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

2. 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

3. 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

4. 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

5. 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

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

7. 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

8. Pathophysiology Gas Exchange
Nonuniform ventilation and ventilation-perfusion mismatching

9. 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

10. 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

12. 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

13. 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

14. 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

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

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