Lecture 13 COPD Pathophysiology Dahri
COPD: preventable & treatable disease
Progressive respiratory disease
Limited airflow associated with inflammatory response of lungs to noxious particles & gases
Not fully reversible
Collectively includes: o Chronic bronchitis (70%) o Emphysema (30%) o 30% overlap between conditions
Severe COPD respiratory failure, hospitalization, and death from suffocation
COPD EPIDEMIOLOGY:
4th leading cause of death
More prevalent in men (5 men: 1 woman)
Multi-factorial risk o Caucasian o Older o Lower socioeconomic status o PRIMARY CAUSE = smoking o Occupational exposure: dust, gas, chemicals o Environmental: air pollution, smog, irritants o Repeated lung infections: bronchitis, pneumonia o Nutrition o Genetics: increased predisposition (2% cases) of AAT
mutation (alpha1 antitrypsin (antiprotease))
AAT normally protects lungs from neutrophil elastase
AAT mutation causes decrease in activity more elastase activity / degradation of lung
COPD & Co-morbidities: COPD pts increased risk…
Myocardial infarction, angina
Osteoporosis
Respiratory infection
Depression
Diabetes
Lung cancer
Systemic effects: weight loss, nutritional abnormalities, skeletal muscle dysfunction
DIAGNOSIS OF COPD:
Post-bronchodilator FEV1/FVC < 0.70 confirms presence of
airflow limitation that is not fully reversible
Spirometry values should be compared to age-related normal values to avoid overdiagnosis of COPD in elderly
Post-bronchodilator FEV1/FVC < 0.70 and….
I: Mild FEV1 ≥ 80% predicted
II: Moderate 50% ≤ FEV1 < 80% predicted
III: Severe 30% ≤ FEV1 < 50% predicted
IV: Very Severe FEV1 < 30% predicted
(or) FEV1 < 50% + chronic respiratory failure
PULMONARY HYPERTENSION IN COPD:
AIRFLOW LIMITATION IN COPD:
REVERSIBLE: inflammation
Mucus & inflammatory cells/mediators in bronchial secretions
Bronchoconstriction
Hyperinflation during exercise
IRREVERSIBLE: damage & remodeling
Fibrosis and narrowing of airways
Reduced elastic recoil with loss of alveolar surface area
Destruction of alveolar support with reduced patency of small airways
AIR TRAPPING IN COPD:
Lecture 13 COPD Pathophysiology Dahri
COPD PATHOPHYSIOLOGY:
CHRONIC BRONCHITIS:
Persistent productive cough
≥ 3 months out of the year
2 or more consecutive years
CAUSE:
Oxidative stress (airway injury)
Free radicals in smog/smoke
Cytokine release/buildup = inflammation
Inflammation of small airways (bronchi & bronchioles) Smooth muscle constriction – REVERSIBLE
Hypertrophy of mucus glands
Impaired healing
Impaired normal “protective” anti-enzyme function
Mucus hypersecretion sputum production
Chronic inflammation leukocyte cytotoxicity
Ciliary dysfunction tissue damage, atrophy
Chronic obstruction
Impaired clearance / build up of airway secretions
EMPHYSEMA:
Destruction and permanent enlargement of terminal bronchioles & alveolar sacs
Fibrosis and scarring
Pulmonary capillary bed destruction
Reduced surface area for gas exchange
INFLAMMATORY CELLS INVOLVED IN COPD:
INFLAMMATION IN COPD EXACERBATIONS:
Inherent inflammation + inflammation due to new factors exacerbation
CHANGES IN LARGE AIRWAYS OF COPD PATIENTS:
CHANGES IN SMALL AIRWAYS OF COPD PATIENTS:
Lecture 13 COPD Pathophysiology Dahri CHANGES IN PULMONARY ARTERIES OF COPD
PATIENTS:
Due to vasoconstriction & increased capacity
CHANGES IN LUNG PARENCHYMA IN COPD:
In addition to small & large airways, you get changes to the lung structures itself (alveoli, capillary beds, large vessels)