Asthma is a chronic inflammatory disease of the airways in which inflammatory cells include eosinophils, mast cells, T lymphocytes, and neutrophils. Chronic inflammation causes increased airway reactivity, reversible airflow limitation, episodes of wheezing, chest tightness, and cough; symptoms may resolve spontaneously or with treatment; long-term recurrent episodes produce irreversible airway narrowing (remodeling). Prevalence: 160 million patients worldwide; prevalent in developed countries and cities; 1%-3% prevalence in China; high prevalence in children; equal prevalence in men and women; 40% of patients have a family history. Etiology: genetic factors: airway response, IgE regulation-related genes play an important role; environmental factors: 1, inhalants (dust mites, pollen, fungi, sulfur dioxide, ammonia); 2, infections (bacteria, protozoa, parasites, etc.); 3, food (fish, shrimp, crab, eggs, milk, etc.); 4, drugs (propranolol, aspirin, etc.); 5, climate change, exercise and pregnancy, etc. Pathogenesis: (1) Immunological mechanisms (humoral and cellular immunity): rapid response: antigen inhalation of the respiratory tract activates Th2 lymphocytes to release interleukin-4, 5, 10, 13, activates B cells, promotes immunoglobulin E (IgE) production and adheres to mast cells and basophils. Re-inhalation of antigen binds to IgE, causing Ca++ to enter mast cells, causing release of histamine, etc., and spasm of bronchial smooth muscle; delayed reaction: several hours later inflammatory cells (macrophages, eosinophils and neutrophils) infiltrate the bronchial wall, releasing leukotrienes (LTS), prostaglandins (PGS), thromboxane (TX) and platelet-activating factor (PAF), leading to microvascular (2) Airway inflammation: chronic airway inflammation is the essence of asthma; Th2 lymphocytes secrete cytokines that activate mast cells and eosinophils, releasing histamine, prostaglandins, leukotrienes, platelet-activating factors, and eosinophil chemokines; airway epithelial cells secrete endothelin, and transfer growth factor (TGF-b) causes fibroblasts and smooth muscle. ) leading to fibroblast and smooth muscle cell proliferation; endothelial and epithelial cells produce adhesion molecules, leukocyte adhesion, transfer to the site of inflammation. (3) Airway hyperresponsiveness: Airway hyperresponsiveness is a pathophysiological feature of asthma (excessive or premature airway contraction in response to various stimuli); airway inflammation is an important mechanism leading to airway hyperresponsiveness. (4) Neural mechanisms: β-adrenergic receptor hypofunction and vagal tone hyperactivity; increased α-adrenergic neuroresponsiveness; airway epithelial damage with exposed sensory nerve endings. Non-adrenergic non-cholinergic nerves release smooth muscle contractile substances (substance P, neurokinin). Pathology: swollen lungs, bronchi containing mucus and mucus plugs, thickened walls, swollen and congested mucosa; microscopy: bronchial colloid formation, smooth muscle hypertrophy, mucosal edema, epithelial detachment, thickened basement membranes, infiltration of eosinophils, neutrophils and lymphocytes in the walls of the tubes. Clinical manifestations: 1. Symptoms: croup, expiratory dyspnea, cough, forced sitting, cyanosis after exposure to allergens, infections, drugs, occupational dust, fumes, cold air inhalation and exercise. 2. Signs: The thorax is in an inspiratory position during the attack, with extensive croup during the expiratory phase. Dry and wet rales may coexist with co-infection. In severe disease, odd pulse may be present; in severe attacks, croup is reduced due to debilitation and sputum bolus instead. (2) Pulmonary respiratory function tests: FEV1, FEV1/FVC, MMEF and PEFR are reduced and may recover in remission; bronchial excitation test: FEV1 decrease >20% after inhalation of small doses of histamine or acetylcholine is positive; bronchodilator test: FEV1 increase >15% after inhalation of bronchodilator is positive. >15% positive. (3) Arterial blood gas: PaO2 and PaCO2 decrease and PH value increases (respiratory alkalosis). PaCO2 rises with airway obstruction (respiratory acidosis). (4) X-rays: both lung translucency . Pulmonary atelectasis, pneumothorax or mediastinal emphysema. (5) Specific allergen detection: in vitro detection of specific IgE; skin allergen testing (scratch, intradermal test for suspected allergens). Diagnostic criteria: allergens, cold air, physical and chemical stimuli, upper respiratory tract infection or shortness of breath or cough after exercise; remission by self or treatment; diffuse expiratory phase dominant croup in both lungs; positive bronchial excitation test, exercise test, bronchodilator test; diurnal variability ([highest PEF – lowest PEF]/highest PEF´100%) ≥ 20%. Asthma attack severity grading: can be classified as mild; moderate; severe and critical. Asthma severity grading: intermittent attacks; mild persistent; moderate persistent and severe persistent. Differential diagnosis: cardiogenic asthma: hypertension, coronary artery disease and wind heart disease causing left heart failure, coughing pink sputum, blistering sounds and croup in both lungs, gallop rhythm, X-ray showing enlarged heart, pulmonary depression, diagnostic treatment with β2 agonists, avoid epinephrine or morphine until clear; asthmatic slow-onset branch: common in middle-aged and elderly, history of chronic cough, long years of wheezing; upper airway obstruction: hoarseness, inspiratory depression, croup during inspiration. Lung cancer: limited bronchial stenosis, progressive worsening of dyspnea and wheezing, sputum blood, clear sputum exfoliative cells, chest radiograph, CT, MRI or bronchoscopy; metaplastic reactive pulmonary infiltrates, pulmonary aspergillosis. Complications: pneumothorax, mediastinal pneumothorax; pulmonary atelectasis; chronic bronchitis; emphysema; chronic pulmonary origin heart disease. Treatment: Detachment from allergens; elimination of etiology; avoidance of allergens and nonspecific stimuli. Drug therapy (1) Bronchodilators: ① β2 agonists increase intracellular cyclic adenosine monophosphate (cAMP). Short-acting – salbutamol, terbutaline; long-acting – formoterol, salmeterol. Can be quantified aerosol, dry powder inhalation, oral or intravenous. ②Anti-cholinergics: ipratropium bromide, blocking postganglionic vagal pathway, diastolic bronchus, reducing sputum secretion. ③Theophyllines: inhibit phosphodiesterase, increase cAMP concentration in smooth muscle cells, antagonize adenosine receptors, stimulate secretion of adrenaline, and enhance respiratory muscle contraction. Plasma theophylline concentration (safe concentration 6-15mg/l). (2) Control airway inflammation ①Glucocorticoids: inhibit inflammatory cell migration and activation, cytokine production, inflammatory mediator release. Commonly used are beclomethasone, budesonide, fluticasone inhalation. Intravenous methylprednisolone 80-160mg/d with an onset of action of 2-4 hours. Cortical function suppression and osteoporosis may occur with long-term use. (ii) Leukotriene receptor antagonist (montelukast): diastole bronchial smooth muscle. (③Histamine H1 receptor antagonists – loratadine, ketotilol, etc.