COPD PDF

Chronic Obstructive Pulmonary Disease PATHOPHYSIOLOGY  Chronic Obstructive Pulmonary Disease COPD denotes a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways. The most common cause of COPD is smoking, as...

Chronic Obstructive Pulmonary Disease PATHOPHYSIOLOGY  Chronic Obstructive Pulmonary Disease COPD denotes a group of respiratory disorders characterized by chronic and recurrent obstruction of airflow in the pulmonary airways. The most common cause of COPD is smoking, as evidenced by the fact that 85% to 90% of persons with COPD have a history of smoking. The term chronic obstructive pulmonary disease encompasses two types of obstructive airway disease: emphysema, and chronic obstructive bronchitis.  Emphysema Emphysema is characterized by a loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds. Enlargement of the air spaces leads to hyperinflation of the lungs and produces an increase in total lung capacity (TLC). Two of the recognized causes of emphysema are smoking, which incites lung injury, and an inherited deficiency of α1- antitrypsin, an antiprotease enzyme that protects the lung from injury.  Emphysema is thought to result from the break-down of elastin and other alveolar wall components by enzymes, called proteases, which digest proteins. The proteases, are released from polymorphonuclear leukocytes, alveolar macrophages, and other inflammatory cells. Cigarette smoke and other irritants stimulate the movement of inflammatory cells into the lungs, resulting in increased release of elastase and other proteases.  There are two commonly recognized types of emphysema: centriacinar, and panacinar. The centriacinar is the most common type of emphysema and is seen predominantly in male smokers. The panacinar is more common in persons with α1- antitrypsin deficiency.  Chronic Bronchitis Chronic bronchitis represents airway obstruction of the major and small airways. The condition is seen most commonly in middle-aged men and is associated with chronic irritation from smoking and recurrent infections. A clinical diagnosis of chronic bronchitis requires a history of a chronic productive cough that has persisted for at least 3 consecutive months in at least 2 consecutive years. The earliest feature of chronic bronchitis is hypersecretion of mucus in the large airways, associated with hypertrophy of the submucosal glands in the trachea and bronchi.  Manifestations Excessive cough, sputum production, and shortness of breath. Frequent exacerbations of infection and respiratory insufficiency are common.  Diagnosis and Treatment In patients with chronic lung disease, the FVC is decreased, the FEV1.0 is decreased, and the ratio of FEV1.0 to FVC is decreased. Lung volume measurements reveal a marked increase in RV, an increase in TLC, and elevation of the RV-to-TLC ratio. Measures of exercise tolerance, nutritional status, hemoglobin saturation, and arterial blood gases can be used to assess the overall impact of COPD on health status and to direct treatment.  Treatment Smoking cessation is the only measure that slows the progression of the disease. Pulmonary rehabilitation includes breathing exercises that focus on restoring the function of the diaphragm, reducing the work of breathing, and improving gas exchange. Immunization for influenza and pneumococcal infections. Bronchodilators. Corticosteroids.  Bronchiectasis Permanent dilation of bronchi caused by destruction of the bronchial muscle wall and elastic supporting tissue. Secondary to a number of abnormalities, including atelectasis, diffuse bronchitis, and cystic fibrosis. Bronchiectasis often followed a necrotizing bacterial pneumonia. Tuberculosis was also commonly associated with bronchiectasis.  Etiology and Pathogenesis Two processes are critical to the pathogenesis of bronchiectasis: obstruction and chronic persistent infection. Both cause damage to the bronchial walls, leading to weakening and dilation. Bronchial dilation is classified as saccular, cylindrical, or varicose. Saccular bronchiectasis involves the proximal third to fourth generation of bronchi.  These bronchi become severely dilated and end blindly in dilated sacs, with collapse and fibrosis of more distal lung tissue. Cylindrical bronchiectasis involves uniform and moderate dilation of the sixth to eighth generations of airways. It is a milder form of disease than saccular bronchiectasis and leads to fewer symptoms. Varicose bronchiectasis involves the second through eighth branchings of bronchi and results in bronchi that resemble varicose veins.  Bronchiectasis can present in either of two forms: 1. Local obstructive process involving a lobe or segment of a lung. 2. Diffuse process involving much of both lungs. Localized bronchiectasis is most commonly caused by conditions such as tumors, and mucus plugs that produce atelectasis and infection due to obstructed drainage of bronchial secretions. Generalized bronchiectasis usually is bilateral and most commonly affects the lower lobes.  It is due largely to inherited impairments of host mechanisms or acquired disorders that permit introduction of infectious organisms into the airways. They include cystic fibrosis, in which airway obstruction is caused by impairment of normal mucociliary function.  Manifestations Chronic productive cough, often with several hundred milliliters of foul-smelling, purulent sputum a day. Hemoptysis is common. Dyspnea and wheezing occur in about 75% of patients. Weight loss, anemia, and other systemic manifestations are common. Clubbing of the fingers is infrequent in mild cases, but common in severe disease.  Diagnosis and Treatment Diagnosis is based on history and imaging studies. The condition often is evident on chest radiographs. High-resolution CT scanning of the chest allows for definitive diagnosis. Treatment consists of early recognition and management of infections along with regular postural drainage and chest physical therapy.  Cystic Fibrosis Cystic fibrosis (CF), is an inherited disorder involving fluid secretion by the exocrine glands in the epithelial lining of the respiratory, gastrointestinal, and reproductive tracts. In addition to chronic respiratory disease, CF is manifested by pancreatic exocrine deficiency and elevation of sodium chloride in the sweat. Cystic fibrosis is inherited as an autosomal recessive trait.  Etiology and Pathogenesis Cystic fibrosis is caused by mutations in a single gene on the long arm of chromosome 7 that encodes for the cystic fibrosis transmembrane regulator (CFTR). The impact on impaired Cl– transport is relatively tissue specific. Similar transport abnormalities and pathophysiologic events take place in the pancreatic and biliary ducts and in the vas deferens in males.  Manifestations Chronic bronchiolitis and bronchitis. Chronic infection. Pulmonary inflammation is another cause of decline in respiratory function in persons with CF. Exocrine pancreatic function is abnormal in more than 85% of affected children. Steatorrhea, diarrhea, and abdominal pain are common. The degree of pancreatic involvement is highly variable.  Diagnosis and Treatment Diagnosis is based on the presence of respiratory and gastrointestinal manifestations typical of CF. A history of CF in a sibling, or a positive newborn screening test result. Confirmatory laboratory tests include the sweat test and DNA tests for CFTR gene mutations. The sweat test, using pilocarpine iontophoresis to collect the sweat followed by chemical analysis of its chloride content.  Diagnosis and Treatment Treatment measures are directed toward early and aggressive measures to slow progression of secondary organ dysfunction. They include the use of antibiotics to prevent and manage infections, the use of chest physical therapy (chest percussion and postural drainage). Mucolytic agents to prevent airway obstruction, and nutritional therapy including pancreatic enzyme replacement.  Supplemental vitamins and minerals and enteric-coated, pH- sensitive pancreatic enzyme supplements. Progress of the disease is variable. Improved medical management has led to longer survival. Today, many people with the disease can expect to live into their 40s and beyond. Lung transplantation is being used as a treatment for persons with end-stage lung disease.