, respiratory viruses (especially respiratory syncytial virus) are infected, and there are many symptoms of asthma. Asthma caused by parasites such as mites and hookworms is still visible in rural areas.

3, food due to dietary relationship caused by asthma attacks are often seen in asthma patients, especially infants and young children are easy to food allergies, but gradually decrease with age. The most common foods that cause allergies are fish, shrimps, crabs, eggs, milk, etc.

4. Climate change When the temperature, temperature, air pressure and/or air ions change, it can induce asthma, so it is more common in the cold season or autumn and winter climate change.

5, mental factors patients with emotional excitement, nervousness, anger, etc., will promote asthma attacks, it is generally believed that it is caused by cerebral cortex and vagus nerve reflex or hyperventilation.

6. Exercise: About 70% to 80% of asthma patients induce asthma after strenuous exercise, called exercise-induced asthma, or exercise-induced asthma. A typical case is 6 to 10 minutes of exercise, and bronchospasm is most pronounced within 1 to 10 minutes after stopping exercise. Many patients recover spontaneously within 30 to 60 minutes. There is an refractory period of about 1 hour after exercise, during which 40% to 50% of the patients exercise again without bronchospasm. Clinical manifestations include cough, chest tightness, shortness of breath, wheezing, auscultation audible and wheezing. Some patients have no typical asthmatic performance after exercise, but pulmonary function tests before and after exercise can detect bronchospasm. The disease is more common in adolescents. If cromolyn sodium, ketotifen or aminophylline is administered in advance, the onset can be alleviated or prevented. Related studies suggest that due to hyperventilation after strenuous exercise, the moisture and heat of the airway mucosa are lost, and the concentration of molecules in the airway epithelium temporarily appears to be too high, leading to contraction of bronchial smooth muscle.

7, asthma and drugs Some drugs can cause asthma attacks, such as propranolol and other causes of asthma caused by blocking β2-adrenergic receptors. About 2.3% to 20% of asthma patients induce asthma as a result of taking aspirin, called aspirin asthma. Patients with nasal polyps and low tolerance to aspirin are referred to as aspirin triad. Its clinical features are: taking aspirin can induce severe asthma, symptoms appear more than 2 hours after medication, and occasionally as late as 2 to 4 hours. Patients may have cross-reactions with other antipyretic analgesics and non-steroidal anti-inflammatory drugs; children with asthma are mostly before the age of 2, but most of them are middle-aged patients, mostly 30 to 40 years old; more women than men, The ratio of male to female is about 2:3; the attack has no obvious seasonality, the condition is heavier and stubborn, most of them are dependent on hormones; more than half have nasal polyps, often accompanied by perennial allergic rhinitis and/or sinusitis, nasal After polypectomy, asthma symptoms sometimes worsen or trigger; common inhalation allergens are negative in the skin test; serum total IgE is normal; patients with less allergic diseases in the family.

Regarding its pathogenesis has not yet been fully elucidated, it has been suggested that the patient's bronchial epoxidase may be affected by an infectious agent (probably a virus), making the epoxidase susceptible to aspirin inhibition, that is, intolerance to aspirin. Therefore, when patients use aspirin drugs, it affects the metabolism of arachidonic acid, inhibits the synthesis of prostaglandins, deregulates PGE2/PGF2α, and increases the production of leukotrienes, resulting in strong and long-lasting contraction of bronchial smooth muscle.

8. Menstruation, Pregnancy and Asthma Many women with asthma have aggravation of asthma 3 to 4 days before the menstrual period, which may be related to the sudden decline of progesterone in the premenstrual period. If some patients are required to have a monthly dose and the amount of menstruation is small, progesterone may be injected in a timely manner, sometimes preventing severe premenstrual asthma. Pregnancy has no regular effect on asthma. There are asthma symptoms improvement and worsening, but most of the conditions have not changed significantly. The effect of pregnancy on asthma is mainly manifested in mechanical effects and changes in hormones associated with asthma. In the third trimester of pregnancy, as the uterus increases, the position of the diaphragm increases, resulting in different amounts of residual gas, expiratory volume, and functional residual capacity. The degree of decline, and there is an increase in ventilation and oxygen consumption. If asthma is treated properly, it will not have adverse consequences for pregnancy and childbirth.

(A) allergic bronchial asthma is associated with allergic reactions, has been recognized as the main type I allergic reaction. Most patients are atopic, often accompanied by other allergic diseases. When the allergen enters the body to stimulate the body, it can synthesize high titer-specific IgE and bind to the surface of mast cells and basophils. Affinity Fcε receptor (FcεR1); also binds to certain B cells, macrophages, monocytes, eosinophils, NK cells, and low-affinity Fcε receptors (FcεR2) on the surface of platelets. However, the affinity of FcεR2 to IgE is about 10-100 times lower than that of FcεR1. If the allergen re-enters the body, it can cross-link with IgE bound to FcεR, synthesize and release a variety of active mediators, resulting in bronchial smooth muscle contraction, increased mucus secretion, increased vascular permeability and inflammatory cell infiltration. Moreover, inflammatory cells can release a variety of media under the action of the medium, which makes the airway inflammation worse. According to the time of asthma after allergen inhalation, it can be divided into immediate asthma response (IAR), delayed-onset asthma response (LAR) and bipolar asthma response (DAR). IAR reacts almost immediately while inhaling allergens, peaks in 15 to 30 minutes, and gradually returns to normal in about 2 hours. LAR is delayed, about 6 hours, and lasts for several days. Some patients with severe asthma are closely related to delayed type of response. The clinical symptoms are severe, the lung function is impaired and persistent, and it is often necessary to inhale glucocorticoid drugs and other treatments to recover.

In recent years, the clinical importance of LAR has attracted people's attention. The mechanism of LAR is more complicated, not only related to IgE-mediated degranulation of mast cells, but mainly due to airway inflammation, which may involve re-granulation of mast cells and leukotrienes (LT), prostaglandins (PG), thromboxane. Release of delayed media such as (TX). Studies have shown that mast cell degranulation is not unique to immune mechanisms, non-immune stimuli such as exercise, cold air, inhaled sulfur dioxide, etc. can activate mast cells to release particles. It is believed that asthma is a chronic inflammatory disease involving multiple inflammatory cell interactions, many mediators and cytokines involved, LAR is the result of airway inflammation, mast cells are primary effector cells, and eosinophils Cells, neutrophils, monocytes, lymphocytes and platelets are secondary effector systems, which in turn release a large number of inflammatory mediators, activate airway target organs, cause bronchial smooth muscle spasm, microvascular leakage, mucosal edema, The nervous response to mucus hypersecretion is excitatory, and the patient's airway responsiveness is significantly increased. Clinically, general bronchodilators are not easy to relieve, and the use of corticosteroids and sodium cromolyn inhalation can prevent the occurrence of LAR.

The relationship between bronchial asthma and type III allergies is now controversial. Traditionally, exogenous asthma is a type I allergy, manifested as IAR; and endogenous asthma is a type III allergy (Arthus phenomenon), which is expressed as LAR. However, some studies have shown that the vast majority of LAR is secondary to IAR, and LAR has a significant dependence on IAR. Therefore, not all LARs are type III allergies.

(B) airway inflammation Airway inflammation is an important advance in the field of asthma pathogenesis research in recent years. Airway inflammation in patients with bronchial asthma is involved in a variety of cells, especially mast cells, eosinophils and T lymphocytes, and there are more than 50 inflammatory mediators and more than 25 cytokines interacting with an airway chronic non-special Heterologous inflammation. Airway inflammation is an important determinant of airway reversible obstruction and non-specific bronchial hyperresponsiveness in asthmatic patients. The airway inflammatory response process in asthma has three phases, namely, IgE activation and FcεR initiation, inflammatory mediators and cytokine release, and expression of adhesion molecules that promote leukocyte transmembrane movement.

When the allergen enters the body, the B cells recognize and activate the antigen. The activation pathways are: T, B cell recognition antigens, different epitopes, respectively, activation; B cells endocytosis, treatment of antigens and binding to major histocompatibility complexes ( MHC II), this complex is recognized by Th and releases IL-4, IL-5 to further promote B cell activation. The activated B cells produce corresponding specific IgE antibodies, which are then cross-linked with mast cells, eosinophils, etc., and then produce and release inflammatory mediators under the action of allergens. It is known that mast cells, eosinophils, neutrophils, epithelial cells, macrophages, and endothelial cells all have the ability to produce inflammatory mediators, which can be divided into rapid release mediators (such as histamine) according to the sequence of media production. There are three types of secondary producing media (PG, LT, PAF, etc.) and particle-derived mediators (such as heparin). Mast cells are the primary primary effector cells of airway inflammation. After mast cell activation, histamine, eosinophil chemotactic factor (ECF-A), neutrophil chemotactic factor (NCF-A), LT can be released. Such as media. Alveolar macrophages may also play an important role in the initiation of asthma inflammation, which can release mediators such as TX, PG and platelet active factor (PAF) upon activation.

ECF-A chemotaxis of eosinophils and induces release of major base protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), eosinophil neurotoxin ( EDN), PAF, LTC4, etc., MBP, EPO can cause airway epithelial cells to fall off, expose sensory nerve endings, resulting in airway hyperresponsiveness. MBP and EPO can also activate mast cell release media. NCF-A can neutrophil chemotaxis and release LT, PAF, PGS, oxygen free radicals and lysosomal enzymes, etc., aggravating the inflammatory response. LTC4 and LTD4 are extremely strong bronchoconstrictors and promote increased mucus secretion and increased vascular permeability. LTB4 can oxidize, aggregate and secrete mediators of neutrophils and eosinophils. PGD2, PGF2, PGF2α, PGI2 and TX are all powerful airway contractions. PAF can contract bronchial tubes and chemotaxis, activate inflammatory cells such as eosinophils, and induce microvascular oozing. It is one of the important mediators of asthma inflammation.

In recent years, endothelin (ET5) produced in airway epithelial cells and vascular endothelial cells has been found to be an important mediator of airway contraction and reconstruction. ET1 is the strongest bronchial smooth muscle contraction agent known to date, and its contractile strength is LTD4 and nerve. The kinin is 100 times more potent than acetylcholine, and ET also has the effect of promoting the secretion of submucosal glands and promoting the proliferation of smooth muscle and fibroblasts. The pre-inflammatory cytokine TNFα can stimulate the secretion of ET1 by airway smooth muscle cells, which not only aggravates the contraction of smooth muscle, but also enhances the contractile reactivity of airway smooth muscle, and can lead to airway remodeling caused by abnormal proliferation of airway cells, which may become chronic. An important cause of refractory asthma. Adhesion molecules (AMs) are a class of glycoproteins that mediate cell-to-cell adhesion. A large number of studies have confirmed that adhesion molecules play an important role in the pathogenesis of asthma. Molecular mediated adhesion of leukocytes to endothelial cells and trans-endothelial transfer to the site of inflammation.

In short, the inflammatory response of asthma is caused by a variety of inflammatory cells, inflammatory mediators and cytokines, and the relationship is very complicated and needs to be further explored.

(3) Airway hyperresponsive airway reactivity refers to the contractile response of the airway to various chemical, physical or drug stimuli. Airway hyperresponsiveness (AHR) refers to an excessive airway contraction response of a non-antigenic stimulator of the airway that does not normally cause or only causes a mild response. Airway hyperresponsiveness is one of the important features of asthma. AHR often has a family tendency and is influenced by genetic factors, but the role of external factors is more important. Airway inflammation is currently considered to be one of the most important mechanisms leading to airway hyperresponsiveness. When the airway is affected by allergens or other stimuli, AHR is caused by the involvement of various inflammatory cells, inflammatory mediators and cytokines, damage to the airway epithelium and intraepithelial nerves.

It is believed that the autocrine and paracrine secretion of endothelin in airway stromal cells, as well as the interaction of cytokines, especially TNFα, with endothelin play an important role in the formation of AHR. In addition, AHR is associated with hypofunction of β-adrenergic receptors, increased cholinergic neuronal excitability, and defects in the inhibition of non-adrenergic non-cholinergic (NANC) nerves. Stimulation of physical and chemical factors such as viral respiratory infections, SO2, cold air, dry air, hypotonic and hypertonic solutions can increase airway reactivity. The degree of airway hyperresponsiveness is closely related to airway inflammation, but the two are not equivalent. AHR is currently recognized as a common pathophysiological feature of bronchial asthma patients, but not all BHR patients are bronchial asthma, such as long-term smoking, exposure to ozone, viral upper respiratory tract infection, chronic obstructive pulmonary disease (COPD), allergic rhinitis, BHR can also occur in patients with bronchiectasis, tropical pulmonary eosinophilia, and allergic alveolitis, so the clinical significance of BHR should be fully understood.

(4) Neurological factors The autonomic innervation of the bronchi is complex. In addition to the previously known cholinergic and adrenergic nerves, there is also a non-adrenergic non-cholinergic (NANC) nervous system. Bronchial asthma is associated with hypofunction of beta adrenergic receptors and hyperkinetic vagal tone, and may have increased reactivity with alpha-adrenergic nerves. NANC inhibits the nervous system as the main nervous system that produces airway smooth muscle relaxation. Its neurotransmitters have not been fully elucidated. It may be vasoactive intestinal peptide (VIP) and/or peptide histidine methionine, while airway smooth muscle. Shrinkage may be associated with impaired functioning of the system. The NANC excitatory nervous system is an unmyelinated sensory nervous system whose neurotransmitter is substance P, which is present in the C-type afferent fibers that are chemically sensitive to airway vagus nerves.

When the airway epithelium is damaged, C-fiber afferent nerve endings are exposed, stimulated by inflammatory mediators, causing local axonal reflexes, reverse conduction along the afferent nerve lateral cord, and releasing sensory neuropeptides, such as substance P, neurokinin, Calcitonin gene-related peptide results in bronchial smooth muscle contraction, enhanced vascular permeability, and increased mucus secretion. Recent studies have shown that nitric oxide (NO) is the main neurotransmitter of human NANC, and endogenous NO has a dual effect on the airway. On the one hand, it can relax airway smooth muscle and kill pathogenic microorganisms, in airway smooth muscle tension. Regulation and pulmonary immune defense play an important role; on the other hand, local large amount of NO production can aggravate airway tissue damage and induce AHR. The effect may vary depending on local tissue concentration and target site, and may regulate airway NO production. Good for asthma treatment.

The basic pathological changes of the airways are mast cells, pulmonary macrophages, citrate granulocytes, lymphocytes and neutrophil infiltration. Airway mucosal tissue edema, increased microvascular permeability, bronchial endocrine retention, bronchial smooth muscle spasm, ciliated epithelial detachment, basement membrane exposure, goblet cell proliferation and increased bronchial secretion, etc., called chronic exfoliation Eosinophilic bronchitis. The above changes can vary with the degree of airway inflammation. If the asthma is recurrent for a long time, it can enter the irreversible stenosis stage of the airway, mainly manifested as thickening of the bronchial smooth muscle, airway reconstruction under the airway epithelial cells, and support of the surrounding lung tissue to the airway. The effect disappears.

In the early stage of the disease, due to the reversibility of pathology, organic changes are rarely found anatomically. As the disease progresses, pathological changes gradually become apparent. The lungs can be seen with enlarged lung swelling and emphysema. The lungs are soft, loose and elastic. The bronchi and bronchioles contain viscous sputum and mucus plugs. The bronchial wall is thickened, the mucosal congestion and swelling are formed, and the atelectasis can be found locally in the mucus embolism.

symptom:

Typical bronchial asthma, there are aura symptoms such as sneezing, salivation, cough, chest tightness, etc. before the attack, if not treated in time, asthma may occur due to aggravation of bronchial obstruction, severe cases may be forced to take a seat or sitting breathing, dry cough Or a lot of white foam, even purple. However, it can usually be relieved by itself or by treatment with self-administered or anti-asthmatic drugs. Some patients may relapse after a few hours of remission, and even lead to persistent asthma.

In addition, atypical manifestations of asthma also exist clinically. Such as cough variant asthma, patients with no obvious incentives for cough for more than 2 months, frequent attacks at night and in the morning, exercise, cold air and other induced aggravation, airway reactivity determination of high reactivity, antibiotics or antitussive, expectorant Ineffective treatment, effective with bronchial spasmolytic agents or corticosteroids, but need to rule out other diseases that cause cough.

According to the presence or absence of allergens and age of onset, it is clinically divided into exogenous asthma and endogenous asthma. Exogenous asthma often occurs in childhood and adolescents, and there is a history of family allergies, which is type I allergic reaction. Endogenous asthma has no known allergens. It has no obvious seasonality in adults, and has a history of allergies. It may be caused by infection in the body.

Regardless of the type of asthma, mild symptoms can gradually resolve spontaneously, without any symptoms or abnormal signs during the remission period.

diagnosis:

(1) Diagnostic criteria

1, repeated episodes of wheezing, difficulty breathing, chest tightness or cough, and more related to contact with allergens, viral infections, exercise or certain irritants.

2, the attack on both lungs can be heard and scattered or diffuse, with the exhalation period as the main wheezing sound.

3. The above symptoms can be relieved by treatment or relieved by themselves.

4. Eliminate other diseases that can cause wheezing or difficulty breathing.

5, for patients with atypical symptoms (such as no significant wheezing or signs), should have at least one of the following test positive: 1 If the basic FEV1 (or PEF) <80% normal value, increase the FEV1 (or PEF) after inhaling the β2 agonist More than 15%. 2PEF mutation rate (measured by expiratory peak flow meter, once every morning and night) ≥ 20%. 3 bronchial provocation test (or exercise challenge test) is positive.

Identification

Bronchial asthma should be distinguished from asthmatic bronchitis, cardiogenic asthma caused by left heart failure, dyspnea due to airway obstruction caused by airway tumors, pulmonary eosinophilic infiltration, and wheezing caused by bronchiolitis in children .

complication:

Acute complications

1. Sudden death is the most serious complication of bronchial asthma, because it often has no obvious aura symptoms. Once it suddenly occurs, it is often too late to rescue and die. The important reasons for sudden death from asthma can be summarized as:

(1) Specific hypersensitivity reaction: due to the high sensitivity state of the airway, specific or non-specific stimulation, especially when performing airway reactivity measurement, can cause severe laryngeal, tracheal edema and extensive bronchospasm, causing obstruction of the trachea Or induce severe arrhythmia or even sudden cardiac arrest and death.

(2) Locked lung: The side effects of bronchial or isoproterenol can be blocked by extensive tendon plugs. The latter is due to the metabolism of the drug 3-methoxyisoproterenol, not only can not stimulate the beta receptor, but also can play a beta blockade, causing bronchial smooth muscle spasm and ventilatory block.

(3) fatal arrhythmia: can be caused by severe hypoxia, water, electrolyte and acid-base imbalance, can also be caused by improper use of drugs, such as the application of digitalis, bronchodilation, β-receptor stimulant, ammonia tea when combined with heart failure Alkali, etc. If intravenous aminophylline is administered at a blood concentration of >30 mg/L, tachyarrhythmia can be induced.

(4) Outbreak of bronchial asthma: It is often too late to die with medication, and the mechanism is unknown.

(5) Improper application of anesthetics or sedatives: anesthetics can cause respiratory depression or even sudden arrest. Some sedatives also have significant inhibitory effects on the respiratory center, such as barbiturates and chlorpromazines. In the event of sudden death, artificial airways should be established immediately, artificial ventilation should be carried out, and important organs such as the heart and brain should be effectively treated accordingly.

2, lower respiratory tract and lung infection According to statistics, about half of asthma is caused by upper respiratory tract infection. As a result, the immune function of the respiratory tract is disturbed, and it is easy to secondary to the lower respiratory tract and lung infection. Therefore, efforts should be made to improve the immune function of asthma patients, maintain airway patency, clear airway secretions, keep the room clean, prevent colds, to reduce infection; once there is a sign of infection, appropriate antibiotics should be used according to bacteria and drug susceptibility.

3, water and electrolytes and acid-base imbalance due to asthma attacks, hypoxia, inadequate feeding, dehydration, heart, liver, especially respiratory and renal insufficiency, often complicated by water, electrolytes and acid-base imbalance, which are affecting asthma efficacy and prognosis Key factor. Efforts should be made to maintain the balance of water, electrolytes and acid-base. The electrolytes and arterial blood gas analysis should be monitored every day, and abnormalities should be detected in time to be processed in time.

4, pneumothorax and mediastinal emphysema due to asthma, gas retention in the alveolar, so that alveolar gas is excessive, lung pressure increased significantly, chronic asthma has emphysema caused by pulmonary rupture, the formation of spontaneous pneumothorax; application of machinery When ventilating, the peak pressure of the airway and alveoli is too high, and it is easy to cause alveolar rupture and form a barotrauma, causing pneumothorax and even mediastinal emphysema.

5, respiratory failure, severe asthma attacks, inadequate ventilation, infection, treatment and improper medication, complicated pneumothorax, atelectasis and pulmonary edema, are common causes of asthma with respiratory failure. In the event of respiratory failure, asthma treatment is more difficult due to severe hypoxia, carbon dioxide retention and acidosis. It is necessary to eliminate and reduce the incentives, prevention and prevention; after the occurrence, it is necessary to rescue according to respiratory failure.

6, multiple organ dysfunction and multiple organ failure due to severe hypoxia, severe infection, acid-base imbalance, gastrointestinal bleeding and drug side effects, severe asthma often complicated by multiple organ dysfunction or even functional failure. It is necessary to prevent and correct the above incentives and actively improve the functions of important organs.

Long-term complications

1, dysplasia and thoracic deformity in children with asthma, often cause dysplasia and thoracic deformity, the factors are multi-faceted, such as nutritional deficiencies, hypoxemia, endocrine disorders, etc., there are reports of long-term systemic use of corticosteroids, 30% are stunted.

2. The incidence of chronic obstructive pulmonary disease, pulmonary hypertension and chronic pulmonary heart disease is related to long-term or repeated airway obstruction, infection, hypoxia, hypercapnia, acidosis and increased blood viscosity caused by asthma.

treatment:

Western medicine treatment

First, eliminate the cause.

Allergens and other non-specific stimuli that cause asthma attacks should be avoided or eliminated, and various predisposing factors should be removed.

Second, control acute attacks.

In the case of asthma attacks, both antispasmodic, anti-inflammatory, and airway mucus plugs should be taken to keep the airway open and prevent secondary infection. Generally, the following drugs can be used alone or in combination.

(1) Adrenalin drugs: These drugs include ephedrine, adrenaline, isoproterenol and the like.

(B) theophylline (xanthine) drugs: aminophylline.

(C) anticholinergic drugs: commonly used drugs are atropine, scopolamine, 654-2 and ipratropium bromide (ipratropium bromide).

(4) Calcium antagonists: Diltiazem, verapamil, nifedipine or oral inhalation, have a good effect on exercise asthma.

(5) Adrenal glucocorticoids.

(6) Disodium cromolyn.

(7) Ketotifen: This product is taken 2 weeks before the onset of the attack. If it is taken orally for 6 weeks, it can be stopped if it is invalid.

Third, promote drainage.

(1) Tincture: Bromine has been added or ammonium chloride mixture.

(2) Inhalation of aerosol.

(3) Mechanical drainage: After the aerosol is humidified, the nursing staff pays attention to turning over the back, draining the drainage, and if necessary, using a catheter to assist in sucking.

(4) Actively control infection.

Fourth, the treatment of severe asthma is critically ill and the condition is complex, and it must be promptly and reasonably rescued.

V. Remission treatment: The purpose is to consolidate the curative effect, prevent or reduce recurrence, and improve respiratory function.

(A) desensitization therapy: desensitization treatment for allergens can reduce or reduce asthma attacks.

(2) Disodium cromolyn, inhalation of bunone aerosol, oral administration of ketotifen, strong anti-allergic effect, and good preventive effect on exogenous asthma. Others such as astemizole, terfenadine, and Trinister are all H1 receptor antagonists, and have no central sedative effect, and can be used as a preventive medication.

(3) Enhance physical fitness, participate in necessary physical exercise, improve the prevention of health knowledge of the disease, and stabilize emotions.

In recent years, with the in-depth study of the etiology and pathogenesis of bronchial asthma, it is recognized that asthma is a chronic inflammation of the airway and has clinical features of airway hyperresponsiveness, so there is a new aspect in the prevention and treatment of asthma. The concept is that treatment with bronchodilator alone is not comprehensive enough. For moderate to severe asthma, it is even harmful to use bronchodilators (such as β2 agonists) regularly. Because β2 agonists have no anti-inflammatory effects, simple symptomatic treatment can mask the development of inflammation and make airway hyperresponsiveness worse. Combined use of anti-inflammatory drugs. At the same time, in order to evaluate the treatment effect, determine the degree of the disease, determine the treatment and management plan, so be sure to record the patient's diary, adhere to the family measurement of pulmonary function (PEF), and monitor changes in airway responsiveness. If you can adhere to reasonable system control, most asthma patients can effectively control the disease and can live, study and work normally. Repeated episodes are often caused by improper prevention and treatment, often leading to difficult to reverse lung function damage. Therefore, in the prevention and treatment of asthma, it is imperative to do a good job in missionary work, control environmental triggering factors, monitor the condition and systematically treat the disease.

(1) Educating patients to enable medical staff, patients and their families to cooperate continuously, so that patients have a correct understanding of the disease, enhance confidence, consciously cooperate with doctors, insist on recording patient diaries, family monitoring lung function, regular follow-up visits, accept Diagnosis of asthma and the latest prevention and treatment methods.

(2) Controlling environmental triggering factors are mainly to determine, control and avoid exposure to various allergens, occupational sensitizers and other non-specific stimuli.

(3) Drug treatment should be formulated separately for the long-term management of the medication plan and the treatment of the attack period. The main purpose of treatment is to inhibit airway inflammation, reduce airway hyperresponsiveness, control symptoms, prevent asthma attacks, maintain normal lung function, and ensure normal activities. The day and night mutation rate of PEF is less than 20%. Drug treatment should not only be individualized, but also should be adjusted at any time, according to the degree of disease to achieve step-by-step treatment, so that the system can be used rationally, the bronchial dilation of β2 agonist, methylxanthine and anticholinergic drugs can be applied as needed or at the minimum dose. Agent. Inhalation therapy is superior to systemic injection or oral therapy in terms of administration route. The former has the advantages of high drug concentration in the airway, low dosage, and no or little adverse reaction in the whole body.

Inhalation therapy, such as quantitative aerosol (MDI), dry powder and nebulized solution, is used for acute severe asthma patients, and can also be used for children under 5 years old and some seizures are heavier. Asthma. If you have a patient with a difficult dose of aerosol, you can use a mist eliminator to improve the inhalation of bronchodilators, improve clinical efficacy, and reduce possible adverse reactions. After the dry powder is used with the inhaler, the effect is remarkable, and the method is simple and easy to grasp.

1. Glucocorticoid Glucocorticoid is the most effective anti-inflammatory drug for the treatment of asthma. The exact mechanism of action in the treatment of asthma is not fully understood. Its main functions are: inhibiting the metabolism of arachidonic acid and reducing leukotrienes. And prostaglandin synthesis; promote small blood vessels contraction, increase the tightness of the endothelium, reduce vascular leakage; inhibit the directional movement of inflammatory cells; activate and improve the reactivity of respiratory muscle smooth muscle β receptor; prevent cytokine production; inhibit histamine Acid decarboxylase, reduce histamine formation; increase the number of PGE receptors; inhibit the synthesis of acid mucopolysaccharides in bronchial glands; reduce the release of plasma proton activators and the secretion of elastase and collagenase.

Glucocorticoids can be administered systemically or via the airways. In the early stages of acute severe asthma attacks, oral glucocorticoids can prevent the exacerbation of asthma attacks; in the persistent state of asthma, large doses of glucocorticoids should be used for short-term systemic administration. medicine. Long-term low-dose or short-term high-dose inhaled corticosteroids are safe and effective for long-term treatment of asthma. Long-term inhalation of large doses of glucocorticoids is useful for the treatment of chronic severe asthma, reducing the amount of long-term oral glucocorticoids, and Reduce systemic side effects. Studies have suggested that a systemic adverse reaction can occur with a daily inhalation of more than 1 mg of chlorhexidine dipropionate (BDP) or the corresponding hormone. Local side effects of inhaled glucocorticoids are: candida infection of the oropharynx, difficulty in pronunciation, and occasional upper respiratory irritating cough, but when using MDI with a mist eliminator, or switching to a dry powder, it can prevent or To alleviate the above side effects, mouthwash can prevent oral Candida infection. The glucocorticoids contained in the existing MDI and dry powders include perclomethasone propionate (peperidone dipropionate) and dexamethasone (buldenazone). The usual dose for adults is 400-800 μg/ d.

2. Sodium cromolyn is a non-hormonal inhaled anti-inflammatory drug for the treatment of asthma. The exact mechanism of action is not fully understood. The known effect is to inhibit IgE mediated by human mast cells in a dose-dependent manner. Release; cell selective and mediator selective inhibition of inflammatory cells such as alveolar macrophages, eosinophils, neutrophils, and monocytes; reduction of excitability of respiratory receptors or inhibition of vagal reflex arcs Branches have a preventive effect on both IAR and LAR. Inhalation of sodium cromolyn can reduce or remove the amount of glucocorticoids in patients. In order to prevent seasonal attacks of asthma, preventive treatment should be given before the season of good hair. Inhalation of 20mg each time, 3 to 4 times a day, do not prematurely stop the drug, after 4 to 6 weeks of treatment, invalidation can be stopped.

3, β2 agonist has diastolic bronchial smooth muscle, enhance the clearance activity of mucociliary, reduce vascular permeability, and can regulate the release of mediators of mast cells and basophils. This class of drugs is effective in treating IAR, but not in LAR. Short-acting inhaled beta 2 agonists are the drug of choice for the treatment of asthma exacerbations and prophylactic treatment of exercise-induced asthma. The novel long-acting inhaled β2 agonists, formaterol and Shiliwen, inhibit antigen-induced rapid and delayed responses and histamine-induced increase in airway responsiveness, but blood and sputum tests do not reduce inflammatory cellular responses. Long-term regular use of β-agonists can lead to desensitization and down-regulation of β2 receptors in patients, which increases the number of asthma attacks. Therefore, it is now believed that β2 agonists should not be applied in a long-term, regular manner. If long-term application is required, it is advisable to use glucocorticoid, Nedocromil Sodium or ipratropium bromide (isopropyl ipratropium bromide) to prevent desensitization and down-regulation of β2 receptor. The sustained release and controlled release oral administration of the β2 agonist can significantly prolong the duration of action and maintain the effective blood concentration, so it is often used for patients with nocturnal asthma attacks.

4, the role of the xanthine drug aminophylline in relieving bronchospasm has been confirmed by clinical practice for more than half a century, and the understanding of its mechanism of action is deepening. It is conventionally believed that theophylline acts by inhibiting the phosphodiester PDE) and reducing the hydrolysis of C-AMP. However, it has been proved that the concentration of theophylline required for inhibiting PDE in the test tube is much higher than the effective plasma theophylline concentration, so it is difficult to explain completely according to this mechanism.

Studies have shown that theophylline can stabilize and inhibit mast cells, basophils, neutrophils and macrophages, antagonize adenosine-induced bronchospasm, and stimulate the release of catecholamines from chromatin cells other than the adrenal medulla and adrenal glands. It can increase the contractility of the diaphragm of the health or fatigue to low frequency stimulation. Moreover, there is increasing evidence that theophylline not only has bronchodilating effects, but also has anti-inflammatory and immunomodulatory effects. It has been found that the plasma theophylline concentration has not reached the level required for the expansion of the bronchus, and significant anti-asthmatic effects can be observed. Therefore, the plasma theophylline concentration recommended for the treatment of asthma is set at 5-10 mg/L instead of 10-20 mg/L. This can significantly reduce its side effects. Some authors have suggested that oral administration of theophylline should be given at an early stage in the clinical treatment of asthma, while inhaling low doses of glucocorticoids as a basic regimen. At present, there is a sustained release or controlled preparation of theophylline in China, which can be stabilized at 5-10 mg/L by oral administration once or twice a day.

Anticholinergic inhaled anticholinergic drugs (ipratropium bromide) block the vagal pathway emanating from postganglionic neurons, reduce vagal tone in the airways and dilate the bronchus, and block the inhalation stimuli. Reflex bronchoconstriction. Although the drug has a slower onset effect, it has a longer lasting effect, and no drug resistance has been found in long-term administration. For example, in combination with an inhaled β2 agonist, the clinical effect can be improved. The usual amount is 20 to 80 μg per inhalation, 3 to 4 times per day.

prevention:

1. Avoid contact with the allergens after clearing them. For example, if the indoor dust or sputum induces the onset of asthma, the indoors should be kept clean, the sun should be smashed, and the windows should be kept open to keep the indoor air fresh.

2. It is not advisable to keep small animals such as cats and dogs indoors.

3, usually should pay attention to the child's physical exercise, such as the use of cold water bath, dry towel body, etc. for skin exercise, so that the nervous state of the lungs, trachea, bronchial vagus nerves are alleviated.

4, strengthen nutrition, avoid mental stimulation, avoid colds and excessive fatigue also play an important role in the prevention of asthma attacks.