What is bronchial asthma? What are the causes and manifestations?

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 cellular components. Characterized by airway allergic inflammation, airway hyperresponsiveness. It is often characterized by different degrees of reversible airway obstruction symptoms, such as recurrent episodes of wheezing, shortness of breath, chest tightness or cough. The prevalence is mostly thought to be higher in children than in young adults. About 40% of patients have family history. This disease belongs to the category of "croup" in traditional Chinese medicine.

Aetiology and pathogenesis

1. The etiology of asthma is still not very clear. Asthma attacks are influenced by both genetic and environmental factors. Genetic aspects may be related to polygenic inheritance; patients with individual allergic body and environmental influences are often its high-risk factors.

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

2. The pathogenesis of asthma is not completely clear. It is currently believed that asthma attacks are related to allergic reactions, airway inflammation, airway hyperresponsiveness, and neurological factors.

(1) Immunological mechanisms: both humoral and cellular immunity are involved in the process. Antigen activates T cells through antigen-presenting cells, sensitized T cells (mainly Th2 cells) release cytokines such as interleukin (IL), and some of the IL activates B cells, which synthesize and secrete specific IgE, which binds to the IgE receptor expressed by mast cells and basophils. If the body re-enters the same kind of antigen, the antigen and the IgE bound to the cell expression of the coupling, so that the corresponding cells release a variety of inflammatory mediators such as platelet-activating factor, causing increased vascular permeability, inflammatory cell infiltration, bronchial mucosal edema, increased secretion of the glands, and so on, resulting in asthma symptoms.

(2) Airway inflammation: Inflammation stimulation, so that certain cells such as Th2 cells to produce cytokines, these cytokines further activate macrophages, mast cells, basophils, etc., so that these cells and then release a large number of cytokines, aggravate the damage to the tissue. In addition, cytokines and environmental factors make airway epithelial cells secrete endothelin-1 and other fibroblasts and smooth muscle cells under the epithelium of the airway mucosa to proliferate, causing airway remodeling; adhesion molecules produced by vascular endothelial cells and airway epithelial cells cause leukocytes to adhere to vascular endothelial cells and promote leukocytes to enter the site of inflammation and aggravate the inflammatory process in the airway.

(3) Airway hyperreactivity: cytokines and other cytokines released under the action of antigens or other stimuli damage the airway epithelial cells, exposing the subepithelial nerve endings and causing the airway to show hyperreactivity.

(4) Nervous mechanism: the bronchial tubes are innervated by autonomic nerves, including cholinergic nerves, adrenergic nerves, and non-cholinergic non-adrenergic nerves. The occurrence of bronchial asthma is often manifested as β-adrenergic receptor hypofunction, vagal hyperfunction, and non-cholinergic non-adrenergic nerves release of diastolic bronchial smooth muscle neurotransmitters such as nitric oxide and contraction of bronchial smooth muscle neurotransmitters such as neurokinin balance is imbalanced, resulting in the contraction of bronchial smooth muscle.

Pathologic visual observation reveals highly distended alveoli, emphysema, and viscous sputum and mucus plugs in the bronchi, bronchial branches, and terminal fine bronchi. Histologic examination shows thickening of the bronchial wall, hyperplasia of the mucosa and submucosal blood vessels, infiltration of eosinophils, lymphocytes and neutrophils, shedding of ciliated epithelial cells, proliferation of cup cells, and increased bronchial secretions. If asthma long-term recurrent episodes, there can be bronchial smooth muscle hypertrophy, epithelial cell basement membrane thickening, lung tissue remodeling, the surrounding lung tissue to the airway support disappeared.

Clinical manifestations

1. Symptomatic episodes of expiratory dyspnea, often accompanied by rales, and in severe cases, sitting breathing.

Cough, sputum, sweat and other symptoms, and even irritability, confusion and other neurological manifestations. It lasts for minutes, hours, days. It can be relieved on its own or with bronchodilators. A characteristic feature of asthma attacks is an attack or exacerbation at night or in the early hours of the morning.

2. SignsThere are no specific changes on physical examination during non-exacerbation period. During an attack the chest is hyperinflated with prolonged expiration and widespread rales. When asthma symptoms are not severe or severe, the rales may not be heard. In severe cases, there may be cyanosis, increased heart rate, odd pulse, and paradoxical chest and abdominal breathing.

ComplicationsAn attack may be complicated by pulmonary atelectasis, pneumothorax, and mediastinal emphysema. Long-term recurrent episodes and infections can complicate chronic bronchitis, emphysema, and pulmonary heart disease.