Chronic Obstructive Pulmonary Disease

Question 1

Chronic obstructive pulmonary disease (COPD)

Answer 1

persistent airflow limitation that is usually progressive. COPD is associated with an enhanced chronic inflammatory response in the airways and lungs, primarily caused by cigarette smoking and other noxious particles and gases. COPD exacerbations and other coexisting illnesses or co-morbidities contribute to the overall severity of the disease

Question 2

Chronic bronchitis

Answer 2

the presence of cough and sputum production for at least 3 months in each of 2 consecutive years

Question 3

Emphysema

Answer 3

the destruction of the alveoli and is a pathologic term that explains only one of several structural abnormalities in COPD patients.

Question 4

Chronic Obstructive Pulmonary Disease (COPD) Men

Answer 4

COPD is more common in men than in women, but the incidence is not increasing in men. • Fewer men die from COPD than women.

Question 5

Chronic Obstructive Pulmonary Disease (COPD) Women •

Answer 5

The number of women with COPD is increasing. • Increase is probably due to increased number of women smoking cigarettes and increased susceptibility (e.g., smaller lungs and airways, lower elastic recoil). • Women with COPD have lower quality of life, more exacerbations, increased dyspnea, and better response to O2 therapy compared with men.

Question 6

(COPD) Etiology

Answer 6

Cigarette Smoking. The major risk factor for developing COPD is cigarette smoking

Question 7

Cigarette smoke has several direct effects on the respiratory tract

Answer 7

The irritating effect of the smoke causes hyperplasia of cells, including goblet cells, thereby increasing the production of mucus. Hyperplasia reduces airway diameter and increases the difficulty in clearing secretions. Smoking reduces the ciliary activity and may cause actual loss of cilia. Smoking also produces abnormal dilation of the distal air space with destruction of alveolar walls.

Question 8

Passive smoking

Answer 8

the exposure of nonsmokers to cigarette smoke, also known as environmental tobacco smoke (ETS) or secondhand smoke. In adults, involuntary smoke exposure is associated with decreased pulmonary function, increased respiratory symptoms, and severe lower respiratory tract infections (e.g., pneumonia). ETS is also associated with increased risk for lung cancer and nasal sinus cancer.

Question 9

Occupational Chemicals and Dusts.

Answer 9

If a person has intense or prolonged exposure to various dusts, vapors, irritants, or fumes in the workplace, symptoms of lung impairment consistent with COPD can develop. If a person has occupational exposure and smokes, the risk of COPD increases.

Question 10

Air Pollution.

Answer 10

High levels of urban air pollution are harmful to people with existing lung disease. However, the effect of outdoor air pollution as a risk factor for the development of COPD is unclear.

Question 11

Infection.

Answer 11

Infections are a risk factor for developing COPD. Severe recurring respiratory tract infections in childhood have been associated with reduced lung function and increased respiratory symptoms in adulthood. People who smoke and also have human immunodeficiency virus (HIV) infection have an accelerated development of COPD. Tuberculosis is also a risk factor for COPD development.

Question 12

Genetics.

Answer 12

The fact that a relatively small percentage of smokers get COPD strongly suggests that genetic factors influence which smokers get the disease. Because of the genetic-environmental interaction, two people may have the same smoking history, but only one develops COPD. To date, one genetic factor has been clearly identified (see next section).

Question 13

α1-Antitrypsin (AAT) defici­ency

Answer 13

is an autosomal recessive disorder that may affect the lungs or liver. AAT deficiency is a genetic risk factor for COPD.

Question 14

Aging.

Answer 14

As one ages, the number of functional alveoli decreases as peripheral airways lose supporting tissues. The surface area for gas exchange decreases, and the PaO2 decreases. Changes in the elasticity of the lungs reduce the ventilatory reserve. These changes are similar to those seen in the patient with COPD.

Question 15

Asthma.

Answer 15

Patients with COPD may have asthma. Asthma may be a risk factor for the development of COPD. There is a considerable pathologic and functional overlap between these disorders, particularly among older adults, who may have components of both diseases. Recently this disorder has been called asthma-COPD overlap syndrome.

Question 16

Gender.

Answer 16

prevalence is almost equal, reflecting the changing patterns of cigarette smoking. Women may be more susceptible to the adverse effects of smoking.

Question 17

Pathophysiology

Answer 17

COPD is characterized by chronic inflammation of the airways, lung parenchyma (respiratory bronchioles and alveoli), and pulmonary blood vessels. The pathogenesis of COPD is complex and involves many mechanisms. The defining feature of COPD is not fully reversible airflow limitation during forced exhalation. This is caused by loss of elastic recoil and airflow obstruction caused by mucus hypersecretion, mucosal edema, and bronchospasm.

Question 18

In COPD, various processes occur

Answer 18

airflow limitation, air trapping, gas exchange abnormalities, and mucus hypersecretion. In severe disease, pulmonary hypertension and systemic manifestations occur. COPD has an uneven distribution of pathologic changes, with severely destroyed lung areas existing together with areas of relatively normal lung.

Question 19

The inflammatory process starts with

Answer 19

inhalation of noxious particles and gases (e.g., cigarette smoke) but is magnified in the person with COPD. The abnormal inflammatory process causes tissue destruction and disrupts the normal defense mechanisms and repair process of the lung.

Question 20

The inflammatory process may also be magnified by

Answer 20

oxidants, which are produced by cigarette smoke and other inhaled particles and released from the inflammatory cells. The oxidants adversely affect the lungs as they inactivate antiproteases (which prevent the natural destruction of the lungs), stimulate mucus secretion, and increase fluid in the lungs.

Question 21

After the inhalation of oxidants in tobacco or air pollution

Answer 21

the activity of proteases (which break down the connective tissue of the lungs) increases and the antiproteases (which protect against the breakdown) are inhibited. Therefore the natural balance of protease/antiprotease is tipped in favor of destruction of the alveoli and loss of the lungs’ elastic recoil.

Question 22

main characteristic of COPD

Answer 22

Inability to expire air

Question 23

The primary site of the airflow limitation

Answer 23

the smaller airways

Question 24

As the peripheral airways become obstructed

Answer 24

air is progressively trapped during expiration. The volume of residual air becomes greatly increased in severe disease as alveolar attachments (similar to rubber bands) to small airways are destroyed.

Question 25

The residual air, combined with the loss of elastic recoil makes

Answer 25

passive expiration of air difficult. As air is trapped in the lungs, the chest hyperexpands and becomes barrel shaped because the respiratory muscles are not able to function effectively. The functional residual capacity is increased. The patient is now trying to breathe in when the lungs are in an “overinflated” state. Thus the patient appears dyspneic and exercise capacity is limited.

Question 26

Gas exchange abnormalities result in

Answer 26

hypoxemia and hypercapnia (increased CO2) as the disease worsens. As the air trapping increases, walls of alveoli are destroyed, and bullae (large air spaces in the parenchyma) and blebs (air spaces adjacent to pleurae) can form.

Question 27

not all COPD patients have

Answer 27

sputum production.

Question 28

late in the course of COPD

Answer 28

Pulmonary vascular changes resulting in mild to moderate pulmonary hypertension may occur.

Question 29

pulmonary hypertension

Answer 29

The small pulmonary arteries vasoconstrict due to hypoxia. As the disease advances, the structure of the pulmonary arteries changes, resulting in thickening of the vascular smooth muscle. Because of the loss of alveolar walls and the capillaries surrounding them, pressure in the pulmonary circulation increases.

Question 30

Clinical manifestations of COPD

Answer 30

A clinical diagnosis of COPD should be considered in any patient who has chronic cough or sputum production, dyspnea, and a history of exposure to risk factors for the disease (e.g., tobacco smoke, occupational dusts, and chemicals).

Question 31

A chronic intermittent cough

Answer 31

which is often the first symptom to develop, may be present every day as the disease progresses. The cough is often dismissed by patients as they expect it with smoking or environmental exposures. The cough may be unproductive of mucus. However, significant airflow limitation may exist without sputum or cough. Typically dyspnea is progressive, usually occurs with exertion, and is present every day.

Question 32

Patients may complain of

Answer 32

not being able to take a deep breath, heaviness in the chest, gasping, increased effort to breathe, and air hunger

Question 33

In late stages of COPD

Answer 33

dyspnea may be present at rest. As more alveoli become overdistended, increasing amounts of air are trapped. This causes the diaphragm to flatten, and the patient must breathe from partially inflated lungs. Effective abdominal breathing is decreased because of the flattened diaphragm from the overinflated lungs. The person becomes more of a chest breather, relying on the intercostal and accessory muscles. However, chest breathing is not efficient.

Question 34

The person with advanced COPD frequently experiences

Answer 34

Wheezing and chest tightness, fatigue, weight loss, and anorexia.

Question 35

Complications that can occur in patients with COPD

Answer 35

cor pulmonale, acute exacerbations, and acute respiratory failure.

Question 36

Diagnostic Studies

Answer 36

A history and physical examination are extremely important in a diagnostic workup. Spirometry is required to confirm the diagnosis in individuals suspected of having COPD. Spirometry confirms the presence of airflow obstruction and determines the severity of COPD.

Question 37

Classification of COPD

Answer 37

An FEV1/FVC ratio of less than 70% establishes the diagnosis of COPD, and the severity of obstruction (as indicated by FEV1) determines the stage of COPD. The management of COPD is based on the patient’s symptoms, classification, and exacerbation history.

Question 38

Classification of COPD GOLD 1

Answer 38

Mild FEV1 ≥80% predicted

Question 39

Classification of COPD GOLD 2

Answer 39

Moderate FEV1 50%-80% predicted

Question 40

Classification of COPD GOLD 3

Answer 40

Severe FEV1 30%-50% predicted

Question 41

Classification of COPD GOLD 4

Answer 41

Very severe FEV1 <30% predicted

Question 42

Interprofessional Care: Stable COPD

Answer 42

influenza immunization yearly. The pneumococcal vaccine is recommended for all smokers ages 19 or older and all patients with COPD. Smoking Cessation
Bronchodilator drug therapy. Oxygen Therapy. Humidification and Nebulization. Breathing Retraining..
Airway Clearance Techniques. Effective Coughing. Chest Physiotherapy. Airway Clearance Devices

Question 43

Interprofessional Care: COPD Complications Cor Pulmonale.

Answer 43

results from pulmonary hypertension, which is caused by diseases affecting the lungs or pulmonary blood vessels

Question 44

COPD Acute Exacerbations.

Answer 44

is an acute event characterized by a worsening of the patient’s respiratory symptoms. Exacerbations are signaled by an acute change in the patient’s usual dyspnea, cough, and/or sputum (i.e., something different from the usual daily patterns). The primary causes of exacerbations are bacterial or viral infections.11 Exacerbations of COPD are typical and increase in frequency (average one or two a year) as the disease progresses.

Question 45

Acute Respiratory Failure.

Answer 45

Frequently, COPD patients wait too long to contact their HCP when they first develop symptoms suggestive of an exacerbation. Discontinuing bronchodilator or corticosteroid medication may also precipitate respiratory failure