The relationship between bronchial asthma (asthma) and chronic obstructive pulmonary disease (COPD) has been the subject of research and discussion in the respiratory community at home and abroad. As two different respiratory diseases, they share a common dysfunction – airflow limitation. Asthma is characterized by reversible airflow limitation, while COPD is characterized by only partially reversible or even completely irreversible airflow limitation. The following is an introduction to the similarities and differences between asthma and COPD. The American Thoracic Society/European Respiratory Society consensus definition of COPD is: COPD is a preventable and treatable airflow limitation disease, airflow obstruction is not completely irreversible, although COPD mainly affects lung function, but it also has obvious systemic consequences. In fact, airflow limitation is not completely reversible in some asthmatic patients. Therefore, it is sometimes not possible to distinguish asthma with incomplete reversible airflow obstruction from COPD patients. Asthma is a disease characterized by varying degrees of reversible airflow limitation, usually accompanied by airway hyperreactivity and clinically manifested by recurrent episodes of wheezing, shortness of breath, chest tightness and cough. COPD is a disease characterized by incomplete reversibility of airflow limitation, which is often progressive and associated with an abnormal inflammatory response of the lungs to noxious dust particles or gases, and is often, but not always, associated with airway hyperreactivity. hyperresponsiveness. Most patients who do not quit smoking have progressive disease. COPD is often associated with dyspnea, and chronic cough and sputum are present in patients with COPD. The modern view of COPD is that it is a chronic inflammatory disease of the lower respiratory tract. In the stable phase, the airway mucosa is infiltrated by mononuclear cells and the lumen is characterized by neutrophilic cells. Therefore, the airway inflammation of asthma and COPD are obviously different. Airway hyperresponsiveness (AHR): (1) Asthma: AHR can be present in young children, and severe AHR in early life is associated with reduced lung function in the future. Low expiratory volume in one second (FEV1) in childhood predicts more severe AHR in adulthood, showing the complex interaction between lung function and AHR, each of which has an independent effect on asthma. (2) COPD: It is well established that AHR can cause reduced lung function, that the presence of AHR precedes the onset of chronic airway symptoms and predicts an accelerated decline in lung function, and that there is a strong correlation between the severity of AHR and FEV1 levels. Smoking: (1) Asthma: Parental smoking, especially during pregnancy and the first few months of life, is a risk factor for the development of atopic asthma. Parental smoking is a risk factor for disease instability in children who already have asthma. Lung function declines more rapidly in asthmatics who smoke, and asthmatics who smoke frequently are more likely to develop emphysema than nonsmokers. (2) COPD: Low FEV1 in some COPD patients can be present in childhood or at a young age. Smoking in adolescents has an overall negative impact on lung function, while quitting smoking has a positive impact on lung growth. There is a dose correlation between the number of cigarettes smoked and the decline in lung function. In conclusion, epidemiological evidence demonstrates that AHR is an important predisposing factor for asthma and that those with AHR are more susceptible to environmental stimuli that increase the risk of developing obstructive airway disease. Tobacco exposure during pregnancy is a clear risk factor for asthma, and active smoking is an important risk factor for the development of COPD. the interaction of AHR and smoking leads to a more significant decrease in lung function. 3, Pathophysiology of asthma and COPD Inflammation: Asthma airway biopsy specimens show CD4+ lymphocytes, eosinophils, and alveolar macrophages as the predominant inflammatory cells . Airway inflammation in asthma primarily involves the bronchial tree, while the alveoli are rarely affected. However, inflammatory cells in COPD patients are mainly CD8+ lymphocytes and macrophages, and the sites of involvement include the bronchi, fine bronchi and alveoli. increased CD8+ cells are negatively correlated with FEV1. However, increased neutrophils in the lungs are also seen in some patients with severe asthma. Smoking increases sputum neutrophils in asthmatic patients. It is hypothesized that a distinct neutrophil-infiltrating type of asthma may be triggered and that smoking may convert asthma to an insensitive type to hormonal therapy. In turn, some COPD patients also have increased eosinophilia in the lungs, especially in acute exacerbations. These COPD patients respond better to hormone therapy than those without eosinophilia. Airway remodeling: Bronchial mucosal epithelial disruption and detachment are common in asthma, and healing or abnormal repair can cause airway remodeling. In contrast, COPD patients rarely have epithelial shedding of the airway mucosal surface, but often have squamous metaplasia. Thickening of the basement membrane of the airway epithelium is a consistent change in all forms of asthma, whereas it is not commonly seen in COPD. Cytokine infiltration: Tissue inflammation dominated by T helper 2 (Th-2) plays a major role in the pathogenesis of asthma, with increased levels of IL-4, IL-5, IL-9, and IL-13 in the asthmatic airways. In contrast, Th-1-dominant responses, including increased production of interferon γ (IFN- γ ) by CD8+ cells, are present in COPD patients. (1) Bronchial asthma: The clinical features are recurrent episodes of wheezing, shortness of breath, chest tightness and cough. The attacks can be relieved by themselves or by treatment, and the symptoms have a pattern of biorhythmic fluctuations, often occurring at night or early in the morning and worsening. The triggers of attacks are mostly related to exposure to allergens, respiratory infections, physical and chemical stimuli and strenuous exercise. The most typical characteristics of asthma are the high reactivity of airways to various stimuli and the periodicity or episodes of airflow restriction. (2) COPD: Like asthma patients, exercise can cause coughing and wheezing and suffocating symptoms, but COPD patients mostly have these symptoms after exercise or exertion, and rarely have dyspnea at rest. A significant number of patients have chronic bronchitis as the cause and a long history of chronic cough and sputum. Long-term smoking is the primary risk factor for the development of COPD, and winter is often the season when clinical symptoms worsen. The main point of differentiation between the two is the reversibility of the airway. Both asthma and COPD can have airflow limitation, which is manifested as a decrease in FEV1, but the improvement rate of FEV1 in asthma patients is often greater than 12% after inhalation of bronchodilators, which means that the bronchodilator test is positive. COPD is associated with impaired small airway function and decreased diffusion function, and in severe cases, combined with chronic hypoxemia. The main bronchodilators are β2 agonists, anticholinergics and methylxanthines. Bronchodilators increase FEV1 significantly in asthma patients than in COPD, and most of them increase FVC and FEV1 at the same time, while COPD often increases FVC. dynamic hyperinflation of the lungs due to exercise in COPD and asthma patients plays a major role in dyspnea and exercise tolerance, and bronchodilators can reduce dynamic hyperinflation of the lungs. Regular inhalation of bronchodilators in patients with asthma has no benefit, whereas regular administration of bronchodilators in patients with COPD improves lung function and dyspnea, but not exercise capacity. Inhaled long-acting β2 agonists (LABAs) should be used in combination with anti-inflammatory control medications in asthma, while long-acting bronchodilators can be used regularly as single agents or in combination for better symptom control in patients with COPD. Theophylline is effective in both asthma and COPD and can be used as an adjunct to β2 agonists and ICSs. Low doses have both anti-inflammatory and immunomodulatory effects in COPD and asthma. Phosphodiesterase inhibitors inhibit many of the inflammatory and immune cell activities involved in the pathogenesis of asthma and COPD, consistent with the anti-inflammatory effects of ICSs. Late-onset phase asthma has decreased responsiveness to bronchodilators, also bronchodilators, and asthmatics respond better to β2 agonists, whereas COPD responds better to cholinergic antagonists. Anticholinergics had a longer duration of action for COPD than short-acting β2 agonists (SABAs) drugs, increased FEV1 improvement with increased doses of anticholinergics, and long-acting anticholinergics improved dyspnea and improved exercise tolerance and quality of life better than short-acting anticholinergics and salmeterol. In conclusion, there is a significant overlap in bronchodilator responsiveness in patients with asthma and COPD. Treatment of asthma is characterized by suppression of inflammation, and treatment of COPD is characterized by symptom relief. Combining ICSs and LABAs or leukotriene modulators has important benefits for asthma, and combining multiple bronchodilators is effective for symptom relief in COPD. ICSs are the most effective long-term control of chronic inflammation in the asthma airway, reducing asthma symptoms, improving lung function, reducing airway hyperresponsiveness, reducing acute exacerbations, and preventing airway remodeling.LABAs in combination with ICSs are more effective than higher doses of ICSs. Most studies have shown that the use of ICSs in COPD patients reduces the frequency and extent of exacerbations and improves quality of life, but does not alter the long-term decline in FEV1. COPD patients who respond significantly to bronchodilators respond to inhaled glucocorticoids regardless of their clinical presentation or functional parameters. COPD patients who do not respond well to bronchodilators before treatment have little cytological or clinical response to oral or inhaled steroids, or at least the rate of FEV1 reduction and the main clinical indicators do not change much. Long-term regular inhaled glucocorticoids should be applied to COPD of grade III or above, and there are often recurrent clinical exacerbations. 7. Acute exacerbation of asthma and COPD Many factors can lead to acute exacerbation of asthma. In some patients, acute exacerbations are often accompanied by viral respiratory infections. Respiratory viruses can cause lymphocyte and eosinophil infiltration of the bronchial mucosa, which is more persistent in patients with asthma and is accompanied by bronchial hyperresponsiveness. Allergens, sensitizers, and medications can cause acute exacerbations of asthma, which can sometimes be very severe. The most common etiologies of acute exacerbations of COPD are bacterial and viral infections, and some patients have acute exacerbations of unknown origin. In addition to air pollution, certain diseases are more closely related to COPD and may also cause acute exacerbations of COPD, such as pulmonary hypertension and heart failure, airway embolism due to large amounts of mucus, pneumothorax p respiratory muscle fatigue, and thrombosis.