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Semester 2 > Pathology of Obstructive Lung Disease COPY > Flashcards

Pathology of Obstructive Lung Disease COPY 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

Semester 2 (150 decks)

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