COPD

Question 1

What is COPD?

Answer 1

• COPD is a lung disease characterised by chronic obstruction of airflow that interferes with normal breathing and is not fully reversible.

Question 2

COPD is a triad of?

Answer 2

Chronic bronchitis, emphysema and small airway fibrosis.

Question 3

What are the risk factors associated with COPD?

Answer 3

-Smoking.
-Environmental exposure to, for example dust, silica and pollutants.
-Alpha-1 antitrypsin deficiency.

Question 4

What is the clinical diagnosis of chronic bronchitis?

Answer 4

Chronic bronchitis is defined as a productive cough for at least 3 months in 2 consecutive years.

Question 5

What is the pathological diagnosis of emphysema?

Answer 5

Permanent enlargement of air spaces and destruction of alveolar walls.

Question 6

What will an x-ray of emphysema show?

Answer 6

Hyperinflation of the lungs with flattened diaphragms.

Question 7

How does chronic bronchitis cause obstruction?

Answer 7

Hypertrophy and hyperplasia of mucous glands and goblet cells occurs as a response to stimuli (e.g., cigarette smoke). This excessive mucus build-up causing narrowing of the airways.

Question 8

What happens to the cilia in chronic bronchitis?

Answer 8

The irritants (especially smoking) can cause destruction of the cilia causing them to shorten and become less motile > ciliary dysfunction > mucus accumulation in the airways > obstruction.

Question 9

How does air trapping occur in chronic bronchitis?

Answer 9

Because of the mucus obstruction, very little oxygen makes it to the alveoli and very little CO2 can be exhaled (more significant) > air trapping.

Question 10

What does air trapping in chronic bronchitis lead to?

Answer 10

CO2 will build up in the blood and little oxygen will be transported into the blood to perfuse the tissues > hypoxaemia and hypercapnea.

Question 11

How are the elastic fibres destroyed in emphysema?

Answer 11

Macrophages will phagocytose irritant molecules in the airways and release cytokines which will attract neutrophils to the area. Neutrophils then release proteases such as elastase which breaks down elastin.

Question 12

What is the result of elastic fibre breakdown?

Answer 12

-Decreases recoil of the lungs.
-Increased lung compliance.
-Increased air trapping.
-Airway collapse > decreases surface area of alveoli.

Question 13

What part of the respiratory tract is affected in centriacinar emphysema? Whats its aetiology?

Answer 13

The proximal part of the airways such as the respiratory bronchioles, mainly the upper lobes. Aetiology: smoking.

Question 14

What is the affected part of the respiratory tract in panacinar emphysema? Whats the aetiology?

Answer 14

The entire acini from respiratory bronchioles to alveolar duct and alveoli, mainly the lower lobes.
Aetiology: α1-antitrypsin deficiency.

Question 15

What part of the respiratory tract is affected in distal acinar emphysema? Whats the aetiology? What can you develop from this type?

Answer 15

The distal part of the airways, mainly the paraseptal region.
Aetiology: Fibrosis, atelectasis
Can develop pneumothorax from this type.

Question 16

Outline the development of Cor Pulmonale.

Answer 16

-Over time, hypoxaemia will lead to pulmonary hypoxemic vasoconstriction. This widespread vasoconstriction will increase the blood pressure leading to pulmonary hypertension. This will cause the right ventricle of the heart to increase its workload to pump the same stroke volume out against high pressure > right ventricle hypertrophy > heart failure.

Question 17

Outline the development of Cor Pulmonale.

Answer 17

-Over time, hypoxaemia will lead to pulmonary hypoxemic vasoconstriction. This widespread vasoconstriction will increase the blood pressure leading to pulmonary hypertension. This will cause the right ventricle of the heart to increase its workload to pump the same stroke volume out against high pressure > right ventricle hypertrophy > heart failure.

Question 18

What are the common symptoms of COPD?

Answer 18

o Cough.
o Breathlessness.
o Sputum.
o Frequent chest infections.
o Wheezing.

Question 19

What are other symptoms of COPD?

Answer 19

o Weight loss.
o Fatigue.
o Swollen ankles.

Question 20

What are some of the examination findings in diagnosed COPD?

Answer 20

o Cyanosis.
o Raised JVP.
o Cachexia.
o Wheeze.
o Pursed lip breathing.
o Hyperinflated chest.
o Use of accessory muscles.
o Peripheral oedema.

Question 21

Define the investigations used to diagnose COPD.

Answer 21

• There is no single diagnostic test. Instead, the symptoms, history and spirometry are used.
• Diagnosis of COPD if the patient meets all of the following criteria:
  o Typical symptoms.
  o > 35 years old.
  o Presence of risk factor (smoking or occupational exposure) and/or host factor (genetic abnormality).
  o Absence of clinical features of asthma.
  o Airflow obstruction confirmed by post-bronchodilator spirometry.

Question 22

Explain how to assess the severity of acute and chronic COPD.

Answer 22

• Spirometry:
  o Stage 1, mild – FEV1 80% of predicted value or higher.
  o Stage 2, moderate – FEV1 50-79% of the predicted value.
  o Stage 3, severe – FEV1 30-49% of predicted value.
  o Stage 4, very severe – FEV1 less than 30% of predicted value.
• Nature and magnitude of symptoms:
  o MRC breathlessness scale and COPD assessment tool.
• History of moderate and severe exacerbations and future risk:
  o Number per year, hospitalisation?
• Presence of co-morbidity:
  o Heart disease.
  o Atrial fibrillation.
  o Obesity.

Question 23

What are the clinical features differentiating COPD and asthma.

Answer 23

Question 24

Discuss respiratory failure in COPD patients.

Answer 24

• Caused by reduced V/Q.
• Type 1: decreased PO2.
• Type 2: decreased PO2 and increased PCO2 (ventilatory failure).
• Severe ventilatory problems can lead to reduced sensitivity of central CO2 chemoreceptors in medulla therefore some COPD pateints develop a ‘hypoxic drive’ driven by peripheral chemoreceptors in the carotid body and aortic arch.

Question 25

Define the aims of COPD management strategies.

Answer 25

• Relieve symptoms.
• Prevent exacerbations.
• Improve quality of life.

Question 26

• Define the investigations used in the assessment of a COPD exacerbation.

Answer 26

-Spirometry.
-Pulse oximetry.
-Sputum culture: enables targeted antibiotic therapy during exacerbations of COPD.
-ECG.
-Arterial blood gas (ABG): during exacerbations check for respiratory acidosis (PaCO2 >6.0 and pH <7.35).
-Chest x-ray: hyperinflation of lungs and flattened diaphragm.

Question 27

Describe the classes of drugs available in the managment of COPD.

Answer 27

• Short-acting bronchodilators:
  o SABA (e.g., salbutamol).
  o SAMA (e.g., ipratropium).
• Long-acting bronchodilators:
  o LAMA (long-acting anti-muscarinic agents, e.g., umeclidinium, tiotropium etc).
  o LABA (long-acting beta2 agonist, e.g., salmeterol).
• High dose inhaled corticosteroids (ICS) and LABA:
  o Relvar (Fluticasone/vilanterol).
  o Fostair MDI.
• Antibiotics:
  o Most exacerbations are secondary to viral infection.
  o If there is evidence of infection (fever, increase in volume/purulence of sputum).

Question 28

Describe non-pharmacological aspects of COPD management.

Answer 28

• Smoking cessation.
• Vaccinations:
  o Annual flu vaccine.
  o Pneumococcal vaccine.
• Pulmonary rehabilitation.
• Nutritional assessment.
• Psychological support.

Question 29

Most infections causing COPD are

Answer 29

viral.

Question 30

Describe omalizumab.