Chronic obstructive pulmonary disease (COPD)

Question 1

What is COPD?

Answer 1

Chronic, progressive lung disorder characterised by airflow obstruction with CHRONIC BRONHCITIS (chronic cough and sputum production for at least three months per year over 2 years) and/or EMPHYSEMA (pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles).

Question 2

What is the aetiology of COPD? (x5)

Answer 2

• Smoking • Air pollution • Occupation exposures • Alpha1-antitrypsin deficiency • May co-present with asthma

Question 3

What is the pathophysiology of COPD? (x6)

Answer 3

• CHRONIC BRONCHITIS: bronchiole inflammation leads to narrowing of airways with mucosal oedema, mucous hypersecretion, squamous metaplasia and ciliary dysfunction. • Activated macrophages, neutrophils, and leukocytes, oxidative stress and excess of proteases amplify the effects of chronic inflammation.
• Airway remodelling thickens the terminal bronchiole walls leading to loss of patency
• EMPHYSEMA: from elastin breakdown which keeps small airways open during expiration, leading to destruction and enlargement of alveoli.
• Expiratory flow limitation promotes hyperinflation, which alongside the above disease process, predisposes patients to hypoxia.
• Hypoxia causes vascular smooth muscle thickening with subsequent pulmonary hypertension which is a late development of the disease

Question 4

What are acute exacerbations of COPD?

Answer 4

Defined as acute worsening of symptoms from baseline, from increases in airway inflammatory cells and proteins that are triggered by infection, airborne pollutants and other precipitating factors. This leads to concurrent bronchoconstriction and worsening in expiratory airflow limitation which leads to increased restrictive work of breathing, increased ventilation/perfusion mismatch and worsening hyperinflation.

Question 5

What is the epidemiology of COPD: Prevalence? Age? Gender?

Answer 5

Prevalence up to 8%. Presents in middle age or later. More common in males.

Question 6

What are bullae?

Answer 6

Manifestation of emphysema when alveolar spaces have a diameter larger than 1cm.

Question 7

What are the symptoms of COPD? (x4)

Answer 7

• Chronic cough and sputum production (green in acute exacerbations) • SOB • Wheeze • Decreased exercise tolerance

Question 8

What are the signs of COPD? (x4)

Answer 8

• INSPECTION: respiratory distress, use of accessory muscles, barrel-shaped overinflated chest, decreased cricosternal distance, cyanosis
• PERCUSSION: hyper-resonant chest, loss of liver and cardiac dullness
• AUSCULTATION: quiet breath sounds, prolonged expiration, wheeze, rhonchi and crepitations sometimes
• SIGNS OF CO2 RETENTION: bounding pulse, warm peripheries, flapping tremor, signs of right heart failure in later stages
• NO CLUBBING

Question 9

How does COPD present on CXR? (x3)

Answer 9

May appear normal or show hyperinflation (more than 6 ribs visible anteriorly, flat diaphragm), decreased peripheral lung markings (hyperlucency), elongated cardiac silhouette.

Question 10

What do pulmonary function tests show in COPD?

Answer 10

Obstructive picture – low PEFR, low FEV1:FVC ratio, raised lung volumes, carbon monoxide gas transfer coefficient low when alveolar destruction is significant.

Question 11

How is COPD diagnosed?

Answer 11

Post-bronchodilator spirometry is required for confirmation of diagnosis: a post bronchodilator FEV1/FVC less than 70% confirms persistent airflow obstruction.

Question 12

How does FEV1:FVC ratio reflect COPD disease severity? (x3)

Answer 12

Mild is 60-80%, moderate 40-60%, severe less than 40%.

Question 13

What are the other investigations for COPD? (x5)

Answer 13

• BLOOD: high Hb and PCV as a result of secondary polycythaemia
• ABG: hypoxia and normal/raised PaCO2.
• ECG and ECHO: signs of right ventricular hypertrophy, arrythmia and ischaemia
• SPUTUM/BLOOD CULTURES: in acute exacerbations for treatment
• ALPHA1-ANTITRYPSIN LEVELS: should be consider in young patients or minimal smoking history as this would be a more likely aetiology

Question 14

How is COPD severity graded? (x4)

Answer 14

• Mild COPD: FEV1/FVC <0.7, FEV1 % predicted ≥80 percent
• Moderate COPD: FEV1/FVC <0.7, FEV1 % predicted 50–79 percent
• Severe COPD: FEV1/FVC <0.7, FEV1 % predicted 30–49 percent
• Very severe COPD: FEV1/FVC <0.7, FEV1 % predicted <30 per cent, OR less than 50% if patient has respiratory failure

Question 15

How is COPD managed for each GOLD group?

Answer 15

• GROUP A: bronchodilator (SAMA, LABA or LAMA) • GROUP B: long-acting bronchodilator such as LABA or LAMA, and SABA • GROUP C: LAMA, and SABA • GROUP D: LAMA, or LABA+LAMA, or LABA+ICS, and SABA

Question 16

What general management is there for COPD? (x3)

Answer 16

• Smoking cessation
• PULMONARY REHABILITATION: aerobic exercise, strength training, and education
• OXYGEN THERAPY: long term; indicated if PaO2 is less than 7.3 kPa on air during period of clinical stability OR PaO2 between 7.3-8.0 and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension

Question 17

How are acute exacerbations of COPD managed? (x5)

Answer 17

• SABA: MDI in mild exacerbations, nebulised if moderate or severe
• 24% O2 via non-variable flow Venturi mask. Increase slowly if no hypercapnia and still hypoxic (measured by ABG). This is because risk of hypercapnic (type 2) respiratory failure
• Corticosteroids (inhaled or oral) e.g., prednisolone
• Start empirical antibiotic therapy if evidence of infection
• Respiratory physiotherapy to clear sputum

Question 18

How are infective exacerbations prevented? (x2)

Answer 18

Pneumococcal (protects against Strep. pneumoniae which causes some pneumonias) and influenza vaccination.

Question 19

What are the complications of COPD?

Answer 19

Acute respiratory failure, infections, pulmonary hypertension, right heart failure, pneumothorax (from bullae rupture) and secondary polycythaemia.

Question 20

What is secondary polycythaemia?

Answer 20

Too many RBCs

Question 21

What is respiratory failure?

Answer 21

Failure to maintain adequate pulmonary gas exchange in the lungs leading to V/Q inequality.

Question 22

What are the two type of respiratory failure?

Answer 22

Type 1 and 2.

Question 23

What is Type 1 respiratory failure? Causes? (x3)

Answer 23

HYPOXIC respiratory failure with NOMRAL CO2 and LOW O2: Hypoventilation/diffusion issue – CO2 can still diffuse out easily, but OXYGEN MOVING IN IS IMPAIRED. Can be due to pneumonia, pulmonary oedema or atelectasis (collapsed lung).

Question 24

What is Type 2 respiratory failure? Causes? (x4)

Answer 24

HYPERCAPNIC respiratory failure – failure to get CO2 out of alveoli. Oxygen has a greater concentration gradient, so will still be able to exchange, but CO2 has a lower concentration gradient so cannot leave the alveoli (oxygen likely to be low as well). May be a V/Q mismatch if the pulmonary vessels are not well perfused. Hypercapnic failure is usually due to pulmonary fibrosis, neuromuscular disease, obesity or increased dead space (INCREASED CO2 PRODUCTION AND/OR DECREASED ELIMINATION).