Disease of COPD

Zulkarnain Arsyad
Pulmonology Subdivison
of Internal Medicine Medical Faculty
Andalas University M Djamil Hospital
Padang

INTRODUCTION
COPD is the 4thth leading cause of death in the United
States (behind heart disease, cancer, and
cerebrovascular disease).
In 2000, the WHO estimated 2.74 million deaths
worldwide from COPD.
In 1990, COPD was ranked 12thth as a burden of
disease; by 2020 it is projected to rank 5thth.
In Indonesia COPD in the no 6thth of leading cause of
death

Definition
Airflow limitation that is NOT fully
reversible

Progressive
Associated with an abnormal inflammatory
response of the lungs to noxious particles or
gases

Pathogenesis
Three processes:

Oxidative stress
Imbalance of proteinases and anti-proteinases
Chronic inflammation

Cigarette smoke
Biomass particles
Particulates

Pathogenesis of
COPD
Host factors
Amplifying mechanisms

LUNG INFLAMMATION
Anti-oxidants

Oxidative
stress

Anti-proteinases

Proteinases
Repair
mechanisms

COPD PATHOLOGY
Source: Peter J. Barnes,

Chronic Inflammation
Chronic inflammation in airways,
parenchyma, pulmonary vasculature
Inflammatory cells involved are:

Macrophages
T-lymphocytes (CD8)
Neutrophils

leukotriene B4
interleukin 8
TNF-

Inflammatory Cells Involved in

COPD
Cigarette smoke
(and other irritants)

Epithelial
cells

Alveolar
macrophage
Chemotactic factors

CD8+
Fibroblastlymphocyte

Neutrophil

Monocyte
Neutrophil elastase

PROTEASES Cathepsins
MMPs

Mucus hypersecretio
Fibrosis Alveolar wall destruction
(Emphysema)
(Obstructive
bronchiolitis)
Source: Peter J. Barnes,
MD

Risk Factors
Tobacco Smoke

Cigarettes,
Pipes, cigars lower rates than
cigarette smokers but higher
than non-smokers

Occupational dusts and

chemicals

Vapors, irritants, fumes

Need sufficiently intense or

prolonged exposure

Indoor air pollution

Biomass fuel used for cooking

and heating in poorly vented
dwellings

Outdoor air pollution

Minor risk factor Passive

cigarette smoke exposure

Respiratory infections in early

childhood
Lower socioeconomic status

association with COPD

May be secondary to crowding,
poor nutrition, etc.

Risk Factors for

COPD
Nutrition
Infections
Socio-economic
status

Aging Populations

Pathology
Central Airways:

Enlarged mucus secreting

glands
Increase in goblet cells
Mucus hypersecretion

Peripheral Airways

Repeated cycles of injury

and repair

Increased collagen/scarring
in airway wall

Pathology
Pulmonary vascular changes
Thickening of vessel wall (intima)
Increase in smooth muscle
Infiltration of vessel wall by inflammatory cells
As COPD worsens, more smooth muscle, proteoglycans and
collagen further thicken the vessel wall

Changes in Lung Parenchyma in

COPD
Alveolar wall destruction

Loss of elasticity
Destruction of pulmonary
capillary bed
Inflammatory cells
macrophages, CD8+ lymphocytes
Source: Peter J. Barnes, MD

Pathophysiology
Mucus hypersecretion
Ciliary dysfunction
Airflow limitation
Pulmonary hyperinflation
Gas exchange abnormalities
Pulmonary hypertension
Cor pulmonale

Mucus hyperserection & ciliary dysfunction cough, sputum production

Medical History
Exposure to risk factors, incl.
intensity/duration
History of exacerbations or previous
hospitalizations for respiratory
disorder
Past medical history

Asthma, allergies, sinusitis/nasal

polyps, respiratory infections in
childhood
Presence of co-morbid conditions

Heart disease
Rheumatic disease

Family History

COPD
Other chronic respiratory diseases

Social History

Impact of disease on patients life,

inc. activity, missed work and
economic impact
Effect on family routines
Depression/anxiety
Social and family support available
to the patient

Other:

Appropriateness of current medical

treatments
Possibilities for reducing risk
factors, esp. smoking cessation

History of Present Illness

Chronic Cough

Intermittently or every day

Present throughout the day;
seldom only nocturnal

Chronic sputum production

Any pattern

Repeated episodes of acute

bronchitis

Dyspnea on exertion

History of exposure to risk

factors

Chronic cough and sputum production often precede development

of airflow limitation by many years

Not all patients with these symptoms develop

COPD

Progressive
Persistent
Worse with exercise
Worse during respiratory
infections

Tobacco smoke
Occupational dusts and
chemicals
Smoke from home cooking and
heating fuels

Physical Examination
Thorax:

Barrel chest

Lungs

Decreased breath sounds

Wheezing

Cardiac

Right-sided heart failure

Edema, tender liver,

distended abdomen
Physical signs are rarely apparent
until significant impairment of lung
function has occurred

Diagnostic Tests
Chest X-ray

Flattened diaphragms
Use to exclude other diagnoses

High resolution CT

Not routinely recommended

If in doubt about diagnosis of
COPD
If considering bullectomy or lung
volume reduction surgery

CBC

May see increased

hemoglobin/hematocrit secondary to
hemoconcentration

ABG
Spirometry

Spirometry
Measure of FVC and FEV1

FVC = forced vital capacity

Maximum volume of air forcibly exhaled from the point of maximal

inhalation

FEV1 = forced expiratory volume in 1 second

Volume of air exhaled in the 1st second of the FVC maneuver

Calculate the FVC/FEV1 ratio

Normal ratio = 70/80%

COPD ratio = <70% pre-bronchodilator
COPD ratio = <80% post-bronchodilator

FVC & FEV are

both decreased

Essential to making the diagnosis of COPD

Stage I:

Classification of COPD
Severity
by
Spirometry
Mild
FEV /FVC < 0.70
1

FEV1 > 80% predicted

Stage II: Moderate

FEV1/FVC < 0.70

50% < FEV1 < 80% predicted

Stage III: Severe

FEV1/FVC < 0.70

30% < FEV1 < 50% predicted

Stage IV: Very Severe

FEV1/FVC < 0.70

FEV1 < 30% predicted or
FEV1 < 50% predicted plus

Differential Diagnosis of
COPD
Asthma

Reversible airflow limitation

Early onset (childhood)
Symptoms vary day to day

Congestive heart failure

Volume restriction, NOT airflow

limitation
CXR with dilated heart, pulmonary
edema

Bronchiectasis

Large volumes of purulent sputum

Commonly associated with bacterial
infection
Bronchial dilation and bronchial
wall thickening on CXR or CT

Tuberculosis

Onset at all ages

Chest x-ray with infiltrate or
nodular lesions

Obliterative bronchiolitis

Younger patients/non-smokers
May have a hx of rheumatoid
arthritis or fume exposure
CT shows hypodense areas with
expiration

Diffuse panbronchiolitis

Male/non-smokers
Chronic sinusitis
CXR and high resolution CT show
diffuse small centrilobular nodular
opacities and hyperinflation

COPD Management Program

GOLD (Global Initiative for Chronic
Obstructive Lung Disease)
Guidelines

Goals

Prevent disease progression

Relieve symptoms
Improve exercise tolerance
Improve health status
Prevent and treat complications
Prevent and treat exacerbations
Reduce mortality
Prevent or minimize side effects from treatment
Cessation of cigarette smoking

General Principles
Determine disease severity
Implement step-wise
treatment plan
Educate the patient

Improve skills
Improve ability to cope with
illness
Improve health status

Prescribe Treatment

Pharmacologic
Non-pharmacologic

Rehabilitation
Exercise training
Nutrition counseling
education
Oxygen therapy

Surgical interventions

GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention