COPD(Chronic Obstructive Pulmonary Disease)
Dr. Meg-angela Christi Amores
COPD
•Global Initiative for Chronic Obstructive LungDisease (GOLD)
•a disease state characterized by airflowlimitation that is not fully reversible
–Includes:
•emphysema, chronic bronchitis, and small airwaysdisease
COPD
•Emphysema
–an anatomically defined condition characterizedby destruction and enlargement of the lung alveoli
•Chronic Bronchitis
–a clinically defined condition with chronic coughand phlegm
•Small airways disease
– a condition in which small bronchioles arenarrowed
Risk Factors
•Cigarette Smoking
–Intensity: pack years (sticks/day for years)
–most highly significant predictor of FEV1
•Airway responsiveness
–asthma, chronic bronchitis, and emphysema arevariations of the same basic disease
•Respiratory infections
–Remains to be proven
Risk Factors
•Occupational Exposures
–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 onintensity, timing during growth, basal function
Pathophysiology
•Airflow obstruction
–Determined by spirometry: FEV1 and FVC
–chronically reduced ratio of FEV1/FVC
–seldom shows large responses to inhaledbronchodilators
•Hyperinflation
–"air trapping“
–helps to compensate for airway obstruction
Pathophysiology
•Gas Exchange
–Nonuniform ventilation and ventilation-perfusionmismatching
Pathology
•Large Airway
–Cigarette smoking often results in mucous glandenlargement and goblet cell hyperplasia
–proportional to cough and mucus production
•Small Airways
•major site of increased resistance in most individualswith COPD is in airways 2 mm diameter
•goblet cell metaplasia and replacement of surfactant-secreting Clara cells with mucus-secreting andinfiltrating mononuclear inflammatory cells
Pathology
•Lung Parenchyma
–destruction of gas-exchanging airspaces
–walls become perforated and later obliteratedwith coalescence of small distinct airspaces intoabnormal and much larger airspaces
–Macrophages accumulate
–Centriacinar emphysema- most frequentlyassociated with cigarette smoking
–Panacinar emphysema - usually observed inpatients with alpha1AT deficiency
Clinical presentation
•History
•cough, sputum production, and exertional dyspnea
•exertional dyspnea, often described as increased effortto breathe, heaviness, air hunger, or gasping, can beinsidious
•patient's ability to perform them has changed
Clinical presentation
•Physical Findings
–entirely normal physical examination – early
–signs of active smoking, including an odor ofsmoke or nicotine staining of fingernails
–prolonged expiratory phase and expiratorywheezing- more severe
–signs of hyperinflation include a barrel chest andenlarged lung volumes
Laboratory Findings
•hallmark of COPD is airflow obstruction
•Pulmonary function testing shows airflowobstruction with a reduction in FEV1 andFEV1/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