Chronic Obstructive Pulmonary Disease Flashcards
What is COPD?
COPD is a common progressive disorder characterised by irreversible airway obstruction (FEV1 <80% ; FEV1/FVC = 0.7).
It comprises of both emphysema and chronic bronchitis which eventually leads to: => airflow limitation, => destruction of lung parenchyma => resultant hyperinflation of lungs, => ventilation/perfusion mis-match, => increased work of breathing => breathlessness
What is the underlying pathology as a result of COPD?
- Emphysema
- Increased mucus-producing goblet cells in the bronchial mucosa => chronic bronchitis
- Acute & chronic inflammation
(Endobronchial biopsies show predominance of neutrophils)
What is emphysema?
Emphysema is defined as abnormal and permanently enlarged air spaces distal to the terminal bronchiole with destruction of alveolar walls.
=> expiratory airflow limitation and air trapping
=> loss of lung elastic recoil results in an increased total lung volume
=> loss of alveoli decreases capacity for gas transfer
Emphysema is classified according to its distribution in the lungs.
Describe the two types of emphysema.
- Centri-acinar emphysema: Distention and damage of lung tissue concentrated around the respiratory bronchioles.
The more distal alveolar ducts and alveoli are well preserved.
Very common form of emphysema.
- Pan-acinar emphysema: assoc. with alpha-1 antitrypsin deficiency.
Distention and destruction in the whole acinus.
In severe cases, lung is a collection of bullae => severe airflow limitation and mismatch
Rare form of emphysema.
- Irregular emphysema: patchy scarring and damage in lung parenchyma, independent of acinar structure
What is chronic bronchitis?
Chronic bronchitis is clinically defined as cough and sputum production on most days for 3 months of 2 successive years.
What are the causes of COPD?
Long term exposure to toxic particles and gases
- Smoking cigarettes = 90% of COPD in developed countries
* 10-20% smokers develop COPD - suggests there is an underlying susceptibility. - Biomass heating fuels, cooking in poorly ventilated areas, pollution = in developing countries
- Alpha1 anti-trypsin deficiency
How does smoking lead to changes in the lung which lead to COPD
- Increased neutrophil granulocytes found in airways => release of elastase & protease.
Imbalance between protease and anti-protease => causative factors for emphysema.
- Mucous gland hypertrophy = direct response to persistent irritation from inhaling cigarette smoke.
- The smoke affects surfactant levels => over distention of the lungs
What is alpha-1 anti-trypsin?
How does alpha-1 anti-trypsin deficiency lead to emphysema?
Alpha-1 anti-trypsin is a proteinase inhibitor produced in the liver, secreted in the blood and diffused in the lungs.
Alpha-1 anti-trypsin’s role is to inhibit proteolytic enzymes i.e. neutrophil elastase which destroy alveolar wall connective tissue
In alpha-1 anti-trypsin deficiency, the proteins accumulate in the liver => low levels in the lung => increased alveolar destruction due to imbalance between proteolytic and anti-proteolytic enzymes.
Who is COPD commonly seen in?
Smokers (passive or active)
Age of onset >35 years
What are the signs and symptoms of COPD?
Symptoms:
Productive cough with white or clear sputum
Wheeze
Dyspnoea
Prone to lower respiratory infections
Signs:
May be no signs or quiet wheeze
In severe cases:
Tachypnoea with prolonged expiration
Use of accessory muscles of respiration
Hyperinflation
Reduced lung expansion
Resonant or hyper-resonant on percussion
Quiet breath sounds e.g. over bullae
Wheeze
Reduced crico-sternal distance
Cyanosis
Cor pulmonale
What are the systemic effects of COPD?
Hypertension
Osteoporosis
Depression
Weight loss
Reduced muscle mass with general weakness
Right heart failure
What are the complications of COPD?
Acute exacerbations ± infections
Polycythaemia
Respiratory failure
Cor pulmonale (oedema ; increased JVP) => right heart failure as a result to increased pulmonary hypertension
Pneumothorax (ruptured bullae)
Lung carcinoma
Explain the terms and how they differ from each other:
i. Pink puffers
ii. Blue bloaters
i. Pink puffers :
=> Increased alveolar ventilation
=> ~Normal O2
=> Normal or low CO2
They are breathless but not cyanosed => risk of type 1 respiratory failure.
Respiratory centre responsive to CO2
ii. Blue bloaters:
=> Decreased alveolar ventilation
=> Low O2
=> High CO2
They are cyanosed but not breathless => at risk of cor pulmonale
Respiratory centre insensitive to CO2 - rely on hypoxic drive to breathe
8 investigations may be carried out if COPD suspected. These include:
- Lung function test
- Chest X-ray
- CT
- Bloods
- Blood gases
- ECG*
- Sputum test*
- Alpha-1 anti-trypsin levels*
*6-8 are carried out if a complication of COPD is suspected.
Describe the common findings of these tests and when *6-8 is indicated.
- Lung function test: airflow limitation
=> FEV1/FVC ratio is reduced <70%
=> Low peak expiratory flow
*airflow limitations partly reversible
- Chest X-ray: usually normal
=> hyperinflation with low, flattened hemi-diaphragm
=> large bullae
=> large central arteries but decreased peripheral vasculature
- CT:
=> Bronchial wall thickening
=> Scarring
=> Air space enlargement
- Bloods:
=> High haemoglobin levels and packed cell volume (PCV)
=> elevated due to persistent hypoxaemia (secondary polycythaemia)
- Blood gases: respiratory failure
=> Decreased O2
=> ± hypercapnia - ECG: often normal
=> Tall P waves (p pulmonale) in pulmonary hypertension secondary to COPD
=> Right bundle branch block secondary to right ventricular failure - Sputum test:
=> Strep. pneumoniae, H. influenza or Moraxella catarrhalis
=> Cause infective COPD exacerbations - Alpha-1 anti-trypin levels and genotype:
=> measure in lifelong non-smokers
=> measure in premature disease
What are some of the lifestyle management advice for COPD?
- Smoking cessation
- Diet advice ± supplements & exercise (BMI usually low)
- Depression screening - severe but treatable
- Flu & pneumococcal vaccines
DRUG THERAPY
Which drugs are given in COPD and what are their mechanism of action?
- Bronchodilators
=> Beta-adrenoreceptor agonists i.e. salbutamol (SABA) for breathlessness in mild COPD or salmeterol (LABA) for moderate to severe COPD
=> Anti-muscarinic — long acting muscarinic antagonist i.e. tiotropium improves lung function, dyspnoea and quality of life
- Phosphodiesterase type 4 inhibitors
=> used as a adjunct to bronchodilators for maintenance of treatment in FEV1 <50% - Corticosteroids
=> Inhaled corticosteroids in exacerbations or FEV1 <50%
=> High dose linked to increased pneumonia => not advised
=> Oral corticosteroids in acute exacerbations - Antibiotics
=> Shortens acute exacerbations so should always be given in acute episodes - Mucolytic agents
=> Reduce sputum viscosity
=> Reduces number of exacerbations
How do you treat chronic COPD?
Start SABA or SAMA (short acting muscarinic antagonist)
If FEV1 >50%
=> Switch to LABA ± inhaled corticosteroids
or
=> LAMA (long acting muscarinic antagonist)
or
=> LAMA ± LABA & inhaled corticosteroids
If FEV1 <50% => LABA + inhaled corticosteroids or => LAMA or => LAMA ± LABA & inhaled corticosteroids
PULMONARY REHABILITATION
Why is long term oxygen therapy (LTOT) given to COPD patients?
Which 3 group of patients benefit the most from it?
I. >8kPa O2 maintained for 15h a day = 3yr survival improved by 50%
II. Long term oxygen therapy (LTOT) recommended for:
=> Clinically stable non-smokers with O2 <7.3kPa despite max treatment
=> O2 between 7.3-8kPa and pulmonary hypertension (e.g. right ventricular hypertrophy, loud S2) or polycythaemia or peripheral oedema or nocturnal hypoxia
=> For terminally ill patients
Pulmonary rehabilitation
=> Long term O2 therapy (LTOT) if O2 <7.3kPa
=> Non-invasive ventilation if hypercapnia on LTOT
=> Surgery in selected patients i.e. recurrent pneumothoraces, isolated bullae disease, lung volume reduction/endobronchial valve transplant
=> Air travel risky if FEV1 <50% or O2 <6.7kPa
INFO CARD
COMPLICATIONS
How do you manage alpha-1 anti-trypsin deficiency leading to COPD?
Alpha-1 anti-trypsin replacement => weekly or monthly infusions
COMPLICATIONS
How do you manage secondary polycythaemia?
Venesection if packed cell volume >55%
Packed cell volume = volume % of RBC in blood
How do you treat large emphysematous bullae that reduce lung capacity?
Surgical bullectomy => allows adjacent collapsed lung to re-expand, thus restoring function
What investigations are carried out in acute COPD?
ABG CXR FBC: U&E, CRP, theophylline level if patient on therapy ECG Sputum for culture if purulent Blood cultures if pyrexial
What is the management of acute COPD?
Nebulised bronchodilators => Salbutamol + Ipratropium
=> Investigate CXR & ABG
Controlled O2 therapy if O2 <88%
Steroids: IV hydrocortisone or oral prednisolone
Antibiotics if infection
Physiotherapy to aid sputum expectoration
If no response to nebulisers and steroids consider IV aminophyline
If no response still:
1. Consider non-invasive positive pressure ventilation if respiratory rate >30 or pH <7.35 or CO2 rising despite treatment
- Consider respiratory stimulant drug
If not response still consider ventilation/intubation if pH <7.26 and CO2 rising despite non-invasive ventilation
What is the differential diagnosis for acute COPD?
Asthma
Pulmonary oedema
Upper respiratory tract obstruction
Pulmonary embolus
Anaphylaxis
What is the risk of O2 therapy?
Respiratory failure => O2 therapy is the most common cause in COPD
This is because some patients rely on their hypoxic drive to breathe
=> too much O2 leads to reduce respiratory rate and hypercapnia => fall in conscious level
Always prescribe O2 like a drug and monitor (ABG) => careful/withdraw if CO2 retention
What type of respiratory failure occurs as a result of COPD?
How should it be managed?
Type 2 Respiratory Failure
Non-invasive ventilation should be offered if pH <7.35
What are the poor prognosis predictors of COPD?
Increasing age
Worsening airflow limitation i.e. decreasing FEV1
Which predictive index is used in COPD to predict its prognosis?
BODE index
Body mass index, degree of airflow obstruction, dyspnoea and exercise capacity.
