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1. Print a copy of this PDF monograph file which includes the post-test and program evaluation.
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 Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008

James F. Donohue, MD Target Audience

Professor of Medicine This educational activity is designed to meet the needs of primary
Chief, Division of Pulmonary and care physicians, nurses, nurse practitioners, and physician assis-
Critical Care Medicine tants with an interest in the epidemiology, diagnosis, and manage-
University of North Carolina School of Medicine ment of chronic obstructive pulmonary disease or asthma.
Chapel Hill, North Carolina
Learning Objectives
Upon completion of this activity, the participant should be able to:
Ketan Sheth, MD, MBA • Describe the pathophysiology of COPD and asthma, and the
Medical Director unique pathogenic characteristics of each condition
Lafayette Allergy & Asthma Clinic
• Discuss the early diagnosis of COPD, the staging of disease
Lafayette, Indiana
severity, and the use of FEV1 reduction as a prognostic indicator
• Describe the latest pharmacological therapy for mild, moder-
ate, and severe COPD and asthma
Family Medicine Consultant: William A. Schwer, MD • Discuss the optimal smoking cessation approaches that pri-
Chairman Department of Family Medicine mary care providers can adopt for the prevention of COPD in
Rush University Medical Center • Chicago, IL their patients
Interviewer: Seymour I. Schlager, MD, PhD ABBREVIATIONS USED
CONFLICT OF INTEREST STATEMENT AP-1, activated protein 1
James F. Donohue, MD discloses that he has received compensation as a member of speakers’ ATS, American Thoracic Society
bureaus and advisory boards for GlaxoSmithKline.
Ketan K. Sheth, MD, MBA, FAAAAI discloses that he has received compensation as a member of
COPD, chronic obstructive pulmonary disease
speakers’ bureaus for AstraZeneca, GlaxoSmithKline, Pfizer Inc, sanofi-aventis, and Schering- DPI, dry-powder inhaler
Plough; for product consultation for Altana Inc., and GlaxoSmithKline, and as a member of adviso-
ry committees for Altana Inc., and GlaxoSmithKline. He also is a shareholder in Merck & Co., Inc. ERS, European Respiratory Society
William A. Schwer, MD reports that he has no significant financial interest or other relationships FEV1, forced expiratory volume in 1 second
with the manufacturer(s) of any commercial product(s) or service(s) discussed in this educational
presentation or with the commercial supporter of this activity. FDA, Food and Drug Administration
Seymour I. Schlager, MD, PhD discloses that he has received compensation as a product consultant FVC, forced vital capacity
for Abbott Laboratories and is a share holder of Abbott Laboratories and Pfizer Inc.
GOLD, Global Initiative for Chronic Obstructive Lung Disease
This educational activity may contain discussion of published and/or investigational uses of pharma-
ceutical agents. Some uses of these agents may not have been approved by the FDA. Please refer to ICS, inhaled corticosteroid
the official prescribing information for each product for discussion of approved indications, con-
traindications, and warnings. IL, interleukin
LABD, long-acting bronchodilator
CREDIT STATEMENTS
LBA, long-acting beta agonist
Physician CME: This activity has been planned and implemented in accor-
dance with the Essential Areas and polices of the Accreditation Council for LHS, Lung Health Study
Continuing Medical Education (ACCME) through the joint sponsorship of AKH Inc. and Medical
Communications Media, Inc. AKH Inc. is accredited by the ACCME to provide continuing medical MDI, multi-dose inhaler
education for physicians. NHLBI, National Heart, Lung, and Blood Institute
AKH Inc. designates this educational activity for a maximum of 2 AMA PRA Category 1
Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation PFT, pulmonary function test(ing)
in the activity.
ROSU, reliever/oral steroid use
Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008
SABD, short-acting bronchodilator
AAFP CME: This activity has been reviewed and is acceptable for up to 2 Prescribed credits by the
American Academy of Family Physicians. AAFP accreditation begins 8/1/06. Term of approval is TNF, Tumor necrosis factor
for one year from this date with option for yearly renewal.
TORCH, Towards A Revolution in COPD Health study
Physician Assistant CME: This program has been reviewed and is approved for a maxi-
mum of 2 hours of AAPA Category I (Preapproved) CME credit by the Physician
Assistant Review Panel of the American Academy of Physician Assistants. Approval is Supported through an
valid for one year from the issue date of May 28, 2006. Participants may submit the self-assess- educational grant from
ment at any time during that period.
This program was planned in accordance with AAPA’s CME Standards for Enduring Material
Programs and for Commercial Support of Enduring Material Programs.
Published by...
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Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008
tents may be reproduced in any form without prior written permission
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continuing education by the American Academy of Nurse Practitioners. Provider institutions, the publisher, AKH Inc., or GlaxoSmithKline. Any medications, or other diag-
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Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008 clinicians without evaluation of their patients' conditions and of possible contraindications
It should take approximately 120 minutes to listen to the CD discussion, read the monograph and or risks, and without a review of any applicable manufacturer's product information and
complete the self-assessment. Successful completion of the self-assessment, defined as a cumulative comparison with the recommendations of other authorities.
score of at least 70% correct, is required to earn credit. Participation is free.
1
 Introduction
Chronic obstructive pulmonary
disease (COPD) is a syndrome
characterized and defined by a
single physiological parameter:
limitation of expiratory airflow.1
COPD has gained interest as a
major public health concern and
is currently the focus of intense
research because of its persistent-
ly increasing prevalence, mortali-
ty, and disease burden. COPD
currently ranks as the fourth lead-
ing cause of death in the United
States, surpassed only by heart
disease, cancer, and cerebrovascu-
lar disease.2,3 Indeed, COPD is
one of the leading causes of dis-
ability worldwide and the only
disease for which prevalence and
mortality rates continue to rise.
One of the more troubling aspects
of COPD is that it is under-recog-
nized by patients, underdiagnosed
by physicians, and arguably
undertreated. Clearly, it is imper-
ative that primary care providers
understand the pathophysiologic
basis of COPD, how to accurately
diagnose and stage the disease,
and treat it appropriately by
matching therapy to disease
severity. In addition, COPD is a
largely preventable disease, and it
is incumbent on the primary care
provider to appreciate optimal
strategies to help their patients
stop smoking and take other steps
to prevent disease progression.
Similarly, asthma is a complex
syndrome, the incidence of
which has increased over the past
several decades.4 Unlike
COPD, for many patients, asth-
ma has its roots in infancy,
resulting in a complex constella-
2
Prevalence of asthma and COPD in the United States6-10
FIGURE 1
tion of symptoms that may be
found in both adults and chil-
dren.5 To properly manage
patients with this disease, the
primary care provider must com-
prehend the pathogenic mecha-
nisms underlying the many vari-
ants of asthma, identify factors
that initiate, intensify, and modu-
late the inflammatory response
of the airway, and determine how
these immunologic and biologic
processes produce the character-
istic airway abnormalities.5
This monograph is intended to
provide an overview of these two
important obstructive respiratory
diseases with the goal of provid-
ing practical information for the
management of patients with
COPD and asthma in the primary
care setting. The following topics
will be covered; in all cases, simi-
larities and distinctions between
the two conditions will be high-
lighted:
• Prevalence and epidemiology
• Pathogenesis and pathophysi-
ology
• Diagnosis and staging of
the disease
• Prevention and treatment
strategies
Prevalence and
Epidemiology
Obstructive lung diseases such as
asthma and COPD constitute a
serious public health issue with
significant financial and resource
burdens on the health care sys-
tem. In 2002, almost 15 million
adults and more than 6 million
children were diagnosed with
asthma. The disease accounted for
nearly 2 million emergency
department visits, 500,000 hospi-
talizations, and 5,000 deaths each
year, with estimated direct and
indirect annual costs to the health
care system of $14.5 billion
(Figure 1).6-10
Similarly, over 20 million
Americans suffer from some form
of COPD.1,2 COPD is responsible
for more than 1.5 million emer-
gency department visits, 726,000
hospitalizations, 120,000 deaths,
and more than $32 billion in direct
and indirect costs each year
(Figure 1).6-10 The prevalence of
COPD is likely to be underesti-
mated for several reasons, includ-
ing the delay in establishing the
diagnosis, the variability in defin-
ing the disease, and the lack of
age-adjusted estimates. Age
adjustment is important because
the prevalence of COPD in indi-
viduals under the age of 45 years
is low, while the prevalence is
highest in patients over 65 years of
age. Approximately 65% of the
patients treated for COPD in the
Unites States are more than 65
years old and the prevalence of the
disease in those over 65 is four
times higher than in the 45- to 64-
year-old group.11,12 In contrast,
the onset of asthma generally
occurs early in life, although some
patients may present with asthma
for the first time in late adulthood.
In total, data from NHANES III
suggest that approximately 44 mil-
lion Americans (adults and chil-
dren) have evidence of impaired
lung function, involving either
COPD or asthma. 7
Pathogenesis and
Pathophysiology
Both asthma and COPD are char-
acterized by airflow obstruction
and chronic persistent airway
inflammation, and many patients
with asthma have characteristics
of COPD, an overlap that often
makes it difficult to establish an
accurate diagnosis (Figure 2). 13
Indeed, the similarities between
COPD and asthma were noted in
the 1960s with the introduction of
the Dutch hypothesis, suggesting
that various types of airway
obstruction are merely different
expressions of a single disease
spectrum that requires predispos-
ing host-derived and environmen-
tal factors for their onset (e.g.,
genetic factors, airway hyper-
responsiveness, atopy, gender,
age, exposure to allergens, and
smoking).14-16
In 2004, the American Thoracic
Society (ATS) and the European
Respiratory Society (ERS)
described COPD as “…a prevent-
able and treatable disease state
characterized by airflow limita-
tion that is not fully reversible.
The airflow limitation is usually
progressive and is associated with
an abnormal inflammatory
response of the lungs to noxious
particles or gases, primarily
caused by cigarette smoking.
Although COPD affects the lungs,
it also produces significant sys-
temic consequences.”17 The ATS
The overlap of asthma and COPD13
FIGURE 2
/ERS statement also supports the
position that COPD and asthma
often coexist.
COPD typically presents in
midlife and is characterized by
progressive airflow limitation and
airway inflammation leading to a
gradual and irreversible loss of
lung function; the primary condi-
tions that fall under the term
COPD are chronic bronchitis and
emphysema (Figure 2).17 On the
other hand, asthma is character-
ized by chronic airway inflamma-
tion associated with widespread
but variable airflow obstruction.
Most asthmatics suffer from
episodic airway obstruction,
unlike patients with COPD who
have progressive airway obstruc-
tion. Further, unlike COPD, air-
flow obstruction in asthma often
reverses completely either sponta-
neously or with treatment.18,19
Airflow obstruction in COPD is
associated with an abnormal
inflammatory response of the
lungs to toxic particles or gases,
3
 including tobacco smoke (either of these cytokines are potent Although bronchial inflammation
due to directly smoking or from chemoattractants that cause an characterizes both COPD and
second-hand smoke), or through influx of monocytes, neutrophils asthma, the pathogenic inflamma-
occupational exposure to coal and CD8 lymphocytes. These tory processes of these diseases
dust, asbestos, and chemicals.8,15 cells, when acted upon by proin- differ significantly (Table 1).13
Because the majority of diagnosed flammatory cytokines, are stimu- The characteristic physiologic
COPD is related to tobacco expo- lated to release proteinases that abnormality in asthma is
sure, there has been considerable contribute to alveolar septal dis- eosinophilic inflammation;
work to define the link between ruption, fibrosis, and mucus indeed, an increase in activated
tobacco smoke and ongoing air- hypersecretion.13, 22-25 This and degranulating eosinophils has
way and parenchymal remodeling. adaptive immune response con- been demonstrated in bronchial
Multiple pathogenic mechanisms tinues in the peripheral airways biopsies and bronchoalveolar
likely contribute to the develop- of patients with COPD even after lavage of asthma patients.5,13
ment of COPD (see below). smoking cessation.26 Unlike the neutrophil and CD8-
lymphocyte predominance in
In addition, since only 20% of Genetic susceptibility to oxidative COPD, CD4+ lymphocytes
smokers acquire COPD, genetic stress induced by cigarette smoke orchestrate an eosinophilic
predisposition seems to play an may also explain why some inflammation and mast cell
important role in the pathogenesis smokers develop COPD and oth- degranulation that characterize
of this disease.15 For example, ers do not. Smokers who develop the bronchoconstrictor responses
patients with a genetic deficiency COPD appear to have a higher in acute asthma. In addition, IgE
in alpha 1-antitrypsin are prone to degree of oxidative stress than antibodies have been linked to the
develop early-onset emphysema. 15 those with a similar smoking his- initiation and persistence of air-
Another important factor linking tory but no evidence of COPD.26 way responses to allergens.5
smoking to inflammation may be
oxidative stress induced by oxi-
dants found in cigarette smoke; COPD Is a Disease of Inflammation22
reactive oxygen species such as
superoxide anions and hydrogen
peroxide generated as a conse-
quence of oxidative stress can
propagate the inflammatory
response by activating several
redox-sensitive transcription fac-
tors (e.g., NF-kappa B and acti-
vated protein 1 [AP-1]) that can
upregulate expression of a num-
ber of proinflammatory
cytokines.20,21 These cytokines
can trigger and propagate an
inflammatory cascade as shown
in Figure 3.22 Cigarette smoke
induces epithelial cells and alve-
olar macrophages to release
tumor necrosis factor-α (TNFα),
which in turn, increases produc-
tion of interleukin 8 (IL-8); both FIGURE 3

4
 Inflammation - differences between asthma and COPD13
Diagnosis and
Disease Staging
Asthma COPD
COPD
Inflammatory cells Mast cells, EOS, CD4+ (Th2) cells, Neutrophils, CD8+(Tc) cells, The diagnosis of COPD is largely
macrophages + macrophages ++
history- and symptom-driven,
Inflammatory mediators LTB4, histamine, IL-4, IL-5, IL-13 LTB4, TNF-alpha, IL-8, GRO which can be problematic since
eotaxin, RANTES
there is an imperfect relationship
Inflammatory effects All airways Peripheral airways and alveoli between the severity of airflow
Epithelial shedding, fibrosis+, Epithelial metaplasia, limitation and the presence of
No parenchymal involvement, mucus fibrosis ++, parenchymal
destruction, mucus symptoms. However, a diagnosis
of COPD should be suspected in
TABLE 1 any patient presenting with a
chronic cough, sputum production,
In asthma, inhaled allergens COPD. For example, there is or exertional dyspnea, especially if
encounter dendritic cells that line ample literature demonstrating there is a history of exposure to
the airway, and these cells the association of inflammatory cigarette smoke.4 Unfortunately,
migrate to draining lymph nodes mediators such as TNFα and IL- physical examination is a relative-
where they present processed 6 (both markedly increased in ly insensitive means of diagnosing
allergen (antigen) to T- and B- COPD) with abnormalities in COPD, especially in mild to mod-
cells. The B-cells are induced body composition, weight loss, erate disease.33
through a complex series of peripheral muscle wasting and
costimulatory signals to produce loss of performance, and func- In the primary care setting, the
IgE, which binds to high-affinity tional status.27-29 Findings of documentation of airflow obstruc-
receptors on the surface of mast increased muscle apoptosis and tion is a universally-recommended
cells in tissue. When the allergen shifts in muscle fiber composi- requirement for the diagnosis of
subsequently interacts with the tion may be related to the sys- COPD, thus making pulmonary
receptor-bound IgE molecules, temic inflammatory processes function testing (PFT) through the
activation and degranulation of associated with COPD. Other use of spirometry essential to the
the mast cells occur, resulting in manifestations of systemic diagnosis and staging of the sever-
release of histamine and inflammation in COPD include ity of this disease.17 Expert
leukotrienes, and causing smooth an increased prevalence of osteo- guidelines for the diagnosis of
muscle constriction that results in porosis and central nervous sys- COPD are readily available and
the early-phase airway obstruc- tem defects.30,31 Finally, there is relatively straightforward: the
tion seen in asthma.5 Prolonged, a growing interest in the role of diagnosis of COPD can be made
late-stage reactions develop as a inflammation in coronary artery when the ratio between the forced
result of the release of cytokines disease progression and its poten- expiratory volume in 1 second
and chemokines (IL-4, IL-5, IL- tial association with COPD and (FEV1) and the forced vital capac-
13) generated by the resident pulmonary inflammation.32 ity (FVC) falls below 0.7.17
inflammatory cells in the lung Despite these widely-accepted
(Table 1).5 These molecules are recommendations, the utilization
responsible for the maintenance of spirometry in the primary care
of airway obstruction in asthma. setting, where early diagnosis is
most likely to be accomplished,
Moreover, there are systemic remains inconsistent. Recent
consequences of the inflammato- studies have shown that spirome-
ry responses associated with try can be reproducibly performed

5

GOLD Disease Stratification Guidelines for Severity of COPD1,17
GOLD Severity Postbronchodilator
Stage FEV1/FVC
0 At risk > 0.7
1 Mild COPD ≤ 0.7
2 Moderate ≤ 0.7
COPD
3 Severe COPD ≤ 0.7
4 Very Severe ≤ 0.7
COPD
TABLE 2
in the primary care setting with
modest training and with little
additional time per patient; each
PFT assessment can be completed
in 4 minutes or less.34,35
Spirometry is necessary not only
for the diagnosis of COPD, but
also for the assessment of severity
of disease and for following a
patient’s response to therapy.
Recently, the ATS/ERS Task
Force and the NHLBI/WHO
Global Initiative for Chronic
Obstructive Lung Disease
(GOLD) released the GOLD
guidelines—a method of “stag-
ing” COPD patients for severity
of disease.1,17 As shown in Table
2, the GOLD guidelines stratify
COPD by disease severity,
FEV1/FVC ratios, and FEV1 %
predicted (based on the patient’s
age, gender, height, and ethnic
background), and relate these val-
ues to clinical symptoms.1,17 The
value of spirometry in COPD
patients is not only for diagnosis
6
FEV1, Clinical symptoms
% predicted
≥ 80 Asymptomatic smoker, ex-smoker,
or chronic cough/sputum
≥80 Breathlessness when hurrying or
walking up slight hill
50-80 Breathlessness causing patient to
stop after walking about 100 m or
after a few minutes on level ground
30-50 Breathlessness resulting in patient
too breathless to leave the house,
< 30 breathlessness after undressing,
presence of chronic COPD respiratory
failure, or clinical signs of right
heart failure
and staging, but also to predict
the natural history of the disease
in a given patient and to guide
aggressiveness of therapy and
smoking cessation efforts. For
example, a recent retrospective
analysis of more than 15,000
adults with COPD assessed the
relationship between GOLD sta-
tus and clinical outcomes. The
study showed that patients with
GOLD stage 3 or 4 disease
demonstrated the most rapidly
declining lung function over time
(adjusted odds ratio 2.4; 95% CI
2.1-2.7) and an increased risk of
death (adjusted odds ratio 1.4;
95% CI 1.2-1.7) compared with
patients with less severe COPD.36
To complete the diagnostic evalua-
tion of a patient suspected of hav-
ing COPD, a chest X-ray should
be considered to rule out infection,
large airway lesions, heart disease,
obstruction by a foreign object, or
a malignancy as the cause of the
patient’s symptoms.
Asthma
On the other hand, the diagnosis
of asthma depends more on histo-
ry, physical findings, and age-
related factors. Recurrent
episodes of coughing or wheezing
are almost always due to asthma
in children and many adults.4,37
Medical history findings that
increase the probability of asthma
include:
• Episodic wheeze, chest
tightness, shortness of
breath, cough
• Symptoms that worsen in the
presence of allergens, irri-
tants, or exercise
• Symptoms that worsen at
night, awakening the patient
• History of allergic rhinitis or
atopic dermatitis
• Family history of asthma,
allergy, sinusitis, or rhinitis
Similarly, certain physical exami-
nation findings can help in the
diagnosis of asthma:
• Sounds of wheezing
during normal breathing
or a prolonged phase of
forced exhalation
• Increased nasal secretions,
mucosal swelling, sinusitis,
rhinitis, or nasal polyps
• Atopic dermatitis, eczema,
or other signs of allergic
dermatitides
It should be noted that the absence
of physical findings (i.e. a normal
lung examination) does not
exclude the diagnosis of asthma.
As in COPD, spirometry may be
useful, since asthma is strongly
suggested by findings of partially
reversible airflow obstruction.
Here, spirometry should be per-
formed as a 2-stage process:
• First, airflow obstruction
should be established by find-
ing FEV1 < 80% predicted
and FEV1/FVC < 0.65
• Second, reversibility should
be established by demonstrat-
ing that FEV1 increases > 12%
and at least 200 mL after
treatment with a short-acting
inhaled beta2-agonist (e.g.,
albuterol or terbutaline)
In addition, it may be advisable to
perform a broad investigation of
clinical factors that are known to
contribute to asthma in an effort
to reduce or eliminate these
comorbid conditions:
• Allergy testing (skin testing or
in vitro tests)
• Nasal examination and/or
computed tomography of
the sinuses
• Assessment for gastro-
esophageal reflux
In children under 5 years of age,
spirometry is difficult to perform,
so a trial of asthma medications
may aid in the diagnosis when the
history and physical examination
findings listed above are present.
There are several different meth-
ods for determining asthma
severity levels—the patient-
reported severity measures and
the Reliever/Oral Steroid Use
(ROSU) method are the most
useful in that they correlate most
closely with the Asthma Quality
of Life Questionnaire scores, the
Work Performance Scale score, Prevention and
and the Physical and Mental
Component scales of the SF-36
Treatment
disability instrument.37 From Smoking Cessation
this, asthma severity may be The most compelling treatment of
COPD consists of aggressive
staged as mild intermittent, mild
persistent, moderate persistent, approaches to smoking cessation.
The sentinel study in this field is
or severe persistent based prima-
rily on the inhaled beta2-agonist the Lung Health Study (LHS),
which studied nearly 6,000 smok-
use per year, modified secondari-
ers between the ages of 35 and 80
ly by the use of oral steroids (see
years of age with mild airflow
Table 3).37 The most often used
obstruction, and randomized these
method of determining asthma
patients to aggressive smoking
staging is based on the National
cessation therapy versus usual
Heart Lung and Blood Institute’s
care.38 As shown in Figure 4,
(NHLBI) classification of asthma
patients who were able to achieve
severity, which can be found at
an 85% reduction or complete
http://www.nhlbi.nih.gov/
cessation in smoking over the
health/prof/lung/asthma/pract-
long term (sustained quitters) pre-
gde/practgde.pdf (See Table 3).
served a significantly higher per-
Using these parameters, asthma
centage of their lung function
can be classified as mild inter-
compared with those who quit
mittent, mild persistent, moder-
smoking intermittently or not at
ate persistent or severe persist-
all, as measured by FEV1 % of
ent. As in COPD, classification
of asthma severity can be used predicted values.38 Men and
to guide therapy and help women who quit at the beginning
patients understand the nature of the LHS had an FEV1 rate of
of their disease. decline of 30.2mL/year and 21.5
mL/year, respectively, compared
Reliever/Oral Steroid Use (ROSU) Method for
Staging Asthma Severity37
Severity Level Inhaled beta-2 agonist use/yr Oral steroids/yr
Severe persistent > 6 canisters <2 Ô mild persistent
Moderate persistent 4-6 canisters 0 Ô mild persistent
(≤ 24 inhalations/week) ≥ 3 Ô severe
2 Ô moderate
Mild persistent 2-3 canisters
(≤ 12 inhalations/week) ≥ 3 Ô severe
1 Ô mild persistent
Mild intermittent ≤ 1 canister
2 Ô mod persistent
≥3 Ô severe
These guidelines can also be found at: http://www.nhlbi.nih.gov/health/prof/lung/asthma/practgde/practgde.pdf
TABLE 3
7

Loss of Lung Function over 11 Years in the Lung Health Study38
FIGURE 4
with a decline of 66.1 mL/year in
men and 54.2 mL/year in women
who continued to smoke. After
11 years of follow-up, 38% of
continuing smokers had an FEV1
< 60% of the predicted normal
value compared with 10% of the
sustained quitters (Figure 4)38 In
this study, smoking cessation was
also associated with improved
symptoms and improved long-
term mortality (hazard ratio, 1.18;
95% CI 1.02-1.37) compared with
usual care.39
Physicians and other health care
professionals working in the pri-
mary care setting are in a unique
position to identify tobacco users
and provide effective intervention.
In 2000, the efficacy of a variety
of smoking cessation methods
was systematically reviewed by a
United States Public Health
Services (USPHS) committee
during the development of an evi-
dence-based clinical practice
guideline for physicians. The
8
USPHS panel concluded that
there was sufficient clinical evi-
dence supporting the use of 2 dis-
tinct smoking cessation methods:
• Behavioral counseling
• Pharmacotherapy with nico-
tine replacement products uti-
lizing a variety of drug deliv-
ery forms (see below)
A combination of counseling and
pharmacotherapy produced the
best results.40 There was no evi-
dence to support the efficacy of
other methods, such as hypnosis
or acupuncture. The resulting
USPHS clinical guidelines recom-
mend that clinicians routinely and
consistently deliver a brief 5-step
intervention in their office prac-
tice called the “5 A’s”:
• Ask about tobacco use at
every visit
• Advise all tobacco users to stop
• Assess their willingness to
make a quit attempt
• Assist the patient in quitting
• Arrange follow-up contact to
support their efforts
In addition, the USPHS guidelines
suggest that it is important to pro-
vide patients with pharmacologic
aids for smoking cessation; these
are reviewed in Table 4.40 Seven
pharmacologic aids have been
approved by the US Food & Drug
Administration (FDA) for use in
the treatment of nicotine depend-
ence: nicotine replacement thera-
pies delivered by patch, gum,
vapor inhaler, nasal spray, or
lozenge, and a non-nicotine pill
(bupropion). On May 11, 2006,
FDA granted approval to a new
class of agent, varenicline, as a
pharmacologic aid to smoking
cessation therapy (see Table 4).
Full prescribing information for
this new agent can be found at
http://www.chantix.com.
The USPHS panel also identified
the tricyclic antidepressant nor-
triptyline and the antihypertensive
clonidine for which there is evi-
dence of efficacy for smoking
cessation; these agents have not
yet been approved by the FDA for
this indication.40
Pharmacologic Intervention
in COPD
The goals of treatment in COPD
patients include reduction of
symptoms, improvement in physi-
ologic function, limitation of
complications, and arresting exac-
erbations of disease.41 Several
treatment algorithms have been
developed for patients with
COPD. Sutherland and Cherniak
have devised a comprehensive
algorithm that encompasses
 Pharmacologic Aids for Smoking Cessation40

Product Dose Treatment Common Instructions

Duration Side Effects
Nicotine-Replacement Therapies
Transdermal patch*† 7-, 14-, or 21-mg patch worn 8 wk Skin irritation, Every morning, place a fresh patch on a rela-
24 hr (eg, Nicoderm CQ) for 24 hrs insomnia tively hairless area of skin between the waist
16 hr (eg, Nicotrol) 5-, 10-, or 15-mg patch worn and neck. If sleep disruption occurs, remove
for 16 hrs the patch at bedtime. Use a hydrocortisone
cream for minor skin reactions.
Nicotine polacrilex gum 1 piece/1-2 hrs (wks 1-6); 2-4 8-12 wk Mouth irritation, sore Chew the gum slowly until mint or pepper is
(Nicorette)*† hrs (wks 7-9); 4-8 hrs (wks jaw, dyspepsia, hiccups tasted. Then park the gum between the cheek
2 mg (< 25 10-12); up to 24 pieces/day and gum to permit absorption through the oral
cigarettes/day) mucosa. Repeat when taste subsides and con-
4 mg (>/= 25 ciga- tinue for approximately 30 minutes. Avoid eat-
rettes/day) ing or drinking for 15 minutes before and dur-
ing use.
Vapor inhaler (Nicotrol 6-16 cartridges/day (deliv- 3-6 mo Mouth and throat Avoid eating or drinking for 15 minutes before
Inhaler)* ered dose, 4 mg/cartridge); irritation, cough, and during use.
taper use in last 6-12 wks of dyspepsia
therapy
Nasal spray (Nicotrol NS)* 1-2 doses/hr (1 mg total; 3-6 mo Nasal irritation, sneez- Do not sniff, inhale, or swallow during admin-
0.5 mg in each nostril); ing, cough, teary eyes, istration because this increases irritating
minimum treatment: 8 runny nose effects. Tilt the head back slightly during
doses/day; maximum administration.
treatment: 40 mg/day
Lozenge (Commit 1 lozenge/1-2 hrs (weeks 1- 12 wk Insomnia (less than Suck on the lozenge until it dissolves. Do not
Lozenge)*† 6); 2-4 hrs (weeks 7-9); 4-8 5% of users), nausea, bite or chew it like a hard candy, and do not
2 mg (first cigarette > 30 hrs (weeks 10-12) hiccups, coughing, swallow it. Avoid eating or drinking for 15
min waking) heartburn, and minutes before use.
4 mg (first cigarette </= headache
30 min waking)
Non-nicotine Therapies
Sustained-release bupro- 150 mg/day for 3 days, then 7-12 wk (up to Insomnia, dry mouth, Limit alcohol intake.
pion (Zyban or Wellbutrin 150 mg twice a day; treatment 6 mo to main- agitation
SR)* started 1 week before quit date. tain abstinence)
Nortriptyline** 75-100 mg/day‡ 12 wk Dry mouth, sedation, Use may cause sedation, a driving hazard. Risk
dizziness, blurred of overdose should be considered carefully;
vision, shaky hands produces cardiotoxic effects.
Clonidine** 0.1-0.3 mg twice a day; treat- 3-10 wk Dry mouth, sedation, Clonidine lowers blood pressure in most patients
ment started on quit date or dizziness, drowsiness, and so should be monitored when using. Use of
up to 3 days before quit date constipation either oral or transdermal form may cause seda-
tion, a driving hazard. Do not stop using abrupt-
ly as rebound hypertension may result.
Varenicline* (Chantix) 0.5 mg daily for 3 days, then 7-10 weeks Nausea, changes in Varenicline binds to nicotine receptors in the
0.5 mg twice daily for 4 days, dreams, constipation, brain, reducing the need for nicotine during
then 1 mg twice daily until gas, vomiting smoking withdrawal; this binding also
the end of treatment dampens the effects of nictotine derived from
cigarettes in patients who have a relapse
during smoking cessation efforts
* Approved by the FDA as a smoking cessation aid. † Over-the-counter medication. ** Not approved by the FDA as a smoking cessation aid. The USPHS clinical guideline recommends as a second-line drug for smoking cessation.
‡ Treatment should be started 10-28 days before the quit date at a dose of 25 mg per day, and the dose should be increased as tolerated.

TABLE 4
9
 health care maintenance, drug LABDs are preferred agents over bations.39,42 Although the FDA
therapy, and supplemental thera- short-acting agents. Both long- has not approved the use of
py for these patients (Figure 5).41 acting beta-agonists (salmeterol inhaled corticosteroids alone for
Because patients with reduced and formoterol) and a long-acting the treatment of COPD, 2 recent
lung function may be asympto- anticholinergic (tiotropium) have meta-analyses demonstrated that
matic, these authors have con- been shown to result in sustained use of these agents for at least 2
cluded that spirometry is indicat- improvement in lung function, years can reduce the rate in deteri-
ed to guide therapy and treat- health status, and exercise toler- oration of pulmonary function and
ment, and should be initiated ance, and to reduce COPD exacer- result in a 30% decrease in the
whenever reduced lung function
is demonstrated, with or without
A Comprehensive Algorithm for the Treatment of COPD41
the presence of symptoms. This
algorithm suggests that patients
may initially require only as-
needed therapy with a single
short-acting anticholinergic agent
or beta-agonist (Figure 5). As
patients progress to moderate or
severe disease, or for those with
increasing or persistent symp-
toms, an inhaled long-acting
bronchodilator (LABD) or a
combination of a short- or long-
acting anticholinergic agent and a
beta-agonist may be used.41
Table 5 summarizes the most
commonly-used short- and long-
acting inhaled bronchodilators
and their appropriate use.41

In response to advances from epi-

demiologic studies and pivotal,
well-controlled clinical trials, the
FIGURE 5
ATS/ERS updated their standards
for treating COPD patients in
2004.17 While some guidelines Duration and Administration of Inhaled Bronchodilators41
(like the Sutherland and Cherniak
algorithm reviewed above) rely Drug Duration Usual Dose*
heavily on spirometric results for Short-acting
guiding pharmacologic and non- Albuterol sulfate 4-6 hr Two puffs every 4 hr (MDI, 90 µg/puff)
pharmacologic therapies, the Ipratropium bromide 4-6 hr Two puffs every 4 hr (MDI, 18 µg/puff)
ATS/ERS guidelines shown in Long-acting
Figure 6 suggest a predominantly Formoterol fumarate 8-12 hr One inhalation twice daily (DPI, 12 µg/inhalation)
symptom-based approach to treat- Salmeterol xinafoate 8-12 hr One inhalation twice daily (DPI, 50 µg/inhalation)
Tiotropium bromide More than 24 hr One inhalation twice daily (DPI, 18 µg/inhalation)
ment.17 Bronchodilator therapy is
* MDI denotes metered-dose inhaler, and DPI dry-powder inhaler
pivotal in the management of
patients with COPD. Inhaled TABLE 5

10
relative risk of exacerbations.43,44
ATS/ERS Algorithm for Pharmacologic Management
of COPD Patients17
More recently, treatment guide-
lines support the use of combina-
tions of drugs of different classes
to achieve improved clinical out-
comes. For example, the combi-
nation of a long-acting beta-ago-
nist and an inhaled corticosteroid
has been recommended.41 When
administered in combination in a
single inhaler, fluticasone and sal-
meterol resulted in an improve-
ment in FEV1 that was main-
tained for 12 to 24 weeks, com-
pared to either agent alone.45,46
A 3-year prospective study
(TORCH) was initiated to further
evaluate the usefulness of this
combination.47 The initial results
of the TORCH study were pre- FIGURE 6
sented at the American Thoracic
Society Meeting in May 2006;
the results showed that there was GINA/NHLBI Guidelines for the Preferred Treatment of Asthma19
a 17% relative reduction in mor-
tality over 3 years for patients
receiving the combination of sal-
meterol + fluticasone propionate
compared with those treated with
placebo (P=0.052). This was the
first study to investigate the
effects of pharmacotherapy on
all-cause mortality in patients
with COPD.

Pharmacologic Intervention
in Asthma
The guidelines established in 2005
by the Global Initiative for Asthma
(GINA), in conjunction with
NHLBI, are shown in Figure 7.19
A rapid-acting inhaled beta-2
agonist should be used as needed
for most patients with mild inter-
mittent asthma.19 For mild per-
sistent asthma, the guidelines rec-
ommend low-dose inhaled gluco- FIGURE 7

11
 corticoids daily. In a recent
study, the use of once-daily
budesonide by these patients was
shown to decrease the risk of
severe exacerbations.48 Moderate
persistent disease should be treat-
ed with low- to medium-dose
inhaled corticosteroids and long-
acting beta-agonists (Figure 7).
Severe persistent asthma necessi-
tates the use of high-dose inhaled
steroids, an LABD, and an oral
steroid. For all levels of disease
severity, a short-acting inhaled
beta-2 agonist should be used as
needed and be available as a res-
cue medication.19 Two recent
studies (one in the US and one in
Europe) investigated whether
inhaled corticosteroids (ICS)
used in children with a positive
asthma predictive index (e.g., fre-
quent bouts of wheezing and a
positive response to treatment
with fluticasone propionate) and
who were under 3 years of age
would have disease-modifying
activity in these patients.49,50
Both studies concluded that in
preschool children at high risk
for asthma, ICS therapy does not
alter the natural history of the
disease and that the risk of
wheezing will persist beyond the
first years of life in children
treated with ICS therapy.49,50
Nonpharmacologic Interventions
in COPD and Asthma
Aside from smoking cessation
efforts which were discussed
above, other nonpharmacologic
interventions should be instituted
in patients with COPD or asthma.
Pulmonary rehabilitation is
designed to address secondary
conditions associated with COPD,
12
such as cardiac deconditioning,
peripheral muscle dysfunction,
reduction in total and lean body
mass, anxiety, and poor coping
skills. Pulmonary rehabilitation
is most effective when delivered
as a multifaceted program incor-
porating individually tailored aer-
obic physical training, compre-
hensive education about the dis-
ease, psychosocial counseling,
and nutritional support.41 A
healthy lifestyle, physical activity,
and adherence to therapy should
be encouraged. Pulmonary reha-
bilitation efforts have been shown
to improve dyspnea, exercise abil-
ity, and health status, and reduce
health care utilization.17,41
In addition, long-term oxygen
therapy is recommended in
patients in whom the resting par-
tial pressure of arterial oxygen is
55 mm Hg or less or if the oxy-
gen saturation falls below 88%; in
these patients, supplemental oxy-
gen has been shown to improve
survival, exercise, sleep, and cog-
nition.17,41 The guidelines also
support the use of influenza vac-
cination for all patients with
COPD. Patients with COPD or
especially, asthma should be
counseled to avoid exposure to
environmental triggers that might
affect symptom control.
Lung-volume reduction surgery
can reduce hyperinflation and
should be considered in patients
with severe upper-lobe emphyse-
ma, poor exercise tolerance, and
a poor response to pharmacothera-
py alone.41 A small, randomized,
controlled trial that compared
lung-volume-reduction surgery
with medical therapy in patients
with severe emphysema demon-
strated improved lung function,
exercise capacity, and quality of
life 6 to 12 months after surgery.51
Single-lung transplantation is an
alternative surgical option for
patients with end-stage emphyse-
ma who have FEV1 < 25% of pre-
dicted normal value and who have
complications such as pulmonary
hypertension, marked hypoxemia,
and hypercapnia.52
Conclusions
Although COPD and asthma are 2
different forms of chronic pul-
monary disease, there is consider-
able overlap in presentation and
management. Both conditions are
caused by an interaction between
intrinsic, genetic factors and envi-
ronmental exposures. The patho-
physiology of COPD and asthma
involve multiple immunologically-
mediated components, resulting in
airway inflammation, obstruction,
and hyperresponsiveness.
Treatment of these diseases is
similar in that they can both be
managed with pharmacologic and
nonpharmacologic strategies
focused on treating bronchocon-
striction and airway inflammation.
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 Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008

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PLEASE CIRCLE THE MOST APPROPRIATE ANSWER TO THE FOLLOWING QUESTIONS.

1. What percentage of smokers develops COPD, suggesting a 6. The most effective approach(es) to effecting smoking
genetic predisposition for the disease? cessation is (are):
a. 10% b. 20% c. 35% d. Over 50% a. Counseling
b. Pharmacotherapy
2. Oxidative stress is thought to play an important role in the c. Counseling and pharmacotherapy
development of COPD. Oxidative stress: d. Counseling, pharmacotherapy, and hypnotherapy
a. Is induced by oxidants found in cigarette smoke
b. Causes upregulation of proinflammatory cytokines, 7. Which of the following is NOT approved by FDA as
primarily TNFα and IL-8 pharmacotherapy for smoking cessation?
c. Occurs to a higher degree in smokers with COPD than a. Nicotine patch c. Nicotine vapor inhaler
in smokers without COPD b. Bupropion d. Nortriptyline
d. All of the above
8. ATS/ERS guidelines for treatment of persistent symptoms
3. Immunologic distinctions in the pathogenesis of COPD and of COPD recommend starting with a
asthma include: a. Short-acting bronchodilator
a. CD4+ lymphocytes predominate in COPD, but not asthma b. Long-acting bronchodilator
b. IgE antibodies and eosinophils play a pivotal role in asthma c. Inhaled corticosteroid
c. Cytokines are not thought to play a role in late-stage d. Oral theophylline
reactions in asthma
d. All of the above 9. The combination of which of the following in a single
inhaler has been shown to achieve improved clinical
4. The diagnosis of COPD can be made by spirometric outcomes in COPD?
findings that a. Albuterol and ipratropium
a. FEV1 < 0.7 c. FEV1/FVC < 0.7 b. Formoterol and salmeterol
b. FVC < 0.7 d. FVC/FEV1 < 0.7 c. Salmeterol and tiotropium
d. Fluticasone and salmeterol
5. Severe COPD, GOLD Stage 3, is characterized by
a. FEV1 = 30-50% predicted normal value 10. GINA guidelines for treatment of mild persistent asthma
b. Breathlessness when walking up a slight hill recommend starting with
c. FEV1 = 50-80% predicted normal value a. Low-dose inhaled steroid
d. FEV1/FVC > 0.7 b. High-dose inhaled steroid
c. Daily dosing of a long-acting bronchodilator
d. Oral steroid 06 GS COPD PCS-2 15
 Release Date: May 28, 2006 • Credit Expiration Date: May 28, 2008

PROGRAM EVALUATION
Please complete this program evaluation so that we may continue to provide you with high-quality educational activities.

INDICATE YOUR ANSWER BY CIRCLING

THE APPROPRIATE NUMBER. STRONGLY AGREE STRONGLY DISAGREE
1. As a result of my participation in this activity, I am better able to:
Describe the pathophysiology of COPD and asthma, and the unique
pathogenic characteristics of each condition. 5 4 3 2 1
Discuss the early diagnosis of COPD, the staging of disease severity,
and the use of FEV1 reduction as a prognostic indicator. 5 4 3 2 1
Describe the latest pharmacological therapy for mild, moderate, and
severe COPD and asthma. 5 4 3 2 1
Discuss the optimal smoking cessation approaches that primary care
providers can adopt for the prevention of COPD in their patients. 5 4 3 2 1

2. This activity increased my awareness and understanding of the subject matter. 5 4 3 2 1

3. The information provided in this activity will be useful to me professionally. 5 4 3 2 1

q q
4. Do you anticipate any changes in your diagnosis or management of asthma
and COPD as a result of this program? Please explain: Yes No

5. Was the content clear and well organized? If no, please explain: q Yes q No

6. The faculty are knowledgeable and up-to-date. If no, please explain: q Yes q No

7. Was the activity objective and scientifically balanced, and free of commercial bias? q Yes q No
If no, please explain

8. The audio CD and workbook format is an effective way to present this material. q Yes q No

9. What clinical problems related to asthma and COPD are you or your colleagues facing about which you would like to learn more?

10. Additional comments:

16 06 GS COPD PCS-2