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1.5
1.0
0.5
59% 64% 35% +163% 7%
0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Source: NHLBI/NIH/DHHS
Of the six
leading
causes of
death in the
United
States, only
COPD has
been
increasing
steadily since
Source: Jemal A. et al. JAMA
COPD Mortality by
Gender,
U.S., 1980-2000
Number Deaths x
1000
Infections
Socio-economic
status
Aging Populations
Global Strategy for Diagnosis,
Management and Prevention of
COPD
Definition,
Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Practical
Pathogenesis of
Cigarette smoke COPD
Biomass particles
Particulates
Host factors
Amplifying mechanisms
LUNG INFLAMMATION
Anti-oxidants Anti-proteinases
Oxidative
stress Proteinases
Repair
mechanisms
COPD PATHOLOGY
Source: Peter J. Barnes,
Changes in Lung Parenchyma in
COPD
Loss of elasticity
Destruction of pulmonary
capillary bed
Inflammatory cells
macrophages, CD8+ lymphocytes
Pulmonary vasoconstriction
Muscularization
Intimal
Pulmonary hypertension hyperplasia
Fibrosis
Edema
Death
Source: Peter J. Barnes,
MD
ASTHMA COPD
Allergens Cigarette smoke
Y Y
Y
Airflow Limitation
Reversible Irreversible
4. Manage exacerbations
GOALS of COPD
MANAGEMENT
VARYING EMPHASIS WITH DIFFERING
SEVERITY
Relieve symptoms
Prevent disease progression
Improve exercise tolerance
Improve health status
Prevent and treat complications
Prevent and treat
exacerbations
Reduce mortality
Four Components of COPD
Management
4. Manage exacerbations
Management of Stable COPD
Assess and Monitor COPD: Key
Points
A clinical diagnosis of COPD should be
considered in any patient who has
dyspnea, chronic cough or sputum
production, and/or a history of exposure to risk
factors for the disease.
The diagnosis should be confirmed by
spirometry. A post-bronchodilator FEV1/FVC
< 0.70 confirms the presence of airflow
limitation that is not fully reversible.
Comorbidities are common in COPD and
Diagnosis of
COPD
EXPOSURE TO RISK
SYMPTOMS FACTORS
cough tobacco
sputum occupation
shortness of breath
indoor/outdoor pollution
SPIROMETRY
Management of Stable COPD
Assess and Monitor COPD:
Spirometry
Spirometry should be performed after the
administration of an adequate dose of a short-
acting inhaled bronchodilator to minimize
variability.
A post-bronchodilator FEV1/FVC < 0.70
confirms the presence of airflow limitation
that is not fully reversible.
Where possible, values should be compared
to age-related normal values to avoid
overdiagnosis of COPD in the elderly.
Spirometry: Normal and
Patients with COPD
Differential Diagnosis:
COPD and Asthma
COPD ASTHMA
Onset in mid-life Onset early in life (often
childhood)
Symptoms slowly
progressive Symptoms vary from day to day
Long smoking history Symptoms at night/early morning
Dyspnea during exercise Allergy, rhinitis, and/or eczema
also present
Largely irreversible airflow
limitation Family history of asthma
Largely reversible airflow
limitation
COPD and Co-
Morbidities
COPD patients are at increased risk for:
Myocardial infarction, angina
Osteoporosis
Respiratory infection
Depression
Diabetes
Lung cancer
COPD and Co-
Morbidities
COPD has significant extrapulmonary
4. Manage exacerbations
Management of Stable COPD
Reduce Risk Factors: Key
Points
Reduction of total personal exposure to
tobacco smoke, occupational dusts and
chemicals, and indoor and outdoor air
pollutants are important goals to prevent
the onset and progression of COPD.
4. Manage exacerbations
Management of Stable COPD
Manage Stable COPD: Key
Points
The overall approach to managing stable COPD
should be individualized to address symptoms and
improve quality of life.
For patients with COPD, health education plays an
important role in smoking cessation (Evidence A) and
can also play a role in improving skills, ability to cope
with illness and health status.
None of the existing medications for COPD have been
shown to modify the long-term decline in lung
function that is the hallmark of this disease (Evidence
A). Therefore, pharmacotherapy for COPD is used to
decrease symptoms and/or complications.
Management of Stable COPD
Pharmacotherapy:
Bronchodilators
Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A).
They are given on an as-needed basis or on a
regular basis to prevent or reduce symptoms
and exacerbations.
The principal bronchodilator treatments are 2-
agonists, anticholinergics, and methylxanthines
used singly or in combination (Evidence A).
Regular treatment with long-acting
bronchodilators is more effective and convenient
than treatment with short-acting bronchodilators
Management of Stable COPD
Pharmacotherapy:
Glucocorticosteroids
The addition of regular treatment with
inhaled
glucocorticosteroids to bronchodilator
treatment is appropriate for symptomatic
COPD patients with an FEV1 < 50%
predicted (Stage III: Severe COPD and Stage
IV: Very Severe COPD) and repeated
exacerbations (Evidence A).
4. Manage exacerbations
Management COPD Exacerbations
Key Points
An exacerbation of COPD is defined as:
Key Points
The most common causes of an
exacerbation are infection of the
tracheobronchial tree and air pollution, but
the cause of about one-third of severe
exacerbations cannot be identified
(Evidence B).
Key Points
Inhaled bronchodilators
(particularly inhaled 2-agonists
with or without
anticholinergics) and oral
glucocortico- steroids are
effective treatments for
exacerbations of COPD (Evidence
Management COPD Exacerbations
Key Points
Definition,
Classification
Burden of COPD
Risk Factors
Pathogenesis,
Pathology,
Pathophysiology
Management
Global Strategy for Diagnosis,
Management and Prevention of COPD:
Summary
COPD is increasing in
prevalence in many countries
of the world.
COPD is treatable and
preventable.
The GOLD program offers a
strategy to identify patients
and to treat them according to
Global Strategy for Diagnosis,
Management and Prevention of COPD:
Summary
COPD can be prevented by avoidance
of risk factors, the most notable being
tobacco smoke.
Patients with COPD have multiple
other conditions (comorbidities) that
must be taken into consideration.
GOLD has developed a global network
to raise awareness of COPD and
disseminate information on diagnosis
Saudi Arabia Bangladesh
Slovenia Ireland
Australia Germany
Yugoslavia Croatia
Philippines Brazil Canada
Austria Taiwan ROC
United States Portugal
Thailand
Norway Greece Malta
Moldova China
Syria South Africa
United Kingdom Hong Kong ROC
Italy New Nepal Chile Israel
ArgentinaZealand
Mexico
Pakista Russia
United Arab Emirates
n Peru Japan
Poland Korea
GOLD National
Netherland
Leaders Egypt s
Switzerland India Venezuela Georgia
Macedonia France
Czech Iceland Denmark
Turkey Slovakia Belgium
Republic
Romania Columbia Ukraine Singapore Spain
Uruguay Sweden Albania Kyrgyzstan Vietnam
WORLD COPD DAY
November 14, 2007
http://www.goldcopd.or
g
ADDITIONAL SLIDES WITH NOTES
PREPARED BY:
PROFESSOR PETER J. BARNES, MD
NATIONAL HEART AND LUNG
INSTITUTE
LONDON, ENGLAND
Changes in Large Airways of COPD
Patients
Mucus hypersecretion Neutrophils in sputum
CD8+ lymphocytes
Mucus gland hyperplasia
Little increase in
airway smooth muscle
Peribronchial fibrosis
Lymphoid follicle
Loss of elasticity
Destruction of pulmonary
capillary bed
Inflammatory cells
macrophages, CD8+ lymphocytes
Endothelial dysfunction
Intimal hyperplasia
Inflammatory cells
(macrophages, CD8+ lymphocytes)
LUNG INFLAMMATION
Anti-oxidants
Anti-proteinases
Oxidative
stress Proteinases
Repair
mechanisms
COPD PATHOLOGY
Source: Peter J. Barnes,
Inflammatory Cells Involved in
COPD Cigarette smoke
(and other irritants)
Epithelial Alveolar
cells macrophage
Chemotactic factors
CD8+
Fibroblastlymphocyte
Neutrophil Monocyte
Neutrophil elastase
PROTEASES Cathepsins
MMPs
Mucus hypersecretio
Fibrosis Alveolar wall destruction
(Obstructive (Emphysema)
bronchiolitis)
Source: Peter J. Barnes,
MD
Oxidative Stress in COPD
Macrophage Neutrophil
Anti-proteases
SLPI 1-AT NF- B
Mucus secretion
Source: Peter J. Barnes,
MD
Differences in Inflammation and its Consequences: Asthma and COP
ASTHMA COPD
Allergens Cigarette smoke
Y Y
Y
Airflow Limitation
Reversible Irreversible
Source: Peter J. Barnes,
Air Trapping in
Normal COPD
Mild/moderate Severe
Inspiration COPD COPD
small
airway
Expiration
closure
Pulmonary vasoconstriction
Muscularization
Intimal
Pulmonary hypertension hyperplasia
Fibrosis
Edema
Death
Macrophages
Epithelial
cells
TNF- IL-8 IL-6
Neutrophils
Oxidative stress