COPD Flashcards
Define COPD
A disease characterised by persistent respiratory symptoms and airflow limitation
Due to airways and/ or alveolar abnormalities
Caused by significant exposure to noxious particles or gases e.g. smoking 90%
Not one disease but a syndrome, number of distinct pathologies usually co-exist (often emphysema &/or chronic bronchitis)
Aetiology of COPD
smoking 90%
Air pollution
Biomass exposure - especially rural India/ China
Genetic (alpha 1 antitrypsin) <1% accelerated emphysema
Illicit drug use (smoking heroin/ weed) accelerated emphysema
How common is COPD?
Very, third biggest killer worldwide
2% of UK prevalence - increasing each year
Pathophysiology of COPD
Small airways disease (airway inflammation, airway fibrosis, luminal plugs, increased airway resistance)
——>
Parenchymal destruction (loss of alveolar attachments, decrease of elastic recoil)
——->
Airflow limitation
COPD: symptoms, risk factors, diagnosis
Symptoms: Dyspnoea worse exercise & progressive, chronic cough may intermittent/ unproductive, recurrent wheeze, chronic sputum, recurrent LRTIs
Risk factors: host factors e.g. genetic/ congenital, tobacco, occupation e.g. steal workers, indoor/ outdoor pollution, FH, low birthweight, childhood respiratory infections
Use both to assess then:
Spirometry - required to establish diagnosis
How do we measure the severity of COPD?
MRC dyspnoea scale :
Grades 1-5
MRC grade 1 - breathless with strenuous exercise
2 - short of breath when hurrying on the level or walking up a slight hill
3 - walk slower than ppl of the same age on the level bc of breathlessness or have to stop for breath when walking on their own pace on the level,
4 - stop for breath after walking 100m or after few minutes on level
5 - too breathless to leave house/ breathless when (un)dressing
Clinical signs of COPD
Often few or none especially at rest
- clinical observation and on exertion
- pursed lips breathing
- hyperinflation/ barrel- shaped chest
- prolonged expiratory phase
May have wheeze on auscultation
In advanced cases: cyanosis rarely, cor pulmonale (right sided heart failure) e.g. peripheral oedema/ raised JVP
How can we use spirometry to diagnose COPD?
takes deep breath in and blows as hard as possible into tube
Use spirometer volume/ time graph
Obstructive disease: FEV1 will be reduced more than vital capacity (takes longer to expire) FEV1: FVC reduced
Be cautious FEV1 varies with age
How can we use spirometry to measure severity of airflow obstruction?
Classification of airflow limitation severity in COPD (based on post- bronchodilator FEV1)
In patients with FEV1/ FVC <0.7:
GOLD 1 - mild FEV1 _> 80% of predicted
GOLD2 - moderate FEV1 _<50%, <80% predicted
GOLD3 - severe FEV1 _<30%, <50% predicted
GOLD 4 - very severe FEV1 <30% predicted
Severity of airflow obstruction NOT COPD
What other investigations can you carry out for COPD as well as spirometry?
Chest X–ray:
Not diagnostic, May suggest hyperinflation, mandatory to exclude other diagnoses e.g. cancer
High-resolution computed tomography:
Detailed assessment of the degree of emphysema, if suspicion of bronchiectasis, not required for routine assessment
Full pulmonary function tests:
Static lung volumes can assess for hyperinflation, gas transfer to look at alveolar destruction
Arterial blood gas:
If suspicion of respiratory failure e.g. SpO2 <92%
Alpha-1 antitrypsin blood test:
Younger patients/ atypical lower lobe emphysema
Exacerbations of COPD definition, how common, mortality
An acute worsening of respiratory symptoms that result in additional therapy (over day to day variability)
Very vague definition
Second most common cause of admission and highest cause of readmission
11.9% mortality at 90 days
43% readmitted at 90 days
Once admitted for COPD exacerbations
Which patients are most at risk of exacerbations?
- previous exacerbations
- disease severity (airflow obstruction and MRC dyspnoea score)
- gastro-oesophageal reflux
- pulmonary hypertension
- respiratory failure
Aetiology of exacerbations
- common bacteria 30%
E.g. haemophilus influenza, streptococcus pneumoniae, moraxella catarrhalis. (20-30% pts chronically colonised) - common viral pathogens 23% e.g. rhinovirus, influenza
B + V = 25%
None = 31%
- Atypical organisms e.g. mycoplasma pneumoniae, chlamydia spp
- environmental factors e.g. pollution
- eosinophilic e.g. eosinophils modulate type 2 mainly inflammatory pathway ✅ steroids
Therapies that improve symptoms & risk
symptoms:
- pulmonary rehabilitation*
- bronchodilators (beta 2 agonists LABA/ SABA & anti-muscurinics LAMA/ SAMA)
- mucolytics (thin phlegm)
- refractory dyspnoea management (low dose opiates, airflow therapy, CBT/ psychological input)
- lung volume reduction surgery*
- lung transplant*
- palliative care
Risk:
- smoking cessation*
- O2 therapy (long term or ambulatory*)
- anti- inflammatories* (inhaled corticosteroids, long term macrolides)
- non- invasive ventilation (type 2 resp failure)
- flu vaccine (best value non-pharmacological)
- used for both
How does quitting smoking change your FEV1 and management of COPD?
Doesn’t improve it but slows worsening (so rate of decline goes back to similar levels as non-smoker but from a lower starting point)
Reduces mortality, improves symptoms, slows down loss of lung function, reduces exacerbations, drugs work better
Champix reduces addiction
As ciliary regrowth night get more cough & sputum short-term
What is pulmonary rehabilitation?
Exercise:
6-8 week course, hospital/ community, 2 supervised sessions/ week + 1 unsupervised, education, ongoing plan/ referral
83% some improvement
Compare the bronchodilators beta-2 agonists & muscarinic antagonists in COPD
Muscarinic receptors in proximal airways, inhibit bronchoconstriction effect of AcH at M3 R smooth muscle, nonselective so also block M2 & M1
B2- adrenergic receptors more in distal airways, activate B2 R bronchioles -> increased cAMP-> relaxation SM
Increase airway calibre, reduce breathlessness & exacerbation
Long acting: used one or twice a day
What effects do ICS have on inflammatory cells in bronchoalveolar lavage studies?
Reduced neutrophil and lymphocyte counts
Increased macrophage counts
No significant effect on eosinophils
in bronchoalveolar lavage studies
What effects do ICS have on inflammatory cells in bronchial biopsies?
Reduced CD8+, CD4+ lymphocytes
No significant effects on neutrophils, eosinophils and CD68 macrophage counts
What effect do inhaled corticosteroids have on exacerbations?
25% reduction
When and why is long term O2 therapy used?
If someone is persistently hypoxic, non-smokers who don’t retain high levels of CO2 (as can lead to hypercapnia)
PO2 <7.3 KPa at rest (or <8KPa if cor pulmonale)
Extended hypoxaemia cause end-organ damage to heart and kidneys
Improves survival
Minimum 16hrs/ day
Safety- home fire risk assessment
When is ambulatory O2 used and what does it do?
Reduces symptoms
If patients desaturate when walking (>4%), use during exertion
Need to walk further on O2, no prognostic benefit
How to treat severe exacerbations
Hospitalisation - 12% mortality/ 43% readmitted at 3months
Bronchodilators - May nebulised therapy (SABA & SAMA) inhaled directly into lungs mask
Oral corticosteroids - prednisolone 5 days, in future may be based on blood eosinophil count
Controlled O2 if at risk type 2 resp failure - SpO2 88-92% , arterial blood gas
Antibiotics if indicated e.g. CRP/ WBCs raised/ symptoms
Wider therapy - inhaler technique, post pulmonary rehabilitation, smoking cessation
What is non-invasive ventilation and what is it’s function?
Breathing support through a face/ nasal mask - air usually with added O2 given under positive pressure, generally altered depending if inhaling or exhaling
Tidal volume directly proportional to initial inspiratory positive airway pressure (IPAP)
Increased IPAP -> inc tidal volume -> inc minute volume -> dec CO2
Support ventilation and improve ventilatory function, reduce PaCO2 and raise PaO2, improve symptoms, increase life expectancy, reduced hospitalisation
