This document provides an overview of chronic obstructive pulmonary disease (COPD). It defines COPD and its subtypes, and discusses its epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and treatment. COPD is characterized by airflow limitation and includes emphysema and chronic bronchitis. It is caused by cigarette smoking and occupational exposures. Symptoms include cough, sputum production and shortness of breath. Diagnosis is made through spirometry showing reduced airflow. Treatment focuses on smoking cessation, bronchodilators, antibiotics and corticosteroids for exacerbations.

1. Melaku Yitbarek(M.D)
Internal Medicine Unit
March,2018

2. Lecture Outline
• Defintion
• Epidemiology
• Risk factors
• Pathophysiology
• Clinical Presentation
• Diagnosis
• Treatment

3. Definition
 Chronic obstructive pulmonary disease (COPD) is
defined as a disease state characterized by airflow
limitation that is not fully reversible
 COPD includes emphysema, an anatomically defined
condition characterized by destruction and
enlargement of the lung alveoli;
 chronic bronchitis,a clinically defined conditionWith
chronic cough and phlegm; and small airways
disease,a condition in which small bronchioles are
narrowed

4. Definition…

5. Epidemiology
• COPD is the third leading cause of death and affects >10 million
persons in the United States
• COPD is also a disease of increasing public health importance
around the world.
• Estimates suggest that COPD will rise from the sixth to the third
most common cause of death worldwide by 2020.
• In Ethiopia, no adequate epidemiologic data.
• COPD accounted for 3.6% of chest clinic visit at TASH ( 2014)

6. Risk factors
• Cigarette smoking-pack year(dose X years) ↓FEV1 faster
• Airway responsive as in asthma(genetic predisposition)
• Respiratory infections-childhood(initiate/exacerbate)
• Occupational exposure-dust,gold,↓FEV1
• Air pollution town>rural,↑Women( indoor pollution)
• +/_ genetic /environmental+passive
• Genetic –α1 antitrypsin deficiency(emphysema)

7. Pathophysiology

8. release
Inflammatory Process in COPD
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343:269-280.
activates
Neutrophils
Macrophages in
respiratory
tract
Proteases stimulate
release
Parenchymal
Destruction

10. Causes of Airflow
Limitation
 Irreversible
Fibrosis and narrowing of the airways
Loss of elastic recoil due to alveolar destruction
 Destruction of alveolar support that maintains patency
of small airways
 Reversible
Accumulation of inflammatory cells, mucus, and
plasma exudate in bronchi
Smooth muscle contraction in peripheral and
central airways
Dynamic hyperinflation during exercise

11. Pathophysiology in Chronic
bronchitis

12. Normal versus Diseased
Bronchi

13. Pathophysiology in Emphysema

14. Pathophysiology in Emphysema

15. Emphysema

16. Not only smoking but
smoke
Air pollution resulting from the burning
of wood and other biomass fuels is
estimated to kill two million women
and children each year.

17. Natural History
 The effects of cigarette smoking on pulmonary function
appear to depend on the intensity of smoking exposure, the
timing of smoking exposure during growth, and the
baseline lung function of the individual
 The rate of decline in pulmonary function can be modified
by changing environmental exposures (i.e., quitting
smoking), with smoking cessation at an earlier age
providing a more beneficial effect than smoking cessation
after marked reductions in pulmonary function have
already developed.
 Genetic factors likely contribute to the level of pulmonary
function achieved during growth and to the rate of decline
in response to smoking and potentially to other
environmental factors as well

18. Clinical Presentation
History:
 The three most common symptoms in COPD are cough,
sputum production,and exertional dyspnea
 Many patients have such symptoms for months or years
before seeking medical attention.
 Activities involving significant arm work, particularly at or
above shoulder level, are particularly difficult for patients
with COPD
 In the most advanced stages, patients are breathless doing
simple activities of daily living
 Patients may also develop resting hypoxemia and require
institution of supplemental oxygen

19. Clinical Presentation
Physical findings:
 In the early stages of COPD, patients usually have an
entirely normal physical examination
 In patients with more severe disease, the physical
examination is notable for a prolonged expiratory
phase and may include expiratory wheezing.
 In addition, signs of hyperinflation include a barrel
chest and enlarged lung volumes with poor
diaphragmatic excursion as assessed by percussion
 Patients with severe airflow obstruction may also
exhibit sitting in “Tripod postion”

20. Clinical Presenatation
Physical findings:
• Patients may develop cyanosis, visible in the lips and
nail beds
• Advanced disease may be accompanied by cachexia,
with significant weight loss, bitemporal wasting
• Clubbing of the digits is not a sign of COPD, and its
presence should alert the clinician to initiate an
investigation for causes of clubbing.

21. Laboratory findings
 The hallmark of COPD is airflow obstruction
 Pulmonary function testing shows airflow obstruction
with a reduction in FEV1 and FEV/FVC
 With worsening disease severity, lung volumes may
increase, resulting in an increase in total lung
capacity,functional residual capacity, and residual
volume

22. Spirometry

23. Spirometry
Volume,liters
Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV1 = 1.8L
FVC = 3.2L
FEV1/FVC = 0.56
Normal
Obstructi
ve

26. Treatment
Stable phase COPD:
 Only three interventions :smoking cessation, oxygen
therapy in chronically hypoxemic patients, and lung
volume reduction surgery in selected patients with
emphysema—have been demonstrated to influence
the natural history of patients with COPD
 All other current therapies are directed at improving
symptoms and decreasing the frequency and severity
of exacerbations

27. Tx…
Pharmacotherapy:
• Smoking cessation
• Bronchodilators
• Anticholinergics
• Beta agonists
• Inhaled corticosteroids
• Oral corticosteroids
• Theophyline
• O2: has mortality benefit

28. Tx
COPD Exacerbations:
 Exacerbations are a prominent feature of the natural
history of COPD.
 Exacerbations are episodes of increased dyspnea and cough
and change in the amount and character of sputum
 The approach to the patient experiencing an exacerbation
includes an assessment of the severity of the patient’s
illness, both acute and chronic components; an attempt to
identify the precipitant of the exacerbation; and the
institution of therapy.

29. Tx…
Acute COPD Exacerbations:
• Bronchodilators: Inhaled Beta agonists with
anticholinergic agents
• Antibiotics: azithromycine
• Glucocorticoids:
• Oxygen
• Mechanical Ventilatory support: In pts with
respiratory failure, decrease mortality rate

30. Referrences
 Harrison’s Principles of Internal Medicine,19th Edition
 Standard Treatment Guideline for general Hospital
2014
 Uptodate 21.6

31. Thank You…