COPD Flashcards
What is COPD - Chronic Obstructive Pulmonary Disease?
COPD is a progressive disorder characterised by airway obstruction with little or no reversibility. It is the obstruction that causes the disabling symptoms
Two conditions come under COPD:
- Chronic Bronchitis
- Emphysema
How is Chronic Bronchitis defined?
- Chronic Bronchitis involves productive cough and sputum for 3 consecutive months over 2 years
- Also known as Blue Bloaters
What is Emphysema?
- Emphysema is defined radiologically as the permanent dilation of the airways distal to the terminal bronchiole
What are the main clinical features found in those with COPD?
- Increased cough and sputum production
- Breathlessness on exertion
- In advanced disease, breathlessness on minimal exertion or rest
What are the main causes of death in COPD?
- Bronchopneumonia
- Respiratory failure
- Heart Failure
What is the pathophysiology of COPD?
Smoking damages the airway through the respiratory tract, but its affects vary depending on the exact location
BRONCHI - hyperplasia of mucus glands and goblet cells results in increased sputum production
SMALL AIRWAYS - chronic inflammation, leading to fibrosis and eventual stenosis of airway
RESPIRATORY BRONCHIOLES - destruction of walls through loss of elastin, leading to permanent dilation hence emphysema
In emphysema, macrophages release elastase which acts on elastin within alveolar walls - causing breakdown. There is therefore less trapping upon expiration so air trapping occurs
What is the protease/anti-protease hypothesis?
- Smoking increases number of neutrophils
- These neutrophils release elastase
- Smoking also inhibit the lungs’ natural protease inhibitor - a1 anti-trypsin
What can a congenital deficiency in a1 anti-trypsin cause?
Liver cirrhosis and hepatocellular carcinoma in adults
In lungs, panacinar emphysema in the lower lobes
=> More on a1 antitrypsin deficiency:
- Inherited in an autosomal recessive fashion
- Gene for protease is found on chromosome 14
- Manifests in patients with the PiZZ genotype
What are the risk factors of COPD?
- Age
- Genes
- Long term smoking
What are the main causes of COPD?
- Smoking
- Air pollution
- Occupational exposure
- Intolerance of proteases and anti-proteases
What is the formula for calculating pack years?
Pack years = no. of packs per day x years of smoking
What is the role of spirometry in COPD?
In emphysema:
- Increased TLC
- Increased Residual volume
- Decreased diffusing capacity for carbon monoxide
COPD is categorised in terms of severity based on post bronchodilator FEV1 predicted value
> 80% - Stage 1 Mild
50-79% - Stage 2 Moderate
30-49% - Stage 3 Severe
<30% - Stage 4 Very severe
What are the investigations carried out in suspected COPD?
=> CXR
- Hypeinflation
- Flat hemidiaphragm
- Large central pulmonary arteries
=> Blood
- Raised haemocrit
=> ABG
Decreased PaO2 accompanied with possible hypercapnia
=> CT
- Bronchial wall thickening
- Scarring
- Air space enlargement
=> Spirometry
- Obstructive picture
What is the emergency management of the acute exacerbation of COPD?
First step is to provide nebulised bronchodilators - SALBUTAMOL 5mg/4h (SABA) + IPATROPIUM 500mg/6h (LAMA). Then carry out investigations - CXR and ABG
Controlled oxygen therapy if SaO2 < 85% or PaO2 < 7.3 kPa. Oxygen levels adjusted depending on ABG
Administer steroids. IV HYDROCORTISONE 200mg and PO PREDINISOLONE 30mg (ICS)
Give antibiotics if there is evidence of infection
Physiotherapy to aid sputum clearance
If there is no response to bronchodilators or steroids, give IV AMINOPHYLLINE
If there is still no response:
- Consider non invasive positive pressure ventilation
- Consider respiratory drug stimulant
What is the management of more stable and advanced COPD?
General management involves:
- smoking cessation
- influenza vaccine
- one off pneumococcal vaccine
- pulmonary rehabiliation
Bronchodilator therapy:
- SABA or SAMA is first line treatment
- If patient remains breathless or has exacerbations next step is to determine whether they have any asthmatic features triggered by steroids
=> Features suggesting asthmatic steroid responsiveness:
- secure diagnosis of asthma
- high eosinophil count
- substantial variation in FEV1
- substantial diurnal variation in PEF
=> If there are no asthmatic features triggered by steroids:
- Add LABA + LAMA
- If already taking SAMA, discontinue and take SABA instead
=> If there are asthmatic features triggered by steroids:
- LABA + ICS
- If still breathless then triple therapy: LABA + LAMA + ICS