COPD Flashcards
Define chronic bronchitis.
Clinical diagnosis characterised by excessive secretions of bronchial mucosa and productive cough for >3months in 2 consecutive years.
What is COPD?
Chronic airflow obstruction due to chronic bronchitis or emphysema. Usually progressive, +/- accompaniment by airway hyperreactivity (may be partially reversible).
What is the typical FEV1 of COPD?
FEV1 will be less than 80% of expected.
What is emphysema?
Pathologic diagnosis denoting abnormal, permanently enlarged air spaces distal to the terminal bronchiole, with destruction of their walls without obvious fibrosis.
What are the major causes of COPD? Other RFx?
-Inhalational injury (smoking)
-a1-antitrypsin deficiency
RFx:
-Occupational exposure
-Bronchial hyperreactivity
-Passive smoking
-Air pollution
What is the common presentation of COPD?
Patients present with progressively worsening dyspnoea (exertion -> rest).
Vary in appearance: blue bloater (chronic bronchitis, overweight, oedematous,cyanotic) OR pink puffer (emphysema, thin ruddy cheeks).
Consider Dx in anyone with chronic or productive cough, dyspnoea, RFx.
How do ABGs apppear throughout the course of COPD?
Early: Initially normal in early phase
Advanced: hypoxemia and hypercapnia. Often with a chronic compensated respiratory acidosis due to CO2 retention.
What is the 50-50 club?
PaO2 near 50
PaCO2 near 50
Near normal pH
What are the spirometric patterns of obstructive lung disease?
Obstructive diseases have:
- larger lung volumes (TLC normal or increased)
- decreased FER (to
What is the spirometric pattern of restrictive lung disease?
Lower lung volumes (decreased TLC and VC)
What are the underlying principles of COPD management?
Relieving airway obstruction and correcting life threatening gas exchange abnormalities.
What is the Rx (inc non pharmacologic) of COPD?
- Smoking cessation
- Drug therapy: short term exacerbations and long term (FEV1 Bronchodilators
- > Corticosteroids
- > Antibiotics (if infection suspected)
- Oxygen therapy
How should bronchodilators be used in COPD?
- B-adrenergic agonists initially:
- > SABA: (ventolin = Salbutamol);
- > add LABA (serevent = salmeterol) if indicated by mod-severe disease.
- Antimuscarinic agent:
- > e.g (spiriva = Tiotropium; atrovent = ipratropium)
Do anti-muscarinics improve decline in FEV1?
Anti-muscarinic agents e.g. tiotropium improve patient’s function and quality of life but decline in FEV1 is unaffected.
Describe corticosteroid therapy in COPD.
In symptomatic patients with mod-severe COPD –> trial prednisolone 30mg for 2/52.
Measure lung function before and after; improvement FEV1>15% –> replace prednisolone with inhaled beclomethasone 40ug bd.
Does the combination of LABA and inhaled corticosteroid improve mortality?
No. Protects against a decline in lung function but does not improve mortality.
How should antibiotics be used in COPD?
Shortens exacerbations –> always give acutely.
e.g. amoxicillin, co-amoxyclav
Does oxygen use improve mortality? Under what conditions?
Yes. Substantial improvement only when administered 19h daily at flow rate 1-3L/min with 28% O2 mask.
What are the signs of acute respiratory failure?
Tachypnoea (resp >40 breaths/min); inability to speak due to dyspnoea; accessory muscle use with fatigue; confusion; restlesness/agitation/lethargy; rising PCO2 and hypoxia.
How is acute respiratory failure treated?
Endotracheal intubation with ventilatory support (to correct gas exchange disorders).
What are the complications of mechanical ventilation?
Difficulty in extubation, ventilator-associated pneumonia, pneumothorax, ARDS.
What are the long term complications of COPD from hypoxia?
- Pulmonary hypertension
- Secondary erythrocytosis
- Exercise limitation
- Impaired mental functioning
Which interventions have been shown to improve mortality and interrupt natural history of COPD?
Smoking cessation
Supplemental oxygen therapy (if chronic hypoxemia)
Lung volume reduction surgery
When does home oxygen therapy provide benefit?
Patients with resting hypoxemia:
PaO2 <88%
What is the most likely examination finding in COPD?
Diffuse expiratory wheeze, clubbing, bibasal inspiratory crackles + increased JVP, inspiratory stridor, S3.
Diffuse expiratory wheeze.
COPD OBSTRUCTIVE! Most airflow limitation in small airways of LRT –> expiratory wheeze.
Inspiratory stridor = upper airway
Clubbing not generally COPD feature (look for other process e.g. bronchogenic carcinoma)
Crackles, increased JVP and S3 indicate CCF.
Why does nocturnal hypoxia occur in COPD patients?
Alveolar hypoventilation due to:
- inhibition of accessory and intercostal muscles in REM
- shallow breathing in REM reducing ventilation
- increase in upper airway resistance due to decreased muscle tone
What is nocturnal hypoxia?
PaO2 may drop as low as 19mmhg, esp in REM.
COPD patients already hypoxic –> much larger fall in O2 sat due to steepness of HbO2 dissociation curve
What is contraindicated in patients with nocturnal hypoxia?
Sleeping tablets.
Will further depress respiration.
How should acute COPD exacerbation be managed?
- Oxygen therapy (watch PaCO2 levels)
- Removal of retained secretions (cough, physio)
- Respiratory support (e.g. CPAP)
- Drugs: corticosteroids, B-agonists, antibiotics
What are the signs of COPD?
Initially: nothing more than quiet wheeze
Advanced: tachypnoeic, prolonged expiratory phase, accesorry muscle use, intercostal indrawing on inspiration, poor chest expansion, lungs hyperinflated, loss of normal cardiac and liver dullness.a
What are the signs of hypercapnia?
Peripheral vasodilation
Bounding pulse
Coarse flapping tremor (when PaCO2 >10kPa)
Severe: confusion and progressive drowsiness; +/- papilloedema (not diagonstic)
What is cor pulmonale?
Heart disease secondary to disease of the lung.
Characterised by pulmonary HTN –> RVH –> RHF.
What are the examination findings of cor pulmonale?
- Patient is centrally cyanosed (due to lung disease);
- when heart failure develops: increased breathlessness, ankle oedema.
- Prominent parasternal heave due to RVH
- Loud P2
- RHF may lead to tricuspid incompetence with increased JVP, ascites and hepatomegaly.
How is COPD diagnosed?
Usually clinical; GOLD criteria for classification.
Stage I - IV (mild - very severe) based on FEV1/FVC (80 / 50 / 30 /
What investigations are required in COPD?
Lung function tests (show airflow limitation)
CXR: often normal, even in advanced disease. Classically: overinflation with low, flattened diaphragms, +/- bullae.
CT: can show emphyesematous bullae
ABGs: often normal at rest
How is COPD prognosis estimated?
BODE: Body mass index Obstruction (degree of airflow obstruction) Dyspnoe Exercise capacity BODE 0-2, mortality = 10% BODE 7 - 10, mortality = 80% at 4 years
Outline the pathogenesis of COPD.
Noxious agent triggers inflammation in airways, lung parenchyma and pul vessels causing:
i) Small Airway Disease: airway inflammation and remodelling
ii) Parenchymal destruction: loss of alveolar attachments and loss of elastic recoil.
Both precipitate airflow limitation.
What is the mechanism of emphysema?
- Protease /antiprotease imbalance (proteases digest elastin and other structural proteins in alveolar wall)
- M0 and T lymphocytes prominent
What are the different patterns in emphysema?
- Centriacinar (radiates from terminal bronchiole)
- Panacinar (more generalised)
- Bullae
What is FER?
Forced Expiratory Ratio.
=FEV1/FVC (or VC, whichever is larger).
Clinical features distinguishing asthma from COPD?
Cf COPD, asthma has:
- variable course
- onset at young age
- Not ass/w smoking
- Airflow limitation substantially reversible
Pathological features distinguishing COPD from asthma?
Cf COPD, asthma has:
- mostly eosinophilic inflammation affecting ALL airways and doesn’t involve lung parenchyma
- Fibrosis NOT a feature
Pathology of COPD distinguishing from Asthma?
Cf asthma, COPD has:
- Neutrophilic inflamm
- Most pathology in peripheral airways, where there is also fibrosis => obliterative bronchiolitis
- Mucus hypersecretion more prominent
What is the management plan for COPD?
COPD-X
- Confirm Diagnosis
- Optimise lung function
- Prevent deterioration
- Develop support network and self management plan
- eXacerbation - manage appropriately
What is spiriva?
Tiotropium = anticholinergic
What is atrovent
Ipratropium = anticholinergic
Anticholinergic v beta agonist as bronchdilator?
Anticholinergics are:
- Long acting, more convenient
- less dyspnoea
- better exercise
- less exacerbation
What is seretide?
Inhaled fluticasone and salmeterol.
What is symbicort?
Inhaled budesonide and formoterol.
What are the principles of pulmonary rehabilitation?
- Improve fitness
- Education
vaccines for COPD patients?
- Fluvax (yearly)
- Pneumococcal vax (twice, 5years apart)
When and how should home O2 be instituted in COPD therapy?
Oxygen concentrator 2-4L/min via nasal prongs >16h /day. Start when:
-PO2 on air at rest
How is a COPD exacerbation defined?
Anthonisen criteria:
i) increased dyspnoea
ii) increased sputum production
iii) sputum become discoloured
