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04. Year 1: Respiratory System > Pathology of Obstructive Lung Disease > Flashcards

Pathology of Obstructive Lung Disease Flashcards

1
Q

What is localised obstruction?

A

Obstruction of a large airway

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2
Q

What can localised obstruction be caused by?

A

Lung cancer

Inhaled foreign bodies

Chronic scarring diseases like bronchiectasis and secondary tuberculosis

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3
Q

What are examples of chronic scarring diseases?

A

Bronchiectasis

Secondary tuberculosis

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4
Q

What is generalised small airway obstruction?

A

Bronchiolar obstruction

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5
Q

What are some obstructive airway diseases?

A

Chronic bronchitis

Emphysema

Asthma

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6
Q

What is chronic obstructive pulmonary disease?

A

A combination of chronic bronchitis and COPD

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7
Q

What is FEV1?

A

Forced expiratory volume of air exiting the lung in the first second of blowing out of your lungs as fast as possible

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8
Q

What is FVC?

A

Final total amount expirred

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9
Q

What is FEV1 usually?

A

70-80% of FVC

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10
Q

What volume is normal FVC1?

A

3.5-4L

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11
Q

What is normal FVC?

A

About 5L

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12
Q

What is used to measure FEV1 and FVC?

A

Spirometry

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13
Q

What is predicted FVC based on?

A

Age

Sex

Height

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14
Q

What can obstructive lung disease be demonstrated by?

A

Peak expiratory flow rate (PEFR)

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15
Q
A
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16
Q

What is the normal peak expiratory flow rate?

A

400-600L/min

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17
Q

What is the normal range, moderate fail and marked fail of PEFR?

A

80-100% of best value is normal

50-80% is moderate fail

<50% is marked fail

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18
Q

How does obstructive lung disease affect spirometry and peak expiratory flow rate?

A

Always airflow limitations

Peak expiratory flow rate is reduced

FEV1 is reduced

FVC may be reduced

FEV1 is less than 70% of FVC

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19
Q

What is bronchial asthma?

A

Type 1 hypersensitivity in the airways

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20
Q

What is bronchial asthma mediated by?

A

Immunologically mediated, leading to the degranulation of mast cells

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21
Q

What are the effects of degranulation of mast cells?

A

Patterns on inflammation in the airways and bronchial smooth muscle contraction

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22
Q

How does mast cell degranulation affect the airways?

A

Reduce cross sectional area, making breathing difficult

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23
Q

What is important about bronchial asthma?

A

Reversible airway obstruction either spontaneously or as a result of medical intervention

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24
Q

What can bronchial smooth muscle contraction and inflammation be modified by?

A

Drugs

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25
Q

What is the aetiology of chronic bronchitis and emphysema?

A

Smoking

Atmospheric pollution

Occupational dust

Alpha-1-antytrypsin deficiency

Effects of age and susceptability

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26
Q

Do more men or woman have COPD and why?

A

Men because they smoke more

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27
Q

What is chronic bronchitis?

A

Cough production of sputum most days in at least 3 consecutive months for 2 or more consecutive years (excludes TB, bronchiectasis)

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28
Q

What is chronic bronchitis easily confused with?

A

Chronic bronchial asthma

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29
Q

What is morphological?

A

Size, shape and structure of a given organ

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30
Q

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

A

Mucous gland hyperplasia

Goblet cell hyperplasia

Inflammation and fibrosis is a minor component

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31
Q

What is hyperplasia?

A

Enlargement of an organ or tissue caused by an increase in the reproductive rate of its cells

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32
Q

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

A

Goblet cells appear

Inflammation and fibrosis in long standing disease

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33
Q

What is emphysema?

A

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilation of from destruction of their walls and without obvious fibrosis

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34
Q

What is an acinus?

A

Everything beyond the last airway which is surrounded entirely by epithelial

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35
Q

What is the size of the normal acinus duct?

A

1-2cm, cannot see where one ends and where another begins

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36
Q

What disease is this?

A

Emphysema

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37
Q

What are the different forms of emphysema?

A

Centriacinar

Panacinar

Periacinar

Scar ‘irregular’

Bullous emphysema

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38
Q

What are emphysema defined by?

A

Where in the acinus the tissue is lost

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39
Q

What is the most common kind of emphysema?

A

Centriacinar, where tissue is lost in the middle of the acinus

40
Q

What is the process of centriacinar emphysema?

A

1) Begins with bronchiolar dilation
2) Then alveolar tissue is lost

41
Q

What is panacinar emphysema?

A

Whole tissue is wiped out, so huge areas of tissue are lost

42
Q

What is a bulla?

A

Emphysematous space greater than 1cm

43
Q

What is an emphysematous space greater than 1cm called?

44
Q

What term is often used to describe bullas just underneath the pleura?

45
Q

What is periacinar emphysema?

A

Holes against the pleura, where if they burst they cause a pneumothorax

46
Q

What happens if a periacinar emphysema bursts?

A

Pneumothorax

47
Q

What is the difference in an X-ray between someone with emphysema and someone who is healthy?

A

With emphysema can see all of the ribs. whereas can only see 10 posterior ribs in someone who is healthy

48
Q

What is the pathogenesis of emphysema?

A

Smoking

Protease-antiprotease imbalance

Ageing

Alpha-1-antitrypsin deficiency

49
Q

What are elastases?

A

Enzymes that macrophages release

50
Q

What are anti-elastases?

A

Enzymes that get rid of elastases to stop them from dissolving our own tissue

51
Q

Why do elastases not dissolve a lot of our own tissue?

A

They are balanced with anti-elastases that remove them

52
Q

How does smoking change the elastase balance?

A

Inhibits anti-elastase and repair mechanisms

53
Q

What leads to an anti-elastase deficiency?

A

Smoking and alpha-1-antitrypsin deficiency

54
Q

What is the reversible component of COPD?

A

Smooth muscle tone and inflammation

55
Q

What disease is the main cause of COPD?

A

Emphysema (loss of alveolar walls) which is irreversible

56
Q

Why is the loss of alveolar walls irreversible?

A

We cannot grow new lung tissue

57
Q

What keeps bronchioles open?

A

There attachment to alveolar walls, so when the walls are lost they close during the process of breathing out

58
Q

When do bronchioles close once alveolar walls are lost?

A

During expiration

59
Q

Do people with emphysema struggle more with inspiration or expiration?

A

Expiration

60
Q

What is the normal PaO2 value?

A

10.5-13.5kPa

61
Q

What is the normal PaCO2 value?

62
Q

What are the 2 kinds of respiratory failure?

A

Type 1 (PaO2 < 8kPa)

Type 2 (PaCO2 > 6.5kPa)

63
Q

What is type 1 respiratory failure?

A

When PaO2 < 8kPa

64
Q

What is type 2 respiratory failure?

A

PaCO2 > 6.5kPa

65
Q

What are the 4 abnormal states associated with hypoxia?

A

Ventilation/perfusion imbalance (V/Q, airway obstruction)

Diffusion impairment (lost of alveolar surface area)

Alveolar hypoventilation (reduced respiratory drive)

Shunt (only during acute infective exacerbation)

66
Q

What cause ventilation/perfusion imbalance?

A

Airway obstruction

67
Q

What causes diffusion impairment?

A

Loss of alveolar surface area

68
Q

What causes alveolar hypoventilation?

A

Reduced respiratory drive

69
Q

What is the most important driver for breathing?

A

Hydrogen ion concentration in CNS acting on chemoreceptors

70
Q

What happens to people who smoke in terms of their respiratory drive?

A

Become less sensitive to changes in hydrogen ions so rely on peripheral chemoreceptors to breath - and so breath less

71
Q

What is hypoxia during pneumonia caused due to?

A

Ventilation/perfusion mismatch (some ventilation but not enough from abnormal alveoli)

Shunt (no ventilation of abnormal alveoli)

72
Q

What kinds of pneumonia is hypoxaemia caused by ventilation/perfusion mismatch?

A

Bronchitis/bronchopneumonia

73
Q

What kinds of pneumonia is hypoxaemia caused by shunt?

A

Severe bronchopneumonia

Lobar patterns with large areas of consolidation

74
Q

Why does severe bronchopneumonia and lobar pneumonia cause hypoxaemia?

A

Due to shunt

75
Q

Why does bronchitis/bronchopneumonia cause hypoxaemia?

A

Due to ventilation/perfusion mismatch

76
Q

What is the size of a normal breath?

78
Q

What is the normal cardiac output?

79
Q

What is the normal ventilation/perfusion ratio?

80
Q

What is the most common cause of hypoaemia?

A

Low ventilation/perfusion ratio

81
Q

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

A

Increasing FIO2

82
Q

What is shunt?

A

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

83
Q

What is blood passing from the right to the left side of the heart without contacting ventilated alveoli called?

84
Q

How do large shunts respond to increasing FIO2?

A

Poorly because the blood leaving the normal lung is already 98% saturated

85
Q

How does alveolar hypoventilation affect PA and Pa of O2 and CO2?

A

Increases PACO2 and so increases PaCO2

Increase in PACO2 decreased PAO2, which causes PaO2 to fall

Fall in PaO2 corrected by increasing FIO2

86
Q

How is the fall in PaO2 during alveolar hypoventilation corrected?

A

Increasing FIO2

87
Q

What does FIO2 stand for?

A

Fraction of inspired air which is oxygen

88
Q

What are some pulmonary vascular changes in hypoxia?

A

Physiological pulmonary arteriolar vasocontriction

(when oxygen tension falls, can be localised effect, all vessels constrict if there is hypoxaemia)

Protective mechanism

(do not send blood to alveoli short of oxygen)

89
Q

What happens to all vessels during hypoxaemia?

A

They all constrict

90
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 disease primary affecting the left side of the heart or congenital heart disease)

91
Q

What is hypertrophy of the right ventricle called?

A

Chronic cor pulmonale

92
Q

What should a normal right ventricle weigh?

A

Less than 70g

93
Q

Why does the right ventricle weigh more than normal in cor pulmonale?

A

Due to having to work harder to pump blood to the rest of the body against greater resistance

94
Q

What does cor pulmonale lead to?

A

Pulmonary hypertension

95
Q

Why does cor pulmonale lead to pulmonary hypertension?

A

Pulmonary vasocontriction

Muscle hypertrophy and intimal fibrosis of pulmonary arterioles

Loss of capillary bed

Secondary polycythaemia

04. Year 1: Respiratory System (37 decks)

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