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01. Respiratory System > Pathology of Obstructive Lung Disease > Flashcards

Pathology of Obstructive Lung Disease Flashcards

1
Q

What are not primarily obstructive diseases?

A
  • Lung cancer
  • Lung tumours
  • Inhaled foreign bodies
  • Chronic scarring diseases ( bronchiectasis, secondary TB)
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2
Q

What are obstructive airway diseases?

A
  • Chronic Bronchitis
  • Emphysema
  • Asthma
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3
Q

What is similar about chronic bronchitis, emphysema and asthma?

A

Airway obstruction

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4
Q

What is different about chronic bronchitis, emphysema and asthma?

A

The mechanism for obstruction

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5
Q

What are chronic bronchitis and emphysema better known as?

A
  • COPD Chronic Obstructive Pulmonary Disease
  • COLD Chronic Obstructive Lung Disease
  • COAD Chronic Obstructive Airways Disease
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6
Q

FEV1

A

Forced Expiratoy Volume of air exiting your lungs in the first second a maximum expiration

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7
Q

FVC

A

Total amount expires

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8
Q

What are the normal for the FEV1:FVC ration?

A
  • FEV1 is usually 70-80% of FVC
  • Normal FEV1 is about 3.5-4 litres
  • Normal FVC is about 5 litres
  • Normal ratio FEV1:FVC is 0.7-0.8
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9
Q

What is predicted FVC based on?

A

Age, sex and height

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10
Q

What does spirometry test?

A

Test of airflow obstruction

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11
Q

What test is commonly used by asthmatics in the home?

A

Peak Expiratory Flow Rate

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12
Q

What are the ranges for peak flow?

A
  • Normal is 400-600 litres
  • Normal range is 80-100% of best value
  • 50-80% of best is moderate fall
  • <50% best is marked fall
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13
Q

What results would you expect to see in obstructive lung disease?

A
  • There is airflow limitation
  • Peak expiratory flow rate is reduced
  • FEV1 is reduced
  • FVC may be reduced
  • FEV1 is less than 70% of FVC
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14
Q

How does the curve of an FEV:FVC graph differ from normal in obstructive lung disease?

A

The slope is flatter and may have a lower end point

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15
Q

What is bronchial asthma caused by?

A

Type I hypersensitivity in the airways

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16
Q

What contributes to inflammation and therefore bronchial constriction in the smooth muscle of the airways?

A
  • Degranulation of mast cells
  • Mediators and chemotactic factors
  • Spasmogens
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17
Q

Why is bronchial asthma considered reversible?

A

Airway obstruction can be reversed either spontaneously or as a result of medical intervention

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18
Q

What can drugs modify in asthma?

A

Bronchial smooth muscle contraction and inflammation

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19
Q

What causes COPD?

A
  • Smoking
  • Pollution from the atmosphere
  • Occupational dust
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20
Q

What is an extremely rare cause of emphysema?

A

Alpha-1-antiprotease (antitrypsin) deficiency

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21
Q

What leads to a natural decline in FEV1?

A

Age

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22
Q

For someone to become clinically symptomatic what must happen?

A

There must be a large drop in FEV1

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23
Q

What happens to someone’s FEV1 curve when the stop smoking?

A
  • Damage is not reversible

- Their curve will continue to decline but at the same rate as someone who had never smoked

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24
Q

How chronic bronchitis defined clinically?

A

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

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25
Q

When is chronic bronchitis complicated?

A

When mucopurulent or FEV1 falls

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26
Q

What morphological changes do the large airways undergo?

A
  • Mucous gland hyperplasia
  • Goblet cell hyperplasia
  • Inflammation and fibrosis is a minor component
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27
Q

What morphological changed do the small airways undergo?

A
  • Goblet cells appear

- Inflammation and fibrosis in long standing disease

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28
Q

What is the pathological definition of emphysema?

A

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilatation or from DESTRUCTION OF THEIR WALLS and without obvious fibrosis

29
Q

What is the terminal bronchiole?

A

Last conducting bronchiole, full lined by respiratory epithelium

30
Q

What forms of emphysema are there?

A
  • Centriacinar
  • Panacinar
  • Periacinar
31
Q

Where is centriacinar localised?

A

Localised to the proximal respiratory bronchioles with focal destruction and predominantly found in the upper lung zones (apex of upper and lower lobes)

32
Q

How does centriacinar emphysema progress?

A
  • Begins with bronchiolar dilatation

- Then alveolar tissue is lost

33
Q

What is a bulla?

A

An emphysematous space greater than 1cm

34
Q

What is a bleb?

A

A bulla just underneath the pleura

35
Q

What happens when a bleb bursts?

A

Pneumothorax

36
Q

What should you see on a chest X-ray of someone with emphysema?

A

Hyperinflated lungs

37
Q

What does smoking cause?

A

Protease- antiprotesase imbalance

38
Q

What is the pathogenesis of emphysema?

A
  • Smoking
  • Ageing
  • Alpha-1-antitrypsin deficiency
39
Q

What does inflammation (neutrophils and macrophages) result in?

A

Release of elastases (proteases)

40
Q

Normally what happens to the elastase?

A

Their is an equilibrium established between elastase and anti-elastase

41
Q

What does smoking cause a decrease in?

A
  • Anti-elastase
  • Repair mechanisms
  • Elastin synthesis
42
Q

What does smoking cause an increase in?

A
  • Neutrophils and macrophages

- Elastase

43
Q

What does the combined effects of smoking lead to?

A

Tissue destruction which causes tissue destruction

44
Q

What is the most important factor in emphysema?

A

Loss of alveolar attachments

45
Q

What components of COPD may respond to pharmacological intervention?

A
  • Smooth muscle tone in the small airways

- Inflammation in the small airways

46
Q

Why is it not possible to breath out your residual volume?

A

Your small airways shut

47
Q

What are the 4 abnormal states associated with hypoxaemia?

A
  • Ventilation/Perfusion imbalance V/Q
  • Diffusion impairment
  • Alveolar Hypoventilation
  • Shunt
48
Q

Why do the 4 abnormal states lead to hypoxaemia?

A
  • Mismatch: airway obstruction
  • Alveolar hypoventilation: reduced respiratory drive
  • Diffusion impairment: loss of alveolar surface area
  • Shunt: only during acute infective exacerbation
49
Q

When would you see ventilation/ perfusion abnormality?

A

Bronchitis/ Bronchopneumonia

50
Q

When would you see shunt?

A

Severe bronchonpneumonia

51
Q

What happens in ventilation/perfusion abnormality that causes hypoxaemia?

A
  • There is some ventilation of abnormal alveoli, just not enough
  • The body tries to match perfusion to ventilation.
  • For every malfunctioning alveoli a few RBC will get through without being oxygenated
  • The more malfunctioning alveoli, the more RBC that get through that are inadequately oxygenated which leads to hypoxaemia
52
Q

Why is there large areas of consolidation in shunt?

A

A large area/lobe is completely airless, no air, no ventilation, all the venous blood whizzes straight through as the vessels narrow but do not shut. This means there is 0 gas exchange. The venous blood then mixes with oxygenated blood

53
Q

What is normal ventilation/perfusion?

A
  • Normally ventilation is 4l/min
  • Normally cardiac output is 5l/min
  • Normal V/Q is 4/5 or 0.8
54
Q

What is the commonest cause of hypoxaemia clinically?

A

Low V/Q

55
Q

How does low V/Q arise in some alveoli?

A

Due to local alveolar hypoventilation due to some focal disease

56
Q

What does hypoxaemia due to low V/Q respond well to?

A

Small increases in FIO2

57
Q

When will administering oxygen not help hypoxaemia?

A

When it is caused by shunt

58
Q

What is shunt?

A

Blood passing from right to left side of the heart without contacting ventilated alveoli

59
Q

When is there pathological shunt?

A
  • AV malformations
  • Congenital heart disease
  • Pulmonary disease
60
Q

Why do large shunts respond poorly to increases in FIO2?

A

Blood leaving normal lung is already 98% saturated

61
Q

What does FIO2 stand for?

A

Fraction of inspired air which is oxygen

62
Q

What does hypoventilation lead to?

A

-Increases PACO2 and decrease in PAO2

63
Q

How is the fall in PAO2 due to hypoventilation corrected?

A

Raising FIO2

64
Q

Why is it important to monitor someone with COPD placed on oxygen?

A
  • In COPD the respiratory centre becomes inured to the effects of CO2 and H ions and therefore lose their respiratory drive.
  • They rely on hypoxia to breathe
  • Therefore giving them oxygen may cease their breathing altogether
65
Q

What pulmonary vascular changed take place in hypoxia?

A
  • Physiological pulmonary arteriolar vasoconstriction. Occurs when alveolar oxygen tension falls. and it can be a localised effect. All vessels constrict if there is hypoxaemia
  • A protective mechanism: do not send blood to alveoli short of oxygen
66
Q

What is chronic cor pulmonale?

A

Hypertrophy of the right ventricle resulting from disease affecting the function and/or the structure of the lung except where pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease

67
Q

Why must the size of the heart on chest X-rays of COPD patients must be examined?

A

To ensure there is no thickening of the muscle of the right ventricle

68
Q

What causes pulmonary hypertension in hypoxic cor pulmonale?

A
  • Pulmonary vasoconstriction of the pulmonary arterioles leads to muscle hypertrophy and intimal fibrosis
  • There is loss of the capillary bed which leads to secondary polycythaemia.
  • There is an increase in the viscosity of the blood which means the heart has to work harder to pass viscous blood through the narrowed vessels

01. Respiratory System (82 decks)

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