What Is Pulmonary Interstitial Emphysema?

Interstitial lung disease (ILD) is based on diffuse pulmonary parenchyma, alveolar inflammation, and interstitial fibrosis as basic pathological changes, with active dyspnea, diffuse infiltration shadows on chest radiographs, restrictive ventilation disorders, and diffuse (DLCO Reduced function and hypoxemia are the general term for clinical-pathological entities composed of different disease groups with clinical manifestations.

Interstitial lung disease

Interstitial lung disease (ILD) is based on diffuse pulmonary parenchyma, alveolar inflammation, and interstitial fibrosis as basic pathological changes, with active dyspnea, diffuse infiltration shadows on chest radiographs, restrictive ventilation disorder, and diffuse Reduced function and hypoxemia are the general term for clinical-pathological entities composed of different disease groups with clinical manifestations.

ILD is usually not malignant and is not caused by a known infectious pathogen. Although the disease has an acute phase, the onset is often insidious and the course of the disease develops chronically. The body initially responds to the lungs and the alveolar wall as an inflammatory reaction, leading to alveolitis, and eventually the inflammation will spread to the adjacent stroma. Interstitial fibrosis will eventually occur in some parts and blood vessels, leading to scarring and destruction of lung tissue, reducing ventilatory function, and inflammation can also affect trachea and capillary bronchi, often with organizing pneumonia, which is also a manifestation of interstitial pneumonia . This group of diseases has many common characteristics, including similar symptoms, X-ray signs, and pulmonary function tests. Mucus and thick sputum may be accompanied by secondary infections, with systemic symptoms such as weight loss, fatigue, anorexia, and joint pain in the extremities, and fever in the acute phase.

Chinese Medicine Name

Interstitial lung disease

Other name

Interstitial lung disease

Affiliated Department

Internal Medicine-General Medicine

Disease site

Lungs

Contagious

Non-contagious

Whether to enter health insurance

Yes

Onset stage

The exact pathogenesis of ILD has not been fully elucidated. It is assumed that the evolution of ILD can be divided into three phases, namely the initiation phase, the progress phase, and the ending phase.

Startup phase

The pathogenic factors that initiate ILD are usually toxins and / or antigens. Known antigen inhalation such as inorganic dust is associated with asbestos and pneumoconiosis, organic dust is associated with exogenous allergic alveolitis, etc., and idiopathic pulmonary fibrosis Specific antigens such as (IPF) and sarcoidosis are unknown.

Progress stage

Once exposed and exposed to the original pathogenic factors, a complex inflammatory process-alveolitis, is the central link in the pathogenesis of ILD. The nature of alveolitis determines the type of lung injury, the degree of repair, and the formation of fibrosis. Inflammatory and immune cell activation not only releases toxic substances such as oxygen free radicals, directly damages type I alveolar epithelial cells and capillary endothelial cells, but also releases proteases and other direct damage to interstitial tissue, collagen tissue and basement membrane. Simultaneous release of various inflammatory mediators, including monokines, interleukin-1 (IL-1), interleukin-8 (IL-8), interleukin-2 (IL-2), platelet-derived growth factor (platelet-derived growth factor (PDGF)), fibronectin (FN), insulin-like growth factor (IGF-1), mesenchymal growth factor (MGF), transformation Transforming growth factor (TGF-) and -interferon (INF-), etc. According to research, antioxidant enzymes, IL-1, IL-6 in bronchoalveolar lavage of pneumoconiosis , Tumor necrosis factor (TNF), TGF and FN increased significantly, and its lipid peroxidation increased, indicating that the occurrence and development of pneumoconiosis is related to oxidative stress and up-regulation of cytokines and growth mediators. The biological activities and roles of these cytokines in the pathogenesis of ILD have not been fully elucidated, but their secondary and / or feedback effects on inflammatory and immune cells play a regulatory role in amplifying and weakening the alveolar inflammatory response. If the alveolitis is self-limiting, or if the lesions are mild and effectively treated before the lung parenchyma is severely damaged, the alveolitis can be controlled, the structure of the alveoli and small airways can be reconstructed and restored to normal, and lung function is protected from further damage and recovery .

Ending stage

It was found that cell adhesion protein (tenascin) is expressed in newly damaged areas, including intraluminal and loose fiber vesicles, and is distributed within or below regenerated type II alveolar cells. Myofibroblast cell adhesion protein mRNA expression It is stronger than type II alveolar cells, and also has weak cytoadhesin mRNA expression in metaplastic bronchial epithelium and alveolar macrophages, indicating that cytoadhesin is actively synthesized in early cellulosic damage, and myofibroblasts cause cellulose An important source of synthesis.

If the inflammation is extensive and the damage is severe, fibroblasts accumulate and proliferate in the alveolar wall, collagen tissues proliferate, repair disorders and deposits, the alveolar wall thickens, scars and fibrosis are formed, and this damaged alveolar wall will be difficult to repair and recover.

This hypothetical process of "causative agent-alveolar inflammation-fibrosis" is also similar to the pathogenesis of emphysema, acute lung injury, or ARDS, but it is still unclear exactly what fundamental factors determine the final outcome of a causative factor STD Orientation.

Signs: Shortness of breath, cyanosis, Velcro snoring (continuous, high-pitched popping sounds) can be heard in the middle and lower lungs, with clubbing fingers, of which Velcro snoring is the most characteristic.

Classification: The classification of interstitial lung disease is not unified, and can be divided into acute, subacute and chronic according to the severity of the disease.

(1) Classified by pathological changes:

Non-inflammatory and non-tumor diseases: such as sarcoidosis and exogenous allergic granulomatous alveolitis.

Granulomatous interstitial lung disease: such as chronic interstitial pulmonary edema, alveolar proteinosis, primary pulmonary hemoxanthinosis, uremia and so on.

Pulmonary-specific inflammation: such as common interstitial pneumonia, occlusive bronchiolitis and organizing pneumonia (BOOP), exogenous irritating smoke, fluid, and other toxic irritating chronic interstitial pneumonia, acute respiratory distress Syndrome (ARDS), idiopathic pulmonary fibrosis, and pulmonary vasculitis.

Inorganic dust inhalation occupational disease.

Hyperplasia and neoplastic lesions: such as primary bronchioalveolar carcinoma induced interstitial lung lesions, diffuse Hodgkin's lymphoma.

Pulmonary interstitial fibrosis and honeycomb lung (end stage lung).

(2) Classified according to the type of cells accumulated in the alveolar structure:

Macrophage-lymphocyte-neutrophil type: neutrophil-type alveolitis for short. Macrophages still account for the majority, but neutrophils increase, and they accumulate in the alveolar structure for a long time, which is the most typical feature of this type. Diseases belonging to this type are: idiopathic pulmonary fibrosis (cryptogenic fibrosing alveolitis), familial pulmonary fibrosis, chronic interstitial pulmonary fibrosis associated with collagen vascular diseases, histiocytosis X and asbestos lung.

Macrophage lymphocyte type: referred to as lymphocytic alveolitis. Both macrophages and lymphocytes increased, but lymphocytes increased relatively more than macrophages. Neutrophils do not increase. Sarcoidosis, allergic pneumonia, and beryllium poisoning all belong to this type. Acute alveolitis occurs in the lung parenchymal cells by the direct action of a pathogenic factor, or by the indirect effects of inflammation and the immune cell system. During the period of alveolitis, if the cause is removed or treated, the lesions can be reversed; when acute alveolitis becomes chronic, neutrophils secrete collagenase and elastase, destroying type I collagen and alveolar walls, and affect the reversibility of the lesion. If the disease develops further, the collagen fibers in the interstitial tissue are disordered, and a large amount of fibrous tissue is seen on the microscopy, the alveolar septum is destroyed, and cystic fibrosis is formed. The damaged alveolar wall cannot be restored; the lesion further develops into complete damage to the alveolar structure, forming extensive cystic fibrosis.

The term Interstitial lung Disease (ILD) was coined as early as the 18th Aspen Pulmonary Symposium in 1975. After 10 years (1985), the 28th Aspen Pulmonary Symposium discussed ILD again. Although the research on ILD has made great progress in the past ten years, there are still different understandings of its concept and classification, especially the idiopathic pulmonary interstitial fibrosis in ILD (also known as The classification of idiopathic interstitial pneumonia and idiopathic fibrotic alveolitis has been controversial, and no consensus has been reached.

ILD is a group of diseases caused by the alveolar wall as the main lesion. Diffuse pulmonary parenchyma, alveolitis, and interstitial fibrosis are the basic pathological changes. Active dyspnea, X-ray chest X-rays show diffuse shadows, and restrictions. Sexually ventilated disorder, reduced diffusive function (DLCO) and hypoxemia are the general term for the clinicopathological entities composed of different disease groups with clinical manifestations. ILD can be acute, subacute, and chronic. In the acute phase, lesions or inflammatory lesions are the main, and in the chronic phase, fibrotic lesions are the main. The lung parenchyma refers to the bronchial and alveolar structures at all levels. Pulmonary interstitial refers to supporting tissues other than the alveolar and terminal bronchial epithelium, including blood vessel and lymphatic tissue. The normal interstitial lung mainly includes two components: cells and extracellular matrix. Cell components account for 75% of the lung interstitial, of which 30% to 40% are mesenchymal cells; the rest are inflammatory cells and immune-active cells.

Mesenchymal cells include: fibroblasts, smooth muscle cells, and perivascular cells. Inflammatory cells and immune cells include: monocyte macrophages (about 90%) and lymphocytes (about 10%), and a small amount of mast cells. Lymphocytes are mainly T lymphocytes (about 3/4 of the lymphocytes),

A small number of lungs (7% to 8%) are B cells, and the rest are non-T and non-B ineffective cells (about 20%). These inflammatory cells, especially monocytes, can produce many chemical mediators or cytokines. It plays a major role in the pathogenesis of inflammatory lesions of the lung. The extracellular matrix includes extracellular matrix and connective tissue fiber components. The latter is mainly collagen fibers (about 70%), followed by elastic fibers; the former is mainly the basement membrane, some other glycoproteins, laminin, fibronectin, and other matrix proteins or glycoproteins. The space between adjacent alveoli is called the interstitial membrane, and there are capillaries and lymphatic vessels in the cavity. There are endothelial cells on the surface of the pulmonary capillary wall, and the basement membrane is underneath. The connections between the endothelial cells are loose, and there are wide and uneven gaps in the adjacent areas, with an average of 4-5 nm. Inside the plastid cavity. Capillaries are closely attached to the alveolar wall in the interstitial cavity. One side is a thin interstitial cavity to ensure high ventilation efficiency of blood and gas; the other is a thick layer cavity for interstitial fluid storage and blood vessels- Interstitial cavity-regulation of fluid movement between alveoli. The terminal lymph nodes distributed in the interstitial cavity can reach the space of the pulmonary capillary network around the alveoli, attract the water and protein in the interstitial cavity, maintain the water storage in the interstitial cavity, and prevent the interstitial and even alveolar edema. When lung interstitial lesions occur, the number and nature of the above components will change-the activation and participation of inflammatory cells, the destruction of tissue structures, the increase of fibroblasts, the deposition and repair of collagen fibers, etc., together form the tissue of ILD Pathological characteristics. It should be noted that the infiltration of inflammation and the repair of fibers are by no means limited to the interstitial, but can also be seen in the alveoli, alveolar ducts, respiratory and terminal bronchioles.

Celery bream carp: 250 grams of carp, 50 grams of fresh celery, starch, ginger, garlic, soy sauce, sugar, vinegar, refined salt, monosodium glutamate, rice wine, sour pepper, vegetable oil. Cut the carp into shreds, cut the celery into sections, and mix the soy sauce, sugar, vinegar, monosodium glutamate, rice wine, salt, and starch into the soup. Set the wok on the high heat, heat the oil to 50% heat, let the mermaid shred, loosen the remaining oil, put the ginger and sour pepper. Stir-fry the celery section, then cook in the tartar sauce, put in the bright oil, and bring it to the pan. Carp has the effects of clearing heat and detoxifying, diuretic and swelling, cough and lowering qi; celery has the functions of clearing liver and clearing heat, expelling wind and dampness, nourishing qi and nourishing qi. Common carp and celery, suitable for adjuvant treatment of acute and chronic pneumonia.

Shredded rabbit meat and mushrooms: 100 grams of cooked rabbit meat, 50 grams of mushrooms, 25 grams of light white, chili oil, soy sauce, vinegar, sugar, sesame oil, sesame sauce, pepper powder, MSG amount. Shred the cooked rabbit meat and green onions separately and cook the mushrooms. Shallots, mushrooms at the bottom, rabbit silk cover surface, and served in the dish. Use soy sauce to disperse the sesame sauce in portions, mix the sesame oil into a flavor sauce, and drizzle it with rabbit silk. Free meat has the effects of clearing heat and detoxifying, nourishing qi and strengthening the spleen, removing dampness and cooling blood, and facilitating the convenience. Mushrooms have the effects of detoxifying and moisturizing, nourishing spleen, nourishing spleen, and dampening diarrhea. Rabbit meat with mushrooms is suitable for the treatment of acute pneumonia.

Quail Lily Soup: 1 quail, 25 grams of lily, ginger, spring onion, monosodium glutamate, fine salt. After the quail is killed, remove its hair, remove its feet, remove its internal organs, and wash it in boiling water. Remove the cut pieces. Wash the lily petals and wash them for future use. Wash the ginger and shallots, smash the ginger, and cut the shallots into sections. Place the pot on a hot fire, pour an appropriate amount of water, add the quail, boil, boil the lilies, ginger pieces, and spring onions, and simmer over low heat until the quail is cooked. Add salt and MSG for a few minutes. Edible. Quail meat has the effects of nourishing the five internal organs, nourishing the liver and clearing the lungs, clearing away heat and dampness, eliminating diarrhea, and reducing diarrhea; lily has the effects of nourishing the lungs and relieving cough, nourishing yin, clearing heat, and soothing the mind and soothing. The two are the same food, suitable for acute and chronic pneumonia.

Lean meat cabbage soup: 100 grams each of lean meat and cabbage heart, ginger, garlic, salt, monosodium glutamate, and a little chicken oil. Shred lean meat, wash and shred cabbage, put into boiling water, remove when fresh, rinse with clear water, filter and dry the water for later use; Garlic, stir-fry golden brown, add lean meat and stir-fry, add fine salt, cook with soup, boil cabbage heart, add MSG and serve. Lean meat has the effects of tonifying qi, invigorating the intestines and moisturizing the intestines; Chinese cabbage is flat and sweet, and has the functions of clearing heat and detoxifying, resolving phlegm and relieving cough, and removing troubles and laxatives. Lean meat and cabbage together, suitable for acute and chronic pneumonia.

Pathological damage of interstitial pneumonia The pathological damage of interstitial pneumonia is dominated by inflammation of the alveolar wall in the early stage of the disease, diffuse pulmonary interstitial fibrosis in the middle stage, and alveolar wall fibrosis in the later stage. During x-ray lung examination, especially high-resolution CT (HRCT) examination, it can be found that the lung lobes on both sides, especially the lower lung lobes, show dense and fine reticulated nodules. The nodules are more uniform and the boundaries are unclear, or There are cord-like lesions, grid shadows, and honeycomb lungs. The ground-glass changes are not obvious, and those with simple ground-glass changes are easy to recover. Pathological examination of bronchoscopy biopsy (TBLB) showed alveolar atrophy and pulmonary interstitial fibrosis ^[1] .