Silicosis

Silicosis is triggered by the inhalation of unbound (free) dusts which contain crystalline silica, and is characterized by a nodular lung fibrosis. Chronic silicosis caused initially no symptoms or only mild dyspnea, however, can cause over the years to attack almost the entire lung and dyspnea, hypoxemia, pulmonary hypertension and lung injury. The diagnosis is based on history and chest x-ray findings. An effective therapy, there is – apart from the symptomatic treatment and lung transplant as a last resort – not.

Silicosis is triggered by the inhalation of unbound (free) dusts which contain crystalline silica, and is characterized by a nodular lung fibrosis. Chronic silicosis caused initially no symptoms or only mild dyspnea, however, can cause over the years to attack almost the entire lung and dyspnea, hypoxemia, pulmonary hypertension and lung injury. The diagnosis is based on history and chest x-ray findings. An effective therapy, there is – apart from the symptomatic treatment and lung transplant as a last resort – not. Etiology silicosis, which is the longest known occupational disease of the lungs by inhalation of tiny silica particles in the form of unbound (free) crystalline silica (usually quartz) or, more rarely, caused by the inhalation of silicates, bound onto silica minerals such as talc. The most vulnerable workers are those who move the stones and sand or grind (miners, quarrymen, stonemasons) or silica-containing abrasive stone or sand used (sandblaster, glassblowers, caster, gem cutters, ceramic industry workers, pottery). risking coal miners to develop a mixed anthraco and anthracosis (pneumoconiosis of coal miners). Among the factors that affect the likelihood of developing silicosis include duration and intensity of exposure silicon form (contact with crystalline form presents greater risk than with bound form) surface finish (contact with uncoated form presents greater risk than with coated form) time inhalation after comminution of the rock formation and dust inhalation (contact immediately after comminution is greater risk as a delayed contact) pathophysiology alveolar macrophages take inhaled free silicon particles and migrate into lymphatic and interstitial tissue. Macrophages cause the release of cytokines (TNF-?, IL-1), growth factors (TGF-?) and oxidants which cause parenchymal inflammation, collagen synthesis and eventually fibrosis. When the macrophages perish, the silicon dioxide is released into the interstitial tissue around the small bronchioles, resulting in the formation of the pathognomonic Silikoseknötchen. This initial nodes contain macrophages, lymphocytes, mast cells, fibroblasts with unorganized collagen retention and interspersed birefringent particles that can be seen under a polarizing microscope best. During maturation tight balls form in the center of the knot of fibrotic scar tissue with classic onion skin formation, which are surrounded by a wall of inflammatory cells. At low concentration or short-term exposure these nodes remain discreet and do not restrict lung function a (simple chronic silicosis). At higher concentrations or long-term exposure, however (complicated chronic silicosis) confluent nodes, leading to progressive fibrosis and restricted lung volumes (total lung capacity, pulmonary ventilation capacity) in the pulmonary function test or they coalesce occasionally large conglomerate nodes (progressive massive fibrosis called). Silikoseknötche Image courtesy of David W. Cugell, M.D. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/silicotic_nodule_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/silicotic_nodule_high_de.jpg?la = en & thn = 0 ‘, title:’ Silikoseknötche ‘description:’ ‘credits’ image courtesy of David W. Cugell, MD’, hideCredits: false, hideTitle: false, hideFigure: false, hideDescription: true}; var panel = $ (MManual.utils.getCurrentScript ()) Closest ( ‘image-element-panel.’). ko.applyBindings (model, panel.get (0)); Chronic silicosis is the most common and usually develops only after decades of exposure. Acute silicosis and the rarer accelerated silicosis caused by intensive Siliziumdioxidstaubbelastung over short periods of time (several months or years). Mononuclear cells infiltrate the alveolar septa and alveolar filled with a protein-containing material “periodic acid-Schiff” (PAS) stain and the positive found in the pulmonary alveolar proteinosis is similar (Silikoproteinose- Pulmonary alveolar proteinosis). To distinguish a Silikoproteinose of idiopathic variant, it requires a professional history with acute exposure. The Konglomeratsilikose (complicated silicosis), the advanced form of chronic or accelerated silicosis and is characterized by extensive fibrosis node, typically in the upper lung fields. Complications Patients with silicosis are at risk of developing other diseases: TB Nokardiose lung cancer Systemic sclerosis (scleroderma) may RA All patients with silicosis have of developing an approximately 30-fold increased risk of pulmonary TB or nontuberkularer mycobacterial disease, and more likely to develop both lung as well as extra-pulmonary abnormalities. Increased risk may result from reduced macrophage function and increased risk of activation of a latent infection. People who are exposed to silica but have no silicosis, have a 3-fold higher risk of developing tuberculosis than the non-exposed general population. Other complications include spontaneous pneumothorax, Broncholithiasis and tracheobronchial obstruction. Emphysema are common in the immediate vicinity of conglomerate nodes and in districts with progressive massive fibrosis. Symptoms and complaints Chronic silicosis is often asymptomatic, but many patients can gradually develop dyspnea during exercise, which later turns into a resting dyspnea. Productive cough, if present, may be caused even by silicosis, by a coexisting chronic occupational (industrial) or bronchitis from smoking. The breath sounds are quieter when the disease progresses, and it can develop consolidations, pulmonary hypertension and respiratory failure with or without right ventricular failure. Patients with silicosis akzelerierter show the same symptoms as those with chronic silicosis, but the symptoms develop over a shorter period. Patients with acute silicosis show a rapid progression of dyspnea, weight loss and fatigue with diffuse bilateral rales. Frequently, a respiratory failure develops within two years. Konglomeratsilikose leading to severe, chronic respiratory symptoms. Diagnostic Work-related history of silica exposure chest CT or chest X-ray Sometimes tissue biopsy to confirm Further diagnostics to differentiate silicosis from other diseases. Imaging techniques silicosis is detected in patients with a history of exposure usually by chest x-ray or chest CT. CT has a higher sensitivity than an X-ray, esp., When using a spiral or HRCT (thin-section). In most cases, chest CT is preferable because it is more sensitive to the discovery of silicosis and the transition from simple to Konglomeratsilikose. A chest CT can better distinguish asbestosis from silicosis, although both can usually be differentiated already by the X-ray image and the occupational history. In patients develop RA, pulmonary rheumatoid nodules are visible on the chest x-ray or CT of 3-5 mm. The chronic silicosis produces multiple, 1-3 mm wide rounded opacities or nodes visible, normally located on the chest x-ray or CT in the upper lung fields. The severity is classified according to a standardized classification that was developed by the International Labor Organization (International Classification of radio Graphs of Pneumoconioses), examine the X-ray image to the size and shape of the shadows, density of opacities and pleural changes out in the specially trained experts. For the CT there is no corresponding Befundungsschema. Calcified hilar and mediastinal lymph nodes are common and occasionally resemble eggshells. Pleural thickening are, unless a severe parenchymal damage directly adjacent to the pleura, rarely found. Rarely occurs a calcified pleural thickening in patients with mild Parenchymbeteiligung. To the conglomerate knots often form bullae. Trachealabweichungen can occur when the lesions are large and lead to fluid loss. Real caverns can be a sign of tuberculosis. Numerous diseases resemble chronic silicosis on x-rays, including the Siderose the welder, hemosiderosis, sarcoidosis, chronic beryllium disease, extrinsic allergic alveolitis, anthracosis, miliary tuberculosis, fungal diseases of the lung and metastatic cancer. Eggshell-shaped calcifications of the hilar and mediastinal lymph nodes can help to distinguish the silicosis of other lung diseases, but they are no pathognomonic findings and are not common. Silicosis Simple Image courtesy of David W. Cugell, M.D. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/silicosis_simple_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/silicosis_simple_high_de.jpg?la = en & thn = 0 ‘, title:’ silicosis Simple ‘, description:’ ‘credits’ image courtesy of David W. Cugell, MD’, hideCredits: false, hideTitle: false, hideFigure: false, hideDescription: true }; var panel = $ (MManual.utils.getCurrentScript ()) Closest ( ‘image-element-panel.’). ko.applyBindings (model, panel.get (0)); Silicosis Simple (upper lung field) Image courtesy of David W. Cugell, M.D. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/silicosis_simple_upper_lung_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/-/media/manual/professional/images/silicosis_simple_upper_lung_high_de.jpg?la = en & thn = 0 ‘, title:’ silicosis Simple (upper lung field) ‘description:’ u003Ca id = “v37893153 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eNahaufnahme an upper lung field with simple silicosis u003c / p u003e u003c / div u003e ‘credits’. image courtesy of David W. Cugell

Health Life Media Team

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