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Respiratory > 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
What is the aetiology of chronic bronchitis and emphysema?
Smoking Atmospheric pollution Occupational dust Alpha-1-antytrypsin deficiency Effects of age and susceptability
26
Do more men or woman have COPD and why?
Men because they smoke more
27
What is chronic bronchitis?
Cough production of sputum most days in at least 3 consecutive months for 2 or more consecutive years (excludes TB, bronchiectasis)
28
What is chronic bronchitis easily confused with?
Chronic bronchial asthma
29
What is morphological?
Size, shape and structure of a given organ
30
What are morphological changes in the large airways due to chronic bronchitis?
Mucous gland hyperplasia Goblet cell hyperplasia Inflammation and fibrosis is a minor component
31
What is hyperplasia?
Enlargement of an organ or tissue caused by an increase in the reproductive rate of its cells
32
What are morphological changes in the small airways due to chronic bronchitis?
Goblet cells appear Inflammation and fibrosis in long standing disease
33
What is emphysema?
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
34
What is an acinus?
Everything beyond the last airway which is surrounded entirely by epithelial
35
What is the size of the normal acinus duct?
1-2cm, cannot see where one ends and where another begins
36
What disease is this?
Emphysema
37
What are the different forms of emphysema?
Centriacinar Panacinar Periacinar Scar 'irregular' Bullous emphysema
38
What are emphysema defined by?
Where in the acinus the tissue is lost
39
What is the most common kind of emphysema?
Centriacinar, where tissue is lost in the middle of the acinus
40
What is the process of centriacinar emphysema?
1) Begins with bronchiolar dilation 2) Then alveolar tissue is lost
41
What is panacinar emphysema?
Whole tissue is wiped out, so huge areas of tissue are lost
42
What is a bulla?
Emphysematous space greater than 1cm
43
What is an emphysematous space greater than 1cm called?
Bulla
44
What term is often used to describe bullas just underneath the pleura?
Bleb
45
What is periacinar emphysema?
Holes against the pleura, where if they burst they cause a pneumothorax
46
What happens if a periacinar emphysema bursts?
Pneumothorax
47
What is the difference in an X-ray between someone with emphysema and someone who is healthy?
With emphysema can see all of the ribs. whereas can only see 10 posterior ribs in someone who is healthy
48
What is the pathogenesis of emphysema?
Smoking Protease-antiprotease imbalance Ageing Alpha-1-antitrypsin deficiency
49
What are elastases?
Enzymes that macrophages release
50
What are anti-elastases?
Enzymes that get rid of elastases to stop them from dissolving our own tissue
51
Why do elastases not dissolve a lot of our own tissue?
They are balanced with anti-elastases that remove them
52
How does smoking change the elastase balance?
Inhibits anti-elastase and repair mechanisms
53
What leads to an anti-elastase deficiency?
Smoking and alpha-1-antitrypsin deficiency
54
What is the reversible component of COPD?
Smooth muscle tone and inflammation
55
What disease is the main cause of COPD?
Emphysema (loss of alveolar walls) which is irreversible
56
Why is the loss of alveolar walls irreversible?
We cannot grow new lung tissue
57
What keeps bronchioles open?
There attachment to alveolar walls, so when the walls are lost they close during the process of breathing out
58
When do bronchioles close once alveolar walls are lost?
During expiration
59
Do people with emphysema struggle more with inspiration or expiration?
Expiration
60
What is the normal PaO2 value?
10.5-13.5kPa
61
What is the normal PaCO2 value?
4.8-6kPa
62
What are the 2 kinds of respiratory failure?
Type 1 (PaO2 \< 8kPa) Type 2 (PaCO2 \> 6.5kPa)
63
What is type 1 respiratory failure?
When PaO2 \< 8kPa
64
What is type 2 respiratory failure?
PaCO2 \> 6.5kPa
65
What are the 4 abnormal states associated with hypoxia?
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
What cause ventilation/perfusion imbalance?
Airway obstruction
67
What causes diffusion impairment?
Loss of alveolar surface area
68
What causes alveolar hypoventilation?
Reduced respiratory drive
69
What is the most important driver for breathing?
Hydrogen ion concentration in CNS acting on chemoreceptors
70
What happens to people who smoke in terms of their respiratory drive?
Become less sensitive to changes in hydrogen ions so rely on peripheral chemoreceptors to breath - and so breath less
71
What is hypoxia during pneumonia caused due to?
Ventilation/perfusion mismatch (some ventilation but not enough from abnormal alveoli) Shunt (no ventilation of abnormal alveoli)
72
What kinds of pneumonia is hypoxaemia caused by ventilation/perfusion mismatch?
Bronchitis/bronchopneumonia
73
What kinds of pneumonia is hypoxaemia caused by shunt?
Severe bronchopneumonia Lobar patterns with large areas of consolidation
74
Why does severe bronchopneumonia and lobar pneumonia cause hypoxaemia?
Due to shunt
75
Why does bronchitis/bronchopneumonia cause hypoxaemia?
Due to ventilation/perfusion mismatch
76
What is the size of a normal breath?
4L/min
77
78
What is the normal cardiac output?
5L/min
79
What is the normal ventilation/perfusion ratio?
0.8
80
What is the most common cause of hypoaemia?
Low ventilation/perfusion ratio
81
What does hypoxaemia due to low V/Q respond well to?
Increasing FIO2
82
What is shunt?
Blood passing from right to the left of the heart without contacting ventilated alveoli
83
What is blood passing from the right to the left side of the heart without contacting ventilated alveoli called?
Shunt
84
How do large shunts respond to increasing FIO2?
Poorly because the blood leaving the normal lung is already 98% saturated
85
How does alveolar hypoventilation affect PA and Pa of O2 and CO2?
Increases PACO2 and so increases PaCO2 Increase in PACO2 decreased PAO2, which causes PaO2 to fall Fall in PaO2 corrected by increasing FIO2
86
How is the fall in PaO2 during alveolar hypoventilation corrected?
Increasing FIO2
87
What does FIO2 stand for?
Fraction of inspired air which is oxygen
88
What are some pulmonary vascular changes in hypoxia?
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
What happens to all vessels during hypoxaemia?
They all constrict
90
What is chronic cor pulmonale?
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
What is hypertrophy of the right ventricle called?
Chronic cor pulmonale
92
What should a normal right ventricle weigh?
Less than 70g
93
Why does the right ventricle weigh more than normal in cor pulmonale?
Due to having to work harder to pump blood to the rest of the body against greater resistance
94
What does cor pulmonale lead to?
Pulmonary hypertension
95
Why does cor pulmonale lead to pulmonary hypertension?
Pulmonary vasocontriction Muscle hypertrophy and intimal fibrosis of pulmonary arterioles Loss of capillary bed Secondary polycythaemia

Respiratory (37 decks)

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