This document discusses definitions of chronic obstructive pulmonary disease (COPD) from various medical organizations over time. It describes COPD as a progressive lung disease characterized by persistent airflow limitation. The definitions have evolved to emphasize COPD as an inflammatory condition caused by long-term exposure to noxious particles or gases. Exacerbations and comorbidities contribute to COPD severity and impact quality of life. The document also contrasts COPD and asthma, noting their different causes, inflammatory profiles, and treatment responses.

2. Chronic Obstructive Pulmonary Disease
COPD

4. What is it ??? COPD

5. 5

6. November 2012 WHO
Key facts
 Chronic obstructive pulmonary disease
(COPD) is a life-threatening lung disease
that interferes with normal breathing – it is
more than a “smoker’s cough”.
6

7. Several different definitions
exist for COPD.
7

8. Definition of COPD
 COPD is defined as
 ‘a disease state characterised by the
presence of airflow obstruction due to
chronic bronchitis or emphysema
 The airflow obstruction is generally
progressive, may be accompanied by
airway hyper-reactivity, and may be
partially reversible’
American Thoracic Society 1995

9. Definition of COPD
 The definition Include chronic
bronchitis ,emphysema with airflow limitation.
 The definition exclude other causes of chronic
airflow obstruction such as Pulmonary cystic
fibrosis , diffuse panbronchiolitis and
bronchiectasis etc.
American Thoracic Society 1995

10. Definition of COPD
 COPD is a nonspecific term referring to a set
of conditions that develops progressively as
a result of a number of different disease
processes
 It most commonly refers to patients with
chronic bronchitis and emphysema and to a
subset of patients with asthma
American Thoracic Society 1995

11. Non-proportional Venn diagram of COPD produced by ATS.
The subsets comprising COPD are shaded
11
American Thoracic Society 1995

12.  Patients with asthma whose airflow obstruction is
completely reversible (subset 9) are not considered
to have COPD.
 Because in many cases it is virtually impossible to
differentiate patients with asthma whose airflow
obstruction does not remit completely from persons
with chronic bronchitis and emphysema who have
partially reversible airflow obstruction, patients with
unremitting asthma are classified as having COPD
(subsets 6, 7 and 8).
12

13.  Chronic bronchitis and emphysema with airflow
obstruction usually occur together (subset 5), and
some patients may have asthma associated with
these two disorders (subset 8).
 Individuals with asthma who have been exposed to
chronic irritation, as from cigarette smoke, may
develop chronic productive cough, which is a feature
of chronic bronchitis (subset 6 ) , Such patients are
often referred to as having asthmatic bronchitis,
although this terminology has not been officially
endorsed in clinical practice guidelines .
13

14.  Persons with emphysema and/or chronic bronchitis
without airflow obstruction (subsets 1, 2 and 11) are
not classified as having COPD.
 Patients with airway obstruction due to diseases with
known aetiology or specific pathology such as cystic
fibrosis or obliterative bronchiolitis (subset 10) are not
included in this definition.
 Subset areas are not proportional to the actual
relative subset sizes.
14

15. COPD
Chronic bronchitis
Emphysema
Unremitting asthma

17.  GOLD Definition: ( Gold 2001)
 A disease state characterized by airflow
limitation that is not fully reversible
 The airflow limitations is usually both
progressive and associated with abnormal
inflammatory response of the lungs to
noxious particles or gases
17
Definition of COPD
.

18.  Many previous definitions of COPD have
emphasized the terms “emphysema” and
“chronic bronchitis,” which are not included
in the definition used in this GOLD reports.
 This definition does not use the terms
chronic bronchitis and emphysema and
excludes asthma (reversible airflow
limitation)
18

19. COPD is used to describe emphysema, chronic
19
bronchitis or a combination of the two.

21. Overlap between COPD and asthma
COPD ASTHMA
–Neutrophils
–No airway
hyperreactivity
–No bronchodilator
response
–No corticosteroid
response
–Eosinophils
–Airway
hyperreactivity
–Bronchodilator
response
–Corticosteroid
response
~10%
“Wheezy bronchitis”
Barnes, Chest 2000

22. COPD ? Asthma

23. COPD Asthma
ATS
2004

24. ATS 2004
 Asthma differs from COPD in its pathogenic and
therapeutic response, and should therefore be
considered a different clinical entity.
 However, some patients with asthma develop
poorly reversible airflow limitation. These
patients are indistinguishable from patients with
COPD but for practical purposes are treated as
asthma.
24

25. 2014
Diagnosis of asthma, COPD and
asthma-COPD overlap syndrome
(ACOS)
A joint project of GINA and GOLD
GINA Global Strategy for Asthma Management
and Prevention
GOLD Global Strategy for Diagnosis,
Management and Prevention of COPD
© Global Initiative for Asthma3.
GINA 2014

26. Definition of COPD 2006
☻ COPD is a preventable and treatable disease
with some significant extrapulmonary effects that
may contribute to the severity in individual
patients.
☻ Its pulmonary component is characterized by
airflow limitation that is not fully reversible.
☻ The airflow limitation is usually progressive
and associated with an abnormal inflammatory
response of the lung to noxious particles or gases.

27. Definition of COPD 2011
☻ COPD, a common preventable and treatable
disease, is characterized by persistent airflow
limitation that is usually progressive and associated
with an enhanced chronic inflammatory response
in the airways and the lung to noxious particles or
gases.
☻ Exacerbations and comorbidities contribute to the
overall severity in individual patients.

28. Definition of COPD 2014
Common preventable & treatable disease
Characterized by persistent airflow limitation that is
usually progressive
Associated with an enhanced chronic inflammatory
response in the airways & the lung to noxious
particles or gases
Exacerbations & comorbidities contribute to the
overall severity in individual patients

29. Will COPD ever go away?
 The term chronic in chronic obstructive lung
disease means all of the time, therefore, you
will have COPD for life.
 While the symptoms sometimes are less after
you stop smoking, they may never go away
entirely. Improvements in symptoms depend on
how much damage has occurred to your lungs.
29

30. COPD is rare ?
Myth
The sad fact is COPD is the fourth leading cause
of death in the U.S. after heart disease, cancer,
and stroke.
Just like heart disease, COPD can be silent for
many years, until it’s nearly too late.
 About 24 million Americans have COPD, but
half of them don’t know it yet.
30

31.  The phrase “preventable and treatable” has
been incorporated following the ATS/ERS
recommendations to recognize need to:
1. Present a positive outlook for patients
2. Encourage the health care community to
take a more active role in developing
programs for COPD prevention and treatment

32. LUNG INFLAMMATION
COPD PATHOLOGY
Oxidative
Anti-proteinases
stress Proteinases
Repair
mechanisms
Anti-oxidants
Host factors
Amplifying mechanisms
Cigarette smoke
Biomass particles
Particulates
Pathogenesis of
COPD

34. Chronic Inflammation plays a central role
in COPD
Smoke Pollutants
Inflammation
Chronic inflammation
Structural changes
Key inflammatory cells
Neutrophils
CD8+ T-lymphocytes
Macrophages
Systemic
inflammation
Bronchoconstriction,
oedema, mucus,
emphysema
Airflow limitation
Acute
exacerbation
Adapted from Barnes PJ, in Stockley, et al (editors), Chronic Obstructive Pulmonary Disease. Oxford, England: Blackwell Publishing; 2007

35. ASTHMA
Allergens
Mast cell
CD4+ cell
(Th2)
Eosinophil
Ep cells
Bronchoconstriction
AHR
COPD
Cigarette smoke
Alv macrophageEp cells
CD8+ cell
(Tc1)
Neutrophil
Small airway narrowing
Alveolar destruction
Reversible Airflow Limitation Not fully reversible

36. COPD IS NOT ASTHMA !
• Different causes
• Different inflammatory cells
• Different inflammatory mediators
• Different inflammatory consequences
• Different response to treatment

37. COPD is a multicomponent disease
Inflammation
Airway
obstruction
Structural
changes
Airflow limitation
Muco-ciliary
dysfunction
Cazzola and Dahl, Chest 2004

40. Mechanical Origins of Airflow Limitation
Flow = Pressure
Resistance
In Respiratory Function
Chronic Airflow Limitation
(Flow)
Is Determined By
Loss of Elastic Recoil
(Pressure)
Airway Narrowing
(Resistance)

41. -Chronic Bronchitis predominant
-Airway obstruction is the main problem
Normal
Elastic Recoil
Increased airway resistance
due to thickened wall and
secretions
Elastic Recoil
Chronic Bronchitis

42. -Emphysema Predominant
-This results in a loss of the elastic recoil of the lungs on expiration
-This also results in loss of tethering or support of the most distal
portions of the airway leading to collapse on expiration
Normal
Elastic Recoil
Airway supported
by connective
tissue
Decreased
Elastic Recoil =
Lower Flow
Loss of support = Airway
collapses= Air gets trapped in lung

43. Causes of Airflow Limitation
 Irreversible
1. Fibrosis and narrowing of the airways
2. Loss of elastic recoil due to alveolar
destruction
3. Destruction of alveolar support that
maintains patency of small airways

44. Causes of Airflow Limitation
 Reversible
1. Accumulation of inflammatory cells,
mucus, and plasma exudate in bronchi
2. Smooth muscle contraction in peripheral
and central airways
3. Dynamic hyperinflation during exercise

45.  The chronic airflow limitation characteristic of
COPD is caused by a mixture of small airway
disease (obstructive bronchiolitis) and
parenchymal destruction(emphysema),
 The relative contributions of which vary from
person to person
45

46. COPD Pathophysiology
AIRFLOW OBSTRUCTION
Alveolar Wall Destruction
Air Spaces Enlargement
Alveolar Attachments
Loss
Capillary Network
Reduction
HIGH VA/Q RATIOS
AIRFLOW
OBSTRUCTION
Small Airways
Narrowing-Distortion
Nonhomogeneous
Inspired Air Distribution
Reduced Ventilation
In Dependent Alveoli
LOW VA/Q RATIOS
AIR TRAPPING-LUNG
HYPERINFLATION
Rodríguez-Roisin and MacNee. ERM 1998; 6
AIR TRAPPING
LUNG HYPERINFLATION

47. COPD is a Complex Disease
Progressive Loss of Lung Function
Reduced Quality of Life
Exacerbations
Mortality
Broncho-constriction
Inflammation
Structural
Changes
Airflow
Limitation &
Hyperinflation

48. Clinical Course of COPD
COPD
Expiratory Flow Limitation
Air Trapping
Hyperinflation
Breathlessness
Inactivity
Deconditioning
Reduced Exercise
Capacity
Poor Health-Related Quality of Life
EXACERBATIONS
Disability Disease progression Death

49. Is it Inevitably All Downhill ?
49

50. Disease Progression in COPD
Am. J. Respir. Crit. Care Med. 2002; 166: 675-679
Lung Function
Continuous smokers
Years
FEV1 (L)
2.9
2.8
2.7
2.6
2.5
2.4
2.3
2.2
2.1
2.0
0 1 2 3 4 5 6 7 8 9 10 11

52. COPD progression
Age (year)
FEV1 % of value at age 25 yr
100
75
50
25
Disability
Death
25 50 75
Adapted from:Fletcher C,et al.Br Med J.1977;1:1645-1648
Nonsmokers
20-30 ml/year
COPD
60 mL/year
symptoms

53. Age 40-50 50-55 55-60 60-70
Age (years)
Symptoms
Disability
Death
Never smoked or
Susceptible Not Susceptible
Smokers
Stopped smoking
at 45 (mild COPD)
Stopped smoking
at 65 (severe COPD)
30 40 50 60 70 80 90
80
60
40
20
0
20
100
Adapted from Fletcher CM, Peto R. BMJ 1977

54. What is Progression of COPD?
Incident Disease
Progressive Disease
*GOLD Guidelines. Am J Respir Crit Care Med.
0
At Risk
I
Mild
II
Moderate
III
Severe
IV
Very Severe
Health
Prevalent Disease
Death
???

55. COPD: Progressive Disease
อาการ/ lung function
Acute exacerbation
ระยะเวลา

56. Disease Trajectory of a Patients
56
Symptoms
Exacerbations
Exacerbations
Exacerbations
Deterioration
End of Life
with COPD

57. Impact of Exacerbations
Decline in lung function Increased symptoms
Social withdrawal
Worsening quality of life
More exacerbations
Increased risk of hospitalisation
Greater anxiety
(I.e. breathlessness)
Increased risk of mortality

58. Frequent exacerbations are associated
with increased mortality
p < 0.0002
p = 0.069
A = No exacerbations B = 1-2 exacerbations C = 3 or more exacerbations
Soler-Cataluna JJ, et al. Thorax 2005;60:925-931.
p < 0.0001
1.0
Probability of surviving
0.8
0.6
0.4
0.2
0.0
0 10 20 30 40 50 60
Time (months)
A
B
C

59. The ‘frequent exacerbator phenotype’:
Frequency/severity by GOLD Category (1)
7
18
33
22
33
47
50
40
30
20
10
0
GOLD II
(N=945)
GOLD III
(N=900)
GOLD IV
(N=293)
% of patients
p<0.01
Hospitalised for exacerbation in yr 1 Frequent exacerbations (2 or more)
ECLIPSE 1 year data Hurst et al. N Engl J Med 2010

60. Assess Risk of Exacerbations
High risk of exacerbations
 > 2 exacerbations within the last year or
 FEV1 < 50 % of predicted value
GOLD revised 2011

61. Global Strategy for Diagnosis, Management
and Prevention of COPD. Updated 2011
C: Less symptoms, high risk
Risk
(GOLD Classification of Airflow Limitation)
D: More Symtoms, high risk
Risk
(Exacerbation
history)
> 2
B: More symtoms, low risk
1
0
(C) (D)
(A) (B)
A: Les symptoms, low risk
mMRC 0-1
4
3
2
1
CAT < 10 or CCQ<1
mMRC > 2
CAT > 10 or
CCQ>1
Symptoms

62. COPD and Comorbidities
 Because COPD often develops in long-time
smokers in middle age, patients often have a
variety of other diseases related to either
smoking or aging.
 COPD itself also has significant extrapulmonary
(systemic) effects that lead to comorbid
conditions
62

63. Aging
 Almost one-half of people aged > 65 years have
> 3 chronic medical conditions, and one-fifth
have five or more
 Aging itself is associated with a chronic low-grade
inflammatory status and the theory that
systemic inflammation is the common driver of
chronic diseases would explain the high
prevalence of chronic diseases with increasing
age
Nussbaumer-Ochsner Y and Rabe KF. Chest 2011;139;165-173

64. Definitions
 “Systemic effects”
Extrapulmonary manifestations which is the
consequence of COPD
 “Comorbidities”
highly prevalent diseases in COPD (e.g.
cardiovascular, metabolic, muscular, and bone
disorders) in aged patients represent the co-ocurrence.
Alvar Agustı´ A and Faner R. Proc Am Thorac Soc Vol 9, Iss. 2, pp 43–46, May 1, 2012

65. SYSTEMIC EFFECTS OF COPD
Liver
IL-6 IL-6, TNF-α, IL-1β
CRP
Skeletal
muscle
Cardiovascular disease Muscle wasting
Other
Inflammatory
diseases
Circulation

66. COPD has significant extrapulmonary
(systemic) effects including:
☻Weight loss
☻Nutritional abnormalities
☻Skeletal muscle dysfunction

67. Assess COPD Comorbidities
COPD patients are at increased risk for:
☻Cardiovascular diseases
☻Osteoporosis
☻Respiratory infections
☻Anxiety and Depression
☻Diabetes
☻Lung cancer
GOLD revised 2011

68. COPD is: More than just a lung disorder
Respiratory system
QuickTime™ an d a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Systemic
inflammation
COPD is:
a multi- component disease
Target organs
with systemic involvement & inflammation

69. Systemic Effects of COPD:
Lung Infections
Lung Cancer
Angina
Acute coronary
syndromes
Diabetes
Metabolic syndrome
Systemic
Inflammation
Oxidatitive Stress
Weight loss
Muscle weakness
Osteoporosis
Depression
Peptic ulceration Depression

71. Comorbidity and Mortality in COPD
Related Hospitalizations
Mortaliyty (%)
Holguin et al. CHEST 2005; 128:2005
COPD Non-COPD
40
30
20
10
0
RF Pneum HF IHD Hypert TM Diabetes PVD

72. Assessing Comorbidities in
COPD
COPD Comorbidities
Agusti A and Jardim J, personal communication.
Look for
Look for
If Smoker

73. COPD components that contribute to the
symptoms of the disease
Structural
changes
Airflow limitation
Broncho-constriction
Systemic
component
Mucociliary
dysfunction
Symptoms
Airway
inflammation
1. Agusti AGN et al. Respir Med 2005; 99: 670–682.
Disease progression
Death

74. COPD is a multicomponent disease with
inflammation at its core leading to mortality
Declining lung function
Symptoms
Exacerbations
Decreased exercise tolerance
Deteriorating health status
and increasing morbidity
Mortality
Airflow
limitation
Structural
changes
Systemic
component
Mucociliary
dysfunction
Airway
inflammation
Agusti. Respir Med 2005
Agusti et al. Eur Respir J 2003
Bernard et al. Am J Respir Crit Care Med 1998

76. COPD: old definition
.…airflow obstruction due to
emphysema and chronic
bronchitis

77. Chronic Bronchitis
 Chronic bronchitis is defined clinically as the
presence of a cough productive of sputum on
most days for at least 3 consecutive months in
each of 2 successive years, in a patient in whom
other causes of chronic cough (eg, bronchiectasis
or TB) have been excluded .

78. Chronic bronchitis
 is a clinical and epidemiological term
 Is not necessarily associated with air flow
limitation.
 It may precede or follow development of
airflow limitation
78

79. Chronic Bronchitis
Classification:
1. Simple chronic bronchitis
2. Chronic mucopurulent bronchitis
3. Chronic bronchitis with obstruction
4. Chronic bronchitis with obstruction and
airway hyperreactivity.

80. Chronic Bronchitis
1. Simple chronic bronchitis : mucoid sputum with
no airway obsturction
2. Chronic mucopurulent bronchitis: cough +
sputum with pus
3. Chronic obstructive: bronchitis with outflow
obstruction
4. Chronic asthmatic bronchitis: intermittent
episodes with airway hyperresponsiveness
(similar to asthma)
 It may Coexistent emphysema

81. Chronic Bronchitis
Pathogenesis
 Hypersecretion of mucus, beginning in large
airways
 Hypertrophy of mucus glands
 Goblet cell hyperplasia in surface epithelium
 Inflammation, growth factor upregulation
 Secondary microbial infection

82. Chronic Bronchitis
pathology
 Mucosa
 Mucopurulent secretions
 Swelling and hyperemia
 Increased number of inflammatory cells
 Increase number of goblet cells
 Loss of ciliated cells
 Squamous metaplasia

83. Chronic Bronchitis
Pathology
 Submucosa
• Enlargement of mucus secreting glands (Reid
index)
 In small bronchioles ( bronchiolitis)
• Inflammation, fibrosis and smooth muscle
hyperplasia
• Peribronchial fibrosis, luminal narrowing,airflow
obstruction

84. NORMAL EPITHELIUM OF
RESPIRATORY TRACT

86. 86

87. 87

88. 88

91. 91

93. Chronic Bronchitis
Pathological Features of CB:
 Initially:
Hypersecretion of mucus (Proteases from PMNs)
Hypertrophy of submucosal glands in trachea
and bronchi
 With chronicity:
Marked increase in goblet cells of small airways

94. Chronic Bronchitis
 Increase in globlet cells and hypertrophy of
submucosal glands are of protective
metaplastic reaction against the irritants
 Irritants > EGF receptor stimulation > up
regulation of MUC 5AC gene (a mucin gene)
 Hypersecretion of mucus is the basis for smaller
air way obstruction

95. Characteristic histological feature:
 Enlargement of mucus secreting glands of trachea
and bronchi i.e. Increased size of mucous glands
 REID Index : Ratio of the thickness of the mucous
gland layer to the thickness of the wall between
the epithelium and the cartilage
 REID Index: Normal is 0.4 and is increased in chronic
bronchitis.
Chronic Bronchitis

96. REID Index
bc/ad
Gland/Wall

98. REID Index

100. The Reid Index
 Is a mathematical relationship that exists in a
human bronchus section observed under the
microscope.
 It is defined as ratio between the thickness of
the submucosal mucus secreting glands and
the thickness between the epithelium and
cartilage that covers the bronchi.
10
0

101.  The Reid index is not of diagnostic use in vivo,
but it has value in post mortem evaluations and
for research
 A normal Reid Index should be smaller than 0.4,
the thickness of the wall is always more than
double the thickness of the glands it contains.
A greater value is the most pathognomonic
indicator of chronic bronchitis.
10
1

103. Pathological processes in
chronic bronchitis
 Mucus hypersecretion
 Epithelial / ciliary dysfunction
 Airway mucosal inflammation / oedema
 Airway fibrosis / remodelling
 Bronchoconstriction
 Ventilation - perfusion mismatch
 Hypoxic pulmonary vasoconstriction
 Cor pumonale

104. Chronic bronchitis: the ‘blue bloater’

105. COPD : Archetypes –
The Blue Bloater
• COPD Type B –
Chronic Bronchitis
• Decreased V/Q
• Poor ventilation / High CO
• Cyanosis
• CO2 retention
• Acidosis
• Pulmonary arteriolar
constriction
• Right heart failure

106. Relatively normal
lung region, normal PAO2
normal
CaO2
Airway narrowing
Bronchitis
 PAO2
 CaO2
 V´
norm
V´
norm Q´ norm Q´
 CaO2
Pulm. a. Pulm. v.

107. Ventilation-perfusion defects
 Alveoli that are ventilated but not perfused is
ventilatory “dead space”
 Alveoli that are perfused but not ventilated
leads to “shunting” of non-oxygenated blood
from pulmonary to systemic circulation ( a
mechanism of cyanosis)

108.  Emphysema frequently occurs in association with
chronic bronchitis .
 These 2 entities have been traditionally grouped
under the umbrella term COPD.
 In patients with COPD either of those conditions
may be present , However, the relative contribution
of each to the disease process is often difficult to
10 discern.
8
Emphysema

109. Emphysema
 An abnormal permanent enlargement of
airspaces distal to the terminal bronchioles,
accompanied by destruction of alveolar
walls, without obvious fibrosis
 A pathological term

110. Weibel's lung model
 The airways consists of a series of branching
tubes – this process continues down to terminal
bronchioles which are the smallest airways
without alveoli
 All these bronchi make up the conducting
airways-their function is to lead inspired air to
gas exchanging regions
11
0

112. Respiratory Conducting

113.  The conducting airways contain no alveoli
therefore take no part in gas exchange –
they constitute the anatomical dead space
11
3

115.  The first 16 generations make up the conducting
airways ending in the terminal bronchioles
 The next 3 generations constitute the respiratory
bronchioles-in which the degree of alveolation
steadily increases –this is the transitional zone
11
5
Weibel's lung model

116.  Finally there are 3 generations of alveolar ducts
and one generation of alveolar sacs-these last
four generationte the true respiratory zone
 In some regions of the human lung there are
fewer than 23 generations from the trachea to
the alveolar sacs where as other regions
contain more generations
11
6
Weibel's lung model

118. 11
8

120. 12
0

121. 12
1

122. 12
2

123. The respiratory acinus
 Cartilage is present to
level of proximal
bronchioles
 Beyond terminal
bronchiole gas
exchange occurs
 The distal airspaces are
kept open by elastic
tension in alveolar walls

124. 12
4

125. 12
5

126. 12 Secondary pulmonary lobule
6

127.  The terminal bronchiole leads to several orders
of respiratory bronchioles which in turn open into
alveolar ducts (AD) and alveolar sacs (AS)
 The Respiratory air spaces arising from a single
terminal bronchiole constitute the secondary
lung lobule
 The secondary lung lobule is an old anatomical
unit –it does seem to comprise about a dozen
12 acini
7

128. Emphysema
 The part of the lung involved in emphysema is the
acinus which is defined as the unit of the lung
structure distal to the terminal bronchiole and that
consists of 3 orders of respiratory bronchioles-a
single order of alveolar duct followed by alveolar
sacs and finally the alveoli
 The way in which the acini is involved determine
12 the classification of emphysema
8

130. Emphysema
 Classified according to the pattern of
involvement of the acini distal to terminal
bronchiole.
 Types: (1) Centrilobular
(2) Panlobular
(3) Paraseptal
(4) Irregular
 Pulmonary acinus Synonyms: primary pulmonary
lobule, respiratory lobule

131. Emphysema

132. Emphysema

134. 13
4

135. Distal acinar Emphysema

136. Distal acinar Emphysema
 or paraseptal emphysema, is the least common
form and involves distal airway structures, alveolar
ducts, and sacs.
 This form of emphysema is localized to fibrous septa
or to the pleura & leads to formation of bullae.
 The apical bullae may cause pneumothorax.
 Paraseptal emphysema is not associated with
airflow obstruction.

138. 13
8

139. 13
9

140. 14
0

141. Loss of surface area (emphysema)

142. Emphysema
Centriacinar Alv
Paraseptal
Panacinar
TB
Original
Emphysematous
RB
BR
RB
Alv
Alv

145. Pathology of Emphysema
Normal Lung
Mild Emphysema
Severe Emphysema

146. What is Emphysema?
Specifically, two things combined:
☻ Permanent abnormal
enlargement of the
acini
 Destruction of alveolar
walls without obvious
fibrosis
)
Image from www.nucleusinc.com

148. Types of Respiratory air space
enlargement
1) Simple air space enlargement
 Is defined as enlargement of the air spaces
without destruction
 Congenital
Down syndrome
Congenital lobar over inflation
 Acquried
Secondary to loss of lung volume (over distention
14 of the remaining lung following pneumonectomy)
8

149. 2) Emphysema
 Proximal acinar (Centrilobular ) or
Cenritiacinar
 Panacinar (Panlobular )
 Distal acinar (Paraseptal) or periacinar
14
9

150. 3) Air space enlargement with fibrosis
 This form may be associated with infectious
granulomatous disease such as TB and non
infectious granulomatous disease such as
sacoidosis
 Air space enlargement with fibrosis was formerly
termed Irregular or paracicatricia emphysema
or Scar emphysema
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151.  Paracicatricia emphysema is used to describe
enlarged air spaces around the margins of a scar
and unrelated to the structure of the acinus
 Paracatricial airspace enlargement (so-called
irregular or “scar ” emphysema
 This lesion is excluded from the current defintion
of emphysema
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152.  Destruction of alveolar walls ( to exclude
Down syndrome –Congenital lobar over
inflation –Senile emphysema )
 Without obvious fibrosis ( to exclude
paracicatricial emphysema )
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153.  Exclusion of obvious fibrosis was intended to
distinguish the alveolar destruction due to
emphysema from that due to the interstitial
pneumonias
 While emphysema can exist in individuals who
do not have airflow obstruction, it is more
common among patients who have moderate
or severe airflow obstruction
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154.  Emphysema, defined as destruction of the
alveoli, is a pathilogical term that is sometimes
(incorrectly) used clinically and describes only
one of several structural abnormalities present
in patients with COPD – but can also be found
in subjects with normal lung fuction
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155.  Destruction is defined as nonuniformity in the
pattern of respiratory air space enlargement so
that the orderly appearance of the acinus and its
components is disturbed and may be lost
 Enlargement of air spaces unaccompanied by
destruction – is now being termed over inflation
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156. Emphysema & Overinflation
 Emphysema:
Increased air space with destruction
 Overinflation:
Increased air space without destruction

157. Obstructive Emphysema
Emphysema
without
Obstruction
senile
emphysema(Physiological)
Interstitial Emphysema
Compensating Emphysema
Scarred Emphysema

158. Overinflation: enlarged spaces without
destruction of the tissue.
 If a part of the lung collapses or removed the
remaining lung can expand to fill the increased
amount of space available a process known as
Compensatory overinflation
 No tissue distruction has occurred and by
definition this is not emphysema
 Compensatory overinflation is caused by
response to a lobectomy/unilateral
pneumonectomy.

159.  Obstructive emphysema: is a misnomer, better
termed hyperinflation, since the distal air ways
are dilated but not destroyed.
 Occurs due to one-way “ball valve” mechanism
in a main bronchi due to a foreign body or
Endobronchial tumor, allow air- entry in one way
only. So lung distal to obstruction becomes
hyperinflated.

160.  In both Compensatory overinflation and
Obstructive overinflation-the lung contains
too much air per unit of lung tissue
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161.  Unilateral emphysema is believed to result
from a severe bronchiolitis in childhood that
prevented normal maturation of the lung on
that side.
 “Congenital lobar emphysema” of infants is
usually a misnomer, since there is no
alveolar destruction.. The lobes are over
inflated rather than emphysematous

162. Congenital lobar emphysema

163. Congenital lobar emphysema
 is a condition characterized by progressive
overdistention of a lobe or, occasionally, two lobes.
 Many cases seem to be due to obstruction of a
bronchus by a ball valve mechanism. Postulated
causes of this obstruction include bronchial cartilage
deficiency, dysplasia, or immaturity; inflammatory
exudates; inspissated mucus; mucosal fold or web;
bronchial stenosis; extrinsic vascular compression;
and extrinsic mass compression.

164.  Senile emphysema according to the current
definition of emphysema is a misnomer , as there
is no destruction of alveolar walls.
 The "senile lung" does not manifest itself clinically
as emphysema
 Alveolar surface area decreases, and alveolar
ductular size increases, progressively after the
age of 30 years. This process is one of normal
senile involution and is not a disease.

165.  Senile emphysema is a misnomer , Senile lungs
are characterized by a homogeneous
enlargement of the alveolar airspaces, without
fibrosis or destruction of their walls

166. Interstitial emphysema.
 This refers to inflation of the interstitium of the
lung by air, and is most commonly due to
traumatic rupture of an airway or spontaneous
rupture of an emphysematous bulla.
 Interstitial emphysema may spread to the
mediastinum or subcutis, giving the
characteristic spongy crepitus on palpation.
the term emphysema really being a misnomer

167. Pulmonary interstitial emphysema
• Mechanical ventillation of premature infant
with RDS (hyaline membrane disease)
• Rupture of overdistended alveoli with
dissection of air along the pulmonary
interstitium.
Pathology
• Premature infant in NICU.
• Neonatal respiratory distress.
C.P
• Focal or diffuse.
• Unilateral or bilateral.
• No specific lobar predilection.
Location
• Cystic or linear translucencies radiating from
the hilum.
CXR
• Pneumothorax.
• Pneumomediastinum.
• Pneumopericardium.
• Pneumoperitoneum.
• Subcuatneous emphysema.
Complications

168. Pathogenesis
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169. 16
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170. Pathophysiology

171. Pathological processes in
emphysema
 Loss of alveolar surface area
 Loss of lung elasticity
 Hyperinflation causing mechanical
inefficiency
 Muscle weakness / cachexia
 Small airways collapse
 Dynamic hyperinflation

172. Emphysema Impairs Respiratory
Function
 Diminished alveolar surface area for gas
exchange (decreased Tco)
 Loss of elastic recoil and support of small
airways leading to tendency to collapse
with obstruction

173. As disease advances….
Pa O2 leads to:
 Dyspnoea and increased respiratory rate
 Pulmonary vasoconstriction (and pulmonary
hypertension)

174. Emphysema - the ‘pink puffer’

175. COPD : Archetypes – The Pink Puffer
• COPD Type A –
Emphysema
• Hyperinflation/barrel
chest
• Tachypnea/pursed lips
• Increased V/Q
• Tachypnea / Low CO
• Systemic hypoxia (low CO)
• Weight loss
• Problems eating & breathing at
same time?

176. 17
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177. 177

178. 17
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