Please enable JavaScript.
Coggle requires JavaScript to display documents.
Chronic Obstructive Pulmonary Disease (COPD) (Pathophysiology…
Chronic Obstructive Pulmonary Disease (COPD)
Key Facts
The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases
Associated with the development of both:
Chronic Bronchitis - cough with sputum for 3 months for 2 or more years
Emphysema - Histologically its enlarged airspaces distal to thermal bronchioles, with destruction of alveolar walls
A disease state characterised by airflow limitation that is not fully reversible
Epidemiology
Alpha-1 antitrypsin deficiency causes early onset COPD
Otherwise patients are rarely symptomatic before middle-age
Chronic exposure to - pollutants at work, outdoor air pollution, inhalation of smoke from biomass fuels
Alpha-1 antitrypsin deficiency
A rare cause of cirrhosis (due to accumulation of the abnormal protein in the liver)
Mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to reduced hepatic production of alpha-1 antitrypsin which normally inhibits the proteolytic enzyme - neutrophil elastase
Causes early onset COPD (due to proteolytic lung damage)
Cigarette smoking is the major cause of COPD and is related to the daily average of cigarettes smoked and years spent smoking
Pathophysiology
The combination of the two results in severe airflow limitation
V/Q mismatch is partly due to damage and mucus plugging of smaller airways from chronic inflammation
Most have both emphysema and chronic bronchitis
CO2 excretion is less affected by V/Q mismatch
Emphysema - results in loss of elastic recoil, which normally keeps the airways open during expiration. This is due to dilation and destruction of lung tissue
Other patients fail to maintain their respiratory effort and then their PaCO2 levels increase
Chronic Bronchitis - there is airway narrowing and hence airflow limitation as a result of hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema
This rise in CO2 leads to stimulation of respiration
In more advanced cases the bronchi become overtly inflamed and pus is seen in the lumen
Such patients appear breathless and because of renal hypoxia, they start to retain fluid & increase erythrocyte production
There is increased numbers of mucus-secreting goblet cells in COPD within the bronchial
Pathogenesis
Cigarette smoke - causes mucus gland hypertrophy in the larger airways, and leads to increase in neutrophils, macrophages and lymphocytes in the airways and walls. These cells release inflammatory mediators that attract inflammatory cells, which break down connective tissue
Respiratory infections - are a precipitating cause of acute exacerbations
Clinical Presentation
Systemic effects include - hypertension, osteoporosis, depression, weight loss, reduced muscle mass with general weakness
On examination a patient with severe disease is breathless at rest with prolonged expiration, chest expansion is poor and the lung are hyper inflated (barrel chest)
Symptoms can be worsened by cold or damp weather and atmospheric pollution
Pursed lips on expiration help to prevent alveolar and airway collapse
Colds seem to settle on the chest and frequent infective exacerbations occur, with purulent sputum (contains pus)
Later stages are characterised by the development of respiratory failure:
PaO2 less than 8kPa
PaCO2 greater than 7kPa
Characteristic symptoms are productive cough, with white or clear sputum, wheeze and breathlessness, usually following many years of a smokers cough
Those with advanced disease may develop pulmonary hypertension which is defined as symptoms and signs of fluid overload secondary to lung disease
Differential Diagnosis
Asthma, congestive heart failure, bronchiectasis, allergic fibrosing alveolitis, pneumoconiosis, asbestosis
Diagnosis
High resolution CT scans are used particularly to show emphysematous bullae
Haemoglobin & PCV may be high as a result of persistent hyperaemia and secondary polycythaemia
Chest X-ray - may be normal or show hyper inflated lungs indicated by low, flattened diaphragms. May be reduced peripheral lung markings
Arterial blood gases may be normal or show hypoxia with or without hypercapnia in advanced cases
Lung function test
FEV1/FVC less than 0.7 - airway obstruction
Stages - 1 (FEV1 less than 80% of predicted), 2 (FEV1 50-79%), 3 (FEV1 30-49%)
Multiple peak flow measurements may be necessary to exclude asthma
FEV less than 80% predicted value
Shows progressive airflow limitation with increasing severity and breathlessness
ECG is often normal
In the absence of a history of cigarette smoking then asthma is a more likely explanation, unless there is a family history suggesting alpha-1 antitrypsin deficiency
Alpha-1 antitrypsin levels and genotypes are worth measuring in premature disease or lifelong non-smokers
Based on a history of breathlessness and sputum production in a chronic smoker
Treatment
Oxygen therapy - long term domiciliary oxygen therapy has survival benefits
Antimucolytic agents can help by reducing sputum viscosity
Prevention of infection - exacerbations are commonly due to bacterial or viral infection. Vaccines should be received.
Diuretics can be used to treat oedema
Corticosteroids - in symptomatic patient with moderate/severe COPD, a trial of corticosteroids is recommended since a proportions of patients will have a reversible element
Pulmonary rehabilitation can modestly increase exercise capacity with a diminished sense of breathlessness and improved general wellbeing
Bronchodilators - a long acting anti-muscarinic is used as a initial therapy with a rescue short acting B2 agonist to prevent or reduce acute symptoms
Good diet to reduce weight and obesity
Smoking cessation is most useful, even in advanced disease this may slow down the rate of deterioration and prolong the time before disability and death occur
Alpha-1 antitrypsin replacement