英文精品课件chronicobstructive pulmonary disease （33p）

COPD SS Visser, Pulmonology Internal Medicine UP Chronic Obstructive pulmonary Disease w Two distinct processes are involved, most often in combination. w Chronic Bronchitis dx on history w Emphysema dx previously on histology, nowadays clinically (good clinical-pathologic- radiologic correlation) Def: Chronic Bronchitis w Excessive tracheobronchial mucus production sufficient to cause cough with expectoration for most days of at least 3 months of the year for 2 consecutive years. w Classification: w Simple chronic bronchitis w Chronic mucopurulent bronchitis w Chronic bronchitis with obstruction w Chronic bronchitis with obstruction and airway hyperreactivity. Def: Emphysema w Permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa (containing alveolar capillaries) and attachments to the bronchial walls. w Classification: w Centriacinar ( centrilobular) emphysema w Panacinar emphysema w Paraseptal emphysema w Senile emphysema Def: COPD w Chronic obstruction to airflow due to chronic bronchitis and/or emphysema. w Degree of obstruction may be less when the patient is free from respiratory infection and may improve with bronchodilator drugs w Significant obstruction is always present Epidemiology of COPD w 30% of smokers develop COPD w 20% of adult males have COPD w 15% of COPD patients are severely symptomatic w 4 th leading cause of death (USA) w Mortality rate still rising w prevalence in low birth weight and low socioeconomic status w Tuberculosis in smokers predisposes to COPD Pathogenesis:Effects of Smoking -1 w Oxidative stress: O2-, OH-,H2O2, HOCl; source of Fe2+ catalizes production of OH- by neutrophils, eosinophils, alveolar macrophages; tar (cigarettes) contains NO and induces iNOStoxic peroxynitrites w Elastin breakdown- activated neutrophils neutrophil elastases and oxidants; -1-AT and metalloproteinase inhibitors (lung defenses) inactivated by smoke w Chemoattractant, upregulation of adhesion molecules neutrophil sequestration in lungs w expression of pro-inflammatory mediators: IL-8, NF-B recruitment of N, B, E and T lymphocytes Effects of smoking -2 w levels of myeloperoxidase and eosinophilic cationic protein bronchoconstriction w levels of TGF- (transforming growth factor) fibrogenesis w Lipid peroxidation and DNA damage point mutations 0f the p53 gene locus epithelial dysplasia and lung cancer w ciliary function retained secretions; airway resistance vagal-mediated smooth muscle contraction w Hypertrophy and hyperplasia of mucus secreting glands secretions Pathogenesis-3 w Air pollution exacerbations of CB related to heavy pollution with SO2 and NO2 w Occupation exposure to organic and inorganic dust or noxious gases accelerated decline in lung function w Infection even mild viral respiratory infections ( rhino virus) may be a major factor associated with etiology as well as progression of disease; severe viral pneumonia early in life may lead to COPD w Genetic factors: - -1-antitrypsin deficiency PIZZ, PISZ, PI00 (PI null null), susceptibility to effects of smoking Pathophysiology w Air trapping- RV and FRC elevated w Hyperinflation TLC elevated w elastic recoil pressure dynamic collapse of airways during expiration ineffective cough mechanism and pursed lips breathing (emphysema) w compliance (emphysema) w airway resistance w Prolonged forced expiratory time (N= 50 Y) w Periacinar/paraseptal E- distention of alveolar spaces adjacent to septal and pleural surfaces Physical signs of COPD w Ronchi- in early disease present on forced expiration, later present in inspiration and expiration w Prolonged forced expiratory time ( 6 seconds) w Hyperinflation: cardiac dullness, liver dullness displaced downwards, A-P chest diameter, heart and breath sounds, Hoover sign w Inspiratory crepitations (lung bases) w Pursed lips breathing ( dynamic airway collapse) w Use accessory respiratory muscles w Signs of cor pulmonale and PHT Emphysema:ChronicBronchitis Emphysema = pink puffer Age (Dx) 60 + y Rest dyspnea mild- mod Exer dyspnea severe Cough Sputum scanty, mucoid Resp infect less often Resp failure terminal Cor pulmonale terminal Chronic Bronchitis = blue bloater 50 y none moderate prominent large volume, purulent often repeatedly common Emphysema:Chronic Bronchitis PHT (rest) 0-mild (exertion) moderate Build Asthenic, cachectic Hematocrit35-45 Breath pattern use accessory muscles of respiration Sleep pattern Normal XRC Hyperinflation Bullae Mild-moderate severe obese, cyanosed 50-55 do not use accessory muscles of respiration sleep apnea bronchovascular markings Emphysema:Chronic Bronchitis Blood gas: PaO2 65 mm Hg PaCO2 35-40 Elastic recoil AW resistance N- Diffusion Cap FEV1 Bronchodilator response Poor 45-60 50-60 Normal N- Better but 55) w Pulmonary rehabilitation and education ( improving quality of life)- exercise program and improved nutrition w Prevention and treatment of complications (cor pulmonale) and limitation of disease progression Treatment -3 w Glucocorticoids only 10% of COPD patients show subjective benefit and improved lung function (FeV1 increase of 20% or more) on systemic GCs; with COPD exacerbation a course of prednisone 40 mg/d for 2 weeks are usually prescribed w Inhaled GCs may severity of exacerbations and need for hospitalisation. Benefit of 10-14 day trial of 30-40mg prednisone for Stage III COPD patients remains to be proven. w Lung volume reduction surgery w Transplantation Airway Diseases - COPD w Smoking w Hyperinflation w Airwa