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COPD Common progressive disorder of airway obstruction with little or no reversibility
- FEV1 < 80% predicted
- Fev1/FVC ratio <0.7 COPD vs Asthma
- Patients usually have COPD OR Asthma (not both)
- COPD favoured by o Age of onset > 35 yrs o Smoking o Chronic dyspnea o Sputum production o No marked diurnal/day to day variation in FEV1 Aetiology
- Smoking
- Long term exposure to toxic particles or gases
- Alpha 1 anti-tripsin deficiency predisposes to early development Pathophysiology
- Chronic bronchitis o Defined clinically as a cough with sputum production daily for 3 months of 2 successive years
- Emphysema o Defined histiologically as enlarged air spaces distal to the terminal bronchioles with destruction of alveolar walls 3 Mechanisms suggested for airflow limitation 1) Mucus secretion blocks airways a. Hypertrophy in number of mucus secreting goblet cells of bronchial tree 2) Inflammation + scarring causes narrowing of small airways a. Infiltration of acute and chronic inflammatory cells b. Ulcerated epithelium c. Ulcers heal with squamous epithelium replacing columnar d. Scarring + remodeling 3) Emphysematous change a. Causes loss of elastic recoil of lungs with collapse of small airways during expiration + air trapping b. Classified according to site of damage i. Centri-acinar = damage around resp. bronchioles ii. Pan-acinar = damage involves whole of acinus iii. Irregula = damage affects lung parenchyma patchily c. Loss of elastic recoil = increased lung V/Q compliance mismatch d. Loss of alveoli = decreased gas exchange Cigarette smoking
- Irritation = hypertrophy of mucus glands
- Increase in elastases + proteases, decrease in alpha 1 antitripsin (antiprotease)

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