Chronic Obstructive Pulmonary Disease .: Swathi Swaroopa. B

CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
by Dr.Swathi Swaroopa. B
MORPHOLOGY OF LUNGS
INTRODUCTION
 Chronic obstructive pulmonary disease (COPD) is 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.
 Cigarette smoking (> 20 PACK YEAR)is the primary cause of

COPD
 Chronic obstructive pulmonary disease generally refers to

Emphysema or Chronic bronchitis.
 Emphysema is characterized by alveolar wall destruction and
abnormal, permanent enlargement of air–space.
 Chronic bronchitis associated with chronic or recurrent

excess mucus secretion into the bronchial tree with chronic
cough for at least 3 months for 2 consecutive years.
PATHOLOGICAL CHANGES
Effect 4 different compartments of lungs:
• Central airways
• Peripheral airways
• Lung parenchyma ( Bronchioles, alveoli, capillaries)
• Pulmonary vasculature
PATHOPHYSIOLOGY
• Noxious Agent
• Inflammation
• Hyperinflation and Hypersecretion
• Airflow Obstruction
• Gas exchange abnormalities
1. Noxious particles and gas inhalation
Activation of neutrophils, macrophages, and CD8 + lymphocytes,
Release tumor necrosis factor-α , interleukin-8, and leukotriene B
Inflammation
Increased number and size of goblet cells and mucus glands
Smooth muscle& connective tissue thickening in airways
Scarring and fibrosis.

2.Oxidative stress
Increased oxidants
Damage various proteins and lipids
Cell and tissue damage.
OXIDANTS Promote inflammation
Inhibit antiprotease activity.
Increase protease-antiprotease imbalance

Proteases and antiproteases imbalance
• Antiprotease a1-antitrypsin (AAT) is an antiprotease enzyme
which inhibit the proteases (neutrophil elastase).
• Neutrophil elastase is a potent elastolytic enzyme that attack elastin

which leads to tissue damage and loss of elasticity.
• Elastin is a major component of alveolar walls.
• Cigarette smoke activate and attract inflammatory cells into the

lung, thereby promoting the release of proteases such as elastase.
• Other proteases, including cathepsins and metalloproteinases.
• A hereditary deficiency of AAT results in an increased risk for

premature development of emphysema.
BRONCHIAL WALL
CHRONIC BRONCHITIS
 Excess mucous secretions

 Inflamated lung endothelium
 Damaged cilia
 Tissue destruction
 Airway obstruction
 Decreases gas exchange
 Infections
 Hypoxemia
 Pulmonary hypertension
 Polycythemia
EMPHYSEMA
 Destructive enlargement of air sacs

 Dilation and destruction
 Impaired gas exchange
 Breakdown of elastin
 Loss of elasticity
 Lack of alpha1 anti trypsin
2 types
CENTRILOBULAR:
Dilation & destruction of bornchioles,
alveolar ducts, alveoli. In COPD
PANACINAR:
Destruction of whole acinus ( airway
ending). In alpha1 antitrypsin
deficiency.
• Centrilobular emphysema that primarily affects respiratory
bronchioles
• Panlobular emphysema is seen in AAT deficiency and extends to

the alveolar ducts and sacs.
PINK PUFFERS BLUE BLOATERS
EMPHYSEMA CHRONIC BRONCHITIS

STRUCTURAL CHANGES IN ALVEOLI
RISK FACTORS
Host Factors
• Genetic predisposition (alfa1-antitrypsin)
• Airway hyper responsiveness
• Impaired lung growth
Exposures
• Environmental tobacco smoke
• Occupational dusts and chemicals
• Air pollution
AETIOLOGY
1. Smoking
Major cause of COPD and risk increases
pack years = Number of cigarettes per day x number of years smoked ÷ 20
2. Age
Increasing age results in ventilatory impairment
3. Gender
Women have greater airway reactivity and experience faster declines in
FEV1 and are at more risk than men.
4. Occupation
Coal and gold mining, cement & cotton industries, farming
and grain handling.
Aetiology …
5. Genetic factor
Deficiency of α1 antitrypsin ( strongest risk factor)
Genetic disorders involving tissue necrosis factor,
6. Air pollution
Death rates are higher in urban areas than in rural areas
Indoor air pollution from burning fuel biomass ( In underdeveloped
areas)
7. Socio-economic status
More common in individuals of low socio-economic status
8. Airway- hyper responsiveness &allergies

Smokers show high IgE & eosnophils & airway hyper responsiveness
SYMPTOMS
• Chronic cough
• Dyspnea
• Sputum production
• Bluish discoloration of lips and nail beds
• Increased resting respiratory rate
• Shallow breathing
• Pursed lips during expiration
• Weight loss
SPIROMETER

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CHRONIC OBSTRUCTIVE

 The airflow limitation is usually both progressive and associated

 Cigarette smoking (> 20 PACK YEAR)is the primary cause of

 Chronic obstructive pulmonary disease generally refers to

 Chronic bronchitis associated with chronic or recurrent

Activation of neutrophils, macrophages, and CD8 + lymphocytes,

Release tumor necrosis factor-α , interleukin-8, and leukotriene B

Increased number and size of goblet cells and mucus glands

Smooth muscle& connective tissue thickening in airways

Scarring and fibrosis.

Damage various proteins and lipids

Cell and tissue damage.

OXIDANTS Promote inflammation

Inhibit antiprotease activity.

Increase protease-antiprotease imbalance

• Neutrophil elastase is a potent elastolytic enzyme that attack elastin

• Elastin is a major component of alveolar walls.

• Cigarette smoke activate and attract inflammatory cells into the

• Other proteases, including cathepsins and metalloproteinases.

• A hereditary deficiency of AAT results in an increased risk for

 Excess mucous secretions

 Destructive enlargement of air sacs

• Panlobular emphysema is seen in AAT deficiency and extends to

EMPHYSEMA CHRONIC BRONCHITIS

8. Airway- hyper responsiveness &allergies

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