CHRONIC OBSTRUCTIVE

PULMONARY DISEASE
(COPD)

Dr. Xing Lihua

Contents
• Definition
• Epidemiology
• Pathogenesis
• Pathology
• Clinical Manifestations
• Laboratory examination
• Diagnosis and Differential diagnosis
• Treatment
Definition
Chronic bronchitis,
Emphysema ,
Asthma
 Definitions of Chronic bronchilitis

• Chronic bronchitis is a clinical diagnosis

based on the symptoms of chronic cough
and sputum production.
• The American Thoracic Society(ATS)
defines chronic bronchitis as the
persistence of cough and excessive mucus
secretion on most days over a 3-month
period for at least 2 successive years.
Other causes, such as infection with

Mycobacterium ,
tuberculosis,
carcinoma of the lung,
or chronic heart failure,

have been excluded.

 Definition of emphysema
• The diagnosis of emphysema is based on
pathologic, rather than clinical criteria.
• The ATS defines emphysema as airspace
enlargement distal to the terminal
bronchiole and destruction of the alveolar
wall; later refinements of the definition
include the requirements that the airspace
enlargement is permanent and that fibrosis
is not a feature.
 Definition of asthma

Asthma is characterized by airway

inflammation that is manifested by airway
hyperresponsiveness to a variety of stimuli
and by airway obstruction that is reversible
spontaneously or in response to treatment;
reversibility may be incomplete in some
patients.

“Asthmatic COPD”
 Definition of COPD

COPD is a disease state characterized

by airflow limitation that is not fully
reversible. The airflow limitation is
usually both progressive and
associated with an abnormal
inflammatory response of the lungs to
noxious particles or gases.
Relationship of chronic bronchilitis, emphysema
and asthma

COPD

Fig 1. Venn diagram illustrating the overlap between the

diagnosis of chronic bronchilitis, emphysema and asthma,and
their contribution to COPD.
Epidemiology
prevalence, incidence, and mortality rates of
COPD increase with age
higher in males than in females
higher in whites than in nonwhites
higher in blue-collar workers than in white-
collar workers
aggregate in families independently of α1 -

antitrypsin (α 1-antiprotease inhibitor)

deficiency
 Fig. 2 Percent Change in Age-Adjusted
Death Rates, U.S., 1965-1998

3.0
Coronary Stroke Other CVD COPD All Other
2.5 Heart Causes
Disease
2.0

1.5

1.0

0.5
–59% –64% –35% +163% –7%
0
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Pathogenesis
Risk Factors

Host Factors

Exposures
Host Factors

Genes (e.g., alpha-1antitrypsin deficiency)

Airway Hyperresponsiveness
Lung Growth
Exposures

Tobacco Smoke
Occupational Dusts and Chemicals
Indoor and Outdoor Air Pollution
Infections
Socioeconomic Status
Pathology
Pathological Changes
Changes of chronic bronchitis
Changes of emphysema
Changes of chronic bronchitis

the submucosal glands are enlarged

squamous metaplasia replace pseudostratified
columnar epithelium
neutrophils and lymphocytes infiltrate
airway smooth muscle hypertrophy
goblet cell metaplasia
the terminal and respiratory bronchioles
distort
 Classification of emphysema

Panacinar emphysema (PAE)

affects all of the acinus

Centrilobular emphysema (CLE)

begins in the respiratory bronchiole and spreads
peripherally
the most common form of emphysema in smokers
 Fig. 3 Pathological Changes of the Peripheral Airways in COPD

(A) a nearly normal airway;

(B) a plug of mucoid exudate in the lumen with little or no evidence of inflammation
in the wall;
(C) the presence of an inflammatory exudate in the wall and lumen of the airway;
(D) an airway with reduced lumen, structual reorganization of the airway wall,
increased smooth muscle, and depostition of peribronchial connective tissue.
 Fig 4.Dissecting microscopic appearance of the cut
surface of a normal(A) and emphysematous(B) lung.
Clinical Manifestations
Symptoms
Cough: always morning
Sputum: usually mucoid

purulent during an exacerbation

Wheezing: when airway infected, there is too

much secretion. It makes airway narrow.

Breathlessness or dyspnea

exertion , progressive
outstanding symptom of COPD
Weight loss ， anorexia
Signs

Early in COPD, physical examination of

the chest may be normal.

As COPD progresses, abnormal signs

become remarkable.
Inspection ： barrel chest ， superficial and
fast respiration, expiration often occurs through
pursed lips
Palpation : tactile fremitus decreases
Percussion: hyperresonant note ，
Auscultation ：
breath sounds are decreased
heart sounds become distant
rhonchi and crackles, often at the lung bases
Laboratory examination
Pulmonary function testing (spirometry)

-------gold standard
 Fig 5. Pulmonary function tests
---Static lung volumes in a normal subject(A) and a patient

with COPD
Fig 6. Time-volume curves showing the FEV1 and FVC in

a normal subject and in patient with COPD

 0
FEV 1 FVC FEV 1/ FVC
Normal 4.150 5.200 80 %
1 COPD 2.350 3.900 60 %

2
FEV 1
Liter

3
COPD
4 FVC
FEV 1

5 Normal
FVC
1 2 3 4 5 6 Seconds
FEV1/FVC
FEV1% predicted

The presence of a postbronchodilator

FEV1 < 80% of the predicted

value in combination with an FEV1/FVC

< 70% confirms the presence of airflow
limitation that is not fully reversible.
Chest radiograph
hypertranslucent lung fields
disorganization of the vasculature
widening of the retrosternal air space
a low and flat diaphragm
bullae (larger than 1cm in diameter
and surrounded by arcuate hairline
shadows)
Arterial blood gas analysis

hypoxemia
hypercapnia
acid-base imbalance
respiratory failure
Sputum examination

Gram stains
 bacteria cultures
 Diagnosis
Differential diagnosis
Key Indicators for Considering a Diagnosis of COPD
Chronic cough: Present intermittently or every day
Often present throughout the day
seldom only nocturnal
Chronic sputum Any pattern of chronic sputum production
production: may indicate COPD
Dyspnea Progressive (worsens over time)
Persistent (present every day)
Described by the patient as an increased

effort to breathe,heaviness, air hunger,

or .gasping
Worse on exercise.
Worse during respiratory infections
History of Tobacco smoke
exposure to Occupational dusts and chemicals
 For the diagnosis and assessment of COPD,
spirometry is the gold standard as it is the most
reproducible, standardized, and objective way of
measuring airflow limitation.

FEV1/FVC < 70% and a postbronchodilator

FEV1 < 80% predicted confirms the presence of
airflow limitation that is not fully reversible.
 Figure 4. Classification of Severity of COPD

Stage Characteristics

0: normal spirometry
At Risk chronic symptoms (cough, sputum production)

I: FEV1/FVC < 70%

Mild COPD FEV1 ≥ 80% predicted
with or without chronic symptoms (cough, sputum production)
II: FEV1/FVC < 70%
Moderate 50% ≤ FEV1 < 80% predicted
COPD with or without chronic symptoms (cough, sputum production)
III: FEV1/FVC < 70%
Severe COPD 30% ≤ FEV1 < 50% predicted
with or without chronic symptoms (cough, sputum production)
IV: FEV1/FVC < 70%
Very Severe FEV1 ≤ 30% predicted or FEV1 < 50% predicted plus chronic
COPD respiratory failure
Staging of COPD
Exacerbation
increased breathlessness, is
often accompanied by wheezing
and chest tightness,
increased cough and sputum,
change of the color and/or
tenacity of sputum,
Stable
feverCOPD
etc.
Differential diagnosis of COPD

• Asthma
• Bronchiectasis
• Tuberculosis
• Carcinoma of the bronchus
• Congestive Heart Failure
COPD Asthma
Onset in mid-life Onset early in life
(often childhood)
Symptoms slowly Symptoms at
progressive night/early
morning
Dyspnea during Allergy, rhinitis,
exercise and/or eczema also
present
Long smoking Family history of
history asthma
 Bronchiectasis

Large volumes of purulent sputum

Commonly associated with bacterial infection

 Coarse crackles/clubbing on auscultation

Chest X-ray/CT shows bronchial dilation,

bronchial wall thickening

Tuberculosis

Onset all ages

Chest X-ray shows lung infiltrate
Microbiological confirmation
High local prevalence of tuberculosis
Treatment
• The aim of treatment
 Control of symptoms
 Prevention of progression
 Maintain suitable lung function
 Improve quality of life
 Manage stable COPD

Education
smoking cessation; reducing risk factors
Bronchodilators ß2-agonist, anticholinergic, theophylline
Mucolytic (mucokinetic, mucoregulator) agents
Oxygen Therapy 1-2 L/min, > 15 hours per
day
PaO2 at or below 55 mm Hg or SaO2 at or below 88%, with
or without hypercapnia
PaO2 between 55 mm Hg and 60 mm Hg, or SaO2 of 89%, if
there is evidence of pulmonary hypertension, peripheral
edema suggesting congestive cardiac failure, or polycythemia
(hematocrit > 55%)
Other Pharmacologic Treatments
Vaccines, Antioxidant agents, Immunoregulators
Manage exacerbations
Assessment of Severity
Bronchodilator Therapy
Antibiotics
Controlled oxygen therapy
nasal catheter ， Venturi
masks
28%-30%

Glucocorticosteroids
Oral or intravenous glucocorticosteroids
Ventilatory support
COPD
as “silent disease”
COPD can be present without significant physical
impairment, particular in early phases

COPD is often not clinically apparent until it is

moderately advanced
 "Breathless not Helpless!"
The Global Initiative for Chronic Obstructive Lung Disease (GOLD)