Ionizing radiation (X-ray beam), breast, lung, esophageal cancers and is often used for the treatment of lymphoma. This treatment can cause lung and some injuries.
The beam of radiation dose applied to the lung tissue reaction brought husule, the duration varies depending on the status and treatment before the lung. Pnömonitis'i radiation or radiation from the reaction of the lung husule fibrosis'i called.
Many times the radiation treatment is done with 3000 rad, 6000 rad'dan pnömonitisine more radiation therapy can cause serious radiation.
Radiation dose and duration of light is important in the development of fibrosis'in. 3000 rad is given at a time, for example, consists of extensive fibrosis. 15 fractions are given the same dose (5 days a week 200 rad / day total of 3 weeks), radiation fibrosis'i rare. Beam at a dose of 3500 rad or more fibrosis, more frequently observed.
Usually 3-4 months after the initiation of X-ray therapy starts clinical and radiological manifestations. In some cases, this period is shorter, in some cases longer.
Before radiation therapy in patients with radiation pneumonitis in the lungs of chronic bronchitis is a more serious reaction. Because of the mediastinum underwent radiation adenopathy, mediastinal lymphatics and bilateral lung disease causes blockages in bringing husule.
Pathology
Before kapillerinde lung damage, destruction and necrosis occurs. Kolagen tissue capillaries takes place in the devastated. Within the alveolar exudate and hyaline-membrane occurs later. And the alveolar connective tissue and lymphatic infiltration septalarında develops. Then, a fibrous tissue invasion of lung parenkimasını is widespread and intense.
Clinical symptoms
There is a significant number of patients in clinical symptoms. Exertional dyspnea and the first clinical manifestation. In some cases, disappear every few weeks. Progressively increasing dyspnea at rest or in some cases, shows itself. Dry cough, in some cases, chest pain, weakness, subfebril fever, hemoptysis, tachycardia, and rarely comes husule. Early stage, patients may have temporary difficulties in swallowing. Radiation treatment of rib fractures in 10% of the cases come husule. Fracture is a serious chest pain that occurs in the region. This pain is increased more than inspiration.
Physical examination findings are usually minimal to slight. Initially, radiation can be heard in the area Railer age. This decrease Railer usually disappear. Because of intensive radiation therapy in advanced disease, fibrosis of the lung volume is reduced, pulled aside the trachea and mediastinal radiation, or dullness in that area has submatite decreased breath sounds and, in some cases, frotman heard.
Radiological findings
Pnömonotisinin the acute phase of radiation lung volume reduction parenkimasında concentration and monitored. This decrease in topo-segment or lobe of x-ray does not show compliance. Patchy or may be larger than the combined concentration of Parenchyma. The size and intensity of the radiation dose and lung lesions varies according to the reaction. Spatial loss comes from the widespread nature bronchiole blockage and reduction of surfactant material. Spatial reduction in almost every case, an air bronchogram was seen in the region.
Characteristic late appearance of radiation fibrosis. All the normal structure of fibrous tissue invaded the lung. Pleural thickening commonly seen.
Lung function tests
An improvement in lung function tests before income husule. This improvement is about the effect of radiation therapy in cancer tissue. The next period is reduced diffusing capacity and restrictive functional abnormality occurs, especially vital capacity and air flow is reduced. Generally, the fibrous tissue is proportional decrease in vital capacity and diffusion.
Treatment
Radiation fıbrosisini steroid treatment to prevent or pmömonitisini achieved a successful outcome in those very times. Acute oxygen therapy for hypoxemia in the growing and widely utilized in cases of fibrosis.
Showing posts with label Other Lung Diseases. Show all posts
Showing posts with label Other Lung Diseases. Show all posts
What is Bisinosis
Cotton, flax and hemp is a pneumonia caused by inhalation of dust konyosistir. Dust inhalation rate and severity of disease increases intensified. There is an interesting patogenesi disease, a healthy person, cotton, flax and hemp dust inhaled when the disease does not occur immediately. After working for a long time a serious cough, chest tightness, wheezing, and exertional dyspnea husule income. These symptoms are similar to the work week begins Monday holiday ends Astmaya occurs. Usually the other days of the week will be lost. Therefore, this disease, "Mondays fire" is also known as.
Pathological evaluation of patients with chronic bronchitis and emphysema patients with long-term results are observed. Allergic reaction to some substances in the dust of the disease has to do with textiles. The suspension will be lost from the study of disease symptoms.
Extrinsic Allergic Alveolitis
(Hypersensitivity pneumonitis)
Farmers lung
Upon specific antigens in the alveoli of inhaled organic powders allergic diseases "extrinsic allergic alveolitis" or "hipersesitive pneumonitis" is called.
Farmers lung
Extrinsic allergic alveolitise a disorder that causes.
Moldy hay or other moldy vegetable powders, a lung disease caused by inhalation. The disease in damp and moldy hay and other nebatta thermophilic some actinomycosis occurs by inhalation of antigens.
Pathology
Topographical distribution of lung lesions similar to bronchopneumonitises. Alveolar kapillerinde acute vasculitis, fibrin, neutrophils, eosinophils and monocyte infiltration of leuko-have-site. Obstructive bronchiolitis developed in the middle of these lesions. After this period, the disease is an acute granulomatous interstitial pneumonitis and non-granuloma develops. The disease increasingly fibrosis, pneumonitis, and emphysema in a mixture of tissue change.
Clinical symptoms
Clinical symptom usually occurs when two groups of acute and chronic. 4-8 hours after inhalation of antigens by acute symptoms of dyspnea, cough, fatigue, chills, fever, and sometimes followed by hemoptysis. It shows the most common chronic formada going insidious disease, progressive dyspnea, cough, weight loss, chills, fever, fatigue and pain are like the local and systemic symptoms. Despite the importance of clinical symptoms, but rarely crepitan Railer Auscultation sounds. Especially in the history of clinical symptoms of allergy in some patients with "asthma bronşitine" similar. Acute and subchronic repeated inhalation of antigen leads to an increase in symptoms and lung fıbrosis'in. The story of moldy straw work is important in the diagnosis of the disease. Serum of these patients are presipitinler. Patient serum thermophile actinomycosis presence of anti-jenleriyle karşılaştınlırsa presipitinlerin understood.
Radiological findings
Chest radiograph in the acute phase of the disease to spread in both lungs shows granular or nodular. Floors and apex lesions is almost negligible. Some lesions are similar to parts of the sarcoidosis in the snow. However, hilar or mediastinal adenopathy seen farmers' lung. The location of antigens away from the patient returns to normal chest radiography. Antigen inhalasy to ten common rough location of the patients in the radiographic findings of nodular lesions in a reticular infiltrates (interstitial fibrosis) and emphysema change is monitored.
Lung function tests
In particular, diffusing capacity is reduced. Furthermore, vital capacity, expiratory air flows decrease in ex-tracked. Function abnormalities may develop in some cases, obstructive. Chest radiograph abnormalities disappeared in pulmonary function returns to normal.
Treatment
Aeration of the sites must be thoroughly dry thoroughly and store hay. Allergic patients and warned those who had the disease should run for other tasks. For this purpose, a significant number of the masks kullanılmasiyle antigen inhalation of dust is reduced. Steroid therapy in patients with acute and subacute multiple times provided a good result.
Pathological evaluation of patients with chronic bronchitis and emphysema patients with long-term results are observed. Allergic reaction to some substances in the dust of the disease has to do with textiles. The suspension will be lost from the study of disease symptoms.
Extrinsic Allergic Alveolitis
(Hypersensitivity pneumonitis)
Farmers lung
Upon specific antigens in the alveoli of inhaled organic powders allergic diseases "extrinsic allergic alveolitis" or "hipersesitive pneumonitis" is called.
Farmers lung
Extrinsic allergic alveolitise a disorder that causes.
Moldy hay or other moldy vegetable powders, a lung disease caused by inhalation. The disease in damp and moldy hay and other nebatta thermophilic some actinomycosis occurs by inhalation of antigens.
Pathology
Topographical distribution of lung lesions similar to bronchopneumonitises. Alveolar kapillerinde acute vasculitis, fibrin, neutrophils, eosinophils and monocyte infiltration of leuko-have-site. Obstructive bronchiolitis developed in the middle of these lesions. After this period, the disease is an acute granulomatous interstitial pneumonitis and non-granuloma develops. The disease increasingly fibrosis, pneumonitis, and emphysema in a mixture of tissue change.
Clinical symptoms
Clinical symptom usually occurs when two groups of acute and chronic. 4-8 hours after inhalation of antigens by acute symptoms of dyspnea, cough, fatigue, chills, fever, and sometimes followed by hemoptysis. It shows the most common chronic formada going insidious disease, progressive dyspnea, cough, weight loss, chills, fever, fatigue and pain are like the local and systemic symptoms. Despite the importance of clinical symptoms, but rarely crepitan Railer Auscultation sounds. Especially in the history of clinical symptoms of allergy in some patients with "asthma bronşitine" similar. Acute and subchronic repeated inhalation of antigen leads to an increase in symptoms and lung fıbrosis'in. The story of moldy straw work is important in the diagnosis of the disease. Serum of these patients are presipitinler. Patient serum thermophile actinomycosis presence of anti-jenleriyle karşılaştınlırsa presipitinlerin understood.
Radiological findings
Chest radiograph in the acute phase of the disease to spread in both lungs shows granular or nodular. Floors and apex lesions is almost negligible. Some lesions are similar to parts of the sarcoidosis in the snow. However, hilar or mediastinal adenopathy seen farmers' lung. The location of antigens away from the patient returns to normal chest radiography. Antigen inhalasy to ten common rough location of the patients in the radiographic findings of nodular lesions in a reticular infiltrates (interstitial fibrosis) and emphysema change is monitored.
Lung function tests
In particular, diffusing capacity is reduced. Furthermore, vital capacity, expiratory air flows decrease in ex-tracked. Function abnormalities may develop in some cases, obstructive. Chest radiograph abnormalities disappeared in pulmonary function returns to normal.
Treatment
Aeration of the sites must be thoroughly dry thoroughly and store hay. Allergic patients and warned those who had the disease should run for other tasks. For this purpose, a significant number of the masks kullanılmasiyle antigen inhalation of dust is reduced. Steroid therapy in patients with acute and subacute multiple times provided a good result.
What is asbestosis
Inhalation of asbestos dust caused by a pnömokonyosistir. Asbestos iron, silicate, magnesium, nickel and calcium in the form of fiber found in nature and is a substance from a mixture husule. In areas where the rock fragmentation process in industry because of asbestos and asbestos dust from the environment is distributed. Asbestos heat, acid and alkali resistant and durable material that is used increasingly in industry and therefore increasing pnömokonyosisi asbestos.
Some regions in Turkey, for example, in Diyarbakir and the villagers around Nevsehir whitewash their homes to do with asbestos, and asbestosis related cancer incidence in these regions, who work to increase the importance of Turkish Doctors (S. Yazid and Rel. Peace) by the proven.
Asbestos fibers are 20-50 microns long, although respira-inflammatory bronchioles and alveoli have access to. These fibers 3-10 microns in diameter, this allows you to be.
Pathology
20-40 years after inhalation of asbestos dust consists of increasing fibrosis. As the disease progresses and the honeycomb microcystic appearance (bronşiolektazi) increases. Asbestos fibers are seen in both the interstitium and the alveoli. Asbestos fibers are thickened pleura with pleural penetration. Pleura asbestos fibers are seen and objective diagnostic biopsy is performed in these cases is provided.
Clinical symptoms
Clinical symptoms are usually 20-40 years after asbestos inhalation begins. The main clinical symptom, exertional dyspnea gradually increases. In some cases, cough, sputum and chest pain are. Toraksda deformity due to pleural disease are seen. Despite this deformity in most patients, there is a complaint about the disease. Railer crepitan bilateral lung bases is heard. In most patients husule clubbing of income. Disease proceed loss of appetite, weight loss and syanoz develops. Cases may be complicated by cancer hemop-treble. Cases of pleural thickening or mesotelyoma dullness and decreased breath sounds in the region are related.
Radiological findings
The first radiographic abnormality in the developing regions of the lower lobe reticular-s appearance. Furthermore, the lung is a "ground glass" appearance is, pleura ililgidir kalınlaşmasıyle. The next period will be more pronounced interstitial Retin-vascular appearance. The concentration limits of the heart and diaphragm and pleura husule Parenchyma partially obscure makes. Such a view of the heart "rough heart" is called. Reticular infiltration in the later period of the disease progresses to the middle and upper loblara, more focused, heart and diaphragm borders belirsizleşir thoroughly.
Radiography of pleural thickening greater than 90% of cases are observed. Approximately half of the cases seen in both pleural and parenchymal lesions. % Of cases of heart view of the rough on the 20th followed. Advanced stages of the disease develop lung parenkimasında microcystic and honeycomb change.
Pleural thickening or pleural plaques are usually bilateral, are monitored more frequently in the lower half of the thorax and rib borders in a way that fits. In some cases, is pleural calcification. Multiple pleural plaques is an important finding for the diagnosis of disease. Pleural-parietal pleural plaques are composed of ordinary Asbestosis'de. These plaques are monitored more frequently than the dome of the diaphragm.
Lung function tests
Vital capacity and diffusing capacity is reduced. In some cases, depending on changes in emphysema secondary to the income tests husule disorder. Venti-lasyon/perfüzyon balance is disrupted in the early stages of the disease.
Asbestosis and cancer
The incidence of cancer of the lung disease after smoking asbestosistir most. The most common neoplasms of asbestosis and bronchial cancer mesotelyoma'dır. 10-fold higher incidence of cancer in workers with asbestos. Oat cell carcinoma or anaplastic bronchial cancer, the most common species. Cuticle-moid carcinoma and adenocarcinoma may also occur. 20 years after the cancer develops from asbestos inhalation. How much and long-term inhalation of asbestos in the incidence of cancer is so much. Incidence in smokers is more.
Mesotelyoma and pleural thickening and pleural biopsy needle to separate the objective is sufficient. The higher incidence of peritoneal Asbestosis'de mesotelyoma.
Asbestosis treatment
There is no possibility of improvement in the disease after coming husule. Periodic clinical and radiological examination of employees' asbestos work should be done, this kind of showing suspicious changes in work places must be removed. Asbestos inhalasoynu cut will stop the progression of the disease. The most successful method to reduce the dust of war, disease, and workers in asbestos work places to ensure that less dust inhaled.
Cancer in asbestos workers who smoke are seen more of these workers should not smoke. Must be trained on this subject. Bırakmayanlar smoking should be checked more closely.
Some regions in Turkey, for example, in Diyarbakir and the villagers around Nevsehir whitewash their homes to do with asbestos, and asbestosis related cancer incidence in these regions, who work to increase the importance of Turkish Doctors (S. Yazid and Rel. Peace) by the proven.
Asbestos fibers are 20-50 microns long, although respira-inflammatory bronchioles and alveoli have access to. These fibers 3-10 microns in diameter, this allows you to be.
Pathology
20-40 years after inhalation of asbestos dust consists of increasing fibrosis. As the disease progresses and the honeycomb microcystic appearance (bronşiolektazi) increases. Asbestos fibers are seen in both the interstitium and the alveoli. Asbestos fibers are thickened pleura with pleural penetration. Pleura asbestos fibers are seen and objective diagnostic biopsy is performed in these cases is provided.
Clinical symptoms
Clinical symptoms are usually 20-40 years after asbestos inhalation begins. The main clinical symptom, exertional dyspnea gradually increases. In some cases, cough, sputum and chest pain are. Toraksda deformity due to pleural disease are seen. Despite this deformity in most patients, there is a complaint about the disease. Railer crepitan bilateral lung bases is heard. In most patients husule clubbing of income. Disease proceed loss of appetite, weight loss and syanoz develops. Cases may be complicated by cancer hemop-treble. Cases of pleural thickening or mesotelyoma dullness and decreased breath sounds in the region are related.
Radiological findings
The first radiographic abnormality in the developing regions of the lower lobe reticular-s appearance. Furthermore, the lung is a "ground glass" appearance is, pleura ililgidir kalınlaşmasıyle. The next period will be more pronounced interstitial Retin-vascular appearance. The concentration limits of the heart and diaphragm and pleura husule Parenchyma partially obscure makes. Such a view of the heart "rough heart" is called. Reticular infiltration in the later period of the disease progresses to the middle and upper loblara, more focused, heart and diaphragm borders belirsizleşir thoroughly.
Radiography of pleural thickening greater than 90% of cases are observed. Approximately half of the cases seen in both pleural and parenchymal lesions. % Of cases of heart view of the rough on the 20th followed. Advanced stages of the disease develop lung parenkimasında microcystic and honeycomb change.
Pleural thickening or pleural plaques are usually bilateral, are monitored more frequently in the lower half of the thorax and rib borders in a way that fits. In some cases, is pleural calcification. Multiple pleural plaques is an important finding for the diagnosis of disease. Pleural-parietal pleural plaques are composed of ordinary Asbestosis'de. These plaques are monitored more frequently than the dome of the diaphragm.
Lung function tests
Vital capacity and diffusing capacity is reduced. In some cases, depending on changes in emphysema secondary to the income tests husule disorder. Venti-lasyon/perfüzyon balance is disrupted in the early stages of the disease.
Asbestosis and cancer
The incidence of cancer of the lung disease after smoking asbestosistir most. The most common neoplasms of asbestosis and bronchial cancer mesotelyoma'dır. 10-fold higher incidence of cancer in workers with asbestos. Oat cell carcinoma or anaplastic bronchial cancer, the most common species. Cuticle-moid carcinoma and adenocarcinoma may also occur. 20 years after the cancer develops from asbestos inhalation. How much and long-term inhalation of asbestos in the incidence of cancer is so much. Incidence in smokers is more.
Mesotelyoma and pleural thickening and pleural biopsy needle to separate the objective is sufficient. The higher incidence of peritoneal Asbestosis'de mesotelyoma.
Asbestosis treatment
There is no possibility of improvement in the disease after coming husule. Periodic clinical and radiological examination of employees' asbestos work should be done, this kind of showing suspicious changes in work places must be removed. Asbestos inhalasoynu cut will stop the progression of the disease. The most successful method to reduce the dust of war, disease, and workers in asbestos work places to ensure that less dust inhaled.
Cancer in asbestos workers who smoke are seen more of these workers should not smoke. Must be trained on this subject. Bırakmayanlar smoking should be checked more closely.
Silicosis Disease
Disease called silicosis caused by inhalation of silica dust. Silica dust is widely available around us. Pnömokonyosisdir silicosis one of the most common. Quarries, mines, brick, tile, pottery, clay works are workers.
Fibrous particles of silica in the lungs of their coal pnömokonyosisinden more intense and widespread reaction. Autoimmune reaction to form the fibrous silica powders and macrophages zedelen-mesiyle related imbalance.
Pathological
The characteristic lesions of the lung nodules of connective tissue in silicosis. As an onion on top of layers of connective tissue accumulation creates a nodule. These nodules are 2-3 mm in diameter than the upper lung regions parahiler foblarında and collected. Silica dust next to the alveolar walls of small vessels are collected several times. Perivascular lymph roads clogged artery walls and wear, would be devastated. NodüUerde, preskalen to hilar lymph nodes are silica powders.
In the fine silica powder how intense and how it develops in such a widespread fibrosis. Inhalation of silica nodules as we continue to expand, and with each other combine to increase the number of large, dense masses occurs. Upper or middle parts of the lung lesions in this large dollars. Conglomerated silicosis cases of tuberculosis infection is very common. The period of active and progressive cavitary lesions of tuberculosis occurs. Lymph nodes, hilar lymph nodes, especially early in the disease expands. Higher incidence of cancer in silicosis.
Clinical symptoms
X-ray micro-nodular lung disease, the diagnosis of silicosis is usually a change is made and the history of professional self. Clinical symptoms after 20-30 years is certain. If the patient smokes, this period, frequent lung infeksi-tions, such as cough and sputum in chronic bronchitis symptoms are observed. These symptoms are connected to smoking, the diagnosis of silicosis remains hidden. Proceed, however, the disease cough, sputum production, and increasing dyspnea of exertion increases, and the evening comes, and chest radiography husule nodules indicates that they come together and look conglomerate. Emphysema and chronic bronchitis is a progressive illness develops. The enlarged barrel-shaped thorax, decreased expansion. Hipersonorite percussion is taken. Auscultation decreased breath sounds and prolonged ekspiras-direction is heard. Parenkimasının progressive lung damage with a fibrous tissue, chronic bronchitis and emphysema, progressive pulmonary hypertension, cor pulmonale and right heart failure and then come husule.
Other environmental diseases in a separate feature in the progression of silicosis after years of ayınldıktan over study of fibrous reaction. For this reason, the patient should ask the former to the years of the professional resume carefully.
Radiological findings
Radiographic signs of silicosis disease usually occurs after 10-20 years of interest. Reticular and radiological changes in the beginning is difficult to decide what is normal or abnormal. Then, with multiple nodular shadows appear. During this period, the diagnosis of the disease remains questionable. Reticular or nodular change and the disease "simple silicosis is called. After this period, and gain a view conglomerated nodules combined with "complicated silicosis" means husule. Diameters of the lesions are homogeneous nature conglomerate with more than one part, some of them large enough to cover a lobe. There are distributions do not comply with the anatomy of the segment or lobe. Are usually localized in the upper lobes. Environments with multiple outputs are intizamsızdır and lesion boundaries. Increases, and the radiographic appearance of fibrous reaction is dominated by the disease progresses. Coal workers pnömokonyosis'inde as "progressive massive fibrosis (PMF) consists of shirt.
Silikosis'de hilar adenopathy are seen. Around 5% of cases, enlarged lymph glands are calcified, and there is a lesion with lymphadenopathy parenkimada this. This view is "egg shell" is like a fairly pathognomonic for the diagnosis of silicosis. Egg shell mediastinal lymphadenopathy, chest wall and peritoneum may also occur. Advanced stages of the disease consists of chronic obstructive pulmonary disease and air regions and the bullae are seen more as a radiograph about it. Tuberculosis and ischemic necrosis in cases with widespread lesions husule Intracavernous income.
Lung function tests
Prenodüler and nodular pulmonary function tests are usually normal period. The disease is complicated by widespread and progressive fibrosis in the lung function tests show restrictive abnormality. Lung hacımları, especially vital capacity is reduced. More advanced cases, compliance, and diffusion capacity is reduced. The other is a functional disorder in patients with obstructive husule this nature. Silicosis patients, ventilation / perfusion imbalance in respiratory function is an important abnormality.
Treatment of silicosis
Patients diagnosed with silicosis silica dust away from the position effective treatment. Micronodular do not need any treatment period. Conglomerate and massive fibrosis should be carefully monitored during the nu complication of tuberculosis. Returnees or those with positive tuberculin reactions, prophylactic treatment should be more strongly. If the patient has clinical symptoms, for example, night sweat, weight loss, fatigue, loss of appetite and quality of radiographic changes of tuberculosis treatment of tuberculosis is the first year. Examination of Koch's bacillus in sputum culture, and resistance to antituberculosis drugs according to the result set type and duration of treatment.
Fibrous particles of silica in the lungs of their coal pnömokonyosisinden more intense and widespread reaction. Autoimmune reaction to form the fibrous silica powders and macrophages zedelen-mesiyle related imbalance.
Pathological
The characteristic lesions of the lung nodules of connective tissue in silicosis. As an onion on top of layers of connective tissue accumulation creates a nodule. These nodules are 2-3 mm in diameter than the upper lung regions parahiler foblarında and collected. Silica dust next to the alveolar walls of small vessels are collected several times. Perivascular lymph roads clogged artery walls and wear, would be devastated. NodüUerde, preskalen to hilar lymph nodes are silica powders.
In the fine silica powder how intense and how it develops in such a widespread fibrosis. Inhalation of silica nodules as we continue to expand, and with each other combine to increase the number of large, dense masses occurs. Upper or middle parts of the lung lesions in this large dollars. Conglomerated silicosis cases of tuberculosis infection is very common. The period of active and progressive cavitary lesions of tuberculosis occurs. Lymph nodes, hilar lymph nodes, especially early in the disease expands. Higher incidence of cancer in silicosis.
Clinical symptoms
X-ray micro-nodular lung disease, the diagnosis of silicosis is usually a change is made and the history of professional self. Clinical symptoms after 20-30 years is certain. If the patient smokes, this period, frequent lung infeksi-tions, such as cough and sputum in chronic bronchitis symptoms are observed. These symptoms are connected to smoking, the diagnosis of silicosis remains hidden. Proceed, however, the disease cough, sputum production, and increasing dyspnea of exertion increases, and the evening comes, and chest radiography husule nodules indicates that they come together and look conglomerate. Emphysema and chronic bronchitis is a progressive illness develops. The enlarged barrel-shaped thorax, decreased expansion. Hipersonorite percussion is taken. Auscultation decreased breath sounds and prolonged ekspiras-direction is heard. Parenkimasının progressive lung damage with a fibrous tissue, chronic bronchitis and emphysema, progressive pulmonary hypertension, cor pulmonale and right heart failure and then come husule.
Other environmental diseases in a separate feature in the progression of silicosis after years of ayınldıktan over study of fibrous reaction. For this reason, the patient should ask the former to the years of the professional resume carefully.
Radiological findings
Radiographic signs of silicosis disease usually occurs after 10-20 years of interest. Reticular and radiological changes in the beginning is difficult to decide what is normal or abnormal. Then, with multiple nodular shadows appear. During this period, the diagnosis of the disease remains questionable. Reticular or nodular change and the disease "simple silicosis is called. After this period, and gain a view conglomerated nodules combined with "complicated silicosis" means husule. Diameters of the lesions are homogeneous nature conglomerate with more than one part, some of them large enough to cover a lobe. There are distributions do not comply with the anatomy of the segment or lobe. Are usually localized in the upper lobes. Environments with multiple outputs are intizamsızdır and lesion boundaries. Increases, and the radiographic appearance of fibrous reaction is dominated by the disease progresses. Coal workers pnömokonyosis'inde as "progressive massive fibrosis (PMF) consists of shirt.
Silikosis'de hilar adenopathy are seen. Around 5% of cases, enlarged lymph glands are calcified, and there is a lesion with lymphadenopathy parenkimada this. This view is "egg shell" is like a fairly pathognomonic for the diagnosis of silicosis. Egg shell mediastinal lymphadenopathy, chest wall and peritoneum may also occur. Advanced stages of the disease consists of chronic obstructive pulmonary disease and air regions and the bullae are seen more as a radiograph about it. Tuberculosis and ischemic necrosis in cases with widespread lesions husule Intracavernous income.
Lung function tests
Prenodüler and nodular pulmonary function tests are usually normal period. The disease is complicated by widespread and progressive fibrosis in the lung function tests show restrictive abnormality. Lung hacımları, especially vital capacity is reduced. More advanced cases, compliance, and diffusion capacity is reduced. The other is a functional disorder in patients with obstructive husule this nature. Silicosis patients, ventilation / perfusion imbalance in respiratory function is an important abnormality.
Treatment of silicosis
Patients diagnosed with silicosis silica dust away from the position effective treatment. Micronodular do not need any treatment period. Conglomerate and massive fibrosis should be carefully monitored during the nu complication of tuberculosis. Returnees or those with positive tuberculin reactions, prophylactic treatment should be more strongly. If the patient has clinical symptoms, for example, night sweat, weight loss, fatigue, loss of appetite and quality of radiographic changes of tuberculosis treatment of tuberculosis is the first year. Examination of Koch's bacillus in sputum culture, and resistance to antituberculosis drugs according to the result set type and duration of treatment.
Fat Embolism Syndrome
Small vessels of the lungs into the circulation due to trauma tıkamasıdır oil droplets. So many times, breaking the bones of the femur or tibia is the result. Embolism as well as review the other escaped many times, they are not diagnostic. For example, 80% of cases of external cardiac massage autopsy showed pulmonary fat embolism.
Two days after a trauma, cough, dyspnea, hemoptysis, pleural pain, fever, tachycardia, and dry Railer age, clinical symptoms, such as occurs frotman. In some cases, heart failure, circulatory shock and the acute cor pulmonale syanoz and monitored. Other organs, signs of embolism after cardiopulmonary symptoms are seen. Confusion, loss of consciousness, cerebral symptoms such as delirium and coma, and petechiae on the skin major systemic symptoms. In one patient two days after a trauma, cardiopulmonary, cerebral and skin for signs of fat embolism occurs triad'dır pathognomonic. Oil droplets can be found in the urine, the diagnosis of disease in this case is finalized.
Chest radiograph bilateral alveolar edema as a result of Konso-idasyon are common. Consolidation of lung periphery is more. Concentration of cardiac origin, pulmonary edema is more pronounced in floors. Lung fat embolism in cases of heart enlargement, venous hypertension or interstitial edema, perivascular there. These findings are evidence that the pulmonary edema of cardiac origin. Clinical symptoms and radiologic abnormalities, trauma occurs after one or two days a week and 1-4 disappear.
Two days after a trauma, cough, dyspnea, hemoptysis, pleural pain, fever, tachycardia, and dry Railer age, clinical symptoms, such as occurs frotman. In some cases, heart failure, circulatory shock and the acute cor pulmonale syanoz and monitored. Other organs, signs of embolism after cardiopulmonary symptoms are seen. Confusion, loss of consciousness, cerebral symptoms such as delirium and coma, and petechiae on the skin major systemic symptoms. In one patient two days after a trauma, cardiopulmonary, cerebral and skin for signs of fat embolism occurs triad'dır pathognomonic. Oil droplets can be found in the urine, the diagnosis of disease in this case is finalized.
Chest radiograph bilateral alveolar edema as a result of Konso-idasyon are common. Consolidation of lung periphery is more. Concentration of cardiac origin, pulmonary edema is more pronounced in floors. Lung fat embolism in cases of heart enlargement, venous hypertension or interstitial edema, perivascular there. These findings are evidence that the pulmonary edema of cardiac origin. Clinical symptoms and radiologic abnormalities, trauma occurs after one or two days a week and 1-4 disappear.
What is Oxygen Toxicity
High concentrations (70% or more) and for a long time (48 hours) consists of oxygen toxicity in the lungs of adults given continuous oxygen. The main pathological findings of intra-alveolar hemorrhage, alveolar and interstitial fibroblastic proliferation and hyaline-membrane husule is that the tissue.
And adults that use high concentrations of oxygen for a long time, but some of the toxicity of oxygen occur. The role of personal factors in the development of this disease has.
Clinical symptoms vary according to the disease requiring oxygen therapy. Usually, these patients with acute respiratory failure (dyspnea, syanoz, wheezing and respiratory acidosis further periods: drowsiness, mental disorders and coma) has symptoms.
Radiologic manifestations of the disease varies according to reason. Oxygen therapy is applied is one of the rapidly growing abnormal radiographic interstitial fibrosis in oxygen toxicity.
Prevansiyon and treatment of
Oxygen treatment when necessary to ensure that arterial blood pressure of 65-75 mm Hg, oxygen should be given oxygen. Frequent arterial blood analysis, and accordingly by adjusting the inspired oxygen concentration of 65-75 mm Hg, arterial oxygen pressure and thus tried to keep the oxygen toxicity is avoided. Hypoxemia in some patients, however, even though treatment is given for the high concentration of oxygen to meet the needs of physiological levels of oxygen in arterial blood is low. And the fatal hypoxemia (arterial blood oxygen pressure of less than 40-50 mm Hg) are available. Oxygen concentration of oxygen toxicity in these patients, fearing azaltmamalıdır definitely. Hypoxemia because the patient dies. Hypoxemia should be treated first and then the toxicity of oxygen. These patients are treated in intensive care units.
And adults that use high concentrations of oxygen for a long time, but some of the toxicity of oxygen occur. The role of personal factors in the development of this disease has.
Clinical symptoms vary according to the disease requiring oxygen therapy. Usually, these patients with acute respiratory failure (dyspnea, syanoz, wheezing and respiratory acidosis further periods: drowsiness, mental disorders and coma) has symptoms.
Radiologic manifestations of the disease varies according to reason. Oxygen therapy is applied is one of the rapidly growing abnormal radiographic interstitial fibrosis in oxygen toxicity.
Prevansiyon and treatment of
Oxygen treatment when necessary to ensure that arterial blood pressure of 65-75 mm Hg, oxygen should be given oxygen. Frequent arterial blood analysis, and accordingly by adjusting the inspired oxygen concentration of 65-75 mm Hg, arterial oxygen pressure and thus tried to keep the oxygen toxicity is avoided. Hypoxemia in some patients, however, even though treatment is given for the high concentration of oxygen to meet the needs of physiological levels of oxygen in arterial blood is low. And the fatal hypoxemia (arterial blood oxygen pressure of less than 40-50 mm Hg) are available. Oxygen concentration of oxygen toxicity in these patients, fearing azaltmamalıdır definitely. Hypoxemia because the patient dies. Hypoxemia should be treated first and then the toxicity of oxygen. These patients are treated in intensive care units.
Wegener's granulomatosis
Wegener's granulomatosis with pulmonary eosinophilia group, even though there were some features of this group is divided into diseases.
There are three pathological features of the disease: 1) associated with aseptic necrosis of the upper respiratory tract and lung granulomatosis, 2) widespread arteritis, and 3) glomerulonephritis. Cause of the disease is unknown. Developing mechanism is thought to be related to an abnormal immune.
The disease is more in men aged 40-50 and most of the body may develop localized in any organ. The three main symptoms are characteristic: 1) persistent and sinüsitis rinitis, 2) nodular pulmonary lesions, and 3) the terminal uremia. The first symptoms usually occur in the respiratory tract: common cold, sinusitis, cough, hemoptysis, pleurisy or pneumonia. Otitis can in some cases, deafness. Hoarseness and swallowing difficulties may develop. Gums can be painful and ulcerations. Eye lesions are common.
Typical lesions in the lungs so many times in the form of a circular density granülomatosis'dir necrosis. There are in the middle of Intracavernous. The lesions are usually bilateral. Kavemlerin thick walls. Furthermore, scattered bronchopneumonitises infiltrates or nodular lesions are seen peribronişiyal. Secondary bacterial or fungal infections are common.
Skin, joint and muscle lesions are too.
Progressive nature of kidney disease. During the terminal uremia and other symptoms of the disease seen in general arteritis. High fever, arteritis, hemorrhagic lesions on the skin and mucous membranes, anemia, and leukocytosis are.
Wegener's granulomatosis disease prognosis is poor. Untreated cases, death is 6-8 months. Worse prognosis in patients with kidney disease. Effective treatment is provided by cyclophosphamide. Oral or intravenous drug use cases, showing very rapid progress. 1-3 weeks of treatment, improvement in clinical symptoms observed. WBC count should be carefully monitored and adjusted dose of cyclophosphamide to be kept up from 3.000/mm3. 1.000-1.500/mm3 should not fall down from the number of lymphocytes, so that the patient would be protected from infections. The other is an immunosuppressive drug azathioprine Siklofosfamid'e patients without tolerance. This is the same dose of the drug siklofos-famidin. If the disease is a severe at the beginning of cyclophosphamide together with corticosteroids, the dose of 1 mg / kg / day in reducing the clinical symptoms-lınca or disappeared (about 2 weeks) corticosteroid is reduced gradually, the day is over and then cut off. A full recovery after treatment with cyclophosphamide husule should continue for at least another year. Cyclophosphamide treatment improved the prognosis of Wegener's granulomatosis disease, most patients live for many years after discontinuation of medication.
There are three pathological features of the disease: 1) associated with aseptic necrosis of the upper respiratory tract and lung granulomatosis, 2) widespread arteritis, and 3) glomerulonephritis. Cause of the disease is unknown. Developing mechanism is thought to be related to an abnormal immune.
The disease is more in men aged 40-50 and most of the body may develop localized in any organ. The three main symptoms are characteristic: 1) persistent and sinüsitis rinitis, 2) nodular pulmonary lesions, and 3) the terminal uremia. The first symptoms usually occur in the respiratory tract: common cold, sinusitis, cough, hemoptysis, pleurisy or pneumonia. Otitis can in some cases, deafness. Hoarseness and swallowing difficulties may develop. Gums can be painful and ulcerations. Eye lesions are common.
Typical lesions in the lungs so many times in the form of a circular density granülomatosis'dir necrosis. There are in the middle of Intracavernous. The lesions are usually bilateral. Kavemlerin thick walls. Furthermore, scattered bronchopneumonitises infiltrates or nodular lesions are seen peribronişiyal. Secondary bacterial or fungal infections are common.
Skin, joint and muscle lesions are too.
Progressive nature of kidney disease. During the terminal uremia and other symptoms of the disease seen in general arteritis. High fever, arteritis, hemorrhagic lesions on the skin and mucous membranes, anemia, and leukocytosis are.
Wegener's granulomatosis disease prognosis is poor. Untreated cases, death is 6-8 months. Worse prognosis in patients with kidney disease. Effective treatment is provided by cyclophosphamide. Oral or intravenous drug use cases, showing very rapid progress. 1-3 weeks of treatment, improvement in clinical symptoms observed. WBC count should be carefully monitored and adjusted dose of cyclophosphamide to be kept up from 3.000/mm3. 1.000-1.500/mm3 should not fall down from the number of lymphocytes, so that the patient would be protected from infections. The other is an immunosuppressive drug azathioprine Siklofosfamid'e patients without tolerance. This is the same dose of the drug siklofos-famidin. If the disease is a severe at the beginning of cyclophosphamide together with corticosteroids, the dose of 1 mg / kg / day in reducing the clinical symptoms-lınca or disappeared (about 2 weeks) corticosteroid is reduced gradually, the day is over and then cut off. A full recovery after treatment with cyclophosphamide husule should continue for at least another year. Cyclophosphamide treatment improved the prognosis of Wegener's granulomatosis disease, most patients live for many years after discontinuation of medication.
Loeffler Syndrome
Chest radiograph of a temporary nature are infiltration and increased eosinophils in the blood. The disease typically recover up to 2 weeks. The main clinical symptom of a mild cough, fever and fatigue sübfebril. Sometimes these symptoms are absent or hard to overlook nature. Chest X-ray in the infiltration kuşkulanılır disease. Approximately 20% of blood eosinophils and the patient's own history supports the diagnosis of allergy. Radiograph infiltrates in the mobile, temporary and homogeneous nature. Concentration limit is not specific, may be single or multiple. Show the localization of a segment. Concentration is reduced after a few days and 6-12 days will be lost. Lung infiltration-tions in some cases, nodular or round.
20,000 or more have increased blood leukocytes and leukocytosis related to the increase in eosinophils.
Loeffler's syndrome may be caused by the different nature of many allergens. Ascaris lumbricoides is one of them (page 58), other parasites, and some medications such paraaminosalisilik acid (PAS), aspirin, penicillin, sulfonamides, and Loeffler's syndrome can lead to some pollens and inhaled allergens.
Chest X-ray diagnosis of pneumonia, tuberculosis, and away from the shadow of a temporary nature. Loeffler's syndrome supports the increase of eosinophils in the blood.
20,000 or more have increased blood leukocytes and leukocytosis related to the increase in eosinophils.
Loeffler's syndrome may be caused by the different nature of many allergens. Ascaris lumbricoides is one of them (page 58), other parasites, and some medications such paraaminosalisilik acid (PAS), aspirin, penicillin, sulfonamides, and Loeffler's syndrome can lead to some pollens and inhaled allergens.
Chest X-ray diagnosis of pneumonia, tuberculosis, and away from the shadow of a temporary nature. Loeffler's syndrome supports the increase of eosinophils in the blood.
What is Sarkoidosis
Common systemic granulomatous disease of unknown cause Sarkoidosis are placed in the pulmonary infiltrates. The main places to be seen in lung and intrathoracic lymph nodes.
Mediastinum, hilar and perihilar lymph nodes, lung, liver, spleen, skin, eyes, phalangeal bones, and parotid glands are the organs that the disease most chosen. Sarcoidosis is found in almost every country. However, Scandinavia, Britain and the United States are at an increased. 5-10/100.000 incidence is.
Turkey is a rare disease with increasing frequency monitored. Men, women, blacks and whites, 30-40 years of age are more numerous, but can be seen at any age.
Sarcoidosis Etiology
Sarcoidosis is a definite cause of disease to be determined.
Some genetic, immunological problems, the effects of a growing assumption in the etiology of the disease.
Incidence of sarcoidosis in some areas, people have a lot of families, and supports this hypothesis.
Pathology
About 90% of cases of sarcoidosis in lung and hilar lymph nodes loka-lize. Other organs also settles. Casein-Fi histopathological feature of the disease, non-necrotic granulomatous inflammatory tissue reaction. Sometimes it may occur less caseation qualifications. Epithelioid cell granuloma, or tubercle Langhans giant cells and inclusion bodies found in the nature of the tissue. Pathognomonic for this disease is not seen in sarcoidosis epithelioid tubercles. Other diseases such as tuberculosis, diseases and Hodgkin'de fiıngus can be seen.
Clinical symptoms of Sarcoidosis
Clinical symptoms and general symptoms often related to the localization of other organs. For example akut.dönemde approximately 30% of cases seen in erythema nodosum. Fatigue, anorexia, weight loss, fatigue and general symptoms such as fever sübfebril often insidious nature. All of these symptoms are not together. For example, 50% of fever cases are observed.
Lung symptoms
Clinical symptoms of the respiratory system depends on the particular formation of lung parenkimasında inifiltrasyonunun. Pulmonary symptoms such as dry cough and dyspnea seen in 25% of cases. Hemoptysis is rare. Physical examination, there is a glimpse of the early stages of the disease.
Depending on the degree of localization of the disease and sibilan, ronflan and age Railer be heard.
75% of patients with peripheral lymphadenopathy in sarcoidosis has LenfadenopatL. Most hilar and paratracheal lymphadenopathy is seen in the region. This adenopa-depressive symptoms often bilateral and symmetrical.
Eye lesions. Characteristic eye lesions, uveitis. Seen in 25% of cases. Conjunctiva, sclera, retina, the lesion may be.
Skin lesions. Nodozumdur one characteristic erythema, temporary nature and usually occurs in the lower extremities. In some cases of acute sarcoidosis, erythema nodosum, fever, arthralgia, and hilar lymphadenopathy are with. The front faces of the legs tight, bright red nodules typical lesion of erythema nodosum usually bilateral. Arm, calf and can be found in the body.
The nodules appear suddenly, but slowly heal. Recovered before the tension is reduced erythema, dark ecchymotic consists of a color, and then heal without leaving a trace or no complication.
Erythema nodosum is a skin lesion is not specific for sarcoidosis. Tuberculosis, kolagen disease, ulcerative colitis, bacterial, viral and fungal infections and drug-ment may be related to a reaction. For example, sulfonamide, iodine, bromide, tetracycline and oral contraceptives can create erythema nodosum.
Liver and spleen lesions. Biopsy and autopsy cases, 75% of the lesions of sarcoidosis are the liver and dalakda. However, such a possibility with the clinical examination in 25% of cases are observed.
Bone and joint lesions. Especially the large joints such as knees, ankles and mono-or polyarticular arthritis symptoms observed in acute or chronic nature. In these cases, granulomatous sarcoid-lomasım sinovia membrane biopsy shows. Hands and feet of cystic bone lesions, such as the terminal falankslarında staple holes for a typical finding in sarcoidosis, but 5% of cases seen in these lesions.
Lesions of salivary glands. 5% of cases in the parotid, sublingual glands and submaksiler husule asimptomatik revenue growth. However, the growth of mumps parotid painful.
Growth of salivary glands, glands in some cases, the growth of eye, uveitis, and fever that accompany it are called uveoparotid fire.
Kidney and heart complications of sarcoidosis, or can be monitored.
Lezyonlaru different nature of the nervous system, most commonly seen facial paralysis. One way or bilateral, often heal spontaneously.
Radiological findings. In the case of about 90% of intrathoracic sarcoidosis lesions have the radiological examination in the diagnosis of disease is important. In the bilateral hilar adenopathy with right paratracheal adenopathy is a common finding.
Sarkoidosis Laboratory
Sarcoidosis is a two-thirds of patients with late skin reactions, for example, tuberculin skin test (PPD) was negative. TEMPERATURE circulating T lymphocytes are closely related to a reduction in skin anergy.
In most patients, increased sedimentation rate. Electrophoresis of serum gamma and beta fraction of 50% of cases are seen hyperglobulinemia.
Kveim test in sarcoidosis cases 2 / 3 'in the positive. For this test, spleen or lymph nodes of patients with human sarcoidosis tissue suspension (antigen) is injected into the skin. Papulonodular granulomatous lesion develops 4-6 weeks after the examination of tissue necrosis seen in non-positive for the diagnosis of sarcoidosis. However, the standard for a long time to wait for the result of people have power because of antigen Kveim test increasingly applied to a lesser extent.
And angiotensin converting enzyme in lung tissue retention Galium'un (ACE) tests are tests to help. These tests and the Kveim test is not specific qualifications.
Lung function tests
Pulmonary function abnormalities increases with increasing infiltration of lung parenkimasında sarcoidosis. These abnormalities are usually restrictive nature: vital capacity, diffusion capacity and compliance is reduced. Hypoxemia at rest and after exertion before the more advanced stages of the disease occurs. Diffusion capacity is an important test for the evaluation of treatment effect and prognosis.
Diagnosis
Two findings are important for diagnosis: 1 Clinical and radiological findings, in accordance with the non-granulomatous lesions kazeifıkasyonu. 2. Of granulomatous inflammation in the absence of other diseases.
Direct biopsy of lymph nodes or tissues obtained by bronchoscopy or medias-tinoskopide non-caseating granulomatous tissue appearance of sarcoidosis is diagnosed. These biopsies are negative, liver biopsy may be helpful in diagnosis.
Bronchoalveolar lavage (BAL), a finding in accordance with the high rate of diagnosis of the disease seen in lymphocytes.
Treatment and prognosis
Asymptomatic patients do not need treatment. There is no cure for sarcoidosis spesiifık. However, to prevent and reduce disease activity in corticosteroid has no effect. Corticosteroid treatment indications: 1 Active eye lesions, 2.İlerleyici lung lesions, 3 Persistent hypercalcemia or hiperkal-siüri, 4 Central nervous system lesions and functional abnormalities of the 5th Fever, systemic symptoms such as weight loss, 6 Significant cardiovascular abnormalities.
Start with 40-50 mg daily prednisone therapy. 2 weeks after the drug every 2 days by reducing 5 mg, 30 mg / day for 2 weeks of treatment is continued. And then in the same way by reducing the 10-20 mg / day prednisone maintenance dose is applied. Prednisone therapy improves clinical symptoms in 1-2 weeks. A few months after the disease will decline. Corticosteroid therapy should continue for at least 6 months. The dose and duration of improvement in chest radiographs, pulmonary function and systemic symptoms, according to the set. In some cases, healing occurs 12-18 months, in some cases take longer. In some cases, good results can be taken with a maintenance dose every other day.
Mediastinum, hilar and perihilar lymph nodes, lung, liver, spleen, skin, eyes, phalangeal bones, and parotid glands are the organs that the disease most chosen. Sarcoidosis is found in almost every country. However, Scandinavia, Britain and the United States are at an increased. 5-10/100.000 incidence is.
Turkey is a rare disease with increasing frequency monitored. Men, women, blacks and whites, 30-40 years of age are more numerous, but can be seen at any age.
Sarcoidosis Etiology
Sarcoidosis is a definite cause of disease to be determined.
Some genetic, immunological problems, the effects of a growing assumption in the etiology of the disease.
Incidence of sarcoidosis in some areas, people have a lot of families, and supports this hypothesis.
Pathology
About 90% of cases of sarcoidosis in lung and hilar lymph nodes loka-lize. Other organs also settles. Casein-Fi histopathological feature of the disease, non-necrotic granulomatous inflammatory tissue reaction. Sometimes it may occur less caseation qualifications. Epithelioid cell granuloma, or tubercle Langhans giant cells and inclusion bodies found in the nature of the tissue. Pathognomonic for this disease is not seen in sarcoidosis epithelioid tubercles. Other diseases such as tuberculosis, diseases and Hodgkin'de fiıngus can be seen.
Clinical symptoms of Sarcoidosis
Clinical symptoms and general symptoms often related to the localization of other organs. For example akut.dönemde approximately 30% of cases seen in erythema nodosum. Fatigue, anorexia, weight loss, fatigue and general symptoms such as fever sübfebril often insidious nature. All of these symptoms are not together. For example, 50% of fever cases are observed.
Lung symptoms
Clinical symptoms of the respiratory system depends on the particular formation of lung parenkimasında inifiltrasyonunun. Pulmonary symptoms such as dry cough and dyspnea seen in 25% of cases. Hemoptysis is rare. Physical examination, there is a glimpse of the early stages of the disease.
Depending on the degree of localization of the disease and sibilan, ronflan and age Railer be heard.
75% of patients with peripheral lymphadenopathy in sarcoidosis has LenfadenopatL. Most hilar and paratracheal lymphadenopathy is seen in the region. This adenopa-depressive symptoms often bilateral and symmetrical.
Eye lesions. Characteristic eye lesions, uveitis. Seen in 25% of cases. Conjunctiva, sclera, retina, the lesion may be.
Skin lesions. Nodozumdur one characteristic erythema, temporary nature and usually occurs in the lower extremities. In some cases of acute sarcoidosis, erythema nodosum, fever, arthralgia, and hilar lymphadenopathy are with. The front faces of the legs tight, bright red nodules typical lesion of erythema nodosum usually bilateral. Arm, calf and can be found in the body.
The nodules appear suddenly, but slowly heal. Recovered before the tension is reduced erythema, dark ecchymotic consists of a color, and then heal without leaving a trace or no complication.
Erythema nodosum is a skin lesion is not specific for sarcoidosis. Tuberculosis, kolagen disease, ulcerative colitis, bacterial, viral and fungal infections and drug-ment may be related to a reaction. For example, sulfonamide, iodine, bromide, tetracycline and oral contraceptives can create erythema nodosum.
Liver and spleen lesions. Biopsy and autopsy cases, 75% of the lesions of sarcoidosis are the liver and dalakda. However, such a possibility with the clinical examination in 25% of cases are observed.
Bone and joint lesions. Especially the large joints such as knees, ankles and mono-or polyarticular arthritis symptoms observed in acute or chronic nature. In these cases, granulomatous sarcoid-lomasım sinovia membrane biopsy shows. Hands and feet of cystic bone lesions, such as the terminal falankslarında staple holes for a typical finding in sarcoidosis, but 5% of cases seen in these lesions.
Lesions of salivary glands. 5% of cases in the parotid, sublingual glands and submaksiler husule asimptomatik revenue growth. However, the growth of mumps parotid painful.
Growth of salivary glands, glands in some cases, the growth of eye, uveitis, and fever that accompany it are called uveoparotid fire.
Kidney and heart complications of sarcoidosis, or can be monitored.
Lezyonlaru different nature of the nervous system, most commonly seen facial paralysis. One way or bilateral, often heal spontaneously.
Radiological findings. In the case of about 90% of intrathoracic sarcoidosis lesions have the radiological examination in the diagnosis of disease is important. In the bilateral hilar adenopathy with right paratracheal adenopathy is a common finding.
Sarkoidosis Laboratory
Sarcoidosis is a two-thirds of patients with late skin reactions, for example, tuberculin skin test (PPD) was negative. TEMPERATURE circulating T lymphocytes are closely related to a reduction in skin anergy.
In most patients, increased sedimentation rate. Electrophoresis of serum gamma and beta fraction of 50% of cases are seen hyperglobulinemia.
Kveim test in sarcoidosis cases 2 / 3 'in the positive. For this test, spleen or lymph nodes of patients with human sarcoidosis tissue suspension (antigen) is injected into the skin. Papulonodular granulomatous lesion develops 4-6 weeks after the examination of tissue necrosis seen in non-positive for the diagnosis of sarcoidosis. However, the standard for a long time to wait for the result of people have power because of antigen Kveim test increasingly applied to a lesser extent.
And angiotensin converting enzyme in lung tissue retention Galium'un (ACE) tests are tests to help. These tests and the Kveim test is not specific qualifications.
Lung function tests
Pulmonary function abnormalities increases with increasing infiltration of lung parenkimasında sarcoidosis. These abnormalities are usually restrictive nature: vital capacity, diffusion capacity and compliance is reduced. Hypoxemia at rest and after exertion before the more advanced stages of the disease occurs. Diffusion capacity is an important test for the evaluation of treatment effect and prognosis.
Diagnosis
Two findings are important for diagnosis: 1 Clinical and radiological findings, in accordance with the non-granulomatous lesions kazeifıkasyonu. 2. Of granulomatous inflammation in the absence of other diseases.
Direct biopsy of lymph nodes or tissues obtained by bronchoscopy or medias-tinoskopide non-caseating granulomatous tissue appearance of sarcoidosis is diagnosed. These biopsies are negative, liver biopsy may be helpful in diagnosis.
Bronchoalveolar lavage (BAL), a finding in accordance with the high rate of diagnosis of the disease seen in lymphocytes.
Treatment and prognosis
Asymptomatic patients do not need treatment. There is no cure for sarcoidosis spesiifık. However, to prevent and reduce disease activity in corticosteroid has no effect. Corticosteroid treatment indications: 1 Active eye lesions, 2.İlerleyici lung lesions, 3 Persistent hypercalcemia or hiperkal-siüri, 4 Central nervous system lesions and functional abnormalities of the 5th Fever, systemic symptoms such as weight loss, 6 Significant cardiovascular abnormalities.
Start with 40-50 mg daily prednisone therapy. 2 weeks after the drug every 2 days by reducing 5 mg, 30 mg / day for 2 weeks of treatment is continued. And then in the same way by reducing the 10-20 mg / day prednisone maintenance dose is applied. Prednisone therapy improves clinical symptoms in 1-2 weeks. A few months after the disease will decline. Corticosteroid therapy should continue for at least 6 months. The dose and duration of improvement in chest radiographs, pulmonary function and systemic symptoms, according to the set. In some cases, healing occurs 12-18 months, in some cases take longer. In some cases, good results can be taken with a maintenance dose every other day.
What is Sjogren's Syndrome
Artritis'in be considered a variant of rheumatoid disease, Sjogren's syndrome, a kolagen consists of 3 main abnormality: 1 Keratoconjunctivitis, tear glands related lesions, 2 Xerostomia (dry mouth), related to abnormalities of the salivary glands, 3 Rheumatoid arthritis. The discovery of two of these three indications that the disease is diagnosed. A rare disease that occurs in women more.
Sjogren's syndrome, scleroderma, polimyositis, Lupus Erythematosus, or polyarteritis nodosa can be found with the disease.
Sjogren's Disease
Salivary glands because of abnormalities in patients with chewing and swallowing difficulties, dental caries, gingivitis, oral mucosa ulcerations husule income. Dry mouth up, respiratory, larynx, trachea and bronchi can cause infections.
The blood of rheumatoid factor, antinuclear factor increased. Approximately one-third of the patients in the reticulo-nodular pulmonary radiography kolagen diseases are an anomaly.
Treatment is symptomatic. Serious and life-threatening cases, corticosteroids are used. Progressive nature of disease. Death is usually related to complications of pneumonia.
Sjogren's syndrome, scleroderma, polimyositis, Lupus Erythematosus, or polyarteritis nodosa can be found with the disease.
Sjogren's Disease
Salivary glands because of abnormalities in patients with chewing and swallowing difficulties, dental caries, gingivitis, oral mucosa ulcerations husule income. Dry mouth up, respiratory, larynx, trachea and bronchi can cause infections.
The blood of rheumatoid factor, antinuclear factor increased. Approximately one-third of the patients in the reticulo-nodular pulmonary radiography kolagen diseases are an anomaly.
Treatment is symptomatic. Serious and life-threatening cases, corticosteroids are used. Progressive nature of disease. Death is usually related to complications of pneumonia.
Polimyositis and Dermatomyositis
This muscle striated muscle diseases, the immune düzensizliğiyle ilgilidir.Polimyositis and dermatomyositis dejeneresansa widespread and symmetrical, proximal muscle weakness and atrophy is caused in particular.
Polimyositis a rare disease. In women than in men. In some cases, Systemic Lupus Erythematosus, rheumatoid arthritis or are close affinity skleroder-yeast.
Fıbrosis'in idiopathic interstitial pulmonary histopathology is the same. Soft tissue calcification is commonly observed. Furthermore, early in the disease, pulmonary alveolar cells and desquamation husule arteriolitis income.
Polymyositis, the most-watched ever-increasing clinical symptoms of dyspnea and cough. Approximately 40% of patients are seen before the symptoms of lung disease, skin and muscle.
Attenuation of proximal muscles develops. November abnormalities niteliğindedir a connective tissue disease, myasthenia gravis, myopathies, and other similar.
Radiography of the common interstitial lung fibrosis, scleroderma, or idiopathic widespread reticular or reticulonodular interstitial pulmonary fıbrosis'e shows that a similar abnormality.
Corticosteroids, may be effective in 50% of patients.
Polimyositis a rare disease. In women than in men. In some cases, Systemic Lupus Erythematosus, rheumatoid arthritis or are close affinity skleroder-yeast.
Fıbrosis'in idiopathic interstitial pulmonary histopathology is the same. Soft tissue calcification is commonly observed. Furthermore, early in the disease, pulmonary alveolar cells and desquamation husule arteriolitis income.
Polymyositis, the most-watched ever-increasing clinical symptoms of dyspnea and cough. Approximately 40% of patients are seen before the symptoms of lung disease, skin and muscle.
Attenuation of proximal muscles develops. November abnormalities niteliğindedir a connective tissue disease, myasthenia gravis, myopathies, and other similar.
Radiography of the common interstitial lung fibrosis, scleroderma, or idiopathic widespread reticular or reticulonodular interstitial pulmonary fıbrosis'e shows that a similar abnormality.
Corticosteroids, may be effective in 50% of patients.
What is Disease Scleroderma (Systemic Sclerosis)
Kolagen Sekleroderma a disease that can cause organ atrophy and sclerosis. Skin, gastrointestinal tract, especially esophageal, lung, no other muscle, bone, heart, kidney and other organs are systemic spread. Middle age is more common in women than in men.
Scleroderma Systemic Lupus Erythematosus disease, there are aspects of rheumatoid lung and similar diseases such as Sjogren's syndrome. A rare disease, the incidence is less than 3/100.000. Associated with the immune disorder of unknown cause. Histopathology 90% of cases there are changes in lung fibrosis. However, 25% of all cases and 15% of clinical symptoms, radiographic abnormalities are observed.
Pathology
In the early period are the connective tissue edema and cell infiltration. Develop the disease progresses, a fibrous reaction. Consists of more advanced periods of atrophy. Widespread interstitial fibrosis in the lungs, alveoli, thickening of the walls of the artery and vein is husule. Parenkiması further periods of lung connective tissue is infested with, narrowing and blockage of blood vessels develops. These changes followed the same as in idiopathic pulmonary interstitial fibrosis. Skleroderma'nın morphological abnormalities in other organs, causing the separation of idiopathic interstitial allows fibrosis'den.
Clinical symptoms of Scleroderma Lung
Clinical diagnosis of extrapulmonary organs, especially the skin is determined anormallirlerle. Thickened skin, the flexibility is lost, there is a view, especially the face and extremities, wax, bronze skin color would be like so many times. Most patients have Raynaud's syndrome, many times before skin lesions are seen. Raynaud's syndrome, cold, excitement, and factors such as smoking spasmıdır small vessels, especially the fingers. Raynaud's syndrome related to these factors, the fingers iskemiyle syanotik, consists of a purple appearance. Factors improves the color of the fingers disappeared.
Esophageal dilatation and dysphagia and dyspepsia due to a decrease of peristaltic movements occur. Lesions in the duodenum and the columns developed ileus, diverticulitis, constipation or diarrhea can cause such symptoms.
Scleroderma lung disease symptoms are not specific, as well as other organs. A mild cough, sputum, and there is a progressive dyspnea. In some cases, chest radiographs show a change in certain patients, but started to dyspnea.
Radiological findings
Period of the disease is about to change according to radiographic interstitial fibrosis, reticular or reticulonodular changes are seen. İdyo-booties interstisiel fibrosis as fine reticular pattern early in the disease has been localized in the lower lobes, upper lobes are normal. Next in the reticular and fibrous infiltration becomes more prevalent and increasing lung volume is decreased. Between reticular and nodular infiltrates and cystic fibrosis husule a change in income. Cysts are more localized to the lung periphery and the diameter is usually smaller than 1 part. Other kolagen pleuritis and pleural diseases, scleroderma, although rarely observed liquid.
Esophageal dilatation and swallowing difficulties as a result of peristaltic movements, reduction of income husule. In some cases, radiographic findings can be seen in the dilated esophagus with air contrast (air özofagogram'ı). Taken in the expansion of esophageal baryumla opera is better.
Phalanx joints such as rheumatoid artritis'deki 25% of the cases observed changes.
Lung function tests and laboratory findings
Function abnormalities, and especially the reduction in diffusion capacity has Skleroderma'da restrictive. Compliance is reduced. First, exertion, hypoxemia develops disease istirahatda proceed. In some cases, radiographic findings of pulmonary function abnormalities, especially before the observed decrease in diffusion.
In some cases, LE cells, latex test is positive and in some cases. Protein electrophoresis globülin'in gamma increases.
Scleroderma Treatment
Corticosteroid in the treatment of scleroderma lung disease have been some successful results. The dose and duration of the disease are the same as other kolagen. Salicylate joint symptoms, Raynaud's, such as reserpine vascular events has resulted in some cases.
Scleroderma Systemic Lupus Erythematosus disease, there are aspects of rheumatoid lung and similar diseases such as Sjogren's syndrome. A rare disease, the incidence is less than 3/100.000. Associated with the immune disorder of unknown cause. Histopathology 90% of cases there are changes in lung fibrosis. However, 25% of all cases and 15% of clinical symptoms, radiographic abnormalities are observed.
Pathology
In the early period are the connective tissue edema and cell infiltration. Develop the disease progresses, a fibrous reaction. Consists of more advanced periods of atrophy. Widespread interstitial fibrosis in the lungs, alveoli, thickening of the walls of the artery and vein is husule. Parenkiması further periods of lung connective tissue is infested with, narrowing and blockage of blood vessels develops. These changes followed the same as in idiopathic pulmonary interstitial fibrosis. Skleroderma'nın morphological abnormalities in other organs, causing the separation of idiopathic interstitial allows fibrosis'den.
Clinical symptoms of Scleroderma Lung
Clinical diagnosis of extrapulmonary organs, especially the skin is determined anormallirlerle. Thickened skin, the flexibility is lost, there is a view, especially the face and extremities, wax, bronze skin color would be like so many times. Most patients have Raynaud's syndrome, many times before skin lesions are seen. Raynaud's syndrome, cold, excitement, and factors such as smoking spasmıdır small vessels, especially the fingers. Raynaud's syndrome related to these factors, the fingers iskemiyle syanotik, consists of a purple appearance. Factors improves the color of the fingers disappeared.
Esophageal dilatation and dysphagia and dyspepsia due to a decrease of peristaltic movements occur. Lesions in the duodenum and the columns developed ileus, diverticulitis, constipation or diarrhea can cause such symptoms.
Scleroderma lung disease symptoms are not specific, as well as other organs. A mild cough, sputum, and there is a progressive dyspnea. In some cases, chest radiographs show a change in certain patients, but started to dyspnea.
Radiological findings
Period of the disease is about to change according to radiographic interstitial fibrosis, reticular or reticulonodular changes are seen. İdyo-booties interstisiel fibrosis as fine reticular pattern early in the disease has been localized in the lower lobes, upper lobes are normal. Next in the reticular and fibrous infiltration becomes more prevalent and increasing lung volume is decreased. Between reticular and nodular infiltrates and cystic fibrosis husule a change in income. Cysts are more localized to the lung periphery and the diameter is usually smaller than 1 part. Other kolagen pleuritis and pleural diseases, scleroderma, although rarely observed liquid.
Esophageal dilatation and swallowing difficulties as a result of peristaltic movements, reduction of income husule. In some cases, radiographic findings can be seen in the dilated esophagus with air contrast (air özofagogram'ı). Taken in the expansion of esophageal baryumla opera is better.
Phalanx joints such as rheumatoid artritis'deki 25% of the cases observed changes.
Lung function tests and laboratory findings
Function abnormalities, and especially the reduction in diffusion capacity has Skleroderma'da restrictive. Compliance is reduced. First, exertion, hypoxemia develops disease istirahatda proceed. In some cases, radiographic findings of pulmonary function abnormalities, especially before the observed decrease in diffusion.
In some cases, LE cells, latex test is positive and in some cases. Protein electrophoresis globülin'in gamma increases.
Scleroderma Treatment
Corticosteroid in the treatment of scleroderma lung disease have been some successful results. The dose and duration of the disease are the same as other kolagen. Salicylate joint symptoms, Raynaud's, such as reserpine vascular events has resulted in some cases.
Rheumatoid Lung Disease
Common cases of interstitial pulmonary fibrosis due to approximately 20% of rheumatoid arthritis. A non-specific interstitial pneumonia in the first period of the disease has. The disease progresses, fibrous tissue increases the "honeycomb" appearance of bronchiectasis develop. In most cases, central necrosis of the granuloma is a thin "rheumatoid granuloma" develops. The most common clinical symptom, exertional dyspnea. In some patients, finger drum, in the form of myth and osteoarthropathy observed deformation. In some cases, LE cells are seen.
Rheumatoid Arthritis Lung Eclipse
Radiography of the disease in subacute nodular lesions are observed. Nodules ufaksa view miiyer tuberculosis, yellow-koidoz nodules greater than or similar to pnömokonyoza. Chronic period, reticular, and "honeycomb" is change. In some cases, pulmonary infiltrates with pleural effusion is located.
Thorax or pleural effusion of rheumatoid artritis'in Plöritis common complications. Exudative pleural effusion is light yellow or yellowish green color. Fluid glucose decreased in a certain way, or even less may be 25 mg%. Chloride is normal (tuberculous pleural fluid glucose and chloride and decreases). Pleural fluid in rheumatoid arthritis leukocytes, particularly lymphocytes, lactate dehydrogenase (LDH), and rheumatoid factor increases. In some cases, although not increased in the blood of rheumatoid factor in pleural fluid may increase. Rheumatoid pleural fluids is less than once to make any clinical symptoms.
Rheumatoid lung nodules are rare, usually are associated with rheumatoid arthritis and subcutaneous nodules. Pathologic features are as subcutaneous nodules. Nodules in the middle of a fibrinoid necrosis and granulation tissue necrosis are intense around. Rheumatoid lung nodules in patients with clinical symptoms usually do not. However, these nodules have grown a lot and when they are infected may develop clinical symptoms. In some cases, may cough and hemoptysis. Sedimentation has generally increased, and anemia. Radiography lung periphery, 3-7 mm in diameter, sübplöral, monitored around the well defined single or multiple nodules. Kavernleşme nodules are common. Kaveri thick wall, the inner boundary is homogeneous. Lung nodules are lost or grow, sometimes with pleural effusion or pneumothorax have.
Rheumatoid pnömokonyosis (Caplan syndrome) is a disease seen in mine workers. Diameter round shadows in the lungs of these patients, 0.5-5 sm (nodules), and there are pnömokonyosis fibrosis'i. The nodules are usually multiple, occur suddenly emerge and grow rapidly. Pulmonary rheumatoid nodules in the middle of necrosis, necrosis around the core of macrophages and polymorphonuclear leukocytes are formed by a granulation tissue. Necrosis of macrophages in the vicinity of the accumulation of dust in the mine is a dark ring husule that allows the separation of other rheumatoid nodules. There is no separation of these nodules Radiography other rheumatoid nodules. In some cases, these lesions disappear.
Pulmonary arteritis with rheumatoid lung disease is a common abnormality. Progression of the disease gradually narrows arteries, pulmonary hypertension and cor pulmonale develops later.
Rheumatoid lung disease are treated with salicylate and kortikosteroid'le. Rheumatoid nodule and Caplan's syndrome is more effective than corticosteroids.
Rheumatoid Arthritis Lung Eclipse
Radiography of the disease in subacute nodular lesions are observed. Nodules ufaksa view miiyer tuberculosis, yellow-koidoz nodules greater than or similar to pnömokonyoza. Chronic period, reticular, and "honeycomb" is change. In some cases, pulmonary infiltrates with pleural effusion is located.
Thorax or pleural effusion of rheumatoid artritis'in Plöritis common complications. Exudative pleural effusion is light yellow or yellowish green color. Fluid glucose decreased in a certain way, or even less may be 25 mg%. Chloride is normal (tuberculous pleural fluid glucose and chloride and decreases). Pleural fluid in rheumatoid arthritis leukocytes, particularly lymphocytes, lactate dehydrogenase (LDH), and rheumatoid factor increases. In some cases, although not increased in the blood of rheumatoid factor in pleural fluid may increase. Rheumatoid pleural fluids is less than once to make any clinical symptoms.
Rheumatoid lung nodules are rare, usually are associated with rheumatoid arthritis and subcutaneous nodules. Pathologic features are as subcutaneous nodules. Nodules in the middle of a fibrinoid necrosis and granulation tissue necrosis are intense around. Rheumatoid lung nodules in patients with clinical symptoms usually do not. However, these nodules have grown a lot and when they are infected may develop clinical symptoms. In some cases, may cough and hemoptysis. Sedimentation has generally increased, and anemia. Radiography lung periphery, 3-7 mm in diameter, sübplöral, monitored around the well defined single or multiple nodules. Kavernleşme nodules are common. Kaveri thick wall, the inner boundary is homogeneous. Lung nodules are lost or grow, sometimes with pleural effusion or pneumothorax have.
Rheumatoid pnömokonyosis (Caplan syndrome) is a disease seen in mine workers. Diameter round shadows in the lungs of these patients, 0.5-5 sm (nodules), and there are pnömokonyosis fibrosis'i. The nodules are usually multiple, occur suddenly emerge and grow rapidly. Pulmonary rheumatoid nodules in the middle of necrosis, necrosis around the core of macrophages and polymorphonuclear leukocytes are formed by a granulation tissue. Necrosis of macrophages in the vicinity of the accumulation of dust in the mine is a dark ring husule that allows the separation of other rheumatoid nodules. There is no separation of these nodules Radiography other rheumatoid nodules. In some cases, these lesions disappear.
Pulmonary arteritis with rheumatoid lung disease is a common abnormality. Progression of the disease gradually narrows arteries, pulmonary hypertension and cor pulmonale develops later.
Rheumatoid lung disease are treated with salicylate and kortikosteroid'le. Rheumatoid nodule and Caplan's syndrome is more effective than corticosteroids.
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