1.What is pulmonary fibrosis? Pulmonary fibrosis is not a separate disease, but a general term for a large group of diseases that are classified as interstitial lung diseases and are the end result of a variety of lung diseases. The end result is simply the replacement of normal lung tissue by an overgrowth of fibrous tissue and the loss of proper function. 2. How does pulmonary fibrosis occur? First, we need to know the structure and function of the lung. The lung is composed of the lung parenchyma (bronchi + alveolar structures at all levels) and the interstitium (supporting tissues other than the alveoli and terminal airways, including blood vessels and lymphatics). The normal lung achieves its function through the exchange of gases between the alveoli and the pulmonary capillaries, through which oxygen inhaled by the body is passed to the capillaries and carbon dioxide from the capillaries is exhaled out of the body. When various pathogens and physical and chemical stimuli occur, they activate the repair mechanisms of the lung, such as the new coronavirus infection, which colonizes the epithelial cells, endothelial cells and smooth muscle cells of the respiratory organs and damages the host cells, leading to alveolitis, and the damaged lung tissue releases inflammatory mediators, such as interleukins, prostaglandins and epidermal growth factor, which recruit platelets and leukocytes to support them. Leukocytes remove pathogens as well as necrotic cells from the injury site, and platelets aggregate to repair the injury site. The fibroblasts in the mesenchyme are transformed into fibroblasts, which proliferate in large numbers through mitosis and begin to synthesize and secrete large amounts of collagen fibers and matrix components to fill the wound tissue defects, creating the basis for tissue cell division and regeneration to cover the injury. On the fibrous mesh scaffold, new tissue cells continue to divide and grow and move across the fibrous mesh scaffold to regenerate the damaged tissue. When this process is completed, the fibroblasts and extracellular matrix gradually fade away, leaving only normal tissue, and the repair of the injury is complete. When the disease is more severe, pathogenic stimuli persist, or there are abnormalities in the repair of the damage, lung tissue cells are necrotic alveolar structure is severely damaged, alveolar epithelium is shed, alveolar capillaries dilate, inflammatory cells infiltrate in large numbers, and alveolar walls widen. Subsequently, type II alveolar epithelial cells and fibroblasts are continuously active and extracellular matrix is deposited. When this continues, it will lead to severe fibrosis of the interstitial lung, thickening of the alveolar-capillary space, and destruction of the alveolar structure, making it impossible to restore normal function. This is the process of pulmonary fibrosis. 3, the impact of pulmonary fibrosis on patients with new coronary pneumonia For for the proportion of the majority of mild, common type of patients, the probability of pulmonary fibrosis is very small or the impact of the lesions on life can be almost negligible; while for patients with severe critical illness, in the recovery process may remain pulmonary fibrosis, after pulmonary fibrosis may be in a period of time or even a lifetime leading to a decline in lung function, that is, labor capacity as well as Exercise tolerance will be reduced.