Chronic obstructive pulmonary disease: An update

Abstract

Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. It is a chronic condition that affects the respiratory
system and worsens over time. The two major risks that are associated with this disease are cigarette smoking and an advancing age.
It is concerning that the global incidence of this chronic illness is on the rise, with current projections indicating that it will become the
third-leading cause of death by the year 2020. Inflammatory changes underlie the pathophysiology of COPD, with irreversible damage
and a progressive narrowing of the air passages that follow. COPD is characterised by a progressive loss of lung function. In addition,
the Global Strategy for the Diagnosis, Management, and Disease Prevention of Chronic Obstructive Pulmonary Disease, or GOLD,
released the latest update of their Global Strategy for the Diagnosis, Management, and prevention of Chronic Obstructive Pulmonary
Disease in 2015. This article provides an overview of the causative risk factors, the underlying disease process and pathophysiological
changes, the classification and the management of COPD, including the latest perspectives on this highly-prevalent condition.

Full text

2015 Vol 82 No 6S Afr Pharm J 24
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Introduction
Chronic obstructive pulmonary disease (COPD) is a leading cause
of death worldwide. It is a chronic condition that aects the
respiratory system and worsens over time. COPD encompasses
two clinical entities, namely chronic bronchitis and pulmonary
emphysema. As may be expected from a chronic illness, periods of
stable COPD is interspersed with episodes of acute exacerbations
(i.e. COPD relapses). COPD is largely associated with deterioration
in lung function and typically presents with respiratory symptoms
such as shortness of breath and a productive cough. Chronic
bronchitis is characterised by inammation of the bronchioles and
emphysema by permanently enlarged alveolar air spaces. COPD
exacerbations signicantly increase the rate at which the lung
function deteriorates as well as the mortality rate associated with
this disease.
1-3
COPD is predicted to become the third leading cause of global
mortality by the year 2020; the COPD-associated mortality rate
is currently on the increase. It is associated with a high socio-
economic burden and has a very signicant impact of the quality
of its suerers’ lives. The primary drivers of COPD are cigarette
smoking and old age. The former is associated with the inhalation
of pollutant particles that set pathophysiological changes in
motion, which ultimately result in damage to the lung tissue. For all
practical purposes, current treatment options are only capable of
managing bronchiolar smooth muscle spam and inammation.
1,3,4
Aetiology and pathogenesis
The major risk factors involved in the causation of COPD can be
divided into two groups, namely those that are exposure-related
versus those that are host-related, as depicted in Figure 1.
COPD is mainly characterised by a sequence of pathological
events that trigger inammatory changes within the airway,
with irreversible damage and a progressive narrowing of the air
passages that follow, resulting in an impairment of smooth air ow
through the lower respiratory tract. The major pathophysiological
mechanisms that underlie the development of COPD are
illustrated in Figure 2.
6,7
Chronic obstructive pulmonary disease:
an update
Natalie Schellack, BCur, BPharm, PhD (Pharmacy)
Associate Professor, Department of Pharmacy, Faculty of Health Sciences, Sefako Makgatho Health Sciences University
Gustav Schellack, BCur, Adv Univ Dipl Nurs Sc (HSM), Hons BSc (Pharmacology)
Clinical Research Manager and training specialist in the pharmaceutical industry, with a special interest in clinical research and applied pharmacology
Richard Omoding, BPharm
Academic Intern, Department of Pharmacy, Faculty of Health Sciences, Sefako Makgatho Health Sciences University
Correspondence to: Prof Natalie Schellack, natalie.schellack@smu.ac.za
Key words: chronic obstructive pulmonary disease, COPD, emphysema, chronic bronchitis, SABA, LABA, SAMA, LAMA, methylxanthines
Abstract
Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. It is a chronic condition that aects the respiratory
system and worsens over time. The two major risks that are associated with this disease are cigarette smoking and an advancing age.
It is concerning that the global incidence of this chronic illness is on the rise, with current projections indicating that it will become the
third-leading cause of death by the year 2020. Inammatory changes underlie the pathophysiology of COPD, with irreversible damage
and a progressive narrowing of the air passages that follow. COPD is characterised by a progressive loss of lung function. In addition,
the Global Strategy for the Diagnosis, Management, and Disease Prevention of Chronic Obstructive Pulmonary Disease, or GOLD,
released the latest update of their Global Strategy for the Diagnosis, Management, and prevention of Chronic Obstructive Pulmonary
Disease in 2015. This article provides an overview of the causative risk factors, the underlying disease process and pathophysiological
changes, the classication and the management of COPD, including the latest perspectives on this highly-prevalent condition.
© Medpharm S Afr Pharm J 2015;82(6):24-29
COPD
Figure 1: Risk factors associated with the development of COPD
5
[AAT : alpha-1 antitrypsin]
Exposure:
• Environmental tobacco smoke
• Occupational dust and
chemicals
• Environmental pollution,
including air pollution
Host Factors:
• Airway hyper-responsiveness
• Genetic predisposition (AAT
deciency)
• Impaired lung growth

2015 Vol 82 No 6S Afr Pharm J 25
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Exposure to a variety of air pollutants collectively contributes to
chronic obstructive pulmonary disease, with cigarette smoking
being the major causative factor. By description, there is a gradual
loss of the alveolar surfaces in the lungs, which is also clinically
referred to as emphysema; and the production of mucus that is
accompanied by the inammatory response to the damage that is
caused to the cells of the lung surfaces, may be dened as chronic
bronchitis. Another causative factor for the development of COPD
is attributed to the impact of a genetic mutation; this is, however,
only applicable to a small portion of the population.
6,8
Alpha-1 antitrypsin (AAT) is synthesised and secreted in two major
body organs, namely the lungs and the liver (as well as certain
types of white blood cells), with the liver being the major site of its
synthesis. AAT plays a vital role in the inhibition of the activity of
the enzyme, neutrophil elastase, which has destructive properties
that are meant to form part of normal white blood cell defence
mechanisms against invading pathogens. The neutrophil elastase
has the potential to overreact and damage normal body cells,
which in the case of COPD may be the lung tissues themselves.
Hence, there is a need for alpha-1 antitrypsin to control and
limit this enzyme’s rate of activity and, therefore, avoid ‘self-cell
destruction’ of the lungs. The Z-variant of alpha-1 antitrypsin
(Z-AAT) is an ineective protein that may arise as a consequence of
a genetic point mutation, which results in a decrease in normal AAT
secretion, a greatly reduced ability to inhibit neutrophil elastase,
and an accumulation within the epithelial cells of the bronchioles.
This, in turn, promotes pathogenesis within the pulmonary tissues
and could contribute to the causation of pulmonary emphysema
and chronic bronchitis.
9
Cigarettes contain more than 6000 dierent molecular entities
and multiple toxins that are released in the lungs to initiate an
inammatory response. Smoke interacts with lung macrophages,
as well as the epithelial cells that line the airways and the alveoli,
thus inuencing the release of chemokines that mediate the
inammatory response. Smoke has the potential to cause
activation of humoral inammation, a process that sequentially
leads to the production of C5a, which is a potent chemotactic
agent, which has its eect enhanced by a co-factor, namely the Gc-
globulin. In addition to inammation, lung tissue damage involves
a variety of multifaceted interactions, such as extracellular matrix
proteolysis, apoptosis and autophagic cell death, which result in
a loss of the elastic properties of the lungs, as well as a loss of the
intact structures that maintain normal shape, and therefore leads
to shrinkage.
10,11
Clinical presentation
A diagnosis of COPD will be made, based on the patient’s signs
and symptoms, and lung function tests. These indicators are
used jointly to increase the likelihood of correctly diagnosing the
patient with COPD. The likelihood of COPD increases in patients
over the age of 40 years. Once specic factors have been identied,
spirometry is used to establish the diagnosis of COPD.
6
The key
indicators are described in Table I.
Table I: Indicators that may lead to a diagnosis of COPD
6
Indicator Description Checklist
Dyspnoea That worsens over time (i.e. that is
progressive)

That worsens with exercise or exertion 
That is persistent 
Chronic cough That may be intermittent and may be
unproductive

Chronic sputum
production
Chronic sputum production 
Risk factor
exposure
Tobacco smoke (in any form) 
Smoke from cooking at home and from
heating fuels

Occupational dust and chemicals 
Family history of COPD 
According to the latest guidelines of the Global Strategy for the
Diagnosis, Management, and Disease Prevention of Chronic
Obstructive Pulmonary Disease, or GOLD (2015 update), the use
of screening spirometry is no longer advised; spirometry should
only be used after basic screening of high-risk patients has been
done. Spirometry in the post-bronchodilator setting, as a means of
identifying airow limitation, remains at a level of FEV
1
/FVC of <0.7
and can be used to conrm the diagnosis of COPD. A short-acting
b
2
-agonist at a dosage of 400 mcg, and/or an anticholinergic
(passive bronchodilator) at around 160 mcg can be administered
and the FEV
1
should then be measured. The measurement of the
FEV
1
can be taken 10-15 minutes after the short acting b
2
-agonist,
or 30-45 minutes following administration of the short-acting
anticholinergic, or when a combination of the two has been
administered. Subsequently, the results are then interpreted by
taking in to consideration the patient’s age, height, sex and race.
6
Categorising COPD
To ensure that a proper diagnosis is made, and with the aim
of avoiding errors in the long run, it is recommended that a
spirometry assessment is used once high-risk patients have been
identied. This will assist in evaluating the rate and extent of the
limitation in air ow for each individual patient. The following
should be considered as part of the assessment:
6,12-16
Figure 2: Mechanisms involved in the development of COPD
6
Airflow limitation
Disease of the small airways
Airway inammation; Airway
brosis; Luminal plugs; ↑ airway
resistance
Parenchymal destruction
Loss of alveolar attachments; ↓
elastic recoil
INFLAMMATION

2015 Vol 82 No 6S Afr Pharm J 26
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• An evaluation of lung function with the use of spirometry to
establish the forced expiratory volume in one second (FEV
1
):
Obstruction to airow is a primary parameter, used widely to
measure the extent of exacerbation or the presence of COPD in
the rst place. Resistance to the pulmonary air ow is observed
when the ratio of forced expiratory volume (FEV) in one second
to the forced vital capacity (FVC) is reduced.
• Respiratory symptoms like dyspnoea, coughing and shortness
of breath
• Exacerbation history of the patient, to establish the level of
progression from the initial time of onset or diagnosis of the
disease
• Comorbidity indices, to establish the presence and relate the
eect of any underlying conditions and disease on a given
patient.
Body mass index (BMI) should be considered in the diagnosis, as
patients with a low BMI have a greater risk of COPD exacerbation
and mortality when compared to obese patients. Co-morbid
conditions, such as diabetes and hypertension, also place patients
at a higher risk for COPD exacerbations.
14
Following the GOLD recommendations to include symptoms
and exacerbations in the diagnostic criteria when classifying the
disease severity from A to D (as shown in Figure 3), the assessment
of symptoms may be done in accordance with the COPD
Assessment Test (CAT) or the modied Medical Research Council
(mMRC) dyspnoea scale.
6,12
Guidelines to the results of these assessments indicate that if the
COPD Assessment Test score is ≥10, or if the mMRC dyspnoea scale
value is ≥2, then there is a high incidence of symptom worsening
for patients in risk groups B and D. Exacerbation is assessed, based
on the number of exacerbations experienced by the patient in
the past year, or with the use of the spirometry; the degree of air
ow resistance being determined with the use of severity grades
ranging from 1 to 4. The guidelines indicate that patients classied
in the severity grades of 3 to 4, and those that have experienced
exacerbations for the past two years will fall in to risk groups C
or D. However, with all of these developments, there is some
doubt whether the mMRC value of greater than, or equal to 10
suciently correlates with the CAT value of greater than, or equal
to 2. Hence the approach may not be a very reliable one.
12
The management of COPD patients is based on a combined COPD
assessment, which incorporates both the CAT score and the mMRC
score, and provides for the four categories (A to D) depicted in
Figure 3.
6
Management of COPD
The management of COPD involves setting treatment goals based
on the pathophysiology of the disease and involves reducing the
symptoms, as well as the overall risk, as depicted in Figure 4.
Non-pharmacological management
Smoking cessation is the intervention with the greatest capacity
to alter the progression of the disease. Smoking cessation can be
encouraged using the 5 A’s model. The 5 A’s model can assist in
identifying patients who are ready to quit and proceed to assist
them with advice about tobacco use. ‘Ask’ will systematically
identify all tobacco users visiting the healthcare facility. Inquiries
should be made in a friendly, non-accusing way, and tobacco
use should be indicated on all medical notes. ‘Advise’ should be
tailored to the specic patient, should be clear and strong, and
must be aimed at persuading the patient to quit. ‘Assess’ will be a
measure of the willingness of the patient to make an attempt to
Group A
Low risk, fewer symptoms
GOLD 1 or 2 (mild or moderate airow limitation)
and/or 0-1 exacerbations per year with no
hospitalisations for exacerbation
and CAT score <10 or mMRC grade 0-1
Group B
Low risk, more symptoms
GOLD 1 or 2 (mild or moderate airow limitation)
and/or 0-1 exacerbations per year with no
hospitalisations for exacerbation
and CAT score ≥10 or mMRC grade ≥ 2
Group C
High risk, fewer symptoms
GOLD 3 or 4 (severe or very severe airow
limitation)
and/or ≥2 exacerbations per year or ≥1
hospitalisation for exacerbation
and CAT score <10 or mMRC grade 0-1
Group D
High risk, more symptoms
GOLD 3 or 4 (severe or very severe airow
limitation)
and/or ≥2 exacerbations per year or ≥1
hospitalisation for exacerbation
and CAT score ≥ 10 or mMRC grade ≥2
COPD
Figure 3: The combined COPD assessment
6
Reducing the symptoms:
• Improving exercise tolerance
• Improving health status
• Relieving the symptoms with
minimal side-eects
Reducing the risk:
• Reducing the mortality rate
• Preventing and treating
exacerbations
• Preventing disease progression
Figure 4: Treatment goals for COPD
6

2015 Vol 82 No 6S Afr Pharm J 27
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quit. ‘Assist’ will be the action of the healthcare worker to support
the patient in developing a specic plan to quit, and of providing
support and recommendations on the use of medication. ‘Arrange’
is the planning of follow-up visits or contact with the patient,
either in person or by telephone.
6,17
The 5 R’s model can be used as a guideline towards motivational
intervention in assisting patients who are not ready to quit.
‘Relevance’ is used to point out to the patient how quitting is
personally relevant to him or her. ‘Risks’ will encourage the
patient to identify potential negative consequences of tobacco
use that are relevant to him or her. These risks may include the
cardiovascular threats like myocardial infarction (MI) and stroke,
and other illnesses like lung cancer and COPD, but also a threat to
wealth or the ensuing nancial burden thereof. ‘Rewards’ means
to make the patient aware of the potential benets of stopping
tobacco use, for example improved health, improved sense of
smell and taste, saving money and a general improvement in their
feeling of wellbeing. It is important to identify any ‘Roadblocks’
or barriers to quitting tobacco products and to provide advice
on treatment options to address these barriers, like withdrawal
symptoms, weight gain, depression and the presence of other
tobacco users. ‘Repetition’ is indicated if the patient is still not
ready to quit, in which case the patient should be re-assessed for
his or her readiness to quit and the intervention should therefore
be repeated at a later stage.
17
Identifying patients who are ready to quit smoking and
motivational measures to assist patients to quit smoking should
be every healthcare provider’s responsibility. Motivational
interviewing is an evidence-based approach to assist patients to
change their habits concerning tobacco use. However, counseling
and medication has both been shown to be eective in treating
tobacco dependence, but using medication together with
counseling has been shown to be more eective than either one
alone.
18,19
Older patients and/or patients with severe COPD should be
oered pneumococcal and inuenza vaccines. The vaccinations
can prevent some of the infections that are responsible for the
severe exacerbations of COPD.
5,6
Pharmacological management
In terms of the pharmacological management of COPD a
distinction should be made between the stable form of the
disease, and the management of exacerbations. Pharmacotherapy
should be aimed at:
6
• Achieving a reduction in the severity of the symptoms,
• Reducing the frequency and severity of exacerbations, and
• Improving the overall health status and the patient’s ability to
tolerate physical activities and exercise.
Current treatment options, however, cannot denitively modify
the characteristic reduction in pulmonary function that is seen
in patients suering from this disease. The current mainstay
of COPD treatment consists of two important classes of
pharmacotherapeutic agents, namely the bronchodilators (active
and passive) and the glucocorticosteroids.
6
The bronchodilators
These drugs cause relaxation of the bronchial smooth muscle,
and therefore facilitate bronchodilatation. The bronchial smooth
muscle contains both muscarinic (M
3
) and β
2
-adrenergic receptors.
This provides for two possible mechanisms of drug action, namely
active bronchodilatation and passive bronchodilatation.
3,20
Selective β
2
-receptor agonists: These drugs are selective
agonists at the adrenergic β
2
-receptors (also referred to as the
β
2
-adrenoceptors) of the bronchial smooth muscle when they
are inhaled directly into their biophase (i.e. when a localised
eect is achieved on the smooth muscle of the lower respiratory
tract). When administered intravenously (or even by mouth) they
lose their selectivity and will produce cardiac (β
1
-receptor) and
other systemic eects as well. Examples of short-acting agents
are salbutamol (also known as albuterol), fenoterol, levalbuterol,
hexoprenaline (no longer available) and terbutaline. By increasing
the concentration of cyclic adenosine monophosphate (cAMP),
these drugs act as active bronchodilators. Therefore, they achieve
a functional antagonism of bronchoconstriction. Patients should
be monitored for side-eects such as tachycardia, palpitations,
cardiac dysrhythmias, anxiousness, dizziness and skeletal muscle
tremors.
3,6,20
In contrast to the short-acting β
2
-agonists, which have an average
onset of action of approximately half an hour (or less), and a
duration of action in the range of four to six hours, the long-acting
β
2
-agonists (LABAs) will have a slower onset and more sustained
duration of action, lasting up to 12 hours. Examples of the latter
are salmeterol, formoterol, arformoterol and indacaterol (as well
as vilanterol).
3,6,20
Methylxanthines: Theophylline is a systemic bronchodilator
with a narrow therapeutic index. Therapeutic drug monitoring
is therefore required. It diers from the abovementioned drugs
in that it inhibits the enzyme phosphodiesterase. This produces
non-selective β-receptor eects through an increase in the cAMP
concentration. It is a second-line drug. Caeine is a methylxanthine
as well. Aminophylline is theophylline ethylenediamine, which is
more water soluble and may be administered intravenously. In
addition to their systemic β-adrenergic eects, the methylxanthines
also have a stimulatory eect on the CNS, resulting in increased
levels of alertness, irritability, anxiousness and insomnia, and with
additional side-eects such as tremors, tachycardia, palpitations
and cardiac dysrhythmias; and can cause gastric irritation.
3,6,20
Roflumilast: This is a possible treatment option in certain
patients with COPD, and is a phosphodiesterase type-4 (PDE-4)
inhibitor, as opposed to the methylxanthines that are non-specic
PDE-inhibitors, which therefore have the ability to increase the
concentrations of both cAMP and cGMP. Both roumilast and its
major active metabolite, roumilast N-oxide, are potent, selective
inhibitors of PDE-4, giving rise to increased intracellular levels of
cyclic AMP. PDE-4 is present in bronchial smooth muscle cells,
as well as immune system and pro-inammatory cells, where its
inhibition (and the subsequent rise in the cAMP concentration)
leads to the suppression of a wide variety of pro-inammatory

2015 Vol 82 No 6S Afr Pharm J 28
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responses. This drug can therefore be regarded as a novel anti-
inammatory agent, rather than a bronchodilator.
3,6
Anti-muscarinic (anti-cholinergic) drugs: The short-acting
drug of choice is ipratropium bromide, since it does not cause
thickening of the bronchial secretions. Blocking the muscarinic
receptors will inhibit acetylcholine-induced bronchoconstriction,
and implies that adrenergic stimulation of β
2
-adrenoceptors in the
bronchial smooth muscle will not be opposed by parasympathetic
outow from the vagus nerves. This results in bronchodilatation.
Therefore, ipratropium bromide is a passive bronchodilator
(oxitropium brominde is another example of a SAMA, or short-
acting muscarinic antagonist). Tiotropium bromide is a long-acting
muscarinic antagonist, or LAMA (other examples of LAMAs are
aclidinium bromide, umeclidinium bromide and glycopyrronium
bromide). These drugs are of particular importance in the
management of COPD, and because they are poorly absorbed
following inhalation they cause very few systemic side-eects.
3,6,20
Enhanced bronchodilatation may be achieved when combining
ipratropium bromide with a short-acting, selective β
2
-agonist,
such as salbutamol or fenoterol (or a LABA/LAMA combination
for inhalation), for example, due to the synergism between
their mechanisms of action. There are several other xed-dose
combinations available, including examples such as salbutamol/
ipratropium, formoterol/aclidinium, vilanterol/umeclidinium,
etc.
3,6,20
According to GOLD, bronchodilator therapy is central to the
management of symptoms in COPD, and inhalant therapy is
preferred over the systemic administration of such agents. They
may be prescribed, either for regular use, or on an as-needed
basis to manage symptoms, with the LABAs and LAMAs being
better at achieving sustained symptom relief than the SABAs and
SAMAs. Increased ecacy may be achieved through combination
therapy with bronchodilators from dierent classes, rather than
increasing dosages of a single agent. Roumilast is recommended
to reduce COPD exacerbations in patients with an FEV
1
of less than
50% predicted, chronic bronchitis and regular episodes of COPD
exacerbations.
6
Figure 5 depicts and summarises the major mechanisms of action
of the various classes of bronchodilators.
The ‘disease modifiers’
The inhaled glucocorticosteroids, such as budesonide,
beclomethasone and uticasone, are much safer for long-term
use than systemic corticosteroids. They will alter the course
of the disease process and are life-saving in the long run.
[b-receptor stimulation produces a stimulatory G-protein coupling, which results in the activation of adenylyl cyclase that, in turn, converts intracellular ATP to cyclic adenosine
monophosphate (the second messenger that produces bronchial smooth muscle relaxation). Conversely, stimulation of muscarinic M
3
-receptors will result in bronchial smooth
contraction (the SAMAs and LAMAs, therefore, act as receptor blockers, thereby achieving passive bronchodilatation). The methylxanthines and PDE-4 inhibitors, on the other hand,
prevent the degradation of cAMP to its inactive form, 5’-AMP, through their inhibition of the enzyme, phosphodiesterase. This also facilitates bronchodilatation via an increase in the
concentration of cAMP.]
20
Figure 5: The mechanisms of action of the dierent classes of bronchodilators

2015 Vol 82 No 6S Afr Pharm J 29
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They will, however, not manage acute bronchospasm, but will
decrease bronchial hyper-reactivity and the risk of a relapse.
Inhaled glucocorticosteroids may give rise to oral thrush (i.e. oral
candidiasis) and patients are therefore encouraged to rinse their
mouths with clean water following the use of their steroid inhalers.
Systemic agents include prednisone and methylprednisolone.
3,6,20
According to GOLD, long-term therapy with the inhaled
corticosteroids, in addition to long-acting bronchodilators
is recommended for patients with an increased risk for the
development of COPD exacerbations. Long-term steroid
monotherapy is not recommended.
6
COPD exacerbations
GOLD denes a COPD exacerbation as being: “…an acute event
characterised by a worsening of the patient’s respiratory symptoms
that is beyond normal day-to-day variations and leads to a change in
medication”. The most common trigger factors are viral infections
of the upper respiratory tract and tracheobronchial infections. The
recommendations for the management of a COPD exacerbation
include:
6
• The use of SABAs, with or without concomitant short-acting
anti-muscarinic agents
• Systemic corticosteroids and antibiotics (if indicated): these
agents can achieve positive outcomes in terms of improving the
FEV
1
, P
a
O
2
, the length of hospital stay and the time to recovery
from the relapse.
GOLD also mentions the following ways of reducing the number
of COPD exacerbations and hospitalisations:
6
• Smoking cessation
• Vaccination with pneumococcal and seasonal inuenza vaccines
• Adequate patient education regarding their treatment and the
correct use of their inhalers
• Treatment with long-acting bronchodilators, with or without
inhaled corticosteroids
• Treatment with a PDE-4 inhibitor (e.g. roumilast).
Conclusion
The eective management of COPD requires an accurate and timely
diagnosis, the removal of preventable risk factors, with smoking
cessation being the most notable, and the commencement
of eective pharmacotherapeutic measures in an attempt to
manage the symptoms, reducing the frequency and severity of
exacerbations, and improving the overall quality of life of these
patients. Current treatment options, however, cannot denitively
modify the characteristic reduction in pulmonary function that
is seen in patients suering from this disease. The backbone of
the current approach to the management of COPD remains the
active and passive bronchodilators, and the glucocorticosteroids.
Healthcare professionals need to have a thorough understanding
of the disease, its categorisation, and how the dierent classes of
bronchodilators and the glucocorticosteroids feature in the current
treatment guidelines for COPD. In addition, the signicance of a
COPD exacerbation should be clearly understood and the need for
more intensive therapy recognised. The health burden of COPD
is increasing and this disease will surely require more denitive
management approaches in the future.
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