COPD Flashcards
(228 cards)
1
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
2
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
3
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
4
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
5
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
6
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
7
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
8
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
9
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
10
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
11
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
12
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
13
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
14
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
15
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
16
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
17
Q
What is the definition of COPD?
A
COPD is defined as “progressive airway obstruction which does not change markedly over several months”
It is characterised by persistent airflow obstruction which is poorly reversible and usually progressive, The obstructive elements of the disease is important; it is the obstruction to airflow which causes the disabling symptoms of breathlessness and impairs quality of life.
18
Q
Define chronic bronchitis
A
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
19
Q
Define Emphysema
A
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
20
Q
What is the most common cause of COPD?
A
tobacco smoking
21
Q
Define chronic bronchitis
A
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
22
Q
Define Emphysema
A
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
23
Q
What is the most common cause of COPD?
A
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
24
Q
Define chronic bronchitis
A
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
25
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
26
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
27
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
28
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
29
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
30
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
31
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
32
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
33
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
34
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
35
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
36
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
37
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
38
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
39
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
40
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
41
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
42
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
43
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
44
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
45
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
46
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
47
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
48
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
49
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
50
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
51
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
52
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
53
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
54
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
55
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
56
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
57
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
58
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
59
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
60
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
61
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
62
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
63
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
64
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
65
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
66
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
67
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
68
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
69
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
70
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
71
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
72
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
73
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
74
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
75
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
76
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
77
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
78
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
79
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
80
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
81
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
82
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
83
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
84
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
85
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
86
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
87
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
88
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
89
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
90
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
91
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
92
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
93
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
94
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
95
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
96
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
97
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
98
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
99
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
100
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
101
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
102
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
103
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
104
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
105
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
106
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
107
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
108
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
109
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
110
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
111
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
112
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
113
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
114
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
115
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
116
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
117
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
118
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
119
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
120
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
121
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
122
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
123
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
124
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
125
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
126
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
127
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
128
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
129
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
130
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
131
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
132
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
133
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
134
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
135
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
136
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
137
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
138
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
139
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
140
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
141
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
142
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
143
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
144
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
145
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
146
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
147
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
148
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
149
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
150
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
151
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
152
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
153
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
154
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
155
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
156
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
157
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
158
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
159
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
160
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
161
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
162
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
163
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
164
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
165
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
166
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
167
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
168
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
169
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
170
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
171
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
172
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
173
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
174
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
175
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
176
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
177
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
178
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
179
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
180
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
181
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
182
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
183
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
184
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
185
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
186
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
187
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
188
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
189
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
190
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
191
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
192
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
193
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
194
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
195
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
196
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
197
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
198
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
199
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
200
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
201
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
202
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
203
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
204
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
205
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
206
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
207
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
208
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
209
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
210
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
211
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
212
Define chronic bronchitis
‘cough productive of sputum for 3 consecutive months for 2 consecutive years which cannot be attributed to other cardiac or pulmonary disease’.
213
Define Emphysema
‘permanent dilatation of the airways distal to the terminal bronchiole’. It is an ‘apparent’ dilatation of airspaces but is, in fact, due to destruction of alveolar walls.
214
What is the most common cause of COPD?
Tobacco smoking. Other factors include occupation (especially those associated with dust e.g. mining) and anti-trypsin deficiency.
215
In COPD what causes the airflow obstruction?
The airflow obstruction is the result of damage to both small conducting airways and alveoli.
216
What are the different levels of the airway that are affected by smoking?
Bronchi
Small airways
Respiratory bronchioles
217
How does smoking effect the bronchi in COPD?
Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.
218
How does smoking effect the small airways in COPD?
Chronic inflammation → healing by fibrosis → stenosis of airways.
219
How does smoking effect the respiratory bronchioles in COPD?
Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.
220
What 2 major effects does destruction of the lungs by smoking have?
1. Loss of pulmonary surface area for gas exchange → hypoxia.
2. Loss of the elastic tissue of the terminal airways results in loss of the natural recoil of the lungs → this contributes to the reduction in airflow on expiration ie. airflow obstruction.
Remember: In normal lungs, the elastic recoil acts to collapse the lung and is opposed by negative intrapleural pressure which maintains lung expansion.
221
What is the protease/antiprotease hypothesis?
The protease/antiprotease hypothesis may account for the lung destruction in emphysema. Smoking causes increased number of activated neutrophils in the lung where they release protease enzymes such as elastase. In addition, smoking inhibits the lung's natural protease inhibitor enzymes e.g. a1-antitrypsin.
Therefore, large amounts of active elastase can enter the lung interstitium, bind to and degrade elastin, which results in destruction and enlargement of the distal airspaces.
222
What is a1-antitrypsin deficiency?
It is an inherited deficiency of a1-antitrypsin leading to the premature onset of COPD due to widespread emphysematous change in the lungs. Affected patients may also develop liver cirrhosis.
223
Clinical presentation of COPD
The earliest symptom in the natural history of COPD is usually cough and sputum production – reflecting involvement of larger airways.
If susceptible individuals continue to smoke, their small airways become increasingly obstructed until eventually the patient suddenly develops breathlessness on exertion.
With advanced disease, breathlessness occurs upon minimal exertion and then at rest. Death in COPD is usually from bronchopneumonia, respiratory or heart failure.
224
Role of spirometry in the diagnosis of COPD
Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.
225
Cause of acute exacerbation in COPD?
Infection (either bacterial or viral) is the most common cause of an acute exacerbation of COPD. Other less common causes include pneumothorax, PE, LVF and lung carcinoma.
226
Difference between infection in COPD and infection in pneumonia?
The airways are the focus of infection in an infective exacerbation of COPD - CXR shows clear lung fields - Most common organisms = H. influenzae, M Catarrhalis, S. pneumonia and viruses.
This is different from pneumonia, where the infection is centred on the alveoli - CXR shows consolidation - Most common organisms = S. pneumoniae, H influenzae, viruses, atypical organisms.
227
Long term complications of COPD
COPD is the most common cause of cor pulmonale (right heart failure due to lung disease). COPD causes changes in the pulmonary circulation:
• emphysema causes loss of pulmonary arterioles and capillaries.
• chronic hypoxia causes pulmonary arterial vasoconstriction.
• chronic hypoxia causes increased erythropoietin production by the kidney resulting in increased RBC production (erythrocytosis) and consequently increased blood viscosity.
All these changes contribute to the gradual development of pulmonary hypertension.
228
What is pulmonary hypertension?
Pulmonary hypertension refers to an increase in blood pressure in the pulmonary vasculature (pulmonary arteries, veins and capillaries). It is defined as a resting mean pulmonary artery pressure at or above 25mmHg (normal is in the range of 18-15mmHg).
