Obstructive airway disease

Question 1

Name 3 obstructive airway diseases.

Answer 1

Asthma, chronic bronchitis and emphysema (chronic bronchitis and emphysema usually co-exist and are known as COPD).

Question 2

What is the normal FEV1:FVC ratio?

Answer 2

0.7-0.8 (FEV1 is 70-80% of FVC).

Question 3

What are the values of a normal and abnormal PEFR?

Answer 3

Normal: 400-600l/min. 80-100% of this value is normal, 50-80% is a moderate fall and less than 50% is a marked fall.

Question 4

What happens to PEFR and FEV1:FVC in obstructive lung disease?

Answer 4

There is airflow limitation so PEFR, FEV1 and FVC are all reduced. FEV1 is

Question 5

How does bronchial asthma cause airflow limitation?

Answer 5

Type 1 hypersensitivity reaction to allergens in the conducting airways. IgE binds to these and mast cells degranulate - an inflammatory reaction than reduces the cross-sectional area of the lungs. Also caused by bronchial smooth muscle contraction.

Question 6

How is bronchial asthma treated?

Answer 6

Bronchial smooth muscle contraction and inflammation can be reversed by drugs.

Question 7

What is the main cause of COPD?

Answer 7

Smoking, more common in men than women.

Question 8

Can a patient have emphysema without chronic bronchitis?

Answer 8

Yes, if they have an alpha-1-antiprotease deficiency.

Question 9

What is the clinical definition of chronic bronchitis?

Answer 9

Cough productive of sputum most days for 3 consecutive months, for 2 consecutive years (to cough and produce sputum is always abnormal).

Question 10

What are the 2 main complications of chronic bronchitis?

Answer 10

When there is an acute infective component (mucopurulent) or when FEV1 falls.

Question 11

Describe the changes that occur in the large and small airways during chronic bronchitis.

Answer 11

Large airways: mucous gland and goblet cell hyperplasia, inflammation and fibrosis. Small airways: goblet cells, inflammation and fibrosis in longstanding disease. Most fibrosis is in the small airways.

Question 12

What is the clinical definition of emphysema?

Answer 12

An increase beyond the normal size of airspaces distal to the terminal bronchiole arising from dilation or destruction of their walls without obvious fibrosis (basically the loss of tissue).

Question 13

What is the acinus?

Answer 13

Anything that is beyond the terminal bronchiole. 1 acinus is fed air by 1 terminal bronchiole.

Question 14

Name the 4 types of emphysema.

Answer 14

1) Centriacinar (most commonly associated with smoking), 2) Panacinar (much rarer, people with alpha-1-antitrypsin deficiency get this), 3) Periacinar (occur in acini next to pleura, if they burst can lead to pneumothorax), 4) Scar/irregular/bullous (a bulla is an emphysematous space greater than 1cm).

Question 15

What happens to the lungs during emphysema?

Answer 15

They hyperinflate. Lungs are trying to compensate for the loss of acini, but this means that the heart is not sitting on the diaphragm.

Question 16

Describe the pathogenesis of emphysema.

Answer 16

There is an imbalance of protease and anti-protease caused by smoking (damages anti-protease and increases production of protease)/alpha-1-antiprotease deficiency. Anti-protease makes sure than protease doesn’t cause tissue damage in the lungs. If this is not present lung damage occurs.

Question 17

Can COPD be treated?

Answer 17

Partly - reversible component is inflammation and smooth muscle constriction in the small airways. Can give the same drugs as you would a bronchial asthma patient. Fixed fibrosis and partial collapse of the airway wall on expiration are both irreversible.

Question 18

What is the most important loss in emphysema?

Answer 18

Loss of alveolar attachments - it is small alveolar attachments that keep the airways open. If you get rid of these the airways collapse. These are first lost in centriacinar emphysema and this is especially true during expiration.

Question 19

What are the normal values for PaO2 and PaCO2?

Answer 19

PaO2 10.5-13.5 kPa and PaCO2 4.8-6 kPa.

Question 20

Define the 2 types of respiratory failure.

Answer 20

Type 1 respiratory failure PaO2 6.5 kPa (PaO2 usually low).

Question 21

What is hypoxaemia?

Answer 21

Low O2 in the blood.

Question 22

What are the 4 states associated with hypoxaemia/compromise gas exchange?

Answer 22

VQ mismatch (most common), diffusion impairment, alveolar hypoventilation and shunt.

Question 23

Using COPD as an example, describe the ways in which gas exchange can be compromised?

Answer 23

VQ mismatch due to airway obstruction, diffusion impairment due to loss of alveolar surface area, alveolar hypoventilation due to reduced respiratory drive and shunt during infective exacerbations.

Question 24

How can VQ mismatch lead to hypoxaemia?

Answer 24

WE normally breathe 4L/min and CO is 5L/min so missmatch is 4/5 (0.8). For some reason (disease) there will not be enough ventilation to get to blood in a particular area of the lung - cannot take part in gas exchange. Blood leaves, is pumped around the body and causes hypoxaemia (low O2 and maybe high CO2). Can give patient high flow O2 (responds well to small increases in flO2 - fraction of inspired air which is O2).

Question 25

Describe alveolar hypoventilation.

Answer 25

A global failure to get air in and out of the lungs. Hypoventilation increases PACO2 and therefore increases PaCO2. In turn, this decreases PaO2 and PaO2 - type 2 respiratory failure. CO2 rises as blood is still flowing to the lungs with little/no gas exchange. Patient needs to be ventilated to increase FlO2.

Question 26

What happens to the pulmonary vasculature in hypoxia?

Answer 26

Arterioles constrict when alveolar O2 tension falls. This is protective - do not send blood to alveoli short of O2. Good at a localised level.

Question 27

Define chronic (hypoxic) Cor Pulmonale.

Answer 27

Hypertrophy of the RV due to disease affecting lungs. All arterioles in lungs constrict, right side of heart increases and eventually fails.