COPD Flashcards
What is COPD?
Airflow limitation that is not fully reversible
Usually both progressive and associated with an abnormal inflammatory response of lungs to noxious particles or gases.
It’s an overarching diagnosis of emphysema, small airways disease and chronic bronchitis associated with airflow limitation and destruction of lung parenchyma.
Resultants of the COPD.
Hyperinflation of the lungs
Ventilation/perfusion mismatch
Increased work of breathing
Breathlessness
Co-morbidities of COPD.
Ischaemic heart disease
Hypertension
Diabetes
Heart failure
Cancer
Bronchiectasis
Causes and risk factors of COPD.
Long term exposure to toxic particles and gases.
Over 90% of cases are due to cigarette smoking.
Can also be inhalation of smoke from biomass heating fuels, and cooking in poorly ventilated areas.
Urbanisation, air pollution, socioeconomic class and occupation may also play a role.
Alpha-antitrypsin deficiency.
Structural changes in COPD.
Emphysema
Small airway disease
Increased mucus-producing goblet cells in bronchial mucosa (hyperplasia)
Inflammation (both acute and chronic)
Neutrophils, CD8 predominant lymphocytes, macrophages
Scarring
Fibrosis
Destruction of alveolar walls (emphysema)
Definition of emphysema
Abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, accompanied with destruction of their walls.
Classifications of emphysema.
Centri-acinar emphysema
Pan-acinar emphysema
Irregular emphysema
What is centri-acinar emphysema?
Distension and damage of lung tissue that is concentrated around the respiratory bronchioles.
More distal alveolar ducts and alveoli are usually well-preserved.
This is the most common form.
What is pan-acinar emphysema?
Distension and destruction affecting the whole acinus, in severe cases the lung is just a collection of bullae.
Severe airflow limitation and mismatch occur.
What is pan-acinar emphysema associated with?
Alpha-antitrypsin deficiency
What is irregular emphysema?
Scarring and damage that affect the lung parenchyma patchily and independent of acinar structure.
What does emphysema lead to?
Loss of lung elastic recoil and increase in TLC.
Hyperinflation and in severe cases barrel chest.
Loss of alveoli leading to decreased capacity for gas transfer.
Explain pathogenesis of COPD regarding smoking.
Increase in neutrophil granulocytes. The granulocytes can release elastases and proteases. An imbalance in protease to antiprotease activity leads to emphysema.
Mucuous gland hypertrophy in larger airways is thought to be a direct response to persistent irritation due to the inhalation of cigarette smoke.
The smoke has an adverse effect on surfactant, favouring over-distension of lungs.
Pathogenesis of COPD in regards to infection.
A common precipitating cause of acute exacerbations of COPD.
How can acute exacerbations of COPD due to infection be prevented?
Prompt use of antibiotics
Routine vaccinations against influenza and pneumococci
Explain alpha1-antitrypsin deficiency.
It is a proteinase inhibitor produced in the liver and then secreted into the blood.
It diffuses into the lungs and will inhibit proteolytic enzymes such as neutrophil elastase which can otherwise destroy the aleolar wall connective tissue.
If there is deficiency the alpha1-antitrypsin will accumulate in the liver and not reach the lungs. This leads to emphysema as well as liver disease.
Symptoms of COPD
Productive cough with white or clear sputum
Wheeze
Breathlessness
More prone to LRTI
Hypertension
Osteoporosis
Depression
Weight loss
Reduced muscle mass
General weakness
Right heart failure
Signs in mild COPD
Might be no signs
Quiet wheeze
Signs in severe COPD.
Tachypnoeic
Prolonged expiration
Use of accessory muscles
Intercostal indrawing on inspiration
Pursed lip breathing on expiration
Cricosternal distance reduced
Poor chest expansion
Hyperinflation
Loss of normal cardiac and liver dullness
Features of patients with COPD that remain responsive to CO2.
Usually dyspnoeic and rarely cyanosed.
Heart failure and oedema are rare
Features of patients with COPD who are unresponsive to CO2.
Oedematous
Cyanosed
Not breathless
Features of patients with COPD who are hypercapnic.
Peripheral vasodilation
Bounding pulse
Coarse flapping tremor of outstretched hand
In severe hypercapnia they may be confused and have progressive drowsiness.
Papilloedema might also occur.
Complications in late stages of COPD.
Respiratory failure
Pulmonary hypertension
Cor pulmonale
How is COPD diagnosed?
Based on clinical presentation, PMH, FH, social history (smoking)
This is then supported by spirometry.
How is dyspnoea assessed?
MRC dyspnoea scale
Explain the MRC dyspnoea scale.
1
Not troubled by breathlessness except on strenuous exercise
2
Short of breath when hurrying or walking up a slight hill
3
Walks slower than contemporaries on level ground because of breathlessness, or has to stop for breath when walking at own pace
4
Stops for breath after walking about 100 metres or after a few minutes on level ground
5
Too breathless to leave the house, or breathless when dressing or undressing
Spirometry in support of COPD diagnosis.
Pre and post-bronchodilator spirometry
Obstructive pattern
FEV1/FVC ratio <70%
And reversibility should not be more than 15% on bronchodilators.
Other investigations in COPD
Transfer factor
CXR (often normal, can be hyperfinflation, large bullae, pruned blood vessels and flattened diaphgram)
HRCT scan
Hb levels and PCV (can be elevated in persistent hypoxaemia)
Blood gases
Sputum examination (S. pneumoniae, H. influenzae, Moraxella catarrhalis)
ECG often normal (tall P wave (pulmonary hypertension), right BBB, RV hypertrophy)
Echocardiography
Alpha1-antitrypsin levels
Assessments of severity of COPD
FEV1
Smoking status
Low BMI
Heart disease
Severity and frequency of exacerbations
COPD assessment test
6 minute walk test
Co-morbidities
Explain the COPD Assessment Test (CAT)
How is the severity of airflow limitation assessed?
By GOLD score
Types of management of COPD.
Smoking cessation (very essential)
Drug therapy
Oxygen therapy
Pulmonary rehabilitation
Vaccination
Surgery
What vaccinations are offered in COPD?
Pneumococcal and yearly influenza vaccines
Examples of drugs used in COPD.
Beta agonists
Antimuscarinic drugs
Theophyllines
Phosphodiesterase type 4 inhibitors
Corticosteroids
Antibiotics
Mucolytic agents
Give examples of beta agonists used in COPD.
Salbutamol 200 microgram
LABAs can be used in more severe airway limitation.
Give examples of antimuscarinic drugs used in COPD.
Tiotropium (LAMA) can improve lung fucntion, symptoms of dyspnoea and QOL.
However LAMAs do not prevent the decline in FEV1
When are theophyllines used in COPD?
They are of little benefit so not often used.
Give an examples of a phosphodiesterase type 4 inhibitor used in COPD.
Roflumilast.
They have anti-inflammatory properties.
When is roflumilast used?
As an adjunct to bronchodilators for maintenance treatment in patients with an FEV1 of less than 50% and chronic bronchitis.
When are corticosteroids used in COPD?
Inhaled are recommended in patients with frequent exacerbations, or a FEV1 of less than 50% of predicted.
High-dose inhaled steroid are not advised.
Oral steroids are prescribed in context of an acute exacerbation.
When are antibiotics used in COPD?
Prompt antibiotic use should be done to shorten exacerbations and should always be used in acute episodes.
It can prevent further damage and hospital admissions.
When should patients start antibiotic use?
As soon as their sputum turns yellow or green,
How do mucolytic agents work?
Reduce sputum viscosity and can reduce the number of acute exacerbations.
When might you give a long term azithromycin treatment for people with COPD?
Do not smoke and…
have optimised non-pharmacological management and inhaled therapies, relevant vaccinations and (if appropriate) have been referred for pulmonary rehabilitation.
and…
continue to have 1 or more of the following, particularly if they have significant daily sputum production:
frequent (typically 4 or more per year) exacerbations with sputum production
prolonged exacerbations with sputum production
exacerbations resulting in hospitalisation.
What investigations need to be done before starting azithromycin treatment?
ECG to rule out prolonged QT interval
Liver function test
Explain the non-pharmacological and inhaler-use treatment algorithm in COPD.
In which patients should you consider giving long-term oxygen therapy?
Who do not smoke (< 3% carboxyhaemoglobin) and who:
have a partial pressure of oxygen in arterial blood (PaO2) below 7.3 kPa when stable or
have a PaO2 above 7.3 and below 8 kPa when stable, if they also have 1 or more of the following:
secondary polycythaemia
peripheral oedema
pulmonary hypertension
Why is pulmonary rehab important in COPD?
Improves symptoms of fatigue and dyspnoea as well as exercise tolerance.
It’s a vicious cycle to more severe types of COPD if pulm rehab is not done.
What can be given in alpha1-antitrypsin def?
Weekly or monthly infusion of alpa1-antitrypsin.
Treatment of secondary polycythaemia in COPD.
Venesection if the PCV is >55%
Treatment of sensation of dyspnoea in COPD.
Can be treated with short-acting sedation such as sublingual lorazepam or opiates. These might be a helpful palliative measure of intractable dyspnoea.
How is air travel simulated in order to see if it is safe for a person with COPD?
Breathing 15% oxygen at sea level.
If saturation drops below 85% within 15 minutes the patient should be advised to contact their airline to request supplemental oxygen during their flight.
Give examples of surgeries in COPD.
Surgical bullectomy
Single lung transplantation
Endobronchial valves
Management algorithm in COPD
Management of suspected acute exacerbation of COPD.
Investigations such as:
ABGs
CXR to exclude pneumothorax, and infection.
FBC, U&E, CRP
Theophylline levels if they are on it at home
ECG
Send sputum if it is purulent
Blood cultures if pyrexial
Management of acute exacerbation of COPD.
Nebulised bronchodilators - salbutamol 5mg/4h and ipratropium 500mcg/6h (also do the CXR and ABGs)
Controlled O2 therapy if SaO2 <88% or PaO2 <7 kPa. Start at 24-28% aim sats at 88-92%. Adjust it according to ABGs.
Give steroids IV hydrocortisone 200mg and oral prednisolone 30mg od for 7-14 days.
Give antibiotics if there is evidence of infection. E.g. amoxicillin 500mg/8h or clarithromycin or doxycycline.
Physiotherapy to aid sputum expectoration.
If there is no response to nebulisers and steroids consider IV aminophylline.
If there is still no response…
Consider non-invasive positive pressure ventilation (NIPPV) if RR >30 or pH <7.35
Consider respiratory stimulant drug eg doxapram 1.5-4mg/min IV. This is used only if NIV is not available.
Consider intubation and ventilation if pH <7.26 and PaCO2 is rising despite NIV.
When should NIV be used?
IF a patient has a persisten respiratory acidosis with a pH of <7.35
PaCO2 >6.5kPa
NIV reduces the need for intubation and lowers mortality.
When should assisted ventilation with an endoctracheal tube be used?
If there is very severe respiratory failure.
Even then it is a difficult ethical problem due to the unlikelihood sometimes of reversibility.
What predictive index is used in COPD?
BODE
What does BODE involve?
BMI
Degree of airflow limitation
Dyspnoea
Exercise capacity
What does a score of 0-2 on BODE mean for prognosis?
4 year mortality rate of 10%
What does a score of 7-10 on BODE mean for prognosis of COPD?
80% 4 year mortality rate.
Explain Pink puffers.
Increased alveolar ventilation and near normal PaO2 and normal or low PaCO2.
Breathless but not cyanosed.
Explain blue bloaters.
Decreased alveolar ventilation
Low PaO2 and high PaCO2
Cyanosed but not breathless.
May go on to develop cor pulmonale.
Insensitive to CO2 and relay on hypoxic drive to maintain respiratory efforts.
This means that O2 should be given with care.
Management of COPD according to FEV1.
SABA or SAMA
If FEV1 > 50% give LABA and LAMA
If FEV <50% give LABA + ICS and possibly LAMA
If all fails give all three regardless.
Indications for specialist referral.
Uncertain diagnosis
Rapid decline in FEV1
Onset of cor pulmonale
Bullous lung disease
Assessment for oral corticosteroids, nebuliser therapy or LTOT
<10 pack years smkoing or COPD in patient <40y
Symptoms disproportionate to lung functions tests.
Frequent infections
What does a CXR show in COPD?
Hyperinflation
Flattened hemidiaphragms
LArge central pulmonary arteries
Decreased peripheral vascular markings
Bullae
What does a CT show in COPD?
Bronchial wall thickening
Scarring
Air space enlargement.
