Pathology of Obstructive Lung Disease

Question 1

Give examples of localised obstructive diseases (not necessarily obstructive diseases)

Answer 1

Lung cancer and other tumours, inhaled foreign bodies and chronic scarring diseases (bronchiecstasis and secondary tuberculosis)

Question 2

What are the three main obstructive airway diseases?

Answer 2

Chronic bronchitis Emphysema Asthma (Mechanisms for each are different)

Question 3

What is Chronic Bronchitis and Emphysema also known as?

Answer 3

COPD

Question 4

What are the normal values for FEV1, FVC and the ratio between them?

Answer 4

Normal FEV1 is about 3.5 – 4 litres Normal FVC is about 5 litres Normal ratio FEV1 : FVC is 0.7 – 0.8

Question 5

What is used to predict FVC?

Answer 5

Age, sex and height

Question 6

Besides FEV1/FVC ratio, how else can an obstructive lung disease be demonstrated?

Answer 6

Peak expiratory flow rate

Question 7

What are the normal values for PEFR?

Answer 7

Normal 400 – 600 litres/min Normal range is 80-100% of best value

Question 8

What is a moderate fall in PEFR?

Answer 8

50-80% of best

Question 9

What is a marked fall in PEFR?

Answer 9

<50% of best is a marked fall

Question 10

What is FEV1, FVC, and PEFR in obstructive lung diseases?

Answer 10

There is AIRFLOW LIMITATION Peak Expiratory Flow Rate (PEFR) is reduced FEV1 is REDUCED FVC may be reduced FEV1 is less than 70% of FVC

Question 11

What causes the decrease in diameter size in bronchial asthma?

Answer 11

Degranulation of mast cells and smooth muscle contraction (both reversible by use of drugs, or spontaneously)

Question 12

What type of hypersensitivity is bronchial asthma?

Answer 12

Type 1

Question 13

What physical substances obstruct airways in chronic asthma?

Answer 13

Oedema, mucus, plasma exudation

Question 14

What are the aetiologies of chronic bronchitis and emphysema?

Answer 14

SMOKING Atmospheric Pollution Occupation : dust

Question 15

What is the effect of smoking on alpha-1-antiprotease (antitrypsin)?

Answer 15

Malfuntion of antitrypsin (alpha-1-antiprotease) -= emphysema or COPD

Question 16

What is the result of antitrypsin deficiency?

Answer 16

Neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs. Antitrypsin would normally It protect tissues from enzymes of inflammatory cells, especially neutrophil elastase

Question 17

How does FEV1 change with age?

Answer 17

Reduces

Question 18

What is chronic bronchitis defined as clinically?

Answer 18

It protects tissues from enzymes of inflammatory cells, especially neutrophil elastase

Question 19

What does chronic bronchitis exclude?

Answer 19

TB Bronchiecstasis These may be confused with asthma

Question 20

What is acute exacerbation of COPD?

Answer 20

Sudden worsening of COPD symptoms (shortness of breath, quantity and colour of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Infection is most common cause (75%)

Question 21

How does the frequency of exacerbations change as the COPD progresses?

Answer 21

Exacerbations become more and more frequent

Question 22

What are the morphological changes in large airways in chronic bronchitis?

Answer 22

Mucous gland hyperplasia Goblet cell hyperplasia Inflammation and fibrosis (minor component)

Question 23

What are the morphological changes in small airways in chronic bronchitis?

Answer 23

Goblet cells appear Inflammation and fibrosis in long standing disease

Question 24

What is the pathological definition of emphysema?

Answer 24

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising from wither dilation or from destruction of their walls without obvious fibrosis. Loss in alveolar tissue, more space between alveoli.

Question 25

Define acinus

Answer 25

A region of the lung supplied with air from one of the terminal bronchioles

Question 26

Define centriacinar emphysema

Answer 26

Most common type of pulmonary emphysema mainly localized to the proximal respiratory bronchioles with focal destruction and predominantly found in the upper lung zones. This is because most material inhaled ends up here - max inflammation and destruction occurs here

Question 27

What is a secondary pulmonary lobule?

Answer 27

The subsegment of lung supplied by three to five terminal bronchioles and separated from adjacent secondary lobules by intervening connective tissue (interlobular septa)

Question 28

Define panacinar emphysema

Answer 28

Emphysema affecting all parts of the secondary pulmonary lobule, typically involving the inferior part of the lung and often asociated with a α1-antitrypsin deficiency.

Question 29

What is a Bulla?

Answer 29

Emphysematous space greater than 1 cm

Question 30

What is a bleb?

Answer 30

A Bulla just underneath the pleura

Question 31

What is the pathogenesis of Emphysema?

Answer 31

Smoking (Protease - Antiprotease imbalance) Ageing Alpha-1-antitrypsin deficiency

Question 32

How does antitrypsin deficiency affect this diagram?

Answer 32

Anti-elastase (anti-proteases are reduced)

Question 33

How does smoking affect this diagram?

Answer 33

Decrease in anti-elastase Increase in Elastase and neutrophils and macrophages Decrease in the activity of Repair mechanisms and Elastin synthesis

Question 34

What portion of COPD is reversible?

Answer 34

Smooth muscle tone and inflammation

Question 35

What are the normal reference ranges of PaO2 and PaCO2?

Answer 35

Question 36

What are the two types of respiratory failure?

Answer 36

Question 37

What are the common causes of Hypoxaemia?

Answer 37

Ventilation/perfusion imbalance Diffusion impairment Alveolar Hypoventilation Shunt

Question 38

How does COPD involve V/Q mismatch, aveolar ventilation, diffusion impairment and shunt?

Answer 38

Airway obstruction Reduced Respiratory Drive Loss of alveolar surface area Shunt only during acute infective exacerbation

Question 39

Why does pneumonia cause hypoxaemia?

Answer 39

Ventilation / perfusion abnormality (mismatch) - some ventilation of abnormal alveoli just not enough Shunt - No ventilation of abnormal alveoli

Question 40

What is the commonest cause of hypoxaemia clinically?

Answer 40

LOW V/Q

Question 41

What is the normal percent of blood that is shunted?

Answer 41

2-4%

Question 42

What is meant by Shunt?

Answer 42

•Blood passing from Right to Left side of Heart WITHOUT contacting ventilated alveoli

Question 43

Why does shunt respond poorly to increase in FI O2?

Answer 43

•Blood leaving normal lung is already 98% saturated

Question 44

What is the effect of hypoventilation on PACO2 and PAO2?

Answer 44

* Hypoventilation increases PACO2, and thus increases PaCO2 * Increase in PACO2 decreases PAO2, which causes PaO2 to fall

Question 45

How do you correct a fall in PaO2 due to hypoventilation?

Answer 45

•Raising FIO2

Question 46

What causes physiological pulmonary vasoconstriction?

Answer 46

When alveolar oxygen tension falls

Question 47

How is Physiological pulmonary arteriolar vasoconstriction protective?

Answer 47

Do not send blood to alveoli short of oxygen

Question 48

What is cor pulmonale?

Answer 48

Hypertrophy of the RV resulting from disease affecting the function and/or structure of the lung ## Footnote Except where pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease

Question 49

What causes pulmonary hypertension?

Answer 49

Pulmonary vasoconstriction Pulmonary arterioles - muslce hypertrophy and intimal fibrosis Loss of capillary bed Secondary polycthaemia