Bronchial asthma, referred to as asthma, is a chronic inflammatory disease of the airways involving a variety of cells such as eosinophils, mast cells, airway epithelial cells and cell components. It is characterized by airway allergic inflammation and airway hyperresponsiveness. It often presents with varying degrees of reversible airway obstruction symptoms, such as recurring wheezing, shortness of breath, chest tightness or coughing. It is generally believed that the prevalence is higher in children than in young adults. About 40% of patients have a family history. This disease belongs to the category of "wheezing syndrome" in traditional Chinese medicine.

Cause and pathogenesis

1. Causes The causes of asthma are not well understood. Asthma attacks are influenced by both genetic factors and environmental factors. In terms of genetics, it may be related to polygenic inheritance; the patient's individual allergic constitution and environmental influences are often high-risk factors.

Environmental factors are mainly some allergens, biological allergens such as dust mites, pollen, animal dander, bacteria, viruses, protozoa, some allergenic substances released by some plants, some Food ingredients, etc., non-biological allergens such as certain drugs and certain organic compounds. Climate change, exercise, etc. can trigger asthma attacks.

2． Pathogenesis The pathogenesis of asthma is not fully understood. It is currently believed that asthma attacks are related to allergies, airway inflammation, airway hyperresponsiveness, neurological factors, etc.

(1) Immunological mechanism: Both humoral immunity and cellular immunity are involved in the occurrence process. Antigen activates T cells through antigen-presenting cells. The sensitized T cells (mainly Th2 cells) release cytokines such as interleukin (IL). Some IL reactivates B cells, causing the B cells to synthesize and secrete specific IgE. This IgE-like binds to IgE receptors expressed on mast cells and basophils. If the body enters the same antigen again, the antigen will couple with the IgE that binds to the cell expression, causing the corresponding cells to release a variety of inflammatory mediators such as platelet activating factor, causing increased vascular permeability, inflammatory cell infiltration, bronchial mucosa Edema, increased glandular secretion, etc., produce asthma symptoms.

(2) Airway inflammation: Inflammatory stimulation causes certain cells such as Th2 cells to produce cytokines. These cytokines further activate macrophages, mast cells, basophils, etc., causing these cells to Then a large amount of cytokines are released, aggravating tissue damage. In addition, cytokines and environmental factors cause airway epithelial cells to secrete endothelin-1, which causes the proliferation of fibroblasts and smooth muscle cells under the airway mucosal epithelium, causing airway remodeling; adhesion molecules produced by vascular endothelial cells and airway epithelial cells It causes leukocytes to adhere to vascular endothelial cells, promotes leukocytes to enter the inflammatory site, and aggravates the airway inflammation process.

(3) Airway hyperresponsiveness: Under the action of antigens or other stimuli, the released cytokines damage airway epithelial cells, exposing subepithelial nerve endings, resulting in airway hyperresponsiveness.

(4) Nervous mechanism: The bronchi are innervated by autonomic nerves, including cholinergic nerves, adrenergic nerves, non-cholinergic non-adrenergic nerves, etc. The occurrence of bronchial asthma is often characterized by hypofunction of β-adrenergic receptors, hyperfunction of the vagus nerve, and neurotransmitters released by non-cholinergic and non-adrenergic nerves that relax bronchial smooth muscle, such as nitric oxide, and neurotransmitters that contract bronchial smooth muscle. The balance of substances such as neurokinins is imbalanced, causing bronchial smooth muscle contraction.

Pathological naked eye observation shows high alveolar expansion, emphysema, and thick sputum and mucus plugs in the bronchi, bronchial branches, and terminal bronchioles. Histological examination showed bronchial wall thickening, mucosal and submucosal vascular proliferation, infiltration of eosinophils, lymphocytes, and neutrophils, ciliated epithelial cell shedding, goblet cell proliferation, and increased bronchial secretions. If asthma relapses for a long time, bronchial smooth muscle hypertrophy, epithelial cell basement membrane thickening, lung tissue remodeling, and the loss of the supporting role of the surrounding lung tissue in the airways may occur.

Clinical manifestations

1. Symptoms include paroxysmal expiratory dyspnea, often accompanied by wheezing, and in severe cases, orthopnea may occur.

There may be symptoms such as coughing, sputum production, and profuse sweating, and even neurological manifestations such as irritability and confusion. It can last from minutes to hours to days. It may be relieved on its own or with bronchodilators. A characteristic feature of an asthma attack is that it starts or worsens at night or in the early hours of the morning.

2． There were no special changes in physical examination during the non-ictal period. During the attack, the chest is hyperinflated, with prolonged expiration and widespread wheezing. When asthma symptoms are mild or severe, wheezing may not be heard.

Severe cases may have cyanosis, increased heart rate, abnormal pulse, and abnormal breathing in the chest and abdomen.

Complications may occur with atelectasis, pneumothorax, mediastinal emphysema, etc. Long-term repeated attacks and infections can be complicated by chronic bronchitis, emphysema, pulmonary heart disease, etc.