COPD (emphysema & chronic bronchitis)

Question 1

Describe the etiology of COPD.

Answer 1

• tobacco smoking and second-hand smoke are key underlying factors. Occupational exposures and pollutants can also play a role.
• genetic predisposition is thought to play a role as not all heavy smokers develop COPD (antriypsin 1 deficiency).

Question 2

What is alpha-1 antitrypsin?

Answer 2

An enzyme normally produced in the liver and delivered in the blood to the lungs. In inhibits the action of elastase that is released when airways are inflamed, such as due to a respiratory infection.

Neutrophils contain the enzyme elastase which is effective in causing injury to bacteria. However, elastase also potentially causes breakdown of elastic fibres within airway and alveolar walls. Alpha-1 antitrypsin plays an important role in ‘regulating’ elastase activity and minimizing airway damage when infection and/or inflammation occurs.

Question 3

Define COPD.

Answer 3

A chronic progressive disease characterized by airflow obstruction. Typically a mix of chronic bronchitis and emphysema.

Question 4

What is chronic bronchitis?

Answer 4

An airflow limitation caused by progressive and irreversible inflammation and mucus hyersecretion in response to chronic irritation.

Initially affects the larger bronchi and progresses to affect smaller bronchioles.

Defined clinically as a chronic productive cough for at least 3 consecutive months of the year in at least 2 consecutive years.

Question 5

Describe the pathogenesis of chronic bronchitis.

Answer 5

Persistant irritation results in:

1. Inflammation = causes thickening of airway walls and the narrowing of the bronchial or bronchiolar lumen.
2. Submucosal gland hypertrophy (in walls of bronchi) and goblet cell hyperplasia (respiratory epitehlium) = causes increased mucus production.

NOTE: changes partially reversible with removal of irritant or bronchodilator use

Mucociliary defences are impaired = mucus accumulates and is difficult to clear:
- cilia function is impaired d/t smoking
- ciliated cells are replaced by goblet cells (d/t hyperplasi)
- ciliated epithelium is replaced by stratified squamous (d/t metaplasia)

3. If irritation and inflammation persist, airway remodeling occurs. Involves fibrosis (scarring) and a permanent thickening of airway walls and airway narrowing.

Question 6

What are the effects of chronic bronchitis on ventilation?

Answer 6

• airway obstruction with inflammation and mucus
• air trapped past the obstruction = not all air can be exhaled = lung hyperinflation

Question 7

What is emphysema?

Answer 7

The destruction of elastin fibres distal to the terminal bronchioles, accompanied by alveolar wall destruction and the enlargement of air spaces.

Question 8

Describe the pathogenesis of emphysema.

Answer 8

• tobacco smoke and other irritants cause injury and inflammation
• neutrophils and other inflammatory cells recruited
• cytokines released during the inflammatory response increase protease activity by neutrophils (i.e., elastase from neutrophils
• elastase normally regulated by alpha-1 antitrypsin but antitrypsin decreased with inherited deficiency or effects of smoking

Question 8

What type of genetic disorder is alpha-1 antitrypsin deficiency?

Answer 8

autosomal recessive genetic disorder

Question 8

In what cases does ephysema occur earlier than age 40?

Answer 8

With an alpha-1 antitrypsin deficiency (genetic or smoking)

Question 9

What is the effect of emphysema on gas exchange?

Answer 9

1. Ventilation (early stages)
2. alveolar-capillary diffusion and pulmonary perfusion (later stages)

Question 10

What is the effect of emphysema on ventilation?

Answer 10

Elastin needed for elastic recoil of bronchiole walls which helps move air out of the lungs passively during exhalation.

Loss of elastic recoil = reduced volume of air exhaled passively = air trapped = enlargement of alveoli = lung hyperinflation = harder to move fresh air in

Question 11

Why is there less of a V/Q mismatch with emphysema compared to chronic bronchitis?

Answer 11

Because both ventilation and perfusion decrease.

However, there are fewer functioning alveoli, thus decreasing gas exchange and causing hypoxemia.

Question 12

What are bullae?

Answer 12

Seen on a chest x-ray = air pockets in the lung at least 1cm in diameter and indicative of damage to the alveolar walls secondary to chronic inflammation.

Question 13

Why is purse-lipped breathing recommended to relieve episodes of dyspnea for COPD patients?

Answer 13

Increases pressure inside the alveoli and bronchioles, keeping them open longer (preventing collapse) during exhalation. Slow exhale helps release trapped air in the lungs and expel carbon dioxide.

Question 14

Why should someone with COPD try to prevent recurrent respiratory infections (e.g. with vaccines)?

Answer 14

Increased risk for infection d/t mucus hyersecretion and impaired mucociliary defences. Frequent exacerbations can lead to progressive airway remodeling.