COPD

INTRODUCTION
• airflow limitation that is not fully reversible

• includes emphysema, an anatomicallydefined condition-

destruction and enlargement of the lung alveoli

• chronic bronchitis, a clinically defined condition with chronic

cough and phlegm; and

• small airways disease, a condition in which small bronchioles

are narrowed
 PATHOGENESIS
• Airflow limitation- the major physiologic change in COPD,

• can result from both small airway obstruction and

emphysema

• pathogenesis of emphysema comprises four interrelated

events
 Pathogenesis contd…..
(1) Chronic exposure to cigarette smoke leads to inflammatory
and immune cell recruitment within the terminal air spaces
of the lung

2) These inflammatory cells release elastolytic and other

proteinases that damage the extracellular matrix of the lung
 Pathogenesis contd….
(3) Structural cell death (endothelial and epithelial cells) occurs
directly through oxidant-induced cigarette smoke damage
and senescence as well as indirectly via proteolytic loss of
matrix
attachment.

(4) Ineffective repair of elastin and other extracellularmatrix

components result in air space enlargement that defines
pulmonary emphysema.
 PATHOPHYSIOLOGY
• Airflow limitation---determined by spirometry

• volume of air exhaled withinthe first second of the forced

expiratory maneuver (FEV1)

• total volume of air exhaled during the entire spirometric

maneuver (forced vital capacity [FVC])
 Pathophysiology contd…
• “air trapping”

• progressive hyperinflation

• partial pressure of oxygen in arterial blood (Pao2) usually

remains near normal until the FEV1 is decreased to ~50%

• An elevation of arterial level of carbon dioxide (Paco2) is not

expected until the FEV1 is <25%
 Pathophysiology contd…
• some patients will develop significant pulmonary
hypertension independent of COPD severity
 RISK FACTORS
• CIGARETTE SMOKING

• AIRWAY RESPONSIVENESS AND COPD-many patients with

COPD also share this feature of airway hyperresponsiveness,
Asthma is viewed as largely an allergic phenomenon, whereas
COPD results from smoking-related inflammation and
damage.
 Risk factors contd….
• RESPIRATORY INFECTIONS- important causes of
exacerbations
of COPD
association of both adult and childhood respiratory infections
with the development and progression of COPD remains to be
proven.

• OCCUPATIONAL EXPOSURES-
coal mining, gold mining, and cotton textile dust, have been
suggested as risk factors for chronic airflow obstruction
 Risk factors contd….
• AMBIENT AIR POLLUTION-

Prolonged exposure to smoke produced by biomass

combustion—significant risk factor among women

the relationship of air pollution to chronic airflow obstruction

remains unproved
 Risk factors contd….
• PASSIVE, OR SECOND-HAND, SMOKING EXPOSURE

• GENETIC CONSIDERATIONS-
Severe α1AT deficiency is a proven genetic risk factor for
COPD
 CLINICAL PRESENTATION
• three most common symptoms in COPD are

cough,

sputum production,and

exertional dyspnea
 Clinical presentation contd…
• PHYSICAL FINDINGS:

early stages of COPD- normal physical examination

more severe disease,- prolonged expiratory phase and may

include expiratory wheezing

signs of hyperinflation include a barrel chest

 Clinical presentation contd…
• severe airflow obstruction-accessory muscles of respiration,
sitting in the characteristic “tripod” position to facilitate the
actions of the sternocleidomastoid, scalene, and intercostal
muscles
• may develop cyanosis,
• most patients have elements of both bronchitis and
emphysema
• physical examination does not reliably differentiate the two
entities
 Clinical presentation contd…
• Advanced disease may be accompanied by cachexia,

• Signs of overt right heart failure, termed cor pulmonale

• Clubbing of the digits is not a sign of COPD

 LABORATORY FINDINGS

• Reduction in FEV1 and FEV1/FVC

• lung volumes may increase, resulting in an increase in total

lung capacity, functional residual capacity, and residual
volume

• Arterial blood gases and oximetry may demonstrate resting or

exertional hypoxemia.
 TREATMENT
• Smoking Cessation-significant improvement in the rate of
decline in pulmonary function,

• Bronchodilators

• Anticholinergic Agents

• Beta Agonists

• Inhaled Glucocorticoids

• Oral Glucocorticoids
 Treatment contd…
• Theophylline

• Antibiotics

• Oxygen

• For patients with resting hypoxemia (resting O2 saturation

≤88% or <90% with signs of pulmonary hypertension or right
heart failure),
 Treatment contd…
• NONPHARMACOLOGIC THERAPIES:

• Influenza vaccine annually

• Polyvalent pneumococcal vaccine is also recommended

• Pulmonary Rehabilitation

• Lung Volume Reduction Surgery (LVRS)

• Lung Transplantation