Flashcards in S2: Pathophysiology of COPD Deck (20):
What is Chronic Obstructive Pulmonary Disease (COPD)?
COPD is an umbrella term used for a mixture of chronic bronchitis and emphysema and encompasses a long term, progressive and accelerated decline in respiratory function.
Risk factors for COPD
- Genetic factors e.g. Alpha 1 antitrypsin deficiency
- Enviromental hazards e.g. pollution
Why does smoking harm the respiratory system?
The many harmful constituents of tobacco smoke cause acute damage to respiratory tissue, generating an inflammatory response.
For example, the individual who smokes inhales noxious chemicals and reactive oxygen species.
With repeated exposure the inflammation becomes pathological and generates chronic and irreversible dysfunction.
How does the inflammation observed within the lungs of COPD patients develop?
- Tobacco smoke causes tissue damage
- Tissue damage has cells that release inflammatory mediators which activates macrophages and neutrophils. These immune cells release proteases that digest tissues and cause further tissue damage.
- Also, noxious chemicals and reactive oxygen species (from smoke) inhibit anti-proteases further increasing protease burden.
- Tissue damage starts to damage structures in the lung that help it function.
e.g. impaired mucociliary clearance
- In long term, tissue remodelling occurs where there can be permanent obstruction and change to the airway decreasing respiratory function
Describe the pathological features observed in the airways of chronic bronchitis patients
- Damage to cilia so impaired mucociliary clearance
- Mucus hypersecretion (increased goblet cells and increased mucus gland activation)
- Inflamed and swollen airway tissue and oedema
- Weakened airway structure (loss of elastin) and loss of patency (airway collapse)
Irritation of sensory neurones = cough
Decreased luminal area = increased airway resistance and airway obstruction
What is the consequence of damage to cilia?
Impaired mucociliary clearance means that bacteria and particles trapped in the trachea cannot be removed effectively increase risk of respiratory infection increasing inflammation (excessive mucus, cilia don't waft).
Compare airflow and causes of it in COPD and asthma
Similar to asthma, in chronic bronchitis airflow through the airways is impaired due to reduce airway lumen radius and increase airway resistance. However whilst these changes are typically reversible in asthma, the changes in chronic bronchitis are progressive and irreversible.
The primary cause of the dysfunction also differs: in chronic bronchitis airway lumen size is reduced by excessive mucus secretion, tissue swelling, and degradation of the overall airway structure (resulting in the airway simply collapsing entirely when placed under excessive pressure), rather than being primarily caused by airway smooth muscle contraction, as in asthma.
Why are beta-2 agonist bronchodilators less effective in COPD patients compared to asthmatic patients?
In asthma, airflow is impaired mainly due to airway smooth muscles contraction.
In COPD patients, airway lumen size is reduced by excessive mucus secretion, tissue swelling, and degradation of the overall airway structure.
Describe the pathological features observed in the airways of emphysema patients
Emphysema is where there is airspace enlargement, air trapping on expiration and destruction of capillary bed.
There is decreased surface area and perfusion so gas exchange decreases.
Loss of elastin fibres increases compliance of lungs and decreases recoil. This means that lungs expand with less force but they aren't able to recoil and force out efficiently.
3 effects of COPD on respiratory function
- Airway obstruction + trapping = ↓ventilation = alveolar hypoxia
- ↓ lung recoil = ↑expiratory effort.
Overall = hypoxaemia
What are exacerbations in COPD patients?
Patients experience acute exacerbations characterised by a temporary (duration = several days) but drastic decline in symptoms and respiratory function, due to the acute inflammation brought about by infection. Whilst exacerbations do resolve, patients with already severe COPD are at acute risk of death, and lung function often fails to completely return to previous levels, further hastening long term respiratory decline
- Exacerbation causes a rapid decline
Effects of chronic bronchitis (symptoms)
- Colour dusky to cyanotic
- Recurrent cough and increased sputum production
- Hypercapnia (increase pCO2)
- Respiratory acidosis
- Increase Hbg
- Increase respiratory rate
- Exertional dyspnea
- Increase incidence in heavy cigarette smokers
- Digital clubbing
- Cardiac enlargement - RS heart failure
- Use of accessory muscles to breath
Symptoms are known as the 'blue bloater'
Effects of emphysema (symptoms)
- Increased CO2 retention (pink)
- Minimal cyanosis
- Purse lip breathing
on chest percussion
- Barrel chest
- Exertional Dyspnea
- Prolonged expiratory time
- Speaks in short jerky sentences
- Use of accessory muscles to breath
- Thin appearence
Are chronic bronchitis and emphysema seperate problems?
Debate exists whether these phenotypes really exist – COPD probably always involves a mixture of the two, depending on the individual patients pathology.
What can chronic alveolar hypoxia (result of COPD) lead to?
Chronic alveolar hypoxia can lead to hypoxic vasoconstriction occur across the lung so there is increased pulmonary vascular resistance and the hear has to work harder to pump blood through constricted capillaries of the lungs. This causes pulmonary hypertension and increased right ventricular afterload. Muscle hypertrophy increases the hearts size to help with the pumping of the blood through the lungs eventually leading to right heart failure.
Chronic alveolar hypxoxia can also lead to hypoxaemia, hypercapnia and acidemia. This causes symptoms such as decreased exercise tolerance, fatigue, and a poor quality life.
V/Q ratio in emphysema and chronic bronchitis
Emphysema has a matched V/Q defect
Chronic Bronchitis has a V/Q mismatch
List potential treatment strategies for COPD
- Treat airway obstructions - B2 agonists only effective during exacerbations
- Treat target mucus hypersecretion - LAMAs reduce ChBr symptoms
- Inflammation - ususally corticosteroid resistant
- Lung Transplant
- O2 therapy - Can be effective (depending on V/Q mismatch) but working sections of lungs will deteriorate
- Smoking cessation- slows acceleration of disease
What does efficacy of O2 therapy depend on?
There has to be some ventilation in hypoventilation.
How effective is smoking cessation at treating COPD?
Smoking cessation, only halts acceleration of decline - lung function doesn't regenerate and decline continues but just not as fast.