Chronic Obstructive Pulmonary Disease (COPD) (cont.)
What treatment is available for COPD?
The goals of COPD treatment are 1) to prevent further deterioration in lung
function, 2) to alleviate symptoms, 3) to improve performance of daily
activities and quality of life. The
treatment strategies include 1) quitting cigarette smoking, 2) taking
medications to dilate airways (bronchodilators) and decrease airway
inflammation, 3) vaccinating against flu influenza and pneumonia and 4)
regular oxygen supplementation and 5) pulmonary rehabilitation.
Quitting cigarette smoking
The most important treatment for COPD is quitting
cigarette smoking. Patients who continue to smoke have a more rapid
deterioration in lung function when compared to others who quit. Aging itself can cause a very slow decline in lung
function. In susceptible individuals, cigarette smoking can result in a much
more dramatic loss of lung function. It is important to note that when one stops
smoking the decline in lung function eventually reverts to that of a non-smoker.
Unfortunately, only about one third of the patients can
abstain from smoking long term. Reasons for difficulty in quitting include
nicotine addiction, stress in the
workplace and at
home, depression, peer pressure, and advertising from
cigarette companies.
Nicotine in cigarettes is addictive, and, therefore,
cessation of smoking can cause symptoms of nicotine withdrawal including
anxiety, irritability,
anger,
depression, fatigue, difficulty concentrating or sleeping, and intense craving
for cigarettes. Patients likely to develop withdrawal symptoms
typically smoke more than 20 cigarettes a day, need to smoke shortly after
waking up in the morning, and have difficulty refraining from smoking in
non-smoking areas. However, some 25% of smokers can stop smoking without
developing these symptoms. Even in those smokers who develop symptoms of
withdrawal, the symptoms will decrease after several weeks of abstinence.
To help those patients with symptoms of withdrawal
during the early weeks of smoking cessation, nicotine chewing gum (Nicorette
Gum) and nicotine skin
patches (Transderm Nicotine) are available in the United States. Both the gum
and skin patches can deliver enough nicotine into the blood to reduce but not
totally eliminate withdrawal symptoms. Nicotine replacement methods in
conjunction with intense patient education and behavioral modification programs
have improved the rates at which individuals quit smoking. Nicotine skin patches
are easy to use. They generally are used for four to six weeks, sometimes with a
tapering period of several additional weeks. The addiction potential of nicotine
skin patches is low.
Bupropion (Zyban, Wellbutrin) is an antidepressant that
has been found to decrease cravings for cigarettes. It has been shown to be of
benefit to patients who want to quit smoking. Recently, varencline (Chantix), a
new medication is available to aid in smoking cessation, has been approved for use in the US.
Varenicline works in two ways; by cutting the pleasure of smoking and reducing
the withdrawal symptoms that lead smokers to light up again and again. This
medicine is taken over a 12 week course and can work in ways that bupropion does
not.
In addition to nicotine withdrawal symptoms, quitting
cigarette smoking also may lead to weight gain of about 8-10 pounds on average
though more in some patients. Quitting smoking also can lead to depression and
worsening of symptoms of chronic ulcerative colitis. Therefore
quitting smoking
should be undertaken with a doctor's supervision. Nevertheless, the benefits of
quitting smoking (decreasing the rate of lung deterioration, decreasing risks of
heart attack, lung cancer and other cancers, decreasing the chance of developing
stomach
ulcers, etc.) far outweigh these potential negative effects.
For more information on quitting cigarette smoking, please read the
Smoking
and Quitting Smoking article.
Bronchodilators
Treating airway obstruction in COPD with bronchodilators is similar but not
identical to treating bronchospasm in asthma. Bronchodilators are medications
that relax the muscles surrounding the small airways thereby opening the
airways. Bronchodilators can be inhaled, taken orally or administered
intravenously. Inhaled bronchodilators are popular because they go directly to
the airways where they work. As compared with bronchodilators given orally, less
medication reaches the rest of the body, and, therefore, there are fewer side
effects.
Metered dose inhalers (MDIs) are used to deliver
bronchodilators. An MDI is a pressurized canister containing a medication that
is released when the canister is compressed. A standard amount of medication is
released with each compression of the MDI. To maximize the delivery of the
medications to the airways, the patient has to learn to coordinate inhalation
with each compression. Incorrect use of the MDI can lead to deposition of much
of the medication on the tongue and the back of the throat instead of on the airways.
To decrease the deposition of medications on the throat
and increase the amount reaching the airways, spacers can be helpful. Spacers
are tube-like chambers attached to the outlet of the MDI canister. Spacer devices can hold the
released medications long enough for patients to inhale them slowly and deeply
into the lungs. Proper use of spacer devices can greatly increase the proportion
of medication reaching the airways.
Beta-agonists
Historically, one of the first medications used for
asthma was adrenaline (epinephrine). Adrenaline has a rapid onset of action in
opening the airways. It is still used in certain emergency situations for
attacks of asthma. Unfortunately, adrenaline has many side effects including
rapid heart rate, headache, nausea, vomiting, restlessness, and a sense of
panic. Therefore, it is
not used in the treatment of COPD.
Beta-2 agonists have the bronchodilating effects of
adrenaline without many of its unwanted side effects. Beta-2 agonists can be
administered by MDI inhalers or orally. They are called "agonists" because they
activate the beta-2 receptor on the muscles surrounding the airways. Activation
of beta-2 receptors relaxes the muscles surrounding the airways and opens the
airways. Dilating
airways helps to relieve the symptoms of dyspnea (shortness of breath). Beta-2
agonists have been shown to relieve dyspnea in many COPD patients, even among
those without demonstrable reversibility in airway obstruction. The action of
beta-2 agonists starts within minutes after inhalation and lasts for about 4
hours. Because of their quick onset of action, beta-2 agonists are especially
helpful for patients who are acutely short of breath. Because of their short
duration of action, these medications should be used for symptoms as they
develop rather than as maintenance. Evidence suggests that when these drugs are
used routinely, their effectiveness is diminished. These are referred to as
rescue inhalers. Examples of beta-2 agonists include albuterol (Ventolin,
Proventil), metaproterenol (Alupent), pirbuterol (Maxair), terbutaline
(Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex) is a recently
approved Beta-2 agonist.
In contrast, Beta-2 agonists with a slower onset of action but a longer
period of activity, such as salmeterol xinafoate (Serevent) and formoterol
fumarate (Foradil) may be used routinely as maintenance medications. These drugs
last twelve hours and should be taken twice daily and no more. Along with some
of these inhalers to be mentioned, these are often referred to as maintenance
inhalers.
Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast
heart rate, and low blood potassium.
Anti-cholinergic Agents
Acetylcholine is a chemical released by nerves that attaches to receptors on
the muscles surrounding the airway causing the muscles to contract and the
airways to narrow. Anti-cholinergic drugs such as ipratropium bromide (Atrovent)
dilate airways by blocking the receptors for acetylcholine on the muscles of the
airways and preventing them from narrowing. Ipratropium bromide (Atrovent)
usually is administered via a MDI. In patients with COPD, ipratropium has been
shown to alleviate dyspnea, improve exercise tolerance and improve FEV1.
Ipratropium has a slower onset of action but longer duration of action than the
shorter-acting beta-2 agonists. Ipratropium usually is well tolerated with
minimal side effects even when used in higher doses. Tiotropium (SPIRIVA) is a
long acting and more powerful version of Ipratropium and has been shown to be
more effective.
In comparing ipratropium with beta-2 agonists in the treatment of patients
with COPD, studies suggest that ipratropium may be more effective in dilating
airways and improving symptoms with fewer side effects. Ipratropium is
especially suitable for use by elderly patients who may have difficulty with
fast heart rate and tremor from the beta-2 agonists. In patients who respond
poorly to either beta-2 agonists or ipratropium alone, a combination of the two
drugs sometimes results in a better response than to either drug alone without
additional side effects.
Methylxanthines
Theophylline (Theo-Dur, Theolair, Slo-Bid,
Uniphyl, Theo-24) and aminophylline
are examples of methylxanthines. Methylxanthines are administered orally or
intravenously. Long acting theophylline preparations can be given orally once or
twice a day. Theophylline, like a beta agonist, relaxes the muscles surrounding
the airways but also prevents mast cells around the airways from releasing
bronchoconstricting chemicals such as histamine. Theophylline also can act as a
mild diuretic and increase
urination. Theophylline also may increase the force of contraction of the heart
and lower pressure in the pulmonary arteries. Thus, theophylline can help
patients with COPD who have heart failure and pulmonary
hypertension. Patients who have difficulty using inhaled bronchodilators but no
difficulty taking oral medications find theophylline particularly useful.
The disadvantage of methylxanthines is their side
effects. Dosage and blood levels of theophylline or aminophylline have to be
closely monitored. Excessively high levels in the blood can lead to nausea,
vomiting, heart rhythm problems, and even seizures. In patients with heart
failure or cirrhosis, dosages of methylxanthines are lowered to avoid high blood
levels. Interactions with other medications, such as cimetidine (Tagamet),
calcium channel blockers
(Procardia), quinolones (Cipro), and allopurinol (Zyloprim) also can alter blood
levels of methylxanthines.
Corticosteroids
When airway inflammation (which causes swelling)
contributes to airflow obstruction, anti-inflammatory medications (more
specifically, corticosteroids) may be beneficial. Examples of corticosteroids
include Prednisone and Prednisolone. Twenty to thirty percent of patients with
COPD show improvement in lung function when given corticosteroids by mouth.
Unfortunately, high doses of oral corticosteroids over prolonged periods can
have serious side effects, including osteoporosis, bone fractures, diabetes
mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight
gain. Therefore, many doctors use oral corticosteroids as the treatment of last
resort. When oral corticosteroids are used, they are prescribed at the lowest
possible doses for the shortest period of time to minimize side effects. When it
is necessary to use long term oral steroids, medications are often prescribed to
help reduce the development of the above side effects.
Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer
side effects than long term oral corticosteroids. Examples of inhaled
corticosteroids include beclomethasone dipropionate (Beclovent, Beconase,
Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone
(Flovent), budesonide (Pulmicort), mometasone furoate (Asmanex) and flunisolide
(Aerobid). Inhaled corticosteroids have been useful in treating patients with
asthma, but in patients with COPD, it is not clear whether inhaled
corticosteroid have the
same benefit as oral corticosteroids. Nevertheless, doctors are less concerned
about using inhaled corticosteroids because of their safety. The side effects of
inhaled corticosteroids include hoarseness, loss of voice, and oral yeast
infections. A spacing device placed between the mouth and the MDI can improve
medication delivery and reduce the side effects on the mouth and throat. Rinsing
out the mouth after use of a steroid inhaler also can
decrease these side effects.
Advair, a powered inhaler device, contains both
salmeterol (a long acting beta-agonist) and fluticasone (an inhaled steroid).
This medication has shown to be effective in COPD patients with chronic
bronchitis. Its major side effects include the possible development of thrush
(oral candidiasis) and hoarseness.
Treatment of Alpha-1 antitrypsin deficiency
Emphysema can develop at a very young age in some
patients with severe alpha-1 antitrypsin deficiency (AAT). Replacement of the
missing or inactive AAT by injection can help prevent progression of the
associated emphysema. This therapy is of no benefit in other types of COPD.
Next: What is the role of oxygen as therapy in COPD? »
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