COPD Flashcards
What % of heavy smokers develop COPD?
10-20%
Pathophysiology of COPD
- Increased mucous secreting goblet cells
- Bronchi inflamed
- Infiltration of inflammatory cells
- Lymphocytic infiltrate is mainly CD8+
- Inflammation followed by scarring and thickening of the walls
- Eventually fibrosis occurs
Asthma involves the infiltration of eosinophils, what cell type is seen in COPD?
Neutrophils
What diseases come under the COPD umbrella☂️?
Chronic bronchitis - pink puffer
Emphysema - blue bloater
How does smoking cause COPD?
Cigarette smoke stimulates epithelial cells, macrophages and neutrophils to release inflammatory mediators and proteases - especially neutrophil elastase
Inflammatory mediators destroy lung tissue
Proteases are normal in humans but smokers have soooo many that they overwhelm the anti-proteases = protease-antiprotease imbalance
Cigarette smoke impairs ciliary movement
Discuss a1-antitrypsin deficiency
a1-antitrypsin (acute phase protein produced in the liver) usually acts as an anti-protease in the lung and inhibits neutrophil elastase
Deficiency causes protease-antiprotease imbalance
Deficiency results in early onset emphysema (<40yrs) and death
Autosomal dominant
What is emphysema?
PINK PUFFER
- Permanent enlargement of the air spaces distal to terminal bronchiole
- Due to alveolar spetal destruction because of protease-antiprotease imbalance
- The walls are destroyed and airways collapse - hence the OBSTRUCTION
- Two types:
1. Centriacinar
2. Panacinar
What is chronic bronchitis?
Persistent cough with sputum production for at least 3mo of the year for 2 consecutive years
How does smoking cause chronic bronchitis?
Smoking causes hyperplasia and hypertrophy of mucus-secreting glands found in the submucosa of large airways.
Small airways become blocked with mucous plugs, mucosal oedema and smooth muscle hypertrophy
Bacterial colonisation occurs due to accumulation of secretions
All of the above cause obstruction and increased resistance to airflow
Upon examination of a patient with emphysema, what would you expect?
PINK PUFFER
- Thin: weight loss due to work of breathing
- Marked chest hyperinflation
- Cor pulmonale absent
- Cyanosis absent
- Low PaCO2
Upon examination of a patient with chronic bronchitis, what would you expect?
BLUE BLOATER
- Obese
- Cor pulmonale present
- Central cyanosis
- Raised PaCO2
Complications of COPD
- Exacerbation: acute worsening usually due to infection
- Respiratory failure: unable to maintain normal blood gases - normal type 2 failure, leading cause of death in COPD
- Cor pulmonale: occurs due to pulmonary hypertension which causes RrV hypertrophy and failure
Investigations for COPD
- Spirometry is gold standard and shows an obstructive pattern (reduced FEV1/FVC ratio)
- Diagnosis is made if FEV1/FVC ratio is <70%
- Bronchodilator reversibility should be tested to exclude asthma
- Chest x-ray shows hyperinflation/ flat hemidiaphragm
- FBC may show polycythaemia (RBC+++ due to hypoxia triggering EPO production in kidneys)
Treatment for COPD
- Smoking cessation slows process and is the key intervention
- Bronchodilators: anticholinergics more effective than b2 agonists but a combination may help
- Inhaled corticosteroids: not all patients will respond
- Antibitoics: to shortern exacerbations, always give during acute episodes
- Vaccine: annual flu vaccine
- O2 therapy if necessary
- Surgery
- a1-antitrypsin therapy for those with genetic defect
What are the two types of emphysema?
- Centriacinar: Septal destruction and dilatation limited to centre of acinus, around terminal bronchiole and mainly upper lobes
- Panacinar: Whole of acinus is involved distal to terminal bronchiole, lower lobes mainly
*panacinar emphysema is characteristic of a1 antitrypsin deficiency
