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COPD
Tharun ponnuvel kumar
Types
 COPD can be divided into 2 clinical phenotypes: emphysema and chronic bronchitis.
 Emphysema is defined pathologically as enlargement of distal air spaces.
 Chronic bronchitis is defined clinically as cough productive of sputum occurring on most days in 3
consecutive months over 2 consecutive years.
Emphysema
 Smoking causes inflammation in the airways. Neutrophils and other immune cells are recruited to
the small airways, releasing proteases and oxidative species. Neutrophil elastase breaks down
elastin fibres that normally contributes to the elastic recoil during expiration,
 A1 antitrypsin is a protease inhibitor that keeps elastase activity in check. Al-antitrypsin deficiency is
the best known genetic predisposition to emphysema, especially in smokers with this genetic
disorder. Impaired gas exchange and air trapping are also features
Chronic Bronchitis
 Inflammation from smoke exposure also causes fibrosis of the bronchiolar walls, mucus
hypersecretion, airway edema, and bronchoconstriction. These features make up the small airway
disease component of COPD, known as chronic bronchitis.
 Goblet cell hypertrophy and hyperplasia due to smoking in chronic case it changes to goblet cell
metaplasia
GOLD stages of chronic obstructive
pulmonary disease severity
Stages of copd
Treatment
Bronchodilators
Inhaled β2-agonists (e.g. short-acting salbutamol or long-acting salmeterol) act on β2-receptors on
smooth muscle cells to cause bronchodilation. Inhaled anticholinergics (e.g. short-acting ipratropium or
long-acting tiotropium) act to block acetylcholine’s effect on muscarinic receptors on smooth muscle
cells, allowing bronchodilation. Inhaled β2-agonists and anticholinergics are used for both
symptomatic management, as well as acute exacerbations of COPD. Long-acting bronchodilators are
preferred over short-acting ones because of fewer doses and improved symptom management. For
more effective treat of stable COPD, combination therapy using an inhaled β2-agonist and an
anticholinergic can also be used.

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Chronic obstructive pulmonary disease, or COPD, refers to a group of diseases that cause airflow blockage and breathing-related problems. It includes emphysema and chronic bronchitis

  • 2. Types  COPD can be divided into 2 clinical phenotypes: emphysema and chronic bronchitis.  Emphysema is defined pathologically as enlargement of distal air spaces.  Chronic bronchitis is defined clinically as cough productive of sputum occurring on most days in 3 consecutive months over 2 consecutive years.
  • 3. Emphysema  Smoking causes inflammation in the airways. Neutrophils and other immune cells are recruited to the small airways, releasing proteases and oxidative species. Neutrophil elastase breaks down elastin fibres that normally contributes to the elastic recoil during expiration,  A1 antitrypsin is a protease inhibitor that keeps elastase activity in check. Al-antitrypsin deficiency is the best known genetic predisposition to emphysema, especially in smokers with this genetic disorder. Impaired gas exchange and air trapping are also features
  • 4. Chronic Bronchitis  Inflammation from smoke exposure also causes fibrosis of the bronchiolar walls, mucus hypersecretion, airway edema, and bronchoconstriction. These features make up the small airway disease component of COPD, known as chronic bronchitis.  Goblet cell hypertrophy and hyperplasia due to smoking in chronic case it changes to goblet cell metaplasia
  • 5.
  • 6. GOLD stages of chronic obstructive pulmonary disease severity
  • 9. Bronchodilators Inhaled β2-agonists (e.g. short-acting salbutamol or long-acting salmeterol) act on β2-receptors on smooth muscle cells to cause bronchodilation. Inhaled anticholinergics (e.g. short-acting ipratropium or long-acting tiotropium) act to block acetylcholine’s effect on muscarinic receptors on smooth muscle cells, allowing bronchodilation. Inhaled β2-agonists and anticholinergics are used for both symptomatic management, as well as acute exacerbations of COPD. Long-acting bronchodilators are preferred over short-acting ones because of fewer doses and improved symptom management. For more effective treat of stable COPD, combination therapy using an inhaled β2-agonist and an anticholinergic can also be used.