4. COPD – classification, diagnosis, clinical course

Essay 4- COPD- classification, diagnosis, clinical course

Definition of COPD

• Heterogenous lung condition characterised by chronic respiratory symptoms (dyspnea, cough, sputum production and/or exacerbations) due to abnormalities of the airways and/or alveoli that cause persistent and often progressive airflow obstruction
• Characterised by airway obstruction (FEV1 <80% predicted; FEV1/FVC <0.7)

Etiology

Smoking

• Maf- recruited and release elastase, MMP which destroy wall and elastic fibres
• Neu- release ROS causing oxidative stress. Also release chemokines, GF which causes hypertrophy and hyperplasia of smooth muscle cells
• Epithelial cells- damaged and shed in lumen creating casts in the terminal bronchioles which aggrevate the obstruction
• Lymphoid cells- release growth factors leading to inadequate tissue repair. Bronchial remodelling occurs and
• Air pollution
• Alpha-1 antitrypsin deficiency

What are the mechanisms of development?

• Neu inflammation
• Destruction of alveolar wall
• Inflammation and fibrosis of the bronchial wall
• Hypertrophy of the submucosal glands
• Hypersecretion of mucus
• Loss of elastic lung fibers and alveolar tissue

Emphysema

• Characterized by a loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles
• Enlargement of the air spaces leads to hyperinflation of the lungs and produces an increase in total lung capacity
• Causes- smoking and inherited deficiency of alpha 1 antitrypsin
• Alpha-1 antitrypsin is a protease inhibitor produced primarily in the liver.
• It inhibits the neutrophil elastase activity in the lung and hence can protect it from proteolytic damage
• Decreased levels of enzyme can result in massive release of proteolytic enzymes even due to small amounts of allergens/pollutants
• These enzymes destroy the alveolar septa and reduce SA resulting in impaired gas exchange

Types of emphysema

• Centriacinar- central parts of acini are affected and distal alveoli are spared
• Panacinar- acini are uniformly enlarged
• Distal acinar- proximal portion of acinus is normal but distal is affected
• Irregular- acinus are irregularly involved and there is almost always scarring

Pathogenesis

• Exposure to toxic substances induces ongoing inflammation with accumulation of Neu, Maf and Ly in the lung
• Elastases, cytokines and oxidases are released which cause epithelial injury and proteolysis of the extra cellular matrix
• Increased release of elastase is due to smoking which stimulates movement of inflammatory cells into lungs
• Elastin degradation products further increase the inflammation

Chronic bronchitis

• Defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years
• Airway obstruction is caused by inflammation of the major and small airways
• Smoking is most important cause

Pathogenesis