Pathology of obstructive lung disease

Question 1

List 3 obstructive lung diseases

Answer 1

Emphysema
Chronic bronchitis
Asthma

Question 2

What conditions make up COPD?

Answer 2

Chronic bronchitis + emphysema

Narrowing of small airways (bronchioles)

Question 3

What measurements can be taken to assess COPD and its severity?

Answer 3

FEV1:FVC

PEFR

Question 4

What type of hypersensitivity reaction occurs in asthma?

Answer 4

Type I HS (IgE, mast cell degranulation)

Question 5

What is normal PEFR?

Answer 5

Peak expiratory flow rate

Normal = 400-600L/min

Question 6

What causes chronic bronchitis and emphysema?

Answer 6

Smoking
Air pollution
Occupation
a1-antitrypsin deficiency
Age

Question 7

How is chronic bronchitis defined clinically?

Answer 7

Cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years

Question 8

What are some morphological changes seen in chronic bronchitis?

Answer 8

mucus gland hyperplasia
Goblet cell hyperplasia
Inflammation and fibrosis
Goblet cells in lower airways

Question 9

Define emphysema

Answer 9

Increase in normal size of airspaces distal to the terminal bronchiole arising either from dilatation or destruction of alveolar walls, without obvious fibrosis

Question 10

What are acini?

Answer 10

Terminal ends of bronchioles, containing many lobed sacs of alveoli

Question 11

What are some different forms of emphysema?

Answer 11

Centriacinar - affects central acinar region where inhaled irritants are inhaled, surrounded by relatively healthy lung tissue

Panacinar - affects secondary pulmonary lobule, typically inferior lung, and linked to a1-antitrypsin deficiency

Periacinar - enlarged spaces at lung periphery

Irregular/bullous emphysema - emphysematous space >1cm

Question 12

What do you see on CXR of COPD patients?

Answer 12

Hyperinflated chest
Flattened diaphragm
Blacked out lungs hiding ribcage

Question 13

Describe pathogenesis of emphysema

Answer 13

Smoking decreases reparative elastin synthesis and decreases anti-proteases, leading to damage
Ageing
a1-antitrypsin deficiency- decreases anti-proteases = build up of elastase
Inflammatory cells release elastase as a bystander effect of pollutants etc which can lead to increased damage to tissue

Question 14

Where can we target with therapies for reducing airway obstruction in COPD?

Answer 14

Large airways - little effect

Small airways

• smooth muscle tone
• inflammation
• fibrosis
• partial collapse of airway wall on expiration

Question 15

Why do COPD patients take half breaths?

Answer 15

Alveoli have lost elastic attachments to chest wall, leaving them floppy and cant stay open to allow efficient breathing if they collapse. Therefore patients only do small breaths in order to keep their alveoli partly inflated and prevent their collapse

Question 16

Why is there hypoxaemia in COPD?

Answer 16

V/Q mismatch - airway obstruction
Hypoventilation - reduced RR
Diffusion impairment - loss of alveolar SA
Shunt - only during acute exacerbations

Question 17

Describe some pulmonary vascular changes in hypoxia

Answer 17

Arteries vasoconstrict is area they perfuse is poorly ventilated

Question 18

What is cor pulmonale?

Answer 18

Hypertrophy of right ventricle resulting from disease affecting the function and/or structure of the lung e.g. widespread vasoconstriction due to hypoxia in the lungs