DEFINITION

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable

disease state characterized by airflow limitation that is not fully reversible.1,2 The
airflow limitation is usually both progressive and associated with an abnormal
response of the lungs to noxious particles and gases, primarily caused by cigarette
smoking.
COPD encompasses the clinical disorders of chronic bronchitis and emphysema,
occasionally with elements of bronchiectasis. Cystic fibrosis is a chronic obstructive
pulmonary disease but is not grouped under the COPD spectrum because of its
unique genetic etiology (ie, mutations in the cystic fibrosis transmembrane
conductance regulator [CFTR] protein that affect the chloride channel in exocrine
cells).
Chronic bronchitis is clinically defined by a mucusproducing cough most days of
the month, 3 months of a year for 2 successive years without other underlying
disease to explain the cough.
Emphysema is anatomically defined by abnormal enlargement and inflammatory
destruction of the alveolar walls, ducts, and sacs distal to the small-airway terminal
bronchioles.
Each lung lobule contains approximately 5000 alveoli. The commonest form of
emphysema is the centrilobular (centriacinar) pattern primarily involving the upper
lung lobes. Panlobular (panacinar) emphysema is an anatomical variant involving
destruction of alveolar structures throughout lung lobules in all lung fields,
particularly the bases and is common in smoking subjects with 1-antitrypsin (AAT)
deficiency.
Bronchiectasis is characterized by abnormal dilation of the central and/or
peripheral airways, generally with associated abnormalities in mucociliary
clearance.
EPIDEMIOLOGY
COPD is the fourth leading cause of death in subjects >45 years of age in the
United States and the fourth most frequent cause of death worldwide.1,2 Compared
with declining age-adjusted mortality rates from 1965 1998 for other major chronic
diseases such as coronary heart disease and stroke, COPD-related mortality
increased by 163%.1
Smoking is the commonest risk factor for COPD; approximately 80% to 90% of
COPD deaths are caused by smoking. Female smokers are nearly 13 times as likely
to die from COPD as women who never smoked. In 2000, for the first time, the
number of deaths in the United States from COPD was greater in women than in

men. Male smokers are nearly 12 times as likely to die from COPD as men who
never smoked.3
In 2003, 10.7 million U.S. adults were estimated to have COPD.3 However, close to
24 million U.S. adults with active or previous smoking histories have evidence of
obstructive lung dysfunction, suggesting that COPD is underdiagnosed.
Inhaled tobacco smoke causes airway and lung inflammation. However, clinically
overt, progressive COPD does not develop in approximately 60% of patients with
significant smoking histories. As approximately 40% of those with previous or
ongoing tobacco abuse do not develop COPD, diagnostic spirometry and/or
additional pulmonary function tests of bronchodilator responsiveness, lung volume
determinations, and diffusion

Risk Factors for COPD

HOST
FACTORS
Genetic factors
Gender
Airway
reactivity
IgE and
asthma

EXPOSURES
Smoking
Socioeconomic status
Occupation
Environmental pollution
Perinatal events and childhood
illness
Recurrent bronchopulmonary
infections
Diet

Respiratory Diseases: Summary of Differences

Disease

Bronchitis

Bronchiectasis

Pneumonia

Primary area affected

Membrane lining bronchial

Results

Membrane lining bronchial

tubes
Bronchial tubes (bronchi or

tubes
Bronchial dilation with

air passages)
Alveoli (air sacs)

inflammation
Causative agent invades
alveoli with resultant

outpouring from lung

Emphysema

capillaries into air spaces and

Asthma

Cystic fibrosis

Air spaces beyond terminal

bronchioles (small airways)
Bronchioles (small airways)
Bronchioles

continued healing process

Breakdown of alveolar walls;

air spaces enlarged

Bronchioles obstructed by
muscle spasm, swelling of
mucosa, thick secretions

Bronchioles become
obstructed and obliterated.
Later, larger airways become
involved. Plugs of mucus cling
to airway walls, leading to
bronchitis, bronchiectasis,
atelectasis, pneumonia, or
pulmonary abscess

BRONCHITIS

Clinical Signs and Symptoms of

AcuteBronchitis

Mild fever f r om 1 to 3 days

Malaise
Back and muscle pain
Sore throat
Cough with sputum production, followed by wheezing
Possibly laryngitis

C h r o n i c B r o n c h i t is
Persistent cough with production of sputum (worse in the morning and evening than at midday)
Reduced chest expansion
Wheezing
Fever
Dyspnea (shortness of breath)
Cyanosis (blue discoloration of skin and
mucous membranes)
Decreased exercise tolerance

Bronchiectasis
Clinical signs and symptoms of bronchiectasis
v a r y widely, depending on the extent of the
disease and on the presence of complicating
infection, but may include:
Chronic "wet" cough with copious foulsmelling
secretions; generally worse in the
morning after the individual has been recumbent
for a length of time
Hemoptysis (bloody sputum)
Occasional wheezing sounds
Dyspnea
Sinusitis (inflammation of one or more
paranasal sinuses)
Weight loss
Anemia
Malaise
Recurrent fever and chills
Fatigue

Emphysema
Shortness of breath
Dyspnea on exertion
Orthopnea (only able to breathe in the upright
position) immediately after assuming the
supine position
Chronic cough
Barrel chest
Weight loss

Malaise
Use of accessory muscles of respiration
Prolonged expiratory period (with grunting)
Wheezing
Pursed-lip breathing
Increased respiratory rate
Peripheral cyanosis

Asthma
Listen f o r
Wheezing, however light
Irregular breathing with prolonged expiration
Noisy, difficult breathing
Episodes of dyspnea
Clearing the throat (tickle at the back of the
throat or neck)
Cough with or without sputum production,
especially in the absence of a cold a n d / o r
occurring 5 to 10 minutes after exercise

Look for
Skin retraction (clavicles, ribs, sternum)
Hunched-over body posture; inability to stand,
sit straight, or relax
Pursed-lip breathing
Nostrils flaring
Unusual pallor or unexplained sweating

Askabout
Restlessness during sleep
Vomiting
Fatigue unrelated to working or playing

Pneumonia
Sudden and sharp pleuritic chest pain that is
aggravated by chest movement
Shoulder pain
Hacking, productive cough (rust-colored or
green, purulent sputum)
Dyspnea
Tachypnea (rapid respirations associated with
fever or pneumonia) accompanied by
decreased chest excursion on the affected side
Cyanosis
Headache
Fever and chills
Generalized aches and myalgia that may
extend to the thighs and calves
Knees may be painful and swollen
Fatigue
Confusion in older adult or increased confusion
in client with dementia or Alzheimer's

Tuberculosis

Fatigue
Malaise
Anorexia
Weight loss
Low-grade fevers (especially in late afternoon)
Night sweats
Frequent productive cough
Dull chest pain, tightness, or discomfort
Dyspnea

Cystic Fibrosis

I n Early or U n d i a g n o s e d Stages
Persistent coughing and wheezing
Recurrent pneumonia
Excessive appetite but poor weight gain
Salty skin/sweat
Bulky, foul-smelling stools (undigested fats
caused by a lack of amylase and tryptase
enzymes)

I n O l d e r Child a n d Young A d u l t

Infertility
Nasal polyps
Periostitis
Glucose intolerance

Clinical Signs and Symptoms of

PulmonaryInvolvementin
Cystic F i b r o s is
Tachypnea (very rapid breathing)
Sustained chronic cough with mucus production
and vomiting
Barrel chest (caused by trapped air)
Use of accessory muscles for respiration and
intercostal retraction
Cyanosis and digital clubbing
Exertional dyspnea with decreased exercise
tolerance
Further complications include:
Pneumothorax
Hemoptysis
Right-sided heart failure secondary to pulmonary
hypertension

Lung inflammation

Parenchymal destruction

Airway remodeling

Airflow limitation

Parenchymal destruction