COPD (Chronic Obstructive Pulmonary Disease) Dr. Meg-angela Christi Amores

COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) a disease state characterized by airflow limitation that is not fully reversible Includes: emphysema, chronic bronchitis, and small airways disease

COPD Emphysema Chronic Bronchitis Small airways disease an anatomically defined condition characterized by destruction and enlargement of the lung alveoli Chronic Bronchitis a clinically defined condition with chronic cough and phlegm Small airways disease a condition in which small bronchioles are narrowed

Risk Factors Cigarette Smoking Airway responsiveness Intensity: pack years (sticks/day for years) most highly significant predictor of FEV1 Airway responsiveness asthma, chronic bronchitis, and emphysema are variations of the same basic disease Respiratory infections Remains to be proven

Risk Factors Occupational Exposures Ambient Air pollution general exposure to dust at work coal mining, gold mining, and cotton textile dust Ambient Air pollution living in urban compared to rural areas Remains to be proven Passive, or Second-Hand, Smoking Exposure Genetic Considerations

Natural History Effect of cigarette smoking depends on intensity, timing during growth, basal function

Pathophysiology Airflow obstruction Hyperinflation Determined by spirometry: FEV1 and FVC chronically reduced ratio of FEV1/FVC seldom shows large responses to inhaled bronchodilators Hyperinflation "air trapping“ helps to compensate for airway obstruction

Pathophysiology Gas Exchange Nonuniform ventilation and ventilation-perfusion mismatching

Pathology Large Airway Small Airways Cigarette smoking often results in mucous gland enlargement and goblet cell hyperplasia proportional to cough and mucus production Small Airways major site of increased resistance in most individuals with COPD is in airways 2 mm diameter goblet cell metaplasia and replacement of surfactant-secreting Clara cells with mucus-secreting and infiltrating mononuclear inflammatory cells

Pathology Lung Parenchyma destruction of gas-exchanging airspaces walls become perforated and later obliterated with coalescence of small distinct airspaces into abnormal and much larger airspaces Macrophages accumulate Centriacinar emphysema- most frequently associated with cigarette smoking Panacinar emphysema - usually observed in patients with alpha1AT deficiency

Clinical presentation History cough, sputum production, and exertional dyspnea exertional dyspnea, often described as increased effort to breathe, heaviness, air hunger, or gasping, can be insidious patient's ability to perform them has changed

Clinical presentation Physical Findings entirely normal physical examination – early signs of active smoking, including an odor of smoke or nicotine staining of fingernails prolonged expiratory phase and expiratory wheezing- more severe signs of hyperinflation include a barrel chest and enlarged lung volumes

Laboratory Findings hallmark of COPD is airflow obstruction Pulmonary function testing shows airflow obstruction with a reduction in FEV1 and FEV1/FVC lung volumes may increase

Treatment SMOKING cessation Bronchodilators Anticholinergic agents Beta agonists Inhaled Glucocorticoids Oral Glucocorticoids Theophylline Oxygen

Treatment General Medical Care Pulmonary Rehabilitation Lung Volume Reduction Surgery Lung Transplantation