Chronic Obstructive Pulmonary Disease (Copd)

Chronic obstructive pulmonary disease (COPD) is defined as only partially reversible airway obstruction, which is caused by a pathological inflammatory response to inhaled toxins, often cigarette smoking. ?1-antitrypsin deficiency and a variety of occupational exposures are less common causes in nonsmokers. The symptoms is to productive cough and dyspnea that develop over years; the more common symptoms include soft breath sounds, prolonged expiratory phase and wheezing. Severe cases may be complicated by weight loss, pneumothorax, frequent acute Dekompensationsepisoden, right heart failure and acute respiratory failure. Diagnosis is based on history, physical examination, chest x-ray absorption and lung function tests. Treatment is with bronchodilators, corticosteroids and, if necessary, O2 and antibiotics. About 50% of patients with severe COPD die within 10 years after diagnosis.

COPD includes

Chronic obstructive pulmonary disease (COPD) is defined as only partially reversible airway obstruction, which is caused by a pathological inflammatory response to inhaled toxins, often cigarette smoking. ?1-antitrypsin deficiency and a variety of occupational exposures are less common causes in nonsmokers. The symptoms is to productive cough and dyspnea that develop over years; the more common symptoms include soft breath sounds, prolonged expiratory phase and wheezing. Severe cases may be complicated by weight loss, pneumothorax, frequent acute Dekompensationsepisoden, right heart failure and acute respiratory failure. Diagnosis is based on history, physical examination, chest x-ray absorption and lung function tests. Treatment is with bronchodilators, corticosteroids and, if necessary, O2 and antibiotics. About 50% of patients with severe COPD die within 10 years after diagnosis. COPD includes chronic obstructive bronchitis (clinically defined) emphysema (pathologic or radiographic determined) Many patients show characteristics of both diseases. Chronic obstructive bronchitis is a chronic bronchitis with airway obstruction. Chronic bronchitis is defined as productive cough on most days of the week for at least 3 months total time in two consecutive years. Chronic bronchitis is for chronic obstructive pulmonary disease as soon as spirometry can demonstrate airway obstruction. Chronic bronchitis asthma may have a component that is characterized by chronic productive cough, wheezing and partially reversible airway obstruction. It occurs mainly in smokers with asthma history. In some cases (d. Editor’s note. The “asthmatic bronchitis” does not constitute an independent disease) can range from chronic obstructive pulmonary disease and chronic asthma not be clearly distinguished. Emphysema is a destruction of the lung parenchyma, leading to the loss of elastic restoring forces and of alveolar septa as well as centripetal tensile forces in the airways, which in turn causes an increased tendency to collapse the airway. Hyperinflation, flow limitations and air pockets are the result. The air spaces are larger and in course of time, bullae may form. Epidemiology In the US, about 24 million people airway obstructions, about half of them COPD was diagnosed. COPD was the third leading cause which led to 135,000 deaths in 2010 – compared to 52,193 deaths in 1980. From 1980 to 2000, the mortality rate from COPD has increased by 64% (from 40.7 to 66.9 / 100,000) and since then unchanged remained. Prevalence, incidence and mortality rates increase with age. Prevalence is now higher in women, but the overall mortality is similar in both sexes. Incidence and mortality are generally higher in whites and low-income groups, probably because smoking prevalence is higher in these populations. COPD seems within families, regardless of the presence of ?1-antitrypsin deficiency (Alpha-1 antitrypsin deficiency) occur frequently (?1-anti-protease inhibitor). COPD is increasing worldwide due to the increasing consumption of cigarettes in developing countries, the decreased mortality in infectious diseases and the widespread use of biological fuels such as wood, grass, or other organic materials. COPD mortality can also affect developing countries more than developed nations. COPD affects 64 million people and caused 2005> 3 million deaths worldwide and is expected to be the third leading cause worldwide by the year 2030th Etiology There are several causes of COPD: smoking (and less frequently other inhalational exposures) Genetic factors Inhalation exposure of all inhalation exposure is cigarette smoking in most countries, the primary risk factor, although only about 15% of smokers develop COPD clinically. Exposure history of 40 or more pack-years is especially predictive. Smoke of arises in the home when cooking and heating in developing countries is a key factor that contributes to the development of disease. Smoking with hyperreactive bronchial system (defined by increased sensitivity to inhaled methacholine) run higher risk of developing COPD than without, even without clinically manifest asthma. Low body weight, respiratory diseases in children, second-hand smoke in a high degree, exposure to air pollution and job-related matter (z. B. dusts of minerals or cotton) or inhaled chemicals (z. B. Cadmium) contribute to the risk of disease, but are in comparison to the cigarette smoking is of secondary factors Bedeutung.Genetische the best definierteursächliche hereditary disease is the ?1-antitrypsin deficiency (Alpha-1 antitrypsin deficiency), which is a major cause of emphysema in nonsmokers, and increased susceptibility in smokers. In recent years,> 30 genetic variants were found associated with COPD or decline in lung function in selected populations in context, but none has been shown to be as momentous as ?1-antitrypsin. Pathophysiology Several factors cause airway obstruction and other complications of COPD. Inflammation Inhaled exposure can trigger an inflammatory response in the airways and alveoli, which leads to disease in genetically susceptible people. This operation is to be mediated through increased protease activity and decreased anti-protease activity (alpha 1-antitrypsin deficiency). Lung proteases such as neutrophil elastase, tissue metalloproteinases and cathepsins cleave at physiological repair processes elastin and connective tissue. Their activity is normally regulated by anti-proteases such as ?1-antitrypsin, from the airway epithelium secreted Leukoproteinase inhibitor Elafin and connective tissue metalloproteinase inhibitor. In patients with COPD as part of the inflammatory response proteases are released by activated neutrophils and other inflammatory cells. The activity of the proteases exceeds that of the anti-proteases. The consequences are tissue damage and hypersecretion of bronchial secretions. The activation of neutrophils and macrophages also leads to an accumulation of free radicals, superoxide anions and hydrogen peroxide, which inhibit anti-proteases and cause bronchoconstriction, mucosal edema and mucous hypersecretion. The oxidative damage caused by neutrophils, the release profibrotic neuropeptides (z. B. bombesin), and decreased levels of the derived from the endothelium growth factors could be attributed to the apoptotic destruction of the lung parenchyma. Inflammation in COPD increases as the severity of the disease increases, and does not heal completely in severe (advanced) disease, despite smoking cessation from. This chronic inflammation does not seem to corticosteroids anzusprechen.Infektion respiratory infections (for COPD patients are prone) can enhance the progression of lung destruction. Bacteria, in particular Haemophilus influenzae colonize the lower respiratory tract of approximately 30% of patients with COPD. In more severely affected patients (z. B. after previous hospitalization), is often colonized by Pseudomonas aeruginosa or gram-negative bacteria detected. Smoking and respiratory disorders can lead to impaired Sekretclearance in the lower respiratory tract, which predisposes to infections. Repeated infection relapses increase the burden of inflammatory reactions that accelerate the progression of the disease. Evidence that long-term antibiotics intake slows down the disease process of COPD do not lie, but vor.Atemwegsobstruktion The pathophysiological salient characteristic of COPD is the “airflow limitation” caused by “airway obstruction” and / or loss of elastic restoring forces. An obstruction of the airways caused by inflammation mediated hypersecretion of mucus, accumulation of mucus, mucosal edema, bronchospasm, peribronchial fibrosis, and small airways, or a combination of these mechanisms. Alveolar walls are destroyed, thereby parenchymal additions in the respiratory tract, and thereby the possibility of a closure of the airway during exhalation be reduced. Advanced alveoli can sometimes form bullae which are defined as the air spaces of ? 1 cm diameter. Bullae can be traversed completely empty or strands of lung tissue, by which they are to a localized severe emphysema; occasionally they can occupy the entire hemithorax. These changes lead to a loss of elastic restoring forces and hyperinflation. Increased airway resistances increase the work of breathing as well as hyperinflation. The increased work of breathing can lead to alveolar hypoventilation with accompanying hypoxia and hypercapnia, hypoxia although the wird.Komplikationen caused by the ventilation / perfusion (V / Q) -Missverhältnis side “airflow limitation” and sometimes respiratory failure, pulmonary hypertension complications include infections respiratory weight loss and other comorbidities chronic hypoxemia increased pulmonary vascular tone, which in diffuse distribution for pulmonary hypertension (pulmonary hypertension) and cor pulmonale (cor pulmonale) leads. The increase in pulmonary vascular pressure can be increased by the destruction of the pulmonary capillary bed due to the destruction of the alveolar walls. Viral or bacterial respiratory infections are common in patients with COPD and cause a large percentage of acute exacerbations. It is currently believed that acute bacterial infection caused by the acquisition of new strains of bacteria rather than by overgrowth of chronically colonizing bacteria. There may be weight loss, perhaps in response to a reduced calorie intake and increased levels of circulating tumor necrosis factor (TNF) -?. To the other concomitant diseases or complications that have a negative impact on quality of life and survival, including osteoporosis, depression, coronary heart disease, lung cancer, muscle atrophy and gastroesophageal reflux. The extent to which these diseases are consequences of COPD, smoking and accompanying systemic inflammation is unclear. Symptoms and signs a COPD usually takes years to develop and progress. Most patients have smoked ? 20 cigarettes / day for> 20 years. Productive cough is the first symptom is usually that develops in smokers in the fourth or fifth decade of life. Dyspnea that increases persists, occurs with physical exertion or worsened by respiratory infections, occurs when patients are in their late 5th or 6th decade of life. Symptoms are worse usually quickly in patients who continue to smoke and have a higher tobacco exposure. In advanced disease to develop morning headaches and are an indication of nocturnal hypercapnia or hypoxemia. Acute exacerbations occur sporadically in the course of COPD and are announced by increasing severity of symptoms. The specific cause of acute exacerbation can rarely be determined. But exacerbations often occur in connection with trivial infections of the upper airways, acute bacterial bronchitis or exposure to irritants. With progression of COPD acute exacerbations tend to occur more frequently, an average of about 1-3 episodes / year. Symptoms of COPD include wheezing, increased expiratory phase, hyperinflation, which manifests itself as a decrease in volume of the heart and breath sounds, and an enlarged chest anteroposterior diameter (barrel thorax). Patients with advanced emphysema show weight loss, muscle wasting due to immobility, hypoxia or release of systemic inflammatory mediators such as TNF-?. The symptoms in advanced disease include breathing with pursed lip, the use of the respiratory muscles, paradoxical retractions of the lower intercostal spaces during inspiration (Hoover’s sign) and cyanosis. Findings in pulmonary heart disease are distended neck veins split second heart sound with emphasis on the Pulmonalisanteils, tricuspid regurgitation-noise and peripheral edema. A factual, shifted to the right apical impulse is an unusual finding in COPD because the lungs are overinflated. A spontaneous pneumothorax can occur (perhaps caused by ruptured bullae) and should be considered in all patients with COPD whose pulmonary status suddenly deteriorated. Diagnostic chest X-ray Pulmonary function test The diagnosis is confirmed by medical history, physical examination findings and suggested the chest radiographs and lung function tests. Similar symptoms can be caused by asthma, heart failure and bronchiectasis (see table: Differential Diagnosis of COPD). COPD and asthma are sometimes easily confused. COPD with bullae GJLP / CNRI / SCIENCE PHOTO LIBRARY var model = {thumbnailUrl: ‘/-/media/manual/professional/images/m1500338_copd_with_bullae_x-ray_science_photo_library_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media /manual/professional/images/m1500338_copd_with_bullae_x-ray_science_photo_library_high_de.jpg?la=de&thn=0 ‘, title:’ COPD with bullae ‘, description:’ u003Ca id = “v38395403 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003eDieser chest X-ray shows a large bubble in the upper right lung and two large bubbles in the left lung. u003c / p u003e u003c / div u003e ‘credits’ GJLP / CNRI / SCIENCE PHOTO LIBRARY’

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