COPD

Definition
COPD is defined as a disease state characterized
by the presence of airflow obstruction due to
chronic bronchitis or emphysema.
The airflow obstruction generally is progressive,
may be accompanied by airway hyperreactivity,
and may be partially reversible.
 Definition
Chronic bronchitis is defined clinically as the
presence of a chronic productive cough for 3
months during each of 2 consecutive years (other
causes of cough were excluded).
 Definition
Emphysema is defined as an abnormal, permanent
enlargement of the air spaces distal to the terminal
bronchioles accompanied by destruction of their walls
and without obvious fibrosis.
Chronic bronchitis is defined in clinical terms, and
emphysema is defined in terms of anatomic pathology.
 Emphysema
Emphysema, on the
other hand, is
characterized by
focal destruction
limited to the
airspaces distal to
the respiratory
bronchioles.
 Types
3 described morphological types of
emphysema are centriacinar, panacinar, and
paraseptal.
centriacinar emphysema, begins in the
respiratory bronchioles and spreads
peripherally.
Also called centrilobular emphysema, this
form is associated with long-standing
cigarette smoking and predominantly involves
the upper half of the lungs.
 Panacinar emphysema,
Destroys the entire alveolus uniformly
and is predominant in the lower half of the
lungs.
This type of emphysema generally is
observed in patients with homozygous
alpha1-antitrypsin (AAT) deficiency.
In people who smoke, focal panacinar
emphysema at the lung bases may
accompany centriacinar emphysema.
 Distal acinar emphysema
Paraseptal emphysema
Preferentially involves the distal airway
structures, alveolar ducts, and alveolar sacs.
The process is localized around the septae of
the lungs or pleura.
Although airflow frequently is preserved, the
apical bullae may lead to spontaneous
pneumothorax.
Giant bullae occasionally cause severe
compression of adjacent lung tissue.
 Vascular changes
Develop simultaneously.
Abnormal longitudinal muscle appears in
the intima of arterioles and arteries; these
may show intimal fibrosis and thickening of
the muscular media.
Enlargement of bronchial arteries and veins
occurs in some patients.
Bronchial venous enlargement may cause
shunting of systemic venous blood to the
left atrium.
Pathogenesis of COPD
NOXIOUS AGENT
(tobacco smoke, pollutants, occupational agent)

Genetic factors
Respiratory
infection
COPD Other
 Noxious particles
and gases
Host factors

Lung inflammation
Anti-oxidants Anti-proteinases

Oxidative stress Proteinases

Repair mechanisms

COPD pathology
 INFLAMMATION

Small airway disease Parenchymal destruction

Airway inflammation Loss of alveolar attachments
Airway remodeling Decrease of elastic recoil

AIRFLOW LIMITATION
 ASTHMA COPD
Sensitizing agent Noxious agent

Asthmatic airway inflammation COPD airway inflammation

CD4+ T-lymphocytes CD8+ T-lymphocytes
Eosinophils Macrophages
Neutrophils

Completely Airflow limitation Completely

reversible irreversible
 Pathogenesis
Cigarette smoking
Cigarette smoking leads to neutrophil
activation and retention in the lung
parenchyma.
A number of neutrophil-derived and
macrophage-derived enzymes known
as proteinases and elastases (ie,
proteolytic enzymes) can destroy
various components of the
extracellular matrix of the lung and
cause emphysema..
Age of initiation, total pack years, and
current smoking status predict COPD
mortality.
Smokers have a greater annual decline in
FEV1. Overall, tobacco smoking accounts
for as much as 90% of the risk.
Secondhand smoke or environmental
tobacco smoke increases the risk of
respiratory infections, augments asthma
symptoms, and causes a measurable
reduction in pulmonary function.
 Air pollution
Although the role of air pollution in the etiology of
COPD is unclear, the effect is small when
compared to cigarette smoking.
The use of solid fuels for cooking and heating may
result in high levels of indoor air pollution and the
development of COPD.
Airway hyperresponsiveness

Airway hyperresponsiveness (ie,

Dutch hypothesis) stipulates that
patients who have nonspecific
airway hyperreactivity and who
smoke are at increased risk of
developing COPD with an
accelerated decline in lung function.
 Alpha1-antitrypsin deficiency
AAT is a glycoprotein that is synthesized in the
liver and is secreted into the blood stream.
The main purpose of this is to neutralize
neutrophil elastase in the lung interstitium and to
protect the lung parenchyma from elastolytic
breakdown.
 Alpha1-antitrypsin deficiency
Severe AAT deficiency predisposes to unopposed
elastolysis with clinical sequela of early onset of
panacinar emphysema.
Deficiency of AAT is inherited as an autosomal
codominant condition. The gene is located on the
long arm of chromosome 14
 Persons who use
intravenous drugs
Emphysema occurs in approximately 2% of
persons who use intravenous drugs and is
attributed to pulmonary vascular damage that
results from the insoluble filler
Methadone or methylphenidate.
IV use of cocaine or heroin
Evolution of chronic bronchitis &
emphysema
 Bronchitis Emphysema
General Mesomorphic, Thin, emaciated,
overweight,suffused pursed lip
appearance conjuctiva, warm breathing,prominent
extremities use of acessory
muscles, normal or
cool extremities

Age 40-55 50-75

Onset Cough Dyspnea
Cyanosis Marked Slight to none
Cough More evident than Less evident than
dyspnea dyspnea
Sputum copious Scanty
 Bronchitis Emphysema
URI Common Occasional
Breath sounds Moderately Markedly diminished
diminished
Cor-pulmonale/ RHF common Only during
infection/ terminally

CXR Normal diaphram / Small tubular heart/

cardiomegaly/ lungs- low flat diaphram /
normal or increased areas of
markings hypertranslucency
 Bronchitis Emphysema
Course Ambulatory Severs
Always on verge of breathlessness/ life
RHF / coma threatening URI /
RVF/ coma
Reduced Reduced
FEV1/ FVC
Normal or slightly Markedly increased
FRC/ TLC/ RV
increased

Lung compliance Normal or low Low

MVV Mod. Decreased Markedly decreased
Airway resistance Increased Normal or slightly
increased
DLCO Normal or low Low
 Bronchitis Emphysema
Arterial PO2 Mod. To severely Low to mod.
decreased Reduced
Hypercapnia Chronic Only during ac.
Resp. infection
Hematocrit High Normal or slightly
high

Pulmonary arterial Increased Normal or slightly

pressure high