Pathological & Clinical Aspects of COPD Flashcards
Define COPD [4]
- disease characterised by airflow obstruction that is:
- usually progressive,
- not fully reversible
- does not change markedly over several months
What are the risk factors/causes of COPD? [5]
- Smoking (major)
- Environmental pollution
- Burning of biomass fuels
- Occupational dusts
- Alpha I anti-trypsin deficiency
Describe the effects of cigarette smoke on the lung [6]
- Cilial motility is reduced
- Cilia are damaged/destroyed by smoking which results in:
- increased infections (due to not being able to clear secretions easily)
- damaged lung
- Cilia are damaged/destroyed by smoking which results in:
- Airway inflammation
- Proteases are released from inflammatory cells
- Mucus hypertrophy and hypertrophy of Goblet cells
- Increased protease activity, anti-proteases inhibited
- Oxidative stress → production of free radicals
- Squamous metaplasia → higher risk of lung cancer
What are the 2 clinical syndromes of COPD? [2]
- chronic bronchitis
- emphysema
Define chronic bronchitis [1]
the production of sputum on most days for at least 3 months in at least 2 years
Define emphysema [1]
abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
Describe the main macroscopic features in both early and late chronic bronchitis [5]
- Chronic bronchitis main macroscopic features:
- larger airways > 4mm in diameter
- Inflammation leading to scarring and thickening of airways
- Small airway disease (earlier on)
- “Bronchiolitis” in airways of 2-3 mm
- May be an early feature of COPD
- Narrowing of the bronchioles due to:
- mucus plugging,
- inflammation
- fibrosis
What are the 3 main cell types involved in COPD inflammation? [3]
- Macrophages,
- CD8 (predominately) and CD4 T lymphocytes,
- Neutrophils
What are the inflammatory mediators involved in COPD inflammation? [9]
- TNF, IL-8 and other chemokines
- Neutrophil elastase, proteinase 3, cathepsin G
- (from activated neutrophils)
- Elastase and MMPs
- (from macrophages)
- Reactive oxygen species
Name the 3 types of emphysema [3]
- centri-acinar
- pan-acinar
- para-septal
Describe the features of centri-acinar emphysema [2]
- Dilatation/damage around respiratory bronchioles, the central portion of the acinus
- Present more in upper lobes
Describe the features of pan-acinar emphysema and what is it associated with? [3]
- Uniformly enlarged/damaged of all parts of the acinus from the level of terminal bronchiole distally to the terminal blind alveoli
- Can get large bullae
- Associated with α1 anti-trypsin deficiency
What are bullae? [1]
thin-walled air-filled space within the lung, typical of pan-acinar emphysema
What is para-septal emphysema and what does it increase your risk of? [2]
- Damage round the edges of the lungs
- Increases risk of pneumothorax
What are the 2 types of emphysema that cause airflow obstruction and what is the eventual complication of these types of emphysema? [3]
- centri-acinar
- pan-acinar
- results in consequent loss of surface area for gas exchange → eventually leading to hypoxaemia
Describe the mechanisms of airflow obstruction in COPD [10]
- Loss of elasticity and alveolar attachments due to emphysema resulting in airway collapse on expiration
- causes air trapping and hyperinflation → increased work of breathing → breathlessness
- Goblet cell metaplasia with mucus plugging of lumen
- Inflammation of the airway wall
- Thickening of the bronchiolar wall due to:
- smooth muscle hypertrophy
- peribronchial fibrosis
What features of COPD can be seen on a chest x-ray? [5]
- Over-inflation
- Low and flattened diaphragms
- Bullae
- Pruned blood vessels with large proximal vessels
- Relatively little blood visible in peripheral lungs
What factors should make you consider a diagnosis of COPD? [7]
- Consider the diagnosis of COPD for people who are over 35yrs, and smokers or ex-smokers, with any of:
- exertional breathlessness
- chronic cough
- regular sputum production
- frequent winter ‘bronchitis’
- wheeze
How can COPD be classified in terms of spirometry (after being given a bronchodilator)? [6]
- spirometry shows an obstructive pattern (FEV1/FVC ratio <70%, both reduced)
- Stage 1 (mild) → FEV1 %predicted = 80%
- Stage 2 (moderate) → FEV1 %predicted = 50-79%
- Stage 3 (severe) → FEV1 %predicted = 30-49%
- Stage 4 (very severe) → FEV1 %predicted = <30%
What are the treatment options for COPD? [6]
- Inhaled bronchodilators
- Short-acting: salbutamol
- Long acting: salmeterol, tiotropium
- Inhaled corticosteroids
- Budesonide and fluticasone — combination inhalers
- Oxygen therapy
- Oral theophyllines
- Mucolytics
- carbocysteine
- Nebulised therapy
What are 2 non-pharmacological approaches to the management of COPD? [2]
- smoking cessation
- pulmonary rehabilitation
What are the typical features of type 1 respiratory failure? [9]
- “pink puffer”
- high respiratory drive
- ↓PaO2, ↓PaCO2
- desaturates on exercise
- pursed lip breathing
- use accessory muscles
- wheeze
- indrawing of intercostals
- tachypnoea
What are the typical features of type 2 respiratory failure? [10]
- “blue bloater”
- low respiratory drive
- ↓PaO2, ↑PaCO2,
- cyanosis
- warm peripheries
- bounding pulse
- flapping tremor
- confusion, drowsiness,
- right heart failure
- Oedema, raised JVP
There are key differences between asthma and COPD. What are the defining inflammatory processes in COPD? [6]
- hint:
- what type of agent induces COPD? [1]
- cells involved in COPD airway inflammation [3]
- features of airflow limitation [2]
- noxious agent
- COPD airway inflammation:
- CD8+ T lymphocytes
- neutrophils
- macrophages
- airflow limitation:
- irreversible
- usually progressive if exposure to noxious agents continue
