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

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

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

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

COPD(Chronic Obstructive Pulmonary Disease)

Dr. Meg-angela Christi Amores

Page 2: 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

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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

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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

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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

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Natural History

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

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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

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Pathophysiology

• Gas Exchange– Nonuniform ventilation and ventilation-perfusion

mismatching

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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

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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

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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

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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

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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

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Page 16: COPD (Chronic Obstructive Pulmonary Disease) Dr. Meg-angela Christi Amores.

Treatment

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

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Treatment

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