COPD Flashcards
What is the definition of COPD?
- Airflow obstruction which is progressive, not fully reversible and does not change markedly over several months. Commonly caused by smoking
What are factors involved in the pathogenesis of COPD?
- Smoking (key), air pollution, pathogens, allergens and host susceptibility. This leads to neutrophil predominant inflammation which causes emphysema and/or chronic bronchitis
Explain how smoking can cause COPD
- Cigarettes cause reduced cilia motility, cause airway inflammation, mucus hypertrophy, goblet cell hypertrophy, increased protease activity, inhibition of anti-proteases and cause oxidative stress. This causes squamous metaplasia.
What are the genetic factors which impact the COPD?
Alpha 1 antitrypsin deficiency. Normally alpha 1 antitrypsin is a protective glycoprotein which inhibits serine proteinase.
SS and ZZ homozygotes have the clinical disease which can cause people to develop emphysema in their 30-40s. Smokers will develop it even earlier
What is the definition of chronic bronchitis?
Production of sputum on most days for at least 3 months in at least 2 years.
Affects large airways greater than 4mm in diameter. Inflammation leads to scarring and thickening of airways.
What is the definition of emphysema?
Abnormal, permanent enlargement of airspaces distal to the terminal bronchioles
What are the histological features of chronic bronchitis
- Infiltration with neutrophils and CD8+ lymphocytesm
- Squamous metaplasia
- Loss of interstital support,
- Increased epithelial mucous cells and mucous gland hyperplasia
What is small airway disease?
Narrowing bronchioles due to mucus plugging, inflammation and fibrosis .
May be an early features of COPD
What are the cell types and inflammatory mediators involved in COPD
Cell types - Macrophages, CD8 and CD4 T lymphocytes and neutrophils.
Inflammatory mediators - TNF, IL-8 and other chemokines, neutrophil elastase, proteinases 3 (from neutrophils), elastase released from macrophages and reactive oxygen species
What are the different types of emphysema?
- Centri-acinar: damage occurs around bronchioles more in upper airways. Associated with smoking
- Pan-acinar: Uniformly enlarged from level of terminal bronchiole distally. Large bullae and associated with alpha 1 anti-trypsin deficiency.
- Paraseptal: Bullae are at risk of rupture and causing pneumothroax
Explain the mechanism of airflow obstruction in COPD
- Emphysema causes a loss of elasticity and alveolar attachments which results in airway collapse on expiration. This results in air trapping and hyperinflation which causes increased work of breathing.
- Goblet cell metaplasia and mucus plugging of lumen ccn obstruct airtflow
- Inflammation of airways and thickening of bronchiolar walls also obstruct airflow
When should you consider a differential diagnosis of COPD?
- Patients who are over 35 and smokers/ex-smokers who present with any of the following: exertional breathlessness, chronic cough, regular sputum production, frequent winter bronchitis or wheeze
How is COPD diagnosed?
Spirometry with an obstructive pattern (FEV1/FVC ration < 70%)
Stage 1 (Mild) - FEV1 80% of predicted.
Stage 2 (moderate) - FEV1 50-79% of predicted.
Stage 3 (severe) - FEV1 30-49% of predicted.
Stage 4 (very severe) - FEV1 <30% of predicted or FEV<50% of predicted with respiratory failure
How can you assess the risk of an exacerbation of COPD?
looking at severity of airflow limitations, the number of exacerbations within the last year and their symptoms/breathlessness
Explain the treatment of COPD?
- Inhaled bronchodilaters: Short acting (salbutamol) or long acting (salmeterol or tiotropium-muscarinic antagonist)
- Inhaled corticosteroids: Budesonide and fluticasone combination inhalers
- Oxygen therapy
- Oral theophyllines (phosphodiesterase inhibitor)
- Mucolytics (carbocysteine) which help thin mucus
- Nebulised therapies (for exacerbations)
