COPD

Question 1

What is the definition of COPD?

Answer 1

• Airflow obstruction which is progressive, not fully reversible and does not change markedly over several months. Commonly caused by smoking

Question 2

What are factors involved in the pathogenesis of COPD?

Answer 2

• Smoking (key), air pollution, pathogens, allergens and host susceptibility. This leads to neutrophil predominant inflammation which causes emphysema and/or chronic bronchitis

Question 3

Explain how smoking can cause COPD

Answer 3

• 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.

Question 4

What are the genetic factors which impact the COPD?

Answer 4

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

Question 5

What is the definition of chronic bronchitis?

Answer 5

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.

Question 6

What is the definition of emphysema?

Answer 6

Abnormal, permanent enlargement of airspaces distal to the terminal bronchioles

Question 7

What are the histological features of chronic bronchitis

Answer 7

• Infiltration with neutrophils and CD8+ lymphocytesm
• Squamous metaplasia
• Loss of interstital support,
• Increased epithelial mucous cells and mucous gland hyperplasia

Question 8

What is small airway disease?

Answer 8

Narrowing bronchioles due to mucus plugging, inflammation and fibrosis .
May be an early features of COPD

Question 9

What are the cell types and inflammatory mediators involved in COPD

Answer 9

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

Question 10

What are the different types of emphysema?

Answer 10

• 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

Question 11

Explain the mechanism of airflow obstruction in COPD

Answer 11

• 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

Question 12

When should you consider a differential diagnosis of COPD?

Answer 12

• 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

Question 13

How is COPD diagnosed?

Answer 13

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

Question 14

How can you assess the risk of an exacerbation of COPD?

Answer 14

looking at severity of airflow limitations, the number of exacerbations within the last year and their symptoms/breathlessness

Question 15

Explain the treatment of COPD?

Answer 15

• 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)

Question 16

What are the different endotypes of COPD?

Answer 16

• Persistent systemic inflammation
• Eosinophilic COPD (responds well to steroids)
• Persistent pathogenic bacterial colonisation
• Alpha 1 antitrypsin deficiency

Question 17

What are the features of ‘blue bloaters’

Answer 17

Type 2 respiratory failure (high CO2 and low O2) due to COPD which presents with following symptoms:
- Cyanosis,
- Warm peripheries,
- Bounding pulse,
- Flapping tremor,
- Confusion/drowsiness,
- Right heart failure,
- Oedema
- Raised JVP

Question 18

What are the features of ‘pink puffers’

Answer 18

Type 1 respiratory failure (low O2 and low CO2) due to COPD which presents with following:
- Desaturates on exercise,
- Pursed lip breathing,
- Use of accessory muscles,
- Wheeze,
- Indrawing of intercostals,
- Tachypnoea

Question 19

What is asthma-COPD overlap syndrome

Answer 19

Exactly as it sounds. Patients with asthma develop COPD

Question 20

What is the difference between asthma and COPD?

Answer 20

Asthma - CD4, T lymphocytes and eosinophil mediated reaction which is completely reversible. Commonly presents with night time waking with breathlessness, diurnal variation.
COPD - CD8, T lymphocyte, macrophages and neutrophil mediated reactions which are irreversible. Strong association with smoking, commonly has productive bough and no diurnal variation.

Question 21

What is the only intervention to slow the progression of COPD?

Answer 21

Smoking cessation