COPD in Canada
- COPD under-diagnosed as those with symptoms do not seek treatment or are misdiagnosed
- Affects 700 000 adults (4.4% 35+)
- 4th leading cause of death in females, 5th in males
- Higher prevalence in women (except for 75+ populations) Mortality rates increasing over past 50 years —> especially in women
Causes of COPD
cigarette smoking, genetics, environment
How does cigarette smoke contribute of COPD?
15-20% of smoker will develop COPD
- Nicotine stimulates sympathetic NS causing overall cardiac artery disease
- smoke stimulates inflammatory response = hyperplasia of goblet cells and loss of ciliated cells
- carbon dioxide more readily combines with hemoglobin = decrease oxygen carrying capacity
How does infection contribute to the development of COPD?
recurring resp. Tract infection is major contributing factor for aggravation and progression of COPD
- Childhood recurring tract infections associated w/ reduced lung function, increased respiratory symptoms in adulthood
- Smokers w/ HIV have accelerated development of COPD
- Tuberculosis increase risk of COPD development
How does AAT deficient contribute to the development of COPD?
A1-antitrypsin (AAT) deficiency only known genetic abnormality that leads to COPD
- AAT is major antiprotenase in plasma that inhibits neutrophil elastase
- Produced in liver and normally found in lungs inhibiting action of proteolytic enzymes from neutrophils and macrophages
- Lower AAT = insufficient inactivation of neutrophil elastase = lysis of lung tissue causes destruction of alveoli
- Severe AAT deficiency = early-onset COPD
Treatment: IV or nebulizer AAT (Prolastin) replacement therapy administered weekly
How does aging contribute to COPD development?
changes in lung structure and respiratory muscles cause gradual loss of elastic recoil of lung
- Lungs become smaller and stiffer
- Number of functional alveoli decreases due to loss of alveolar supporting structure
- Thoracic cage changes due to osteoporosis and calcification of costal cartilages = stiff and rigid ribs that are less mobile
- Decreased compliance of chest wall and increase work of breathing
changes similar to emphysema (fewer capillaries for gas exchange, arterial oxygen levels decrease)
What is COPD?
Chronic Obstructive Pulmonary Disease - causing permanent airflow limitations. Involving chronic bronchitis and emphysema
Chronic Bronchitis diagnosis
chronic productive cough for at least 3 consecutive months over 2 consecutive years
What occurs with chronic bronchitis?
Airway inflammation & obstruction of major and small airways = inflammation of airway
mucus hyper secretions, increase # of mucus glands and goblet cells, impaired ciliary function
What is emphysema?
Loss of lung elasticity & abnormal enlargement of airspaces distal to terminal bronchioles with destruction of alveolar walls & capillary beds
Breakdown of elastin in alveolar septa and chronicle walls by protease
Septal destruction destroying capillary bed
decrease elastic recoil in bronchial walls causing air trapping
increased residual volume and total lung capacity
Centriacinar
most common - emphysema where destruction is confined to terminal and respiratory bronchioles (branches of trees expanded)
Panacinar
Emphysema where destruction of peripheral alveolar occurs (tops of trees are destroyed rather that branches).
More common with AAT deficiencies
What causes airflow limitations in COPD (mechanisms)
loss of elastic recoil, peribronchiolar fibrosis, increased airway secretion, airway smooth muscle tone
Acute Exacerbation of COPD
acute changes in symptoms (cough, dyspnea & sputum production) beyond what is considered normal variability in a patent
Therapy for COPD
oxygen therapy, medications, pulmonary rehabilitation
