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)