Chronic Obstructive Pulmonary Disease (COPD) is an irreversible lung disease characterized by limited airflow and an abnormal inflammatory response in the lungs caused by long-term exposure to harmful particles like cigarette smoke. The main symptoms are breathlessness, cough, and wheezing. Diagnosis is based on a history of symptoms and cigarette smoking, and confirmed with lung function tests showing reduced airflow. Treatment focuses on smoking cessation and drug therapy with bronchodilators and corticosteroids to manage symptoms and reduce exacerbations.

1. Chronic Obstructive Pulmonary Disease
Dr. Mazen Al Zo’ubi
Rheumatology and Internal Medicine Senior
Specialist

2. Definition
COPD is an irreversible lung disease characterized by limited airflow
It is progressive and accompanied by an abnormally inflammatory
response of the lungs to toxic substances or gases
Emphysema, small airways disease, and chronic bronchitis are grouped
under the umbrella diagnosis of COPD
Lung hyperinflation, ventilation/perfusion mismatch, increased work of
breathing, and dyspnea follow as a result
The presence of several comorbidities, including cancer, ischemic heart
disease, hypertension, diabetes, and heart failure, suggests that the
condition could be a result of a broad systemic inflammatory response.

3. Epidemiology and Aetiology
Long-term exposure to
harmful chemicals and
particles results in COPD
Over 90% of cases in
developed nations involve
smoking cigarettes
Biomass heating fuels and
cooking smoke in poorly
ventilated locations, play a
role in developing nations
Only 10–20% of smokers
experience the development
of COPD, indicating a
possible underlying
individual predisposition

4. Pathophysiology
Structurally, there may be
evidence of emphysema and
small airways disease, with
increased mucus-producing
goblet cells in the bronchial
mucosa, which may lead to
chronic bronchitis
Pathologically, there is
evidence of both acute and
chronic inflammation
This chronic inflammation
results in scarring and fibrosis
of the small airways. In
addition, there is destruction
of the alveolar walls, which
results in emphysema.

5. Emphysema
It is an abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by
destruction of their walls.
Distension and damage of lung
tissue are concentrated around
the respiratory bronchioles
Distension and destruction affect
the whole acinus, and in severe
cases the lung is just a collection of
bullae
There is scarring and damage that
affect the lung parenchyma
patchily, independent of acinar
structure

6. Pathogenesis
Cigarette smoking
1) Imbalance between protease
and antiprotease activity
2) Mucous gland hypertrophy
Infections
precipitating cause of acute
exacerbations
α-1 antitrypsin
Deficiency
1) It is a proteinase inhibitor.
2) Inhibits proteolytic enzymes
such as neutrophil elastase,
which can destroy alveolar wall
connective tissue.

7. Symptoms
Breathlessness
Productive cough
Wheeze

8. Signs
Early disease
• Asymptomatic
• Quit wheeze
Severe disease
• Tachypnoea
• Prolonged expiration
• Accessory muscle use
• Lips purse
• Reduced cricosternal
distance
• Poor chest expansion
Advanced disease
• Signs of right heart
failure

9. Signs

10. Diagnosis
This is usually clinical
and based on a history
of breathlessness and
sputum production in
a chronic smoker.
In the absence of a
history of cigarette
smoking, asthma is a
more likely
explanation, unless
there is a family
history suggesting α1-
antitrypsin deficiency.

11. Investigations
Show evidence of airflow limitation (FEV1:FVC ratio is reduced)
Often normal
Over-inflation
Flattened diaphragms
Sometimes the presence of large bullae
Useful, particularly when the CXR is normal
helpful to determine if there is any evidence of respiratory failure
worth measuring in premature disease or lifelong non-smokers

12. Classification of airflow limitation severity in
COPD (based on post-bronchodilator FEV1)
Global Initiative for Chronic Obstructive Lung Disease
(GOLD)

13. Management
Healthcare
• The single most useful measure
• Smoke from burning biomass fuels in poorly
ventilated homes should also be reduced
Smoking cessation
• single dose of the polyvalent pneumococcal
polysaccharide vaccine
• Yearly influenza vaccinations
Vaccines

14. Management
Drug therapy
• Mild COPD: short-acting β2 agonist
• Moderate and severe COPD: long-acting β2 agonist
β-Adrenoceptor agonists
• Regular use of a LAMA (such as inhaled tiotropium) improves lung function, symptoms of
dyspnea and quality of life
• Use of a LAMA does not prevent the decline in FEV1
Antimuscarinic drugs
• It is used as an adjunct to bronchodilators for maintenance treatment in those patients with
an FEV1 of less than 50% and chronic bronchitis
Phosphodiesterase type 4
inhibitors
• Inhaled corticosteroids are recommended in patients with frequent exacerbations or a FEV1
of less than 50% predicted
• Demonstration of a blood eosinophilia may identify patients who are more likely to have a
beneficial response to inhaled corticosteroid therapy
Corticosteroids
• Long-acting preparations of theophylline are of little benefit
Theophyllines

15. Management
Oxygen therapy
PaO2 of <7.3 kPa (55 mmHg) when breathing air; measurements should be taken
on two occasions at least 3 weeks apart after appropriate bronchodilator therapy
PaO2 of <8 kPa with secondary polycythemia, nocturnal hypoxemia, peripheral
oedema or evidence of pulmonary hypertension
Carboxyhemoglobin of <3% (i.e., patients who have stopped smoking).
Domiciliary oxygen is best provided via an oxygen concentrator

16. Algorithm for
the treatment
of chronic
obstructive
pulmonary
disease