Pulmonary Pathophysiology - Obstructive Lung Disease

Question 1

Mechanisms of airway obstruction

Answer 1

Secretions / fluid / foreign body within airway

Increased thickness of airway wall

Loss of radial traction of airway secondary to alveolar destruction

Question 2

Examples of causes of increased airway thickness

Answer 2

Hypertrophy of smooth muscle

Chronic bronchitis

Question 3

Example cause of alveolar destruction resulting in reduced airway radial traction

Answer 3

Emphysema

Question 4

COPD components

Answer 4

Mixed picture of emphysema and chronic bronchitis

Question 5

Emphysema definition

Answer 5

Enlargement of air spaces distal to the terminal bronchiole with destruction of their walls

Anatomical diagnosis

Question 6

Distribution / types of emphysema

Answer 6

Centriacinar emphysema

Panacinar emphysema

Bullous emphysema

Paraseptal emphysema

Lower zone emphysema

Question 7

Lower zone emphysema

Answer 7

Primarily lower lung zones affected by emphysema

Caused by alpha 1 antitrypsin deficiency

Question 8

Possible pathogenesis of emphysema (as suggested by alpha 1 antitrypsin deficiency)

Answer 8

Imbalance of protease-antiprotease system

Cigarette smoking causes release of neutrophil elastase

Elastase attacks both elastin and collagen

Type IV collagen in blood gas barrier may be a critical structure

Question 9

Why do neutrophils contain elastase

Answer 9

To break down bacteria

Question 10

Chronic bronchitis definition

Answer 10

Excessive mucus production in the bronchial tree sufficient to cause excessive expectoration of sputum

Clinical diagnosis

Question 11

Pathophysiology of chronic bronchitis

Answer 11

Increased mucus production by mucus glands in response to airway pollutant (cigarette smoke)

Mucus volume overwhelms mucociliary escalator

Question 12

Changes in small airways in chronic bronchitis

Answer 12

Inflammation

Airway wall oedema

Narrowing

Cellular infiltration

Peri-bronchial fibrosis

Question 13

Effect of single cigarette on airway conductance

Answer 13

Significantly reduces airway conductance for around 1 hour after single cigarette

Question 14

Clinical presentations of COPD

Answer 14

Type A (Pink puffer)

Type B (Blue bloater)

Usually patients are a mix of type A and type B

Question 15

Type A COPD presentation

Answer 15

‘Pink puffer’

SOB with high ventilation rate
Maintains relatively normal PaO2 and PaCO2

Question 16

Type B COPD presentation

Answer 16

‘Blue bloater’

Severe chronic bronchitis
PaCO2 higher and lower PaO2
Pulmonary HTN + right heart failure

Question 17

Lung volume changes in COPD

Answer 17

TLC, FRC and RV typically increased

Question 18

Gas exchange changes in COPD

Answer 18

Question 19

Pulmonary circulation changes in COPD

Answer 19

Pulmonary hypertension (Cor pulmonale)

Fluid retention with pulmonary oedema

Right heart failure

Question 20

Causes of pulmonary hypertension in COPD

Answer 20

• Destruction of capillary bed
• Hypoxic vasoconstriction
• Polycythaemia - increases blood viscosity
• Thickening of small artery walls

Question 21

Hypoxic vasoconstriction

Answer 21

Vasoconstriction of poorly ventilated alveoli / lung to maintain V/Q matching

Question 22

Early changes in COPD early stages

Answer 22

Increased resistance in small airways

Question 23

Management of COPD

Answer 23

Lung tissue destruction is irreversible

Abx + prevention of exacerbation for bronchitis

Bronchodilators for reversible bronchoconstriction

LTOT can reduce pulmonary hypertension

Lung volume reduction surgery

Rehabilitation programs

Question 24

Asthma definition

Answer 24

Increased responsiveness of airways to various stimuli.
Manifested by inflammation and widespread airway narrowing that changes in severity either spontaneously or in response to treatment.

Question 25

Clinical features of asthma

Answer 25

Often begins in children but can be any age Can be related to specific allergens General hyper-reactivity of airways May have other atopy features

Question 26

Common triggers for asthma

Answer 26

Smoke Cold air Exercise Aspirin

Question 27

Status asthmaticus

Answer 27

Exacerbation which may last for hours

Question 28

Pathological changes in airways with asthma

Answer 28

Question 29

Pathogenesis of asthma

Answer 29

Airway hyper-responsiveness Airway inflammation May be an allergic basis

Question 30

Possible reasons for increasing incidence of asthma

Answer 30

Environmental factors Pollutants Genetic component

Question 31

Inflammatory mediators involved in asthma

Answer 31

Cytokines associated with T helper cells Interleukins 3, 4, 5 and 13 Arachidonic acid metabolites Leukotrienes, prostaglandins Histamine, platelet activating factor

Question 32

Location of Beta 2 adrenergic receptors

Answer 32

Bronchi Blood vessels Uterus

Question 33

Location of Beta 1 adrenergic receptors

Answer 33

Heart

Question 34

Action of Beta 2 adrenergic receptors

Answer 34

Increase activity of adenyl cyclase -> Raises concentration of cAMP in smooth muscle Also reduce airway inflammation

Question 35

Action of inhaled corticosteroids

Answer 35

Inhibit inflammatory and immune response Enhance Beta 2 receptor expression or function (Minimal systemic absorption)

Question 36

Additional bronchoactive therapies used for asthma

Answer 36

Methylxanthines Anticholinergics Leukotriene receptor antagonists

Question 37

Methylxanthine examples

Answer 37

Theophylline Aminophylline

Question 38

Lung volume changes in asthma exacerbation

Answer 38

FRC and TLC increase Lung compliance increases RV increases as diseases airways close prematurely in expiration

Question 39

Why is it helpful for lung volumes to increase in asthma exacerbation

Answer 39

Increase volume results in increased radial traction on airways and pulls them open to reduce airway resistance

Question 40

Which airways are affected in asthma

Answer 40

Likely all airways of all size are constricted in asthma exacerbations

Question 41

Gas exchange changes in asthma

Answer 41

Uneven distribution of ventilation Ventilation perfusion mismatch Less significant than mechanical changes in asthma mentioned earlier