Bronchial Asthma

Introduction to bronchial asthma Bronchial asthma is defined in the World Health Organization and the National Institutes of Health's revised Global Strategy for Asthma (2002) as "bronchial asthma is a chronic airway inflammation involving multiple cells and cellular components. Inflammation is often associated with increased airway responsiveness, resulting in recurrent wheezing, shortness of breath, chest tightness and/or coughing, mostly at night and/or in the early hours of the morning. These symptoms are often accompanied by extensive and variable airflow. Blocking can be reversed by itself or by treatment." basic knowledge The proportion of children: the prevalence rate of children aged 13-14 is 0-30%, and the prevalence rate of children of the same age is 3%-4%. Susceptible people: no specific population Mode of infection: non-infectious Complications: pulmonary edema

Causes of bronchial asthma

genetic factors:

Asthma is a disease with complex genetic traits with multiple genetic predispositions. It is characterized by: 1 exogenous incompleteness, 2 genetic heterogeneity, 3 polygene inheritance, 4 synergistic effects, which leads to discovery in a group. Genetic linkage, but not found in another different population, the Asthmatic Genetics Collaborative Research Group (CSGA) studied 140 families in 3 races, using 360 autosomal short tandem repeat polymorphism genetic markers Whole genome scanning, the asthma candidate gene was roughly mapped to 5p15; 5q23-31; 6p21-23; 11q13; 12q14-24.2; 13q21.3; 14q11.2-13; 17p11.1q11.2; 19q13.4; 21q21 and 2q33 The genetic susceptibility genes of asthma that may be contained in the chromosomal regions identified by these genetics are roughly classified into three categories: 1 genetic polymorphisms of HLA class II molecular genes (eg, 6p21-23) that determine the susceptibility to allergic diseases; 2T cells Receptor (TcR) is highly diverse and specific IgE (such as 14q11.2); 3 determines cytokine genes and drug-related genes that regulate IgE regulation and the development of characteristic airway inflammation in asthma (eg 11q13, 5q31-33) 5q31 -33 region contains cytokine clusters (IL- 3, IL-4, IL-9, IL-13, GM-CSF), 2 adrenergic receptor, lymphocyte glucocorticoid receptor (GRL), leukotriene C4 synthase (LTC4S), etc. Candidate genes associated with the onset of asthma, these genes are important for the regulation of IgE and the development of inflammation in asthma, so 5q31-33 is also known as the "cytokine gene cluster."

None of the above identified chromosomal regions showed evidence of linkage to more than one ethnic group, indicating that specific asthma susceptibility genes are only of relative importance, and that environmental factors or regulatory genes may be present in different races for disease expression. Differences, while suggesting that asthma and atopy have different molecular genetic basis, these genetic chromosomal regions are large, with an average of >20Mb of DNA and thousands of genes, and many results cannot be repeated due to the limitation of specimen size. It can be seen that there is still a lot of work to be done to find and identify asthma-related genes.

Allergens:

The most important stimulator of asthma may be the inhalation of allergens.

(1) Indoor allergens: The eaves are the most common and most harmful indoor allergens. They are important pathogenic factors for asthma worldwide. There are four common types: house dust mites, dust mites, and dust mites. And more than 90% of the mites are found in house dust. House dust mites are the most important aphids in the continuous humid climate. The main antigens are DerpI and DerpII. The main components are cysteine protease or tyrosine protease. For example, cats, dogs, and birds release allergens in their fur, saliva, urine, and feces. Cats are the most important sensitizers in these animals. Their main allergens are feldl, which has cat hair. And sebum secretions, which are the main risk factors for acute asthma attacks. They are common indoor allergens in Asian countries. Commonly associated with asthma are American cockroaches, German cockroaches, Oriental cockroaches and black-chested cockroaches. Among them, black-breasted cockroaches are most common in China. Fungi are also one of the allergens present in indoor air, especially in dark, humid and poorly ventilated areas, commonly known as Penicillium, Aspergillus, and Alternaria. Branches spores and Candida, among which Alternaria has been identified as a risk factor for asthma, a common outdoor allergen: pollen and grass powder are the most common outdoor allergens that cause asthma attacks. Woody plants (tree pollen) often cause spring asthma, while grasses and alfalfa pollen of grasses often cause autumn asthma. The eastern part of China is mainly ragweed pollen; the northern part is mainly wormwood.

(2) Occupational allergens: common allergens that can cause occupational asthma, grain, flour, wood, feed, tea, coffee beans, silkworms, pigeons, mushrooms, antibiotics (penicillin, cephalosporin) isocyanide Acid salts, phthalic acid, rosin, reactive dyes, persulfates, ethylenediamine, and the like.

(3) Drugs and food additives: Aspirin and some non-corticosteroids are the main allergens of asthma caused by drugs. Food additives such as salicylate, preservatives and stains can also cause acute asthma attacks, royal jelly. Oral liquid is widely used as a health care product in countries and regions of China and Southeast Asia. It has been confirmed that royal jelly can cause acute asthma attacks in some patients, which is an allergic reaction mediated by IgE.

Promoting factors:

(1) Air pollution: Air pollution (SO2, NO) can cause bronchoconstriction, transient airway reactivity is increased and can enhance the response to allergens.

(2) Smoking: Cigarette smoke (including passive smoking) is the main source of indoor triggering factors, and is an important asthma triggering factor, especially for asthmatic children whose parents smoke, often causing asthma attacks due to smoking.

(3) Respiratory virus infection: Respiratory virus infection is closely related to asthma attack. Infant bronchial virus infection is particularly concerned as the starting cause of asthma. Common respiratory viruses include respiratory syncytial virus (RSV), adenovirus, and rhinovirus. Influenza virus, parainfluenza virus, coronavirus, and certain enteroviruses. The viruses associated with adult asthma are mainly rhinovirus and influenza virus; respiratory syncytial virus, parainfluenza virus, adenovirus and rhinovirus are associated with childhood asthma. The seizures are closely related. The syncytial virus is the main pathogen in the first year after birth. It accounts for 44% of infectious asthma under 2 years old, and more than 10% of it is associated with infection in large children's asthma. It has been reported that after RSV infection Nearly 100% of epithelial cells in patients with asthma or bronchiolitis have IgE attachment, and 42% of children hospitalized for acute RSV infection develop asthma after 10 years.

(4) Perinatal fetal environment: T lymphocytes can be produced in the fetal thymus at 9 weeks of gestation. B-lymphocytes have been produced in various organs of the fetus from the 19th to 20th week, due to the main auxiliary in the placenta during pregnancy. Type II T cell (Th2) cytokines, so in the microenvironment of the lung, the Th2 response is dominant. If the mother has a specific constitution, it is exposed to a large number of allergens during pregnancy (such as milk in milk). Globulin, egg protein in eggs or Derp I in aphids, or repeated infection by respiratory viruses, especially syncytial viruses, may aggravate their Th2-regulated allergic reactions and increase the likelihood of postnatal allergies and asthma .

In addition, the intake of polyunsaturated fatty acids in the third trimester of pregnancy will affect the production of prostaglandin E, which may be related to the allergic reaction of Th2 cell regulation. The mother's smoking during pregnancy will definitely affect the fetal lung function and future asthma. The susceptibility to the sound.

(5) Others: strenuous exercise, climate change and a variety of non-specific stimuli such as: inhalation of cold air, distilled water droplets, etc. In addition, mental factors can also induce asthma.

Pathogenesis

Certain environmental factors act on genetically susceptible individuals, and the immune mediator release mechanism (cytokine, inflammatory mediator) regulated by T cells acts on the airway to produce inflammation and airway hyperresponsiveness; meanwhile, airway structural cells, especially airway epithelial cells The interaction with the subcutaneous matrix and immune cells and the abnormalities of airway neuromodulation aggravate the airway hyperresponsiveness, and directly or indirectly aggravate the airway inflammation. Under the further action of environmental factors, the inflammation is aggravated, and the airway is aggravated. Smooth muscle contraction and symptomatic asthma.

1. Immunological mechanism

The immune system is functionally divided into antibody-mediated and cell-mediated immune processes, which are involved in the development of inflammation. B lymphocytes produce and secrete specific antibodies, while T lymphocytes, in addition to controlling the function of B cells, can also By secreting cytokines to exert pre-inflammatory effects, a key step in the immune response is that T cells are activated by antigens, which is achieved by antigen-delivery of antigen-presenting cells such as dendritic cells and macrophages.

(1) Th1/Th2 mechanism: In recent years, significant progress has been made in the understanding of T helper cell function. Studies suggest that allergic reactions such as asthma are driven by Th2 cells, one for harmless antigens or allergens. Highly reactive, CD4 T helper cells are divided into two groups according to their functions: Th1 and Th2, Th1 and Th2 secrete interleukin-3 (IL-3), granulocyte macrophage colony-stimulating factor (GM-CSF) and tumor necrosis. Factor (TNF), Th1 mainly synthesizes interferon (IFN), interleukin-2 (IL-2), regulates immune anti-infective function; Th2 mainly produces IL-4, IL-5, IL-10 and IL-13 Etc., mainly regulates allergic reactions, IFN-r and IL-4 are the characteristic cytokines of Th1 and Th2, respectively. IL-4 is an essential cytokine for the selective development and expansion of Th2 cells. B cell synthesis and secretion-specific IgE are dependent on The presence of IL-4, the expression of IL-4 and IL-4 receptor alpha chain, is the basis of antigen-induced airway inflammation, such as eosinophil accumulation, excessive mucus secretion and airway hyperresponsiveness. -13 is a cytokine closely related to IL-4, and can also bind to the IL-4 receptor alpha chain to induce acute asthma attacks. Shows: antigen priming mechanism cytokines in acute asthma may be mediated by signal transduction pathways IL-4 receptor -chain starting mediated via effects.

As described above, Th1 cells, which function as immunosuppressive anti-infective functions, and Th2 cells that regulate allergic function exhibit an equilibrium state of mutual restraint and mutual growth.

IFN-, IL-12 can promote the development of activated Th0 cells in the direction of Th1, while IL-4 promotes its development in the Th2 direction. In Th1 dominant diseases such as multiple sclerosis, patients with type I diabetes, asthma The incidence rate is low; animal experiments show that type I allergic reactions triggered by allergens are inhibited after infection with M. tuberculosis, because M. tuberculosis can activate Th1 function, newborn or 2 months of birth vaccination BCG can increase the secretion activity of Th1 cytokines. The possible mechanism is that CD14 on the surface of mononuclear cells and macrophages in the early pregnancy is a high-affinity receptor for bacterial lipopolysaccharide (endotoxin). The heterogeneous congenital bacterial infection is a key factor in the immune response, and one of the main active components in BCG is lipopolysaccharide. Although the fetus is in a Th2 dominant environment, non-specific immune stimulation of the bacteria activates CD14 and improves Th1 function.

Under the regulation of Th2 cells, B lymphocytes can be regulated by secreted IL-4 to produce specific IgE, which further binds to specific receptors on mast cells and eosinophils, making them sensitized. Re-exposed to the same antigen, the antigen is cross-linked with cell surface-specific IgE, resulting in a chain reaction of inflammatory mediator release. Histamine, leukotrienes including LTB4, LTC4, LTD4 and LTE4 are early and late phases. The main inflammatory mediators of these mediators, which cause increased airway vascular permeability, mucosal edema, smooth muscle spasm and mucus hypersecretion. This response is immediate, which is the "T-cell regulation, IgE-dependent" mechanism, most recently Studies have shown that IgE can also mediate antigen presentation, allowing Th0 cells to develop in the direction of Th2.

Th2 cells can also directly cause the aggregation and activation of various inflammatory cells through the release of various cytokines (IL-4, IL-13, IL-3, IL-5, etc.), which directly promotes the inflammatory response in this way. - delayed type hypersensitivity, eosinophil aggregation activates and secretes the primary base protein, eosinophil cationic protein and proteolytic enzyme secreted by neutrophils can further aggravate the inflammatory process (T cell regulation, non-IgE-dependent mechanism) ).

(2) Dendritic cells: Dendritic cells are the main antigen-presenting cells in the lung. Studies have shown that these dendritic cells initiate the development of Th2 cells in the respiratory tract, and dendritic cells from the blood circulation are in the airway. A network is formed in the mucosa to ingest and process the inhaled antigen, which in turn migrates to the local lymph node, and delivers the treated antigen to CD4 T cells, dendritic cells of the respiratory tract, or DC2 cells, which are immature on the phenotype. Dendritic cells, which express low levels of surface MHC class II antigens, produce IL-10, but produce only a very small amount of IL-12; this local cytokine environment causes CD4 T cells to develop in the Th2 direction, Dendritic cells in peripheral lymphoid organs, which are mature dendritic cells, can express high levels of MHC class II antigens and produce IL-12, which induces differentiation in the Th1 direction. If CD4 T cells are activated by antigen, IL- is present. In the environment of 12, the cells will differentiate into the Th1 population; in the IL-4 environment, they will develop in the Th2 direction. The study also found that mucosal DC2 cells can stimulate Th2 cell differentiation in a non-IL-4 dependent manner. Prompt Some so-called endogenous asthma may be caused by this route.

(3) GATA-3 and C-Maf: GATA-3 is a key regulator of T cell development, Th2 differentiation and Th1/Th2 balance. GATA-3 belongs to the GATA transcription factor family, which binds to WGATAR (W= A/T, R=A/G) DNA sequence; there is such a GATA binding site in the IL-5 promoter. In a non-Th2 environment, a single GATA-3 is sufficient to activate the IL-5 promoter and induce IL- 5 gene transcription, non-activated CD4 T cells expressed low levels of GATA-3 mRNA, GATA-3 expression was significantly up-regulated when cells differentiated into Th2; and when cells developed toward Th1, GATA-3 expression was significant Downregulated, the development of Th1, such as overexpression of GATA-3, can cause the expression of IL-12 receptor 2 subunit to be blocked, and at the same time cause IFN production disorders. Studies have confirmed that GATA-3 controls Th2 activity by inducing Th2 cytokine gene expression. Furthermore, the induction of Th cell biased to Th2 functional differentiation showed a significant increase in GATA-3 expression in the airways of asthmatic patients, and this increase in expression was significantly associated with IL-5 expression and airway hyperresponsiveness, and inhibition of GATA-3 resulted in Local and systemic Th2 response is slow, local inflammatory response (eosinophil accumulation, excessive mucus Reduced secretion, and a significant reduction in IgE production.

The transcription factor C-Maf is defined as a Th2 specific factor; it has transcriptional activation of the IL-4 promoter. In C-Maf-negative mice, IL-4 production is blocked, but IL-5 and IL-13 expression are normal, so Normal levels of IgE are produced. In addition, other transcription factors: NF-KB, NF-AT, c/EBPB and AP-1 are also important for Th2 gene expression.

2. Inflammatory cell adhesion mechanism

Since cytokines activate capillary microscopic structures of the capillaries (venous end), including the airway epithelium, which leads to increased activity of adhesion molecules, including endothelial-leukocyte adhesion molecule-1 in the E-selectin family, cells in the globulin superfamily Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), etc., promotes the aggregation, adhesion and migration of various white blood cells in the capillary wall, leading to the accumulation of inflammatory cells in the airway.

3. Mechanism of interaction between airway epithelium and matrix

In the airways of asthma, bronchial epithelial cells are highly abnormal; structural changes include the separation of columnar epithelial cells from their basal attachment, functional changes including proinflammatory factors, growth factors, and increased expression of a series of inflammatory mediators. Under the damaged epithelial structure, there is hyperplasia of subepithelial fibroblasts, and thus the thickening of interstitial collagen deposition and the density of subepithelial basement membrane. The characteristic pathological changes of asthmatic airway epithelium may be The main growth factor that regulates epithelial damage repair, the epidermal growth factor (EGF) receptor is impaired, which in turn mediates the abnormal repair of the epithelium. Abnormal expression of the epidermal growth factor receptor may cause a balance between growth factor populations. Changes such as increased EGF production that promote epidermal growth result in increased expression of transforming growth factor (TGF), which promotes proliferation of stromal fibroblasts and smooth muscle cells, and some important factors involved in airway contraction and remodeling such as endothelin- 1, also has the effect of promoting the expression of inflammatory factors, so that epithelial repair continues to be active and tends to an abnormal In the process of integration, under the synergy of the local environment of Th2 cytokines, the exchange between the epithelial mesenchymal nutrient units changes, the subepithelial fibroblasts are activated to deposit excess matrix, and not only the activated epithelial cells and Subcutaneous fibroblasts can also produce large amounts of inflammatory mediators, leading to airway remodeling and expansion to the entire airway, suggesting that protecting the airway mucosa and restoring normal epithelial cell phenotype may be present in future asthma treatments. important position.

4. The neuromodulation mechanism of the airway

Asthmatic patients' airway response threshold to external stimuli is reduced. In the past, it was thought that the excitability of the parasympathetic nervous system was associated with airway hyperresponsiveness. Further studies confirmed that the airway neuromodulation is in addition to the classical cholinergic and adrenal nerves. Outside the system, there are also non-cholinergic, non-adrenergic nervous systems, which can release some neuropeptides, of which substance P, neurokinin A, neurokinin B, calcitonin gene-related peptide can cause Bronchial smooth muscle contraction, excessive mucus secretion, increased vascular permeability; other media including vasoactive intestinal peptide (VIP) and nitrous oxide (NO) can relax bronchial smooth muscle, in which the role of NO is increasingly valued, under normal circumstances The main production of constructive NO (cNO), in the pathogenesis of asthma, cytokines stimulate the induction of NO (iNO) produced by airway epithelial cells, which can dilate blood vessels and aggravate the inflammatory process.

5, pathology

Extensive airway stenosis is the most important basis for the clinical symptoms of asthma. The mechanisms of airway stenosis include: bronchial smooth muscle contraction, mucosal edema, chronic mucus formation, airway remodeling, and loss of elastic support of the lung parenchyma.

Airway stenosis caused by early or acute onset of asthma, mostly airway smooth muscle contraction and mucosal edema, rarely found organic changes, airway stenosis has greater reversibility; as the disease continues, mucosal edema Further development, and due to the accumulation of inflammatory cells, especially eosinophils, hypersecretion of mucus, chronic mucus formation may occur, at which time the clinical symptoms persist and the insufficiency is incomplete. If the asthma recurs, it may enter the irreversible phase of the airway. Mainly manifested as bronchial smooth muscle hypertrophy, fibrosis and airway remodeling under airway epithelial cells, and the supporting effect of surrounding lung tissue on the airway disappeared. At this time, high-dose corticosteroids were used, and the effect was still poor.

Bronchial asthma prevention

Prevention of asthma should include:

1 eliminate or avoid various factors that produce allergies and asthma;

2 early diagnosis, early treatment;

3 actively control airway inflammation and symptoms, prevent the disease from worsening, and avoid complications.

1. Prevent the occurrence of asthma - primary prevention

As mentioned above, asthma in most patients (especially children) is allergic asthma, and the immune response of the fetus is a Th2-preferred response. In the late pregnancy, certain factors such as excessive maternal contact with allergens, viral infections It can enhance the Th2 response and aggravate the imbalance of Th1/Th2. If the mother is an allergic constitution, it is more obvious and therefore avoided as much as possible. In addition, there is sufficient evidence to support the mother's smoking to increase the wheezing of infants and young children after birth. The risk of asthma, and breastfeeding for 4-6 months after birth, can reduce the incidence of allergic diseases in infants, and mothers should avoid smoking during pregnancy. These are important links to prevent asthma, and the maternal diet is relevant. The effects of the fetus still require more observation.

2, to avoid allergens and stimulating factors - secondary prevention

(1) Avoid allergens: especially for patients with specific constitution, eliminate or avoid contact with factors that induce asthma, such as house dust mites, pollen, animal skin, foods that can cause allergies, drugs, etc. Asthmatic patients should be separated from the occupational environment.

As mentioned above, whether allergens of respiratory virus are asthma is still controversial, but it is closely related to the occurrence and development of asthma, especially respiratory syncytial virus in children, rhinovirus in adults, and avoiding respiratory virus infection is also important. Measures to prevent asthma.

(2) Prevention and treatment of allergic rhinitis: Allergic rhinitis has a close relationship with asthma. Some patients with allergic rhinitis have been followed for nearly 20 years, and found that nearly 17% of them develop asthma, which is much higher than the control group. (5%); studies have also shown that 20% to 25% of patients with simple allergic rhinitis have airway hyperresponsiveness (histamine or methotrexate challenge), so that these patients may be considered "subclinical" Asthma", asthma patients with allergic rhinitis accounted for about 28% to 50%, recent data indicate that such patients can actively control rhinitis on the basis of tracheal inhaled corticosteroid treatment (such as oral non-sedating H1 Receptor blockers, nasal inhaled corticosteroids can significantly reduce the frequency of asthma attacks and reduce their symptoms, so active treatment of allergic rhinitis is valuable for the prevention of asthma and reduce its onset.

3, early diagnosis and treatment, control symptoms, prevent the development of the disease - tertiary prevention

(1) Early diagnosis and early treatment: Patients with symptoms that are not obvious or atypical (such as manifested as simple cough, paroxysmal chest tightness or shortness of breath after exercise) should be diagnosed early. The study shows that for patients with confirmed bronchial asthma, The earlier the use of airway anti-infective therapy (inhaled corticosteroids), the lower the damage to future lung function (including the recovery of lung function and the increase in children's lung function with age), and thus the vast majority of patients (except a few) Intermittent "outside", once diagnosed, anti-infective treatment is required. With the standardization of specific immunotherapy, it may become an effective measure for tertiary prevention in patients with allergic asthma.

(2) Do a good job in education management for asthma patients: Asthma is a chronic disease. There is no cure at all. However, effective prevention and treatment measures can promote normal life, work, study and strengthen the education and management of patients. Important, first, educate patients to understand the nature of asthma, the incentives, the signs of the attacks, the types and methods of medication, especially the long-term anti-inflammatory prophylactic treatment, and second, the education patients learn to use the micro-peak flow meter to monitor Your own condition, in order to use the drug in time when the condition changes.

China has gained good experience in implementing the global asthma prevention and control strategy, especially the establishment of the Asthma Home and the Asthma Club, which has strengthened the cooperation between doctors and patients, the frequency of asthma attacks, the rate of emergency and hospitalization, and medical expenses. Both are significantly reduced and will be further promoted throughout the country.

Bronchial complications Complications pulmonary edema

Concurrent bacterial infection, severe asthma can cause pulmonary edema.

Symptoms of bronchial asthma Common symptoms Breathing difficulty Exhalation sound prolongs chest tightness Coughing wheezing sound Dry cough foaming mucus Hair snoring Breathing sound weakening airway hyperresponsiveness

1, symptoms

Asthma manifests as paroxysmal cough, chest tightness and difficulty in breathing. Some patients have more cough than cerebral palsy. If there is no co-infection, it is often white, phlegm, and sometimes grainy or mucous column. The severity and duration of the individual vary greatly. The lighter has only a chest sensation, lasting for a few minutes, and the severe person is extremely dyspnea, lasting for several weeks or longer. The symptoms are characterized by reversibility, that is, after treatment. Relieve in a relatively short period of time, part of the natural relief, of course, a small part does not relieve and is in a continuous state, the attack often has certain predisposing factors, many patients have obvious biological laws, and the attack or aggravation occurs every day from 2 to 6 in the morning. Generally, it occurs in spring/summer handover or in winter. Some women (about 20%) have asthma attacks or exacerbations before or during menstruation. Pay attention to patients with atypical asthma. Some patients often have episodes of cough as the only symptom. Clinically, Often misdiagnosed as bronchitis; some adolescent patients with chest tightness during exercise, tightness is the only clinical manifestation.

2, signs

The sign is an exhalation wheezing, which occurs and disappears at the same time as breathing difficulties. Generally speaking, the higher the wheezing sound is, the finer it appears at the end of expiration, the more severe the asthma symptoms, and the lungs may have excessive inflation and signs such as barrels. Chest chest, percussion of unvoiced sound, weakened breath sounds, etc., respiratory assisted muscle and sternocleidomastoid muscle contraction increased, severe cases may have cyanosis, expiratory jugular vein engorgement, odd pulse, etc., some critically ill patients, severely restricted airflow The wheezing sound disappears, presenting a "silent lung."

Examination of bronchial asthma

Blood routine examination

There may be an increase in eosinophils at the time of onset, but most of them are not obvious. For example, concurrent infection may have an increase in the number of white blood cells and an increase in the proportion of classified neutrophils.

Sputum check

The smear showed more eosinophils under the microscope, and sharp-edged crystals (Charcort-Leyden crystals) formed by eosinophils, mucus plugs (Curschmann spirals) and transparent asthma beads (Laennec beads) were observed. For example, combined with respiratory bacterial infection, sputum smear Gram stain, cell culture and drug sensitivity test will help pathogen diagnosis and guidance treatment.

Respiratory function test

It is a very important test for the diagnosis of asthma. The main pathophysiological features of this disease are obstructive ventilatory disorders and increased airway resistance. The typical lung function changes were: reduced ventilation function, forced expiratory volume in the first second (FEV1), mid-maximal expiratory flow (MMFR), and maximum expiratory flow (V25, V50) at 25% and 50% of vital capacity; Uneven gas distribution; residual volume (RV), functional residual capacity (FRC), and total lung volume (TLC); severe lung capacity (VC) decreased. Several tests are often used clinically to assist in the diagnosis and differential diagnosis, including bronchial provocation test, bronchial dilation test, and peak expiratory flow rate (PEF).

Blood gas analysis

There may be hypoxia in severe asthma attacks, PaO2 and SaO2 are reduced, PaCO2 is decreased due to hyperventilation, and pH is increased, showing respiratory alkalosis. Such as severe asthma, the condition is further developed, airway obstruction is serious, there may be hypoxia and CO2 retention, PaCO2 rises, showing respiratory acidosis. If the lack of oxygen is obvious, metabolic acidosis can be combined.

Chest X-ray

In the early stage of asthma attack, the brightness of both lungs increased and it was over-inflated; there was no obvious abnormality during the remission period. 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.

Detection of specific allergens

Specific IgE can be measured by radioactive allergen adsorption test (RAST). Serum IgE in patients with allergic asthma can be 2-6 times higher than that of normal people. In the remission period, skin allergies can be used to judge related allergens, but allergic reactions should be prevented.

Diagnosis and diagnosis of bronchial asthma

Diagnostic criteria

In the guidelines for the prevention and treatment of bronchial asthma (definition, diagnosis, treatment, and education and management programs for bronchial asthma) developed by the Asthma Group of the Chinese Medical Association's Respiratory Diseases Society in 2008, the diagnostic criteria for asthma are:

1, repeated episodes of wheezing, shortness of breath, chest tightness or cough, and more related to contact with allergens, cold air, physical, chemical stimulation, viral upper respiratory tract infections, exercise and so on.

2, in the onset of the lungs can be heard and scattered or diffuse, with the exhalation-based wheezing sound, exhalation prolonged.

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

4, except for other diseases caused by wheezing, shortness of breath, chest tightness or cough.

5, atypical clinical symptoms (such as no significant wheezing or signs) should have at least one of the following test positive:

Positive bronchial provocation test or exercise test;

Positive bronchodilation test (FEV1 increased by more than 15%, and the absolute value of FEV1 increased by >200ml);

The PEF mutation rate of day and night is 20%.

Those who meet the above 1-4 or 4, 5 can be diagnosed with bronchial asthma. The above three test methods refer to the terms or related works respectively.

Staging and severity grading of bronchial asthma

According to clinical manifestations, bronchial asthma can be divided into acute attack period and remission period. An acute asthma attack refers to an episode of asthma between symptoms within 4 weeks. Remission period refers to treated or untreated symptoms, signs disappear, lung function returns to pre-existing levels, and maintained for more than 4 weeks.

The evaluation of the condition of asthma patients should be divided into two parts:

General evaluation of non-acute episodes: Many asthmatic patients do not have an acute attack at the time of the visit, but for a long period of time there are always different frequencies and/or different degrees of symptoms (wheezing, coughing, chest tightness), so The overall assessment of the condition is based on the frequency, severity, and need for medication and lung function for a period of time prior to the visit.

Severity evaluation of asthma exacerbation: Acute asthma attack refers to sudden onset or aggravation of symptoms such as shortness of breath, cough, chest tightness, and often difficulty breathing and wheezing, accompanied by decreased expiratory flow. A correct assessment of the severity of the condition is the basis for timely and effective treatment. Knowledge of severe asthma is the key to avoiding death from asthma.

Differential diagnosis

1. Breathing difficulty caused by left heart failure

In the past, it became a cardiogenic asthma with similar symptoms to asthma, but its pathogenesis and pathological nature are completely different from those of bronchial asthma. To avoid confusion, the term cardiac asthma is no longer used. Patients with high blood pressure, coronary heart disease, rheumatic heart disease, mitral stenosis and other medical history and signs. Paroxysmal cough, cough pink foam, double lungs can smell a wide range of wet rales and wheezing sounds, the left heart is enlarged, the heart rate is increased, and the apex can be heard and galloped. The condition is allowed to do a chest X-ray examination, which shows that the heart is enlarged and the pulmonary congestion sign helps to identify. If it is difficult to identify at one time, it can be inhaled 2 receptor agonist or intravenous aminophylline to relieve symptoms, further examination, avoid epinephrine or morphine drugs, if it is coronary heart disease, etc. instead of asthma, adrenaline can cause myocardial Hypoxia is further aggravated, exacerbating the condition, and morphine inhibits breathing, causing more severe breathing difficulties.

2. Chronic obstructive pulmonary disease (COPD)

More common in the elderly, with a history of chronic cough, wheezing for many years, there is a period of aggravation. Patients have a history of long-term smoking or exposure to harmful gases. There are signs of emphysema, both lungs or audible and wet rales. However, it is sometimes difficult to distinguish between COPD and asthma clinically. It may be helpful to use bronchodilators and oral or inhaled hormones for therapeutic trials because asthma patients respond well to hormones, while COPD patients are worse. At present, some scholars advocate that patients with COPD should be treated with hormone therapy. It should be noted that COPD can also be combined with asthma.

In addition, there is still a need for external airway diseases (such as benign and malignant tumors of the trachea, foreign bodies, etc.), pulmonary eosinophilia, allergic bronchopulmonary aspergillosis, tracheobronchomalacia, and recurrent multiple cartilage. Inflammation, allergic vasculitis and granulomatosis, allergic granulomatous vasculitis, endobronchial tuberculosis, etc.

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