Everything about Chronic Obstructive Pulmonary Disease totally explained
Chronic Obstructive Pulmonary Disease (
COPD), also known as
chronic obstructive airway diseases (
COAD), is a group of
diseases characterized by the pathological limitation of airflow in the
airway that isn't fully reversible. It refers to an obstruction of airflow, which results in air becoming trapped in the lungs. COPD is the
umbrella term for
chronic bronchitis,
emphysema and a range of other lung disorders. It is most often due to
tobacco smoking, but can be due to other airborne irritants such as
solvents, as well as
congenital conditions such as
alpha-1-antitrypsin deficiency. It is the 4th leading cause of death in the U.S.
Signs and symptoms
The main
symptoms of COPD are
dyspnea (shortness of breath) lasting for months or perhaps years, possibly accompanied by
wheezing, and a persistent
cough with
sputum production. It is possible the sputum may contain blood (
hemoptysis) and become thicker, usually due to damage of the blood vessels of the airways. Severe COPD could lead to
cyanosis (bluish decolorization usually in the lips and fingers) caused by a lack of
oxygen in the blood. In extreme cases it could lead to
cor pulmonale due to the extra work required by the heart to get blood to flow through the lungs.
COPD is particularly characterised by the
spirometric measurement of a ratio of forced expiratory volume over 1 second (
FEV1) to forced vital capacity (FVC) being < 0.7 and the
FEV1 < 80% of the predicted value as measured by a
plethysmograph. Other
signs include a rapid breathing rate (
tachypnea) and a wheezing sound heard through a
stethoscope. Pulmonary emphysema is
not the same as
subcutaneous emphysema, which is a collection of air under the skin that may be detected by the
crepitus sounds produced on
palpation.
- Shortness of breath (dyspnea) persisting for months to years
- Wheezing
- Decreased exercise tolerance
- Cough with or without phlegm
Etiology
Cigarette smoking
A primary risk factor of COPD is chronic tobacco smoking. In the
United States, around 80 to 90% of cases of COPD are due to smoking. Not all smokers will develop COPD, but continuous smokers have at least a 25% risk, after 25 years.
Occupational pollutants
Some occupational pollutants, such as
cadmium and
silica, have shown to be a contributing risk factor for COPD. Coal workers who smoke have increased risk for concomitmant
pneumoconiosis and
emphysema. Asbestos workers who smoke are at increased risk for concomitant
emphysema,
asbestosis and
mesothelioma.
Air pollution
Urban
air pollution may be a contributing factor for COPD as it's thought to impair the development of the lung function. In
developing countries indoor air pollution, usually due to
biomass fuel, has been linked to COPD, especially in women.
Other risk factors
Increasing age, male gender,
allergy, repeated airway
infection and general impaired function are also related to the development of COPD.
COPD as an autoimmune disease
There is mounting evidence that there may be an autoimmune component in individuals with COPD. This is evidenced by the presence of autoreactive T-cells and autoantibodies found in patients. In addition, many individuals who have stopped smoking continue to have chronic inflammation and decline in lung function.
Pathophysiology
Chronic bronchitis
Chronic bronchitis is defined in
clinical terms as a cough with sputum production on most days for 3 months of a year, for 2 consecutive years.
Chronic bronchitis is hallmarked by
hyperplasia (increased number) and
hypertrophy (increased size) of the
goblet cells (
mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction.
Microscopically there's
infiltration of the airway walls with
inflammatory cells, particularly
neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to
metaplasia (abnormal change in the tissue) and
fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow.
Emphysema
Emphysema is defined
histologically as the enlargement of the air spaces
distal to the
terminal bronchioles, with destruction of their walls.
Physical examination
A
systematic review has concluded that no single
medical sign or
symptom can adequately exclude the diagnosis of COPD. One study found that the presence of either "a history of smoking more than 30 pack-years, diminished breath sounds, or peak flow less than 350 L/min" has a
sensitivity of 98 percent.
Management
Although COPD isn't curable, it can be controlled in a variety of ways.
Clinical practice guidelines by
Global Initiative for Chronic Obstructive Lung Disease
(GOLD), a collaboration including the American
National Heart, Lung, and Blood Institute and the
World Health Organization, are available.
Smoking cessation
Smoking cessation is one of the most important factors in slowing down the progression of COPD. Even at a late stage of the disease it can reduce the rate of deterioration and prolong the time taken for disability and death. These drugs relax the
smooth muscles of the airway allowing for improved airflow. The change in
FEV1 may not be substantial, but changes in the
vital capacity are significant. Many patients feel less breathless after taking bronchodilators.
β2 agonists
There are several highly specific β
2 agonists available.
Salbutamol (Ventolin) is the most widely used short acting β
2 agonist to provide rapid relief and should be prescribed as a front line therapy for all classes of patients. Other β
2 agonists are
Bambuterol,
Clenbuterol, Fenoterol, and
Formoterol. Long acting β
2 agonists (LABAs) such as
Salmeterol act too slowly to be used as relief for
dypsnea so these drugs should be used as maintenance therapy in the appropriate patient population. The TORCH study showed that LABA therapy reduced COPD exacerbation frequency over a 3 year period, compared to placebo. An increased risk is associated with long acting β
2 agonists due to decreased sensitivity to inflammation so generally the use of a concomitant
corticosteroid is indicated
(External Link)(External Link)(External Link).
M3 muscarinic antagonists (anticholinergics)
Specific
antimuscarinics were found to provide effective relief to COPD. Inhaled antimuscarinics have the advantage of avoiding
endocrine and
exocrine M
3 receptors. The quaternary M
3 muscarinic antagonist
Ipratropium is widely prescribed with the β
2 agonist
salbutamol.
(External Link). Ipratropium formerly was offered combined with salbutamol (Combivent) and with fenoterol (Duovent) but due to the CFC propellant, these products have been withdrawn.
Tiotropium provides improved specificity for M
3 muscarinic receptors. It is a long acting muscarinic antagonist that has shown good efficacy in the reduction of exacerbations of COPD, especially when combined with a LABA and inhaled steroid.
Cromones
Cromones are
mast cell stabilizers that are thought to act on a
chloride channel found on
mast cells that help reduce the production of
histamine and other inflammatory factors. Chromones are also thought to act on IgE-regulated
calcium channels on mast cells.
Cromoglicate and
Nedocromil, which has a longer half-life, are two chromones available.
Leukotriene antagonists
More recently
leukotriene antagonists block the signalling molecules used by the immune system.
Montelukast,
Pranlukast,
Zafirlukast are some of the leukotrienes antagonists.These agents have not been tested in good, controlled trials, and as such, there's no data to support the use of these agents in COPD.
Xanthines
Theophylline is the prototype of the
xanthine class of drug. Teas are natural sources of methylxanthines, xanthines and
caffeine while
cocoa is a natural source of
theobromine.
Caffeine is approximately 16% metabolized into theophylline. Nebulized theophylline is used in the EMR for treatment of
dyspnea (Difficulty in breathing). Patients need continual monitoring as theophylline has a narrow
therapeutic range. More aggressive EMR interventions include IV H
1 antihistamines and IM
dexamethasone.
Theophylline antagonizes
phosphodiesterase, and small reductions in COPD exacerbation rates have been demonstrated. The investigative phosphodiesterase-4 antagonists,
roflumilast and
cilomilast have completed Phase-2 clinical trials.
Corticosteroids
Enteral and parenteral corticosteroid therapy has long been the mainstay of treatment of COPD, and is known to reduce length of stay in hospital. Similarly, inhaled
corticosteroids (specifically
glucocorticoids) act in the inflammatory cascade and improve airway function considerably, Corticosteroids are often combined with bronchodilators in a single inhaler. Some of the more common inhaled steroids in use are
beclomethasone,
mometasone, and
fluticasone.
Salmeterol and fluticasone are combined (Advair), however the reduction in death from all causes among patients with COPD in the combination therapy group didn't reach the predetermined level of statistical significance.
TNF antagonists
Tumor necrosis factor antagonists (TNF) are the most recent class of medications designed to deal with refractory cases.
Tumor necrosis factor-alpha is a cachexin or cachectin and is considered a so-called biological drug. They are considered immunosopressive with attendant risks. These rather expensive drugs include
infliximab,
adalimumab and
etanercept.Infliximab has been trialled in COPD with no evidence of benefit, with the possibility of harm. This was a relatively small study (77-79 patients in each arm).
Supplemental Oxygen
In general, long-term administration of oxygen is usually reserved for individuals with COPD who have arterial
hypoxemia (
PaO2 less than 55 mm Hg), or a PaO2 between 55 and 60 mm Hg with evidence of
pulmonary hypertension,
cor pulmonale, or secondary
erythrocytosis (hematocrit >55%). In these patients, continuous home oxygen therapy (for >15 h/d) sufficient to correct hypoxemia has been shown to improve survival. The use of low flow oxygen may be necessary in some patients because in the COPD patient,
control of respiration is driven mainly by the blood oxygen level rather than the carbon dioxide level, increased oxygen delivery can diminish this response and cause respiratory failure. The American Thoracic Society Guidelines on COPD cover the use of oxygen therapy and its risks.
Vaccination
Patients with COPD should be routinely
vaccinated against
influenza,
pneumococcus and other diseases to prevent illness and the possibility of death. Pulmonary rehabilitation has been shown to relieve difficulties breathing and fatigue. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.
Diet
A recent French study conducted over 12 years with almost 43,000 men concluded that eating a
Mediterranean diet "halves the risk of serious lung disease like emphysema and bronchitis".
(External Link)
Treatment
Treatment for COPD includes inhalers that dilate the airways (bronchodilators) and sometimes theophylline. The COPD patient must stop smoking. In some cases inhaled steroids are used to suppress lung inflammation, and, in severe cases or flare-ups, intravenous or oral steroids are given.
Antibiotics are used during flare-ups of symptoms as infections can worsen COPD. Chronic, low-flow oxygen, non-invasive ventilation, or intubation may be needed in some cases. Surgery to remove parts of the disease lung has been shown to be helpful for some patients with COPD.
Lung rehabilitation programs may help some patients.
Lung transplant is sometimes performed for severe cases.
Support Groups
The stress of illness can often be helped by joining a support group where members share common experiences and problems.
Prognosis
A good prognosis of COPD relies on an early diagnosis and prompt treatment. Most patients will have improvement in lung function once treatment is started, however eventually signs and symptoms will worsen as COPD progresses. The median survival is about 10 years if two-thirds of expected lung function was lost by diagnosis.
"End Stages" of COPD are diagnosed as the normal ratio of carbon dioxide being inordinately higher than the volume of oxygen in the bloodstream. Although end stage COPD may mean death is imminent in cases dealing with degenerative diseases, forced oxygen therapy and other treatments may successfully be used to prolong life but have not been proven to be successful for the long run. These types of therapy may be successfully used in COPD cases caused by curable diseases such as bronchitis.
Bronchitis
Acute
bronchitis usually resolves in 2-10 years.
Emphysema
The outcome is better for patients with less damage to the lung who stop smoking immediately. Still, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from respiratory failure,
pneumonia, or other complications.
Pneumoconiosis
The outcome is good for patients with minimal damage to the lung. However, patients with extensive lung damage may live for many years so predicting prognosis is difficult. Death may occur from
respiratory failure,
pneumonia,
cor pulmonale or other complications.
Pulmonary neoplasms
The stage of the
tumor(s) has a major impact on
neoplasm prognosis. Staging is the process of determining tumor size, growth rate, potential
metastasis, lymph node involvement, treatment options and prognosis. Two-year prognosis for limited small cell pulmonary neoplasms is twenty percent and for extensive disease five percent. The average life expectancy for someone with recurrent small cell pulmonary neoplasms is two to three months.
(External Link)
The 5-year overall survival rate for pulmonary neoplasms is 14%.
Epidemiology
According to the
World Health Organization (WHO), 80 million people suffer from moderate to severe COPD and 3 million died due to it in 2005. The WHO predicts that by 2030, it'll be the 4th largest cause of mortality worldwide.
Since COPD isn't diagnosed until it becomes clinically apparent, prevalence and mortality data greatly underestimate the
socioeconomic burden of COPD.
In the UK, COPD accounts for about 7% of all days of sickness related absence from work.
Smoking rates in the industrialized world have continued to fall, causing rates of emphysema and pulmonary neoplasms to slowly decline.
Further Information
Get more info on 'Chronic Obstructive Pulmonary Disease'.
|
External Link Exchanges
Do you know how hard it is to get a link from a large encyclopaedia? Well we're different and will prove it. To get a link from us just add the following HTML to your site on a relevant page:
<a href="http://chronic_obstructive_pulmonary_disease.totallyexplained.com">Chronic obstructive pulmonary disease Totally Explained</a>
Then simply click through this link from your web page. Our crawlers will verify your link, extract the title of your web page and instantly add a link back to it. If you like you can remove the words Totally Explained and embed the link in article text.
As long as your link remains in place, we'll keep our link to you right here. Please play fair - our crawlers are watching. Your site must be closely related to this one's topic. Any kind of spamming, dubious practises or removing the link will result in your link from us being dropped and, potentially, your whole site being banned. |
