copd (chronic obstructive pulmonary disease) dr. meg-angela christi amores

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 – 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– 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– 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– 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– 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