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Anaesthetic FRCA Primary - Teaching Days > Pulmonary Pathophysiology - Obstructive Lung Disease > Flashcards

Pulmonary Pathophysiology - Obstructive Lung Disease Flashcards

1
Q

Mechanisms of airway obstruction

A

Secretions / fluid / foreign body within airway

Increased thickness of airway wall

Loss of radial traction of airway secondary to alveolar destruction

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2
Q

Examples of causes of increased airway thickness

A

Hypertrophy of smooth muscle

Chronic bronchitis

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3
Q

Example cause of alveolar destruction resulting in reduced airway radial traction

A

Emphysema

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4
Q

COPD components

A

Mixed picture of emphysema and chronic bronchitis

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5
Q

Emphysema definition

A

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

Anatomical diagnosis

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6
Q

Distribution / types of emphysema

A

Centriacinar emphysema

Panacinar emphysema

Bullous emphysema

Paraseptal emphysema

Lower zone emphysema

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7
Q

Lower zone emphysema

A

Primarily lower lung zones affected by emphysema

Caused by alpha 1 antitrypsin deficiency

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8
Q

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

A

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

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9
Q

Why do neutrophils contain elastase

A

To break down bacteria

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10
Q

Chronic bronchitis definition

A

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

Clinical diagnosis

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11
Q

Pathophysiology of chronic bronchitis

A

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

Mucus volume overwhelms mucociliary escalator

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12
Q

Changes in small airways in chronic bronchitis

A

Inflammation

Airway wall oedema

Narrowing

Cellular infiltration

Peri-bronchial fibrosis

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13
Q

Effect of single cigarette on airway conductance

A

Significantly reduces airway conductance for around 1 hour after single cigarette

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14
Q

Clinical presentations of COPD

A

Type A (Pink puffer)

Type B (Blue bloater)

Usually patients are a mix of type A and type B

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15
Q

Type A COPD presentation

A

‘Pink puffer’

SOB with high ventilation rate
Maintains relatively normal PaO2 and PaCO2

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16
Q

Type B COPD presentation

A

‘Blue bloater’

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

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17
Q

Lung volume changes in COPD

A

TLC, FRC and RV typically increased

18
Q

Gas exchange changes in COPD

A
19
Q

Pulmonary circulation changes in COPD

A

Pulmonary hypertension (Cor pulmonale)

Fluid retention with pulmonary oedema

Right heart failure

20
Q

Causes of pulmonary hypertension in COPD

A
  • Destruction of capillary bed
  • Hypoxic vasoconstriction
  • Polycythaemia - increases blood viscosity
  • Thickening of small artery walls
21
Q

Hypoxic vasoconstriction

A

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

22
Q

Early changes in COPD early stages

A

Increased resistance in small airways

23
Q

Management of COPD

A

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

24
Q

Asthma definition

A

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.

25
Q

Clinical features of asthma

A

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

26
Q

Common triggers for asthma

A

Smoke
Cold air
Exercise
Aspirin

27
Q

Status asthmaticus

A

Exacerbation which may last for hours

28
Q

Pathological changes in airways with asthma

A
29
Q

Pathogenesis of asthma

A

Airway hyper-responsiveness
Airway inflammation
May be an allergic basis

30
Q

Possible reasons for increasing incidence of asthma

A

Environmental factors
Pollutants
Genetic component

31
Q

Inflammatory mediators involved in asthma

A

Cytokines associated with T helper cells

Interleukins 3, 4, 5 and 13

Arachidonic acid metabolites

Leukotrienes, prostaglandins

Histamine, platelet activating factor

32
Q

Location of Beta 2 adrenergic receptors

A

Bronchi
Blood vessels
Uterus

33
Q

Location of Beta 1 adrenergic receptors

A

Heart

34
Q

Action of Beta 2 adrenergic receptors

A

Increase activity of adenyl cyclase
-> Raises concentration of cAMP in smooth muscle

Also reduce airway inflammation

35
Q

Action of inhaled corticosteroids

A

Inhibit inflammatory and immune response

Enhance Beta 2 receptor expression or
function

(Minimal systemic absorption)

36
Q

Additional bronchoactive therapies used for asthma

A

Methylxanthines
Anticholinergics
Leukotriene receptor antagonists

37
Q

Methylxanthine examples

A

Theophylline
Aminophylline

38
Q

Lung volume changes in asthma exacerbation

A

FRC and TLC increase

Lung compliance increases

RV increases as diseases airways close prematurely in expiration

39
Q

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

A

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

40
Q

Which airways are affected in asthma

A

Likely all airways of all size are constricted in asthma exacerbations

41
Q

Gas exchange changes in asthma

A

Uneven distribution of ventilation
Ventilation perfusion mismatch

Less significant than mechanical changes in asthma mentioned earlier

Anaesthetic FRCA Primary - Teaching Days (64 decks)

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