What is the definition of COPD?
A progressive, largely irreversible airflow obstruction due to chronic bronchitis (productive cough ≥3 months for 2 years) and emphysema (destruction of alveolar walls).
What is the main cause of COPD?
Cigarette smoking (≈90%).
Which genetic disorder causes early-onset COPD?
Alpha-1 antitrypsin deficiency causing panacinar emphysema.
What are the key risk factors for COPD?
Smoking, passive smoke exposure, occupational dust/fumes, biomass fuel exposure, A1AT deficiency.
What is the diagnostic spirometry finding in COPD?
Post-bronchodilator FEV1/FVC <0.7 confirming obstruction.
What CXR features are seen in COPD?
Hyperinflation, flattened hemidiaphragms, bullae, hyperlucent lungs.
What blood test helps identify A1AT deficiency?
Serum alpha-1 antitrypsin level.
What symptoms characterise COPD?
Progressive dyspnoea, chronic productive cough, wheeze, frequent infections.
What signs may be present in COPD?
Barrel chest, hyperinflation, pursed-lip breathing, accessory muscle use, wheeze, cyanosis, oedema if cor pulmonale.
What are the GOLD severity stages based on FEV1?
Mild >80%, Moderate 50–79%, Severe 30–49%, Very severe <30%.
What is the first-line bronchodilator in stable COPD?
SABA or SAMA as needed.
What determines inhaler escalation in COPD?
Presence or absence of asthma/steroid-responsive features.
What are steroid-responsive features in COPD?
High eosinophils, atopy, past asthma, >400 mL FEV1 variability, >20% PEF variability.
How is COPD treated if NO steroid-responsive features?
LABA + LAMA.
How is COPD treated if steroid-responsive features?
LABA + ICS, escalating to triple therapy (LABA + LAMA + ICS).
When are mucolytics used in COPD?
Chronic productive cough with symptomatic benefit.
When is azithromycin prophylaxis used in COPD?
Non-smokers with optimised therapy and ≥2 exacerbations despite triple therapy, after CT & sputum culture.
What improves survival in COPD?
Smoking cessation, LTOT, lung volume reduction surgery in selected patients.
What are the LTOT referral indicators?
O₂ sats ≤92%, severe COPD (FEV1 <30%), cyanosis, polycythaemia, cor pulmonale.
What are the ABG criteria for LTOT?
PaO₂ <7.3 kPa OR PaO₂ 7.3–8 kPa with cor pulmonale, oedema, or polycythaemia.
When should LTOT NOT be given?
Patients who continue smoking due to fire risk.
What are the main causes of COPD exacerbations?
Haemophilus influenzae, Strep pneumoniae, Moraxella catarrhalis, rhinovirus.
What are the clinical features of a COPD exacerbation?
Worsening dyspnoea, cough, sputum volume/colour change, fever, wheeze, confusion.
How is an acute COPD exacerbation initially managed?
Oxygen to 88–92%, nebulised salbutamol + ipratropium, prednisolone 30 mg 5 days, antibiotics if sputum purulent.