COPD Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the most common cause of COPD?

A

tobacco smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the protease/antiprotease hypothesis?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the protease/antiprotease hypothesis?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a1-antitrypsin deficiency?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the protease/antiprotease hypothesis?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is a1-antitrypsin deficiency?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Clinical presentation of COPD

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Cause of acute exacerbation in COPD?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Difference between infection in COPD and infection in pneumonia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Long term complications of COPD

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the protease/antiprotease hypothesis?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is a1-antitrypsin deficiency?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Clinical presentation of COPD

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Cause of acute exacerbation in COPD?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Difference between infection in COPD and infection in pneumonia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Long term complications of COPD

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
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’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

97
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

101
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.

102
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.

103
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

104
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

105
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

106
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

107
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

108
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

113
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

117
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.

118
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.

119
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

120
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

121
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

122
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

123
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

124
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

129
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

133
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.

134
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.

135
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

136
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

137
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

138
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

139
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

140
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

145
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

149
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.

150
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.

151
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

152
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

153
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

154
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

155
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

156
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

161
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

165
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.

166
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.

167
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

168
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

169
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

170
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

171
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

172
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

177
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

181
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.

182
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.

183
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

184
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

185
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

186
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

187
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

188
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

193
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

197
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.

198
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.

199
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

200
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

201
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

202
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

203
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

204
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

209
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
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’.

213
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.

214
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.

215
Q

In COPD what causes the airflow obstruction?

A

The airflow obstruction is the result of damage to both small conducting airways and alveoli.

216
Q

What are the different levels of the airway that are affected by smoking?

A

Bronchi
Small airways
Respiratory bronchioles

217
Q

How does smoking effect the bronchi in COPD?

A

Hyperplasia of mucus-producing glands in the submucosa and hyperplasia of goblet cells on the surface epithelium → increased sputum production.

218
Q

How does smoking effect the small airways in COPD?

A

Chronic inflammation → healing by fibrosis → stenosis of airways.

219
Q

How does smoking effect the respiratory bronchioles in COPD?

A

Destruction of the walls with loss of the elastic tissue but without significant fibrosis → airway dilatation → emphysema.

220
Q

What 2 major effects does destruction of the lungs by smoking have?

A
  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
Q

What is the protease/antiprotease hypothesis?

A

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
Q

What is a1-antitrypsin deficiency?

A

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
Q

Clinical presentation of COPD

A

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
Q

Role of spirometry in the diagnosis of COPD

A

Spirometry confirms the diagnosis of COPD by demonstrating airflow obstruction.

225
Q

Cause of acute exacerbation in COPD?

A

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
Q

Difference between infection in COPD and infection in pneumonia?

A

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
Q

Long term complications of COPD

A

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
Q

What is pulmonary hypertension?

A

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).