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Ailments causing Bronchial obstruction- Especially, Chronic Obstructive Pulmonary Diseases (COPD)

Updated on November 11, 2011

clinical findings of Bronchial obstruction

Bronchial lumen view in healthy (a) and asthmatic (b) persons: 1  mucosa, 2  submucosa and 3  smooth muscles; 4  a mucous plug
Bronchial lumen view in healthy (a) and asthmatic (b) persons: 1 mucosa, 2 submucosa and 3 smooth muscles; 4 a mucous plug | Source
Chest radiograph 17 hours after extubation.
Chest radiograph 17 hours after extubation. | Source
Chest radiograph 20 hours after extubation.
Chest radiograph 20 hours after extubation. | Source
 Histopathology of asthma: 1 - normal bronchial cross section; 2, 3, 4, 5 - mechanisms of the bronchial obstruction
Histopathology of asthma: 1 - normal bronchial cross section; 2, 3, 4, 5 - mechanisms of the bronchial obstruction | Source
Posteroanterior chest radiograph shows poorly defined increased opacity of the left hemithorax associated with superior displacement of the left hilum and elevation of the left hemidiaphragm characteristic of left upper lobe atelectasis. The patient
Posteroanterior chest radiograph shows poorly defined increased opacity of the left hemithorax associated with superior displacement of the left hilum and elevation of the left hemidiaphragm characteristic of left upper lobe atelectasis. The patient | Source

Bronchial Obstruction

COPD and Bronchial Asthma are the most common diseases of the Lungs in which 4-10% of Adults in the world are ill of COPD. In Europe, 7.4% of people have COPD and mortality of such patients is 10%. According to Gold (Global initiative for Chronic Obstructive Lung Disease), COPD is a disease which is characterized by combination of clinical signs of chronic obstructive bronchitis (inflammation and narrowing of bronchi) and emphysema (changes of Lung tissue structure)

Etiology of bronchial obstruction: a) spasm; b) mucous odema; c) hypersecretion; d) scar narrowing: e) endobronchial tumor; f) external pressuring of bronchus.

Airways obstruction is mainly caused by: Chronic bronchitis, Emphysema, Cystic fibrosis (mucoviscidosis), Bronchial asthma

Pathogenesis of bronchial obstruction is based on ventilation disturbances caused by etiological factor.

Classification of bronchial obstruction is based on spirography estimation of decrease of FEV1: stage 1 >= 70 %, stage 2– 50-69 %, stage 3– < 50 %.

Clinical signs of syndromes:

Bronchial spasm (paroxysmal and steady) – Expiratory dyspnoe, dry cough, dry rales. Accent of second sound on a. pulmonale, on ECG overloading of right ventricle. X-ray examination – acute enphysema. Decrease of symptoms after administration of broncholytics.

Bronchial inflammation (diffuse and local) – common symptoms of inflammation associated with pain in trachea or bronchi, cough (dry or wet), rales;

Delay of sputum – dry nonproductive cough associated with bed feeling and high temperature changes on large amount of spurum during coughing and relieve of all symptoms (lung abscess, chronic bronchitis etc.).

Obturation and compression of bronchus – Absence of ventilation in part of lung. Symptoms of lung atelectasis.

Trachea and bronchial narrowing– inspiratory dyspnoe, cough, restriction of chest movements. Symptoms of hypoventilation. Atelectasis in perspective (tumor etc.).

Bronchial drainage disturbances– based on bed function of epithelium and suppressed coughing reflex. Cough associated with wet rales. Degenerative changes in epithelium.

Bronchial mucous hypersecretion – deals with changes of neuro-humoral regulation or irritation of mucosa. In sputum: low amount of leucocytes and a lot of fluid;

Hypersensitivity of bronchus – allergic in origin and is reaction on infection or non infection factors. The main symptoms are: sneezing, cough, wheezing after contact with allergen. In sputum: eosinophylia, Sharko-Laiden crystals.

Clinical peculiarities of bronchial disorders in case of bronchitis, pneumonia, bronchial asthma, bronchoectases,tumors.

Bronchitis. There are obstructive and non obstructive bronchitis. The obstructive btonchitis is the main cause of bronchial obstruction. The most common are the syndromes of bronchial inflammation and delay of sputum. Bronchial spasm is not common.

Bronchial asthma. The main syndrom is bronchospasm with dyspnoe of expiratory type associated with allergic inflamation.

Pneumonia. In 55% of patients are bronchial disorders. Pneumonia may worse the previously persisted bronchial obstruction. The syndromes of inflammation and Delay of sputum and sometimes bronchospasm are usual.

Bronchoectases independently don’t course bronchial obstruction but frequently associates with chronic bronchitis, pneumonia or hiredetary abnormalities that course the obstruction or other syndromes.

Tumors frequently compress the bronchus. Hypoventylation, regional pneumatosis and atelectasis subsequently develops. Syndrom of obturation and compression of bronchus are frequent.

Diagnostic value of laboratory and instrumental investigations for bronchial obstruction and it peculiarities in patients with lung diseases is completely described in methodological instructions to lesson 1 in pulmonology. Its necessary to say that the most important methods of diagnostics are spirometry and peakfluorymetry. The perculiarities of diagnostics in cases of different diseases are described in chapters dedicated to this pathology either in methodological instructions or in handbooks.


Clinically significant, irreversible, generalized airways obstruction associated with varying degrees of chronic bronchitis, abnormalities in small airways, and emphy sema. The designation was introduced because chronic bronchitis, small airways abnormalities, and emphysema often coexist and it may be difficult in an individ ual case to decide which is the major factor producing the airways obstruction.

When it is clear that the patient's entire disease can be explained by emphysematous changes in the lung, the diagnosis "chronic obstructive emphysema" is pre ferred to the more general designation COPD. Similarly, the diagnosis "chronic obstructive bronchitis"should be used when the obstructive abnormality is a di rect result of an inflammatory process in the airways.

To avoid the semantic confusion often encountered in discussions of these dis orders, the following definitions are provided. Chronic bronchitis, when unquali fied, is defined as acondition associated with prolonged exposure to nonspecific bronchial irritants and accompanied by mucus hypersecretion and certain structural alterations in the bronchi.Clinically, it is characterized by chronic productive cough and is usually associated with cigarette smoking. Pulmonary emphysema is defined as enlargement of the air spaces distal to the terminal nonrespiratory bronchioles, accompanied by destructive changes of the alveolar walls. Airways obstruction is defined asincreased resistance to air flow during forced expiration. It may result from narrowing or obliteration of the airways secondary to intrinsic bronchial disease or from excessive collapse of airways during forced expiration secondary to pulmonary emphysema.

The interrelationships between chronic bronchitis, pulmonary emphysema, and COPD are depicted inFIG. 34-1. Some degree of emphysematous change is ex tremely common in the general population, but not all patients with emphysema have sufficient airways obstructive problems to be considered as having COPD. Similarly, many cigarette smokers have evidence of chronic bronchitis, but only a minority have clinically significant airways obstruction, usually associated with marked changes in the small airways of the lung. As noted in FIG. 34-1, most patients with clinically significant irreversible airways obstruction (COPD) have some combination of chronic bronchitis and emphysema. It is uncertain, however, whether this overlap results from a common causal factor or whether emphysema and chronic bronchitis predispose to one another.


The development of chronic bronchitis, emphysema, and chronic airways ob struction appears to be determined by a balance between individual susceptibility and exposure to provocative agents.

The basic lesion of emphysema apparently results from the effect of proteolytic enzymes on the alveolar wall. Such enzymes can be released from leukocytes participating in an inflammatory process. Thus, any factor leading to a chronic inflammatory reaction at the alveolar level encourages development of emphysematous lesions. Smoking presumably plays a role due to its adverse effects on lung defense mechanisms (particularly by impairing the function of the alveolar macrophage) permitting low-grade inflammatory reactions to develop with conse quent recurrent or chronic release of leukocytic proteolytic enzymes (see Ch. 48). Fortunately, most people can neutralize such enzymes as a result of antiproteolytic activity of the «i-globulin fraction of their sera. In a rare condition known ashomozygotic antitrypsin deficiency, however, the serum antiproteolytic activity is markedly diminished. In such patients, emphysema may develop by middle age even in the absence of exposure to substances that interfere with lung defense mechanisms. In the absence of severe deficiency of ai-globulin in the serum, however, the factors which make some cigarette smokers more susceptible to develop ment of emphysema than others remain uncertain. It is also uncertain why persons with similar degrees of emphysema may have considerably varying de grees of severity of airways obstruction.

With sufficient exposure to bronchial irritants, particularly cigarette smoke, most persons develop some degree of chronic bronchitis. The lesion essential to development of severe airways obstruction is apparently located in the small air ways and may be basically different from the ordinary large airways abnormality which leads to hypersecretion of mucus in most smokers. The reason why small airways abnormalities develop in some patients with chronic bronchitis is uncer tain, but viral or bacterial pulmonary infections in childhood, an unidentified immunologic mechanism, a mildly impaired ability to inactivate proteolytic en zymes (as in heterozygotic antitrypsin deficiency), or unidentified genetic char­acteristics could be predisposing factors. While typical allergic bronchial asthma is not a common precursor of COPD, the exact interrelationships of these disor ders are not known.


COPD is a major cause of disability and death. In the USA, it is second to heart disease as a cause of disability in Social Security statistics, and reported mortality rates have been doubling about every 5 yr. Its true mortality probably exceeds that from lung cancer. Some of this increase reflects the longer survival of patients who previously would have died of bacterial pneumonia before their COPD became known. Overall, it has been estimated that COPD affects as many as 15% of older men. Symptomatic COPD affects men 8 to 10 times more often than women, presumably as a result of the more frequent, prolonged, and heavier smoking in men; however, the incidence in women is now increasing.


In patients with severe emphysema, the lungs are large and pale and often fail to collapse when the thorax is opened. Microscopic examination reveals "departitioning" of the lung due to loss of alveolar walls. Large bullae may be present in advanced disease. Changes may be most marked in the center of the secondary lobule (centrilobular emphysema) or more diffusely scattered throughout the lobule (panacinar emphysema). In all forms, the normal architecture is destroyed; rupture of septa results in air sacs of various sizes. The number of capillaries in the remaining alveolar walls is reduced, and the pulmonary arterial vessels may show sclerotic changes. These abnormalities lead not only to a reduction in the area of alveolar membrane available for gas exchange, but also to the perfusion of non-ventilated areas and to the ventilation of nonperfused parts of the lung; i.e., ventilation/perfusion abnormalities. They also lead to poor support of the airways of the lung, accounting for excessive collapse of airways on expiration.

In chronic bronchitis, the bronchial walls are thickened, there is mucus in the lumen, and the number of goblet cells and mucous glands is increased. There may be purulent secretions and inflammatory changes in bronchial walls and sur rounding lung parenchyma if infection is present. Such large airways changes do not account for severe airways obstruction, however, and in patients dying of COPD, narrowing or obliteration, or both, of small airways may be observed.

Right ventricular hypertrophy (cor pulmonale) is common in patients with ad vanced respiratory insufficiency.

Clinical pictures of COPD

Smoking and COPD
Smoking and COPD
Pictures Images COPD Chronic Obstructive Pulmonary Disorder Chronic obstructive pulmonary disease COPD refers to chronic lung disorders that result in blocked air flow in the lungs The two main COPD
Pictures Images COPD Chronic Obstructive Pulmonary Disorder Chronic obstructive pulmonary disease COPD refers to chronic lung disorders that result in blocked air flow in the lungs The two main COPD | Source
COPD Chronic Obstructive Pulmonary Disease This colorful anatomical chart displays the signs symptoms and other useful
COPD Chronic Obstructive Pulmonary Disease This colorful anatomical chart displays the signs symptoms and other useful | Source
an active lifestyle Chronic Obstructive Pulmonary Disease COPD According to the Heart Lung and Blood Institute Chronic Obstructive Pulmonary Disease COPD is a lung disease in which the lungs are damaged making it hard to breathe In COPD the
an active lifestyle Chronic Obstructive Pulmonary Disease COPD According to the Heart Lung and Blood Institute Chronic Obstructive Pulmonary Disease COPD is a lung disease in which the lungs are damaged making it hard to breathe In COPD the | Source
aged 18 to 69 years have hypertension The older you are the more likely you are to have hypertension In the 60 69 years age group more than 1 in 2 persons have hypertension Chronic Obstructive Pulmonary Disease COPD Chronic Obstructive Pulmonary Dise
aged 18 to 69 years have hypertension The older you are the more likely you are to have hypertension In the 60 69 years age group more than 1 in 2 persons have hypertension Chronic Obstructive Pulmonary Disease COPD Chronic Obstructive Pulmonary Dise | Source

Different variants of the Chest-X-ray and showing COPD

These radiographs of a patient with chronic obstructive pulmonary disease (COPD) reveal pulmonary hyperinflation. In the PA projection above the diaphragms are at the level of the eleventh posterior ribs and appear flat. The lateral radiograph below
These radiographs of a patient with chronic obstructive pulmonary disease (COPD) reveal pulmonary hyperinflation. In the PA projection above the diaphragms are at the level of the eleventh posterior ribs and appear flat. The lateral radiograph below
These are "Normal" Lungs (notice how clear they are)
These are "Normal" Lungs (notice how clear they are) | Source
These are lungs of Cystic Fibrosis (the cloudiness is scarring)- One of the major complications of COPDs
These are lungs of Cystic Fibrosis (the cloudiness is scarring)- One of the major complications of COPDs | Source
COPD usually happens because of the commitment to smoking habit for too long. It is marked by symptoms such as frequent coughing, increase of slime or sputum, frequent suffocation especially if exercising, tight chest feeling and often having respira
COPD usually happens because of the commitment to smoking habit for too long. It is marked by symptoms such as frequent coughing, increase of slime or sputum, frequent suffocation especially if exercising, tight chest feeling and often having respira | Source
Chest radiograph shows hyperinflation, flattened diaphragms, increased retrosternal space, and hyperlucency of the lung parenchyma in emphysema.
Chest radiograph shows hyperinflation, flattened diaphragms, increased retrosternal space, and hyperlucency of the lung parenchyma in emphysema. | Source
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior (PA) film.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior (PA) film. | Source
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph.
An emphysematous lung shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on lateral chest radiograph. | Source
The differential diagnosis of unilateral hyperlucent lung includes pulmonary arterial hypoplasia and Swyer-James syndrome. The expiratory chest radiograph exhibits evidence of air trapping and is helpful in making the diagnosis. Swyer-James syndrome
The differential diagnosis of unilateral hyperlucent lung includes pulmonary arterial hypoplasia and Swyer-James syndrome. The expiratory chest radiograph exhibits evidence of air trapping and is helpful in making the diagnosis. Swyer-James syndrome | Source
Lateral chest radiograph of Swyer-James syndrome may demonstrate some of the features of emphysema.
Lateral chest radiograph of Swyer-James syndrome may demonstrate some of the features of emphysema. | Source

CT scans showing COPD

High-resolution CT (HRCT) scanning is more sensitive than standard chest radiography. HRCT scanning is highly specific for diagnosing emphysema and outlines bullae that are not always observed on radiographs. A CT scan is indicated when the patient i
High-resolution CT (HRCT) scanning is more sensitive than standard chest radiography. HRCT scanning is highly specific for diagnosing emphysema and outlines bullae that are not always observed on radiographs. A CT scan is indicated when the patient i | Source
Diffuse emphysema secondary to cigarette smoking
Diffuse emphysema secondary to cigarette smoking | Source
A CT scan showing severe emphysema and bullous disease.
A CT scan showing severe emphysema and bullous disease. | Source

Symptoms, Signs, and X-ray Findings

COPD is thought to begin early in life, though significant symptoms and dis ability usually do not occur until middle age. Mild ventilatory abnormalities may be discernible long before the onset of significant clinical symptoms. A mild "smoker's cough" is often present many years before onset of exertional dyspnea.

Gradually progressive exertional dyspnea is the most common presenting com plaint. Patients may date the onset of dyspnea to an acute respiratory illness, but the acute infection may only unmask a preexisting subclinical chronic respiratory disorder. Cough, wheezing, recurrent respiratory infections, or, occasionally, weakness, weight loss, or lack of libido may also be initial manifestations. Rarely, initial complaints are related to congestive heart failure secondary to cor pulmo nale, patients with such complaints apparently ignoring their cough and dyspnea prior to the onset of dependent edema and severe cyanosis.

Cough and sputum production are extremely variable. The patient may admit only to "clearing his chest" on awakening in the morning or after smoking the first cigarette of the day. Other patients may have severe disabling cough. Sputum varies from a few ml of clear viscid mucus to large bronchiectasis-like quantities of purulent material.

Wheezing also varies in character and intensity. Asthma-like episodes may oc cur with acute infections. A mild chronic wheeze that is most obvious on reclining may be noted. Many patients deny having any wheeze.

The physical findings in COPD are notoriously variable, especially in early cases. A consistent abnormality is obstruction to expiratory air flow manifested by a slowing of forced expiration. To demonstrate this, the patient is asked to take a deep breath and then empty his lungs as quickly and completely as possible. Forced expiration is normally virtually complete in < 4 seconds. This test, which should be part of every routine physical examination, may be abnormal even though the patient does not complain of dyspnea.

Other findings, including bronchi, diminished vesicular breath sounds, tachy cardia, distant heart tones, and decreased diaphragmatic motion, are not consis tently present. The typical findings of gross pulmonary hyperinflation, prolonged expiration during quiet breathing, depressed diaphragm, pursed-lip breathing, stooped posture, calloused elbows from repeated assumption of the "tripod posi tion," and marked use of accessory muscles of respiration are seen only in later stages of COPD. A barrel-chested appearance is an unreliable finding since it is often noted in elderly patients without significant respiratory problems. Late in the disease, there may be frank cyanosis from hypoxemia, a plethoric appearance associated with secondary erythrocytosis, and, in patients with severe cor pulmo nale, signs of congestive heart failure. Mild, chronic, dependent edema is quite common and does not necessarily indicate heart failure. It may result from pro longed sitting, elevated intrathoracic pressures, and renal retention of salt second ary to blood gas abnormalities even in the absence of cor pulmonale. X-rayfindings are also variable. In early stages of the disease, the x-ray is often normal. Changes indicative of hyperinflation (e.g , depressed diaphragm, general ized radiolucency of the lung fields, increased retrosternal air space, and tenting of the diaphragm at the insertions to the ribs) are common and suggestive of emphysematous disease, but are not diagnostic. They may also be found in pa dents with asthma and occasionally m healthy persons Localized radioluceno with attenuation of vascular markings is a more reliable indicator of emphysema

Bullae are seen occasionally with COPD. Large bullae are generally well seen on ordinary x-rays, but small ones are more reliably detected with planograms. They may occur as part of a diffuse emphysematous process or as isolated phe nomena and thus do not necessarily indicate a generalized lung disease.

Bronchitis itself does not have a characteristic appearance on ordinary chest x-ray, but bronchogramsmay reveal cylindrical dilation of bronchi on inspiration bronchial collapse on forced expiration, and enlarged mucous ducts Prank: saccular bronchiectasis is unusual and generally occurs only in patients who have had a previous severe respiratory infection.

In patients with recurrent chest infections, a variety of nondescript postinflammatory abnormalities may be noted, such as localized fibrotic changes, hone^ combing, or contraction atelectasis of a segment or lobe.

Isotopic lung scans generally demonstrate uneven ventilation and perfusion Diagnosis COPD should be suspected in any patient with chronic productive cough or exertional dyspnea of uncertain etiology, or whose physical examination reveals evidence of slowing of forced expiration. Definite diagnosis depends on (1) demonstration of physiologic evidence of airways obstruction which persists despite intensive and maximum medical management, and (2) exclusion of any specific disease (e.g., silicosis, tuberculosis, or upper airway neoplasm) as a cause of this physiologic abnormality.

Spirometric testing reveals characteristic obstruction to expiratory air flow with slowing of forced expiration as manifested by a reduced 1-second forced expiratory volume (FEV1) and a low maximum mid-expiratory flow. Slowing of forced expiration is also evident on flow-volume curves. The vital capacity (VC) and forced vital capacity (FVC) are somewhat impaired in patients with severe disease but are better maintained than the measures of the speed of expiration. For this reason, the FEV1/VC and FEV1/FVC ratios are regularly reduced to < 60% with clinically significant COPD. This degree of abnormality should persist despite prolonged, maximal therapy before a diagnosis of COPD is considered confirmed

Maldistribution of ventilation and perfusion occurs in COPD and is manifested m several ways. An excessive physiologic dead space ventilation indicates that there are areas of the lung in which ventilation is high relative to blood flow (a high ventilation/perfusion ratio), resulting in "wasted" ventilation. Physiologic shunting indicates the presence of alveoli with reduced ventilation in relation to blood flow (a low ventilation/perfusion ratio) which allows some of the pulmonary blood flow to reach the left heart without becoming fully oxygenated, resulting in hypoxemia. In late stages of the disease, overall alveolar underventilation with hypercapnia occurs, aggravating any hypoxemia present due to physiologic shunting. Chronic hypercapnia is usually well compensated, and pH levels are close to normal.

The pattern of physiologic abnormality in an individual case depends to some extent on the relative severity of intrinsic bronchial disease and anatomic emphy sema. Diffusing capacity is regularly reduced in patients with severe anatomic emphysema, but is more variable in patients with airways obstruction associated with predominant intrinsic bronchial disease. In patients with severe emphysema. resting hypoxemia is usually mild and hypercapnia does not occur until terminal stages of the illness. In these patients, cardiac output may be quite low, but frank pulmonary hypertension and cor pulmonale are usually late developments. In patients with airways obstruction associated primarily with an intrinsic bronchial disorder, severe hypoxemia and hypercapnia may be noted relatively early. Such patients usually have a well-maintained cardiac output and tend to develop severe pulmonary hypertension with chronic cor pulmonale. The residual volume (RV) and total lung capacity (TLC) are markedly elevated in emphysematous patients, while pulmonary hyperinflation may be relatively slight in bronchitic COPD, but the ratio of RV to TLC tends to be elevated in both types of disease.

Detailed lung function measurements help to determine the severity of emphy sema and intrinsic bronchial disease in an individual case, but are rarely needed for ordinary clinical evaluation. With severe emphysema, pressure-volume curves show a characteristic loss of recoil and increased compliance. Airways resistance measurements made in the body plethysmograph tend to reflect the severity of intrinsic bronchial narrowing.

In a few cases with severe emphysema but little bronchitis or with severe ob structive bronchitis but little, if any, emphysema, it is possible to distinguish emphysematous type (Type A) disease frombronchial type (Type B) disease on the basis of clinical and physiologic findings (see TABLE 1). Unfortunately, most patients appear to have a "mixed" syndrome.

Specific parenchymal lung diseases which may lead to airways obstruction can usually be excluded by chest x-ray. Upper airway lesions (generally associated with stridor) and localized bronchial obstructions (often associated with a local ized wheeze) must also be excluded. It is particularly important to exclude pri mary cardiac disease with congestive failure as a cause of the patient's respiratory insufficiency. A normal or small cardiac silhouette on chest x-ray is characteristic of COPD prior to development of frank cor pulmonale, but is most unusual in patients who are dyspneic as a result of a cardiac disorder.


Emphysematous (Type A)

Age at diagnosis: 55-75

Cough onset: Often after onset of dyspnea

Sputum: Scanty, mucoid

Recurrent infections: Occasional

Chest x-ray: Normal or emphysematous

Pulmonary artery pressure: Normal or slightly high

Chronic cor pulmonale: unusual

Lung compliance: Normal or high

Recoil pressure: Low

Airways resistance: Near normal

Pulmonary overdistention: Marked

Diffusing capacity: Low

Chronic hypercapnia: Unusual

Chronic hypoxemia: Mild or moderate

Bronchial (TypeB)

Age at diagnosis: 45-65

Cough onset: Usually before onset of dyspnea

Sputum: Copious, purulent

Recurrent infections: Frequent

Chest x-ray: Normal or fibrotic

Pulmonary artery pressure: Often very high

Chronic cor pulmonale: Common

Lung compliance: Normal or low

Recoil pressure: Normal or high

Airways resistance: Elevated

Pulmonary overdistention: Mild or moderate

Diffusing capacity: Variable

Chronic hypercapnia: Common

Chronic hypoxemia: Often severe

Homozygotic antitrypsin deficiency should be suspected when there is a family history of obstructive airways disease, or when emphysema occurs in a woman, a relatively young man, or a nonsmoker. The diagnosis may be confirmed by mea suring serum antitrypsin levels or by specific phenotyping.

Course and Prognosis

Some reversal of airways obstruction and considerable symptomatic improve ment can often be obtained initially, but the long-term prognosis is less favorable in patients with persistent obstructive abnormality. After initial improvement, the FEV1 generally falls 50 to 75 ml/yr, which is 2 to 3 times the rate of decline expected from aging alone. There is a concomitant slow progression of exertional dyspnea and disability. The course is punctuated by acute symptomatic exacerba tions, generally related to superimposed bronchial infections.

Prognosis is closely related to the severity of expiratory slowing. When the FEV1 exceeds 1.25 L, the 10-yr survival rate is about 50%; when the FEV, is 1 L, the average patient survives about 5 yr; when there is very severe expiratory slowing (FEV1 about 0.5 L), survival for > 2 yr is unusual, particularly if the patient also has chronic hypercapnia or demonstrable cor pulmonale.


Therapy does not result in cure, but provides symptomatic relief and controls potentially fatal exacerbations. It may also slow progression of the disorder, though this is unproved. Treatment is directed at alleviating conditions which cause symptoms and excessive disability (e.g., infection, bronchospasm, bronchial hypersecretion, hypoxemia, and unnecessary limitation of physical activity).

Infection: An attempt should be made to clear purulent sputum with a broad-spectrum antibiotic (e.g., tetracycline 250 mg q.i.d. for 10 days), the course re peated promptly at the first sign of recurrent bronchial infection or sputum purulence. Ampicillin or cephalothin may be used to treat severe exacerbations Regular courses of a broad-spectrum antibiotic are indicated in patients with frequent infectious exacerbations.

Bronchospasm: The degree of reversibility of airways obstruction can be as sessed only by a vigorous and prolonged therapeutic trial of bronchodilators.

Corticosteroids have a very limited role in treating COPD, but a trial of these agents may be required to prove conclusively that the airways obstruction is not a result of potentially reversible bronchospasm. This is especially true when there is a past history suggesting asthma, eosinophilia, fluctuations in the severity of air ways obstruction, or a good immediate response to inhalation of a bronchodilator. If a corticosteroid trial (e.g., prednisone 30 to 40 mg every morning for 3 wk) is undertaken, its usefulness should be documented by objective improvement w spirometric tests before long-term corticosteroid therapy is recommended, al which time the lowest maintenance dose which sustains improvement is used. In some patients, alternate-day therapy can be used for maintenance.

Bronchial secretions: Adequate systemic hydration is essential to prevent 10-spissation of secretions. In some patients bronchial hygiene may also be improved by inhalation of mist, postural drainage, and chest physical therapy, particularly following bronchodilator inhalation. Saturated solution of potassium iodide 10 drops in H20 t.i.d. is used by some physicians in an attempt to thin bronchial secretions. Despite their wide use, IPPB machines have not been shown to im prove the patient's ability to raise secretions or to affect favorably the overall condition of ambulatory patients with COPD.

Hypoxemia: Severe chronic hypoxemia, often associated with hypercapnia, accentuates pulmonary hypertension and leads to development of cor pulmonale in patients with COPD. Recurrent cardiac failure may develop and necessitate long-term 02 therapy. Low flow (1 to 2 L/min) 02 therapy via nasal prongs for 15 h or more/day (including sleeping hours) may be effective in reversing pulmonary hy­pertension and improving cardiac status. Around-the-clock 02 supplementation has been shown to be preferable for patients with severe chronic hypoxemia (arte rial O2 tensions consistently < 55 mm Hg at rest) and appears to prolong survival. When instituting long-term O2 therapy, it is important to monitor the blood gas responses. No more O2 should be given than is needed to raise the arterial 02 tension to 55 mm Hg. One should also be sure that chronic 02 therapy does not lead to a progressive rise in C02 tension as a consequence of removing hypoxic ventilatory drive; in fact, this has rarely proved to be an important problem.

Even in patients without severe cor pulmonale, O2 may be needed to correct severe exertional hypoxemia when the patient is started on a graded exercise program. Use of 02 for symptomatic relief of dyspnea without verification of severe hypoxemia, however, is unjustified and potentially dangerous.

Hypercapnia: Patients with rapidly developing or worsening hypercapnia re quire immediate hospitalization and intensive therapy, but chronic well-compen sated hypercapnia is generally well tolerated and requires no specific therapy.

Heart failure: The most important measure for controlling heart failure second ary to cor pulmonale is correction of excessive hypoxemia. Diuretic therapy and controlled sodium intake are important adjuncts. Digitalis must be used cau tiously, if at all, since digitalis intoxication readily occurs in patients with COPD, probably as a result of fluctuating blood gas and electrolyte abnormalities.

Exercise tolerance: Prolonged inactivity leads to excessive disability in patients with COPD. As long as there is no severe cardiac disease, it is important to maintain a regular exercise program. This can usually be prescribed directly by the physician. If the patient is severely disabled, however, the program may be more effective if supervised by a trained physical therapist. The exercise program should have a specific meaningful goal (e.g., walking to the store, golfing) and should train those muscles needed for this specific activity. Breathing "exercises" (breathing training) may have a place in treating anxious patients who develop an excessively rapid ventilatory rate during exertion, but such exercises have not been shown to improve ventilatory capacity.

Depression: Periods of severe depression or marked anxiety are frequent in patients with COPD. A vigorous therapeutic program and an enthusiastic physi cian are most helpful. A nihilistic attitude toward management of this disease is inexcusable. The patient must understand the nature of the disease and the goals and expectations of therapy.

Exacerbations: Treat promptly; e.g., if sputum becomes purulent, prescribe a course of broad-spectrum antibiotics and a more intensive program of bronchodilation and bronchial hygiene (see above). Patients with increasing hypoxemia or hypercapnia should be hospitalized promptly for intensive therapy. Sedatives and hypnotics should always be avoided in patients with COPD, particularly during exacerbations, since they increase the risk of acute ventilatory failure

More on COPD

If you smoke regularly, you should realize how black your lungs are becoming.  You keep reducing your lung capacity the more you smoke and should realize that today should be the day you quit.  This product is supposed to shock smokers from realizing
If you smoke regularly, you should realize how black your lungs are becoming. You keep reducing your lung capacity the more you smoke and should realize that today should be the day you quit. This product is supposed to shock smokers from realizing | Source
Over the years smokers have been notified  by their doctors and the FDA of the long term effects of tobacco smoke. There have been constant reminders regarding the effects that smoking has on the lungs, blood pressure, heart and other vital organs.
Over the years smokers have been notified by their doctors and the FDA of the long term effects of tobacco smoke. There have been constant reminders regarding the effects that smoking has on the lungs, blood pressure, heart and other vital organs. | Source
Cough is another major sign of COPD
Cough is another major sign of COPD | Source
Sputum production is another major sign of COPD
Sputum production is another major sign of COPD | Source

Complications, classification by severity and Treatment


Acute Bronchitis, Pneumonia, Pulmonary thromboembolism, and concomitant left Ventricular failure may worsen otherwise stable COPD. Pulmonary hypertension, Cor Pulmonale, and chronic respiratory failure are common advanced COPD. Spontaneous Pneumothorax occurs in a small fraction of patients with emphysema. Hemophysis may result from chronic bronchitis or may signal bronchogenic carcinoma.

Classification of COPD (by severity)

This classification is based on stage and severity.

1. Mild- FEV1<80%, FEV1/FVC <70%. As a rule, chronic cough with sputum usually occurs in this stage.

2. Moderate- 50%<FEV1<80%. FEV1/FVC<70%. Symptoms are more significant, presence of dyspnea during physical activity and exacerbation occur.

3. Severe- 30%<FEV1<50%. FEV1/FVC<70%. Symptoms in this stage cause worsening of Life quality.

4. Very severe- FEV1<30%. FEV1/FVC<70% and Chronic renal failure occurs.


Principles of treatment

I. Increasing of intensity of treatment in correlation with COPD severity.

II. Permanent basis therapy.

III. Individual sensitivity of patients to different medicines leads to necessity of permanent control

IV. Inhaled medicines are useful

Inhaled Cholynolytics

I. SHort action- (Ipratropium bromide, Berodual H) has more slowly beginning but longer action than B2- agonists.

II. Prolonged action- (Thyotropium bromide, spiriva) is active for 24 hours.

Inhaled Broncholytics

I. B-agonists of short action (salbutamol, fenoterol)- fast beginning of action, but duration is 4-6 hours.

II. B2-agonists of prolonged action (Salmeterol, Formoterol) are active for 12 hours.


Theophylines of prolonged action are useful- Teopec, Teotard etc.


Glucocorticosteroids are useful for permanent basis therapy for patients with COPD III- IV stages and basically, inhaled types are used. Prednisome may be used only during exacerbation and is not recommended for basis therapy. Examples of such are Beclomethasone, Budesonid, FLucasone). Seretid is Glucocorticosteroids + Salmeterol, which is used in patients with III- IV stages of COPD and often exacerbations in anamnesis.


Management of Chronic Obstructive Pulmonary Diseases in all severity involves; avoidance of risk factors (smoking cessation, reduction of indoor pollution, reduction of occupational exposure etc) and also influenza vaccination.

I. Stage 0: CHaracterized by chronic symptoms of cough and sputum. No spirometric abnormalities. The recommended treatment is smoking cessation.

II. Stage 1 (Mild COPD): The recommended treatment is administration of short-acting bronchodilator as needed.

III. Stage 2 (Moderate COPD): Recommended treatment is the administration of the following; short acting bronchodilator as needed; regular treatment with one or more long-acting bronchodilators and as well rehabilitation.

IV. Stage 3 (Severe COPD): Recommended treatment is short-acting bronchodilator as needed; regular treatment with one or more long-acting bronchodilators, inhaled glucocorticosteroids if repeated exacerbations occur and also rehabilitation.

V. Stage IV (Very severe COPD): Recommended treatment is by the administration of short-acting bronchodilator as needed. Regular treatment with one or more long-acting bronchodilators. Also administration of inhaled glucocorticosteroids if repeated exacerbations occur. Complications as well should be treated appropriately and long term oxygen therapy should be administered if respiratory failure occurs. Surgical options could as well be considered.

Acknowledgement and Contributors

Great appreciationg to the Pulmonology branch of the department of Internal Medicine; Prof. Smiyan Svitlana (Head of Department), Dr. Andrei Lepyavko Adreivich (M.D) and Dr. Sofia Gusak (MD).
Great appreciationg to the Pulmonology branch of the department of Internal Medicine; Prof. Smiyan Svitlana (Head of Department), Dr. Andrei Lepyavko Adreivich (M.D) and Dr. Sofia Gusak (MD). | Source
The Mukite...
The Mukite... | Source


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    • profile image


      4 years ago

      Thank you Lydia, i als0 purchased this herbs my breathing has improved

    • Sandyspider profile image

      Sandy Mertens 

      7 years ago from Wisconsin, USA

      Very informative hub on COPD.

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      9 years ago from Europe

      Yes, a normal but careful Life can be lived.... Just dont smoke again.

    • profile image

      pat from uk 

      9 years ago

      hi can you give your opinion

      if a person of 64 who smoked for 14 yrs 20 or less a day

      36 yrs ago who has now been told they have copd consider that the copd will stay as it is as in one of the write ups it say the syptoms would get no worse so would a person be able to live out there life normal lifespan with some exercise and diet and healthcare. if the copd was said to be mild - moderate cough gone phlem 80 per cent better breathlessness = maybe when climbing a hill please no scary replys

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      10 years ago from Europe

      thanks emdi

    • emdi profile image


      10 years ago

      Great job.

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      10 years ago from Europe

      "Surprise" is an understatement.... I am overwhelmed!

    • profile image


      10 years ago

      Why do you act surprised, my Doctor? I am not surprised... You are truly exploding.... It seems your community work is now going global

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      10 years ago from Europe

      wooooooooooooooooooooooooooooooooooooow! I have been anticipating this but not so soon! I feel on top of the world right now. Thank you all. I have been thinking of choosing one of these hospitals to do my next summer practical training, now I am very confused. Germany is very close to Ukraine, the UK and USA are English speaking nations, Canada is enticing.... I am just confused. Well! Keep on following even as I continue to publish more and more clinical cases. You guys are making my profile here on hubpages a complete one. Seriously, my hubs together with all these blogs makes a complete research package, I do not think I need to go else where anymore, unless otherwise. Thank you very much for spicing my publications with enough materials and ideas. Continue the good work and of course, so many viewers wil read and come across your various hospitals to know more about them. I am greatly honoured and positively embarassed.

    • profile image

      Klinikums der Universität München 

      10 years ago

      Chronic obstructive pulmonary disease and flying

      If you have COPD and plan to fly then you should discuss this with the airline. Some airlines may request a fitness to fly assessment. Although your GP might be able to give some advice, they are not well placed to make the final decision. Your respiratory specialist may be able to help or alternatively you may need to see a specialist in aviation medicine.

      When travelling by air you should keep your medicines, especially your inhalers, in your hand luggage. If you are on LTOT, you will need to inform the airline. It is possible to use your own oxygen in-flight but individual circumstances may differ. Some people with COPD are more likely to need in-flight oxygen. Some people are more at risk of a punctured lung (pneumothorax) at altitude, despite the fact that the aircraft cabin is pressurised.

      Regular follow-up

      If you have COPD, your GP surgery will probably call you yearly for a check-up or annual review. You can discuss your medication and the GP or nurse might assess your inhaler technique. Regular review allows monitoring of the severity of your COPD, and gives an opportunity for health promotion such as help with stopping smoking or weight control. Reviews should happen more often if you have frequent exacerbations or complications, if you have very severe COPD, or if you have recently been discharged from hospital.

      In summary

      COPD is usually caused by smoking.

      COPD should be considered as a possible diagnosis in anyone aged over 35 years old who smokes, or has ever smoked and has persistent problems such as cough with lots of phlegm, breathlessness or wheeze, and recurrent chest infections.

      Symptoms usually become worse if you continue to smoke.

      Symptoms are unlikely to get much worse if you stop smoking.

      Treatment with inhalers often eases symptoms, but no treatment can reverse the damage to the airways.

      A flare-up of symptoms, often during a chest infection, may be helped by increasing the dose of usual treatments. This may be combined with a short course of steroid tablets and/or antibiotics.

    • profile image

      Cedars Sinai Medical Center  

      10 years ago

      What can I do to help?

      Get immunised

      Two immunisations are advised.

      A yearly 'flu jab' each autumn protects against possible influenza and any chest infection that may develop due to this.

      Immunisation against pneumococcus (a germ that can cause serious chest infections). This is a one-off injection and not yearly like the 'flu jab'.

      Try to do some regular exercise

      Studies have shown that people with COPD who exercise regularly tend to improve their breathing, ease symptoms, and have a better quality of life.

      Any regular exercise or physical activity is good. However, ideally the activity that you do should make you at least a little out of breath, and be for at least 20-30 minutes, at least 4-5 times a week. If you are able, a daily brisk walk is a good start if you are not used to exercise. But, if possible, try to increase the level of activity over time.

      You may be referred for pulmonary rehabilitation or be under the care of a community respiratory team. You will be given exercises and advice to try to help you stay as fit as possible. This is important because, effectively, you may become disabled due to your breathlessness.

      Try to lose weight if you are overweight

      Obesity can make breathlessness worse. If you are overweight or obese it is harder to exercise, and exercise makes you more breathless. It becomes a bit of a vicious cycle. If you are obese the chest wall is made heavy by fat. This means that you have to work much harder to breathe in and take a good breath, to inflate the lungs and expand the chest. A dietician may be able to give you advice on healthy eating and

    • profile image

      Allina Hospitals & Clinics 

      10 years ago

      Other medicines

      Medicines such as morphine and codeine may be prescribed to try to reduce your coughing, and to help with breathlessness. Hyoscine is a medication that can be given to try to dry up secretions from your lungs. Anxiety is a common symptom when you are breathless. Morphine can help the feelings of anxiety. In some cases, other anti-anxiety drugs (such as diazepam) can be given. Depression and anxiety are common in patients with COPD, at all stages of the disease. You may already be prescribed medication for this.

      Other treatments in chronic obstructive pulmonary disease


      This is an option in a very small number of cases. Removing a section of lung that has become useless may improve symptoms. Sometimes large air-filled sacs (called bullae) develop in the lungs in people with COPD. A single large bulla might be suitable for removal with an operation. This can improve symptoms in some people. Lung transplantation is being studied, but is not a realistic option in most cases.

    • profile image

      Chang Gung Memorial Hospital 

      10 years ago

      Home oxygen

      This may help some people with severe symptoms or end-stage COPD. It does not help in all cases. Unfortunately, just because you feel breathless with COPD it does not mean that oxygen will help you. Great care has to be taken with oxygen therapy. Too much oxygen can actually be harmful if you have COPD.

      To be considered for oxygen you would need to have very severe COPD, and be referred to a respiratory specialist (consultant) at a hospital. Your GP cannot just prescribe oxygen to you in this situation. Tests are done to see how bad your COPD is, and how low the oxygen levels in your blood are. This might be done with a pulse oximeter (mentioned earlier) or by taking a sample of blood from an artery in your wrist (blood gases). These tests are needed to decide whether oxygen will help you or not. The monitoring of oxygen levels may take place over a period of several weeks, at rest and with exercises.

      If found to help, oxygen needs to be taken for at least 15-20 hours a day to be of benefit. Oxygen can be given with a face mask or through little tubes (nasal cannulae or 'nasal specs') that sit just under your nostrils. Portable oxygen is available in cylinders, but if you need long-term oxygen therapy (LTOT), for long periods of the day, an oxygen concentrator is required. This is a big machine (about two feet square and two and a half feet tall) that plugs into a normal electrical socket. The concentrator takes oxygen from the air in your room, and concentrates it, meaning that it is separated from other gases in air, so you only have pure oxygen to breathe in. A back-up supply of oxygen cylinders is provided if you have a concentrator, in case of an electrical power cut or machine breakdown.

      Normally, you will only be considered for oxygen if you do not smoke. There is a serious risk of explosion or fire when using oxygen if you smoke.

      Oxygen might be used to treat an exacerbation of COPD in hospital but would not be prescribed short-term for an exacerbation to be used at home. Oxygen might be used in an emergency whilst awaiting transfer to a hospital (for example, by a paramedic).

    • profile image

      University of Wisconsin Health 

      10 years ago

      End-stage chronic obstructive pulmonary disease

      Palliative care

      Palliative care should be discussed with all people with COPD who are likely to die in the coming year. It is always difficult to be accurate about prognosis (outlook). Mostly, health professionals talk in terms of 'days', 'months' or 'years' when discussing prognosis for any particular disease or illness.

      As COPD progresses, the condition becomes more severe. You might have more frequent exacerbations and/or admissions to hospital. These factors can give a clue as to how advanced the illness is. Palliative care us usually started in COPD when you are on the maximum medication and are continuing to deteriorate (get worse). Sometimes in these situations you might choose to remain at home for any/all treatments, rather than having further hospital admissions, as things get worse.

      Palliative care means care or treatment to keep a person as comfortable as possible, to reduce the severity of the disease, rather than to cure it. Mostly it is about helping you with your symptoms, to make them easier to bear. Your quality of life in the end stages of COPD is very important. Palliative care is not quite the same as terminal (end of life care), when someone is dying and death is expected within a few days. Palliative care can be given in a hospice, but is just as likely to be provided by your GP, district nurse or community palliative care team. Palliative care involves not just physical treatments. Psychological and spiritual well-being are important too. The aim is that both you and your family feel supported and that your care is planned. The idea is that a multi-disciplinary team, with different healthcare professionals can anticipate any problems before they happen, and help you with access to medication and any equipment that might be needed.

    • profile image

      Erasmus Medisch Centrum Universitait Medisch Centrum Rotterdam 

      10 years ago

      Admission to hospital

      If your symptoms are very severe, or if treatments for an exacerbation are not working well enough, you may need to be admitted to hospital. In hospital you can be monitored more closely. Often the same drugs are given to you but at higher doses or in a different form. Tests such as a chest X-ray or blood tests to measure how much oxygen there is in your blood (arterial blood gases) can be performed. Chest physiotherapy can be started to help you clear secretions (mucus) from your chest by coughing and suction machines.

      If you are very breathless it may be impossible to use your inhaler. Nebulisers are machines that turn the bronchodilator medicines into a fine mist, like an aerosol. You breathe this in with a face mask or a mouth piece. Nebulisers are no more effective than normal inhalers but they are useful in people who are very fatigued (tired) with their breathing.

      You may need oxygen to help you breathe. Sometimes a special machine called bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP) is used to help you breathe. This is called noninvasive ventilation (NIV). It consists of a close-fitting facemask and drives oxygen into your lungs, forcing the airways open. It can make you feel a bit claustrophobic and it is quite noisy. In very severe cases, you might need more help with breathing, in an intensive care unit (ICU). A tube can be put into your windpipe and connected to a ventilator (a machine that 'breathes' for you). If you have severe underlying COPD (rather than just a severe exacerbation of COPD), this is not always the best option.

      About 2-4 patients in 100 admitted to hospital because of their COPD will die due to that illness. Between 1in 10 and 1 in 4 people admitted to ICU with severe COPD die.

    • profile image

      Lifespan Health System 

      10 years ago


      A short course of antibiotics is commonly prescribed if you have a chest infection, or if you have a flare-up of symptoms which may be triggered by a chest infection.

    • profile image

      Tokyo Women's Medical University Hospital 

      10 years ago

      Steroid tablets

      A short course of steroid tablets called (prednisolone) is sometimes prescribed if you have a bad flare-up of wheeze and breathlessness (often during a chest infection). Steroids help by reducing the extra inflammation in the airways which is caused by infections.

      Steroid tablets are usually taken once per day, often for between 5 to 14 days. Depending on the strength of the tablet, you might need to take 6 or even 8 as a single daily dose. If your symptoms improve quickly, your doctor may tell you to stop taking the steroids at the end of the week. If your problems are more severe, the steroid tablets may be tailed off over several days or weeks. Occasionally, some patients take steroid tablets long-term. This is not always advised as there can be serious side-effects.

      Some important side-effects of steroids include osteoporosis (thinning of the bones due to reduced bone density), bleeding in the stomach (gastrointestinal bleeds), a lowering of the immune system (immunosuppression) - making infections more common, weight gain (and a condition called Cushing's syndrome), and a lowering of the body's natural ability to make certain hormones (adrenal suppression). If you need to have steroid tablets long-term, you will usually be given some medicines to protect your bones and prevent osteoporosis. (See separate leaflet called 'Osteoporosis' for more information.)

    • profile image

      Children's Healthcare of Atlanta Pediatric Hospital 

      10 years ago

      Treatment of exacerbations

      Treatment of an exacerbation of COPD involves adding extra medicines temporarily to your usual treatment. This is usually steroid tablets with or without antibiotics. These medicines are usually taken until your symptoms settle down to what is normal for you.

      If you have frequent flare-ups then your doctor may advise on a self-management plan. This is a written plan of action agreed by you and your doctor on what to do as soon as possible after a flare-up starts to develop. For example, you may be given advice on how to increase the dose of your inhalers when needed. You may also be given some steroid tablets and/or antibiotics to have on standby so that you can start these as soon as possible when a flare-up first develops. You will also be told when you need to seek medical attention - for example if you are concerned that you are not responding to treatment.

    • profile image

      Kaiser Permanente, CA 

      10 years ago

      Mucolytic medicines

      A mucolytic medicine such as carbocisteine (Mucodyne®), erdosteine (Erdotin®) and mecysteine (Visclair®) makes the sputum less thick and sticky, and easier to cough up. This may also have a knock-on effect of making it harder for bacteria (germs) to infect the mucus and cause chest infections. The number of flare-ups of symptoms (exacerbations) tends to be less in people who take a mucolytic. It needs to be taken regularly (usually two or three times per day) and is most likely to help if you have moderate or severe COPD and have frequent or bad flare-ups (exacerbations).


    • profile image

      Inselspital Universitatsspital Bern 

      10 years ago

      Treatments for stable chronic obstructive pulmonary disease

      The main treatments are medications given in devices called inhalers. The medicine within the inhaler is in a powdered form which you breathe in (inhale). Some people find inhalers more difficult than others to use. The medicines in standard inhalers reach the lungs better if used with a spacer device. (See separate leaflet called 'Inhalers for Chronic Obstructive Pulmonary Disease' for more information on the different inhaler medicines and the different inhaler devices.)

      Short-acting bronchodilator inhalers

      An inhaler with a bronchodilator medicine is often prescribed. These relax the muscles in the airways (bronchi) to open them up (dilate them) as wide as possible. The same inhalers may be used if you have asthma. People often call them relievers. They include:

      Beta-agonist inhalers. Examples are salbutamol (brand names include Airomir®, Asmasal®, Salamol®, Salbulin®, Pulvinal Salbutamol® and Ventolin®) and terbutaline (brand name Bricanyl®). These inhalers are often (but not always), blue in colour. Other inhalers containing different medicines can be blue too.

      Antimuscarinic inhalers. For example, ipratropium (brand name Atrovent®).

      These inhalers work well for some people, but not so well in others. Typically, symptoms of wheeze and breathlessness improve within 5-15 minutes with a beta-agonist inhaler, and within 30-40 minutes with an antimuscarinic inhaler. The effect from both types typically lasts for 3-6 hours. Some people with mild or intermittent symptoms only need an inhaler as required for when breathlessness or wheeze occur. Some people need to use an inhaler regularly. The beta-agonist and antimuscarinic inhalers work in different ways. Using two, one of each type, may help some people better than one type alone.

      Long-acting bronchodilator inhalers

      These work in a similar way to the short-acting inhalers, but each dose lasts at least 12 hours. Long-acting bronchodilators may be an option if symptoms remain troublesome despite taking a short-acting bronchodilator.

      Beta-agonist inhalers. Examples are formoterol (brand names Atimos®, Foradil®, and Oxis®) and salmeterol (brand name Serevent® - a green-coloured inhaler). You can continue your short-acting bronchodilator inhalers with these medicines.

      Antimuscarinic inhalers. The only long-acting antimuscarinic inhaler is called tiotropium (brand name Spiriva®). The inhaler device is green-coloured. If you start this medication, you should stop ipratropium (Atrovent®) if you were taking this beforehand. There is no need to stop any other inhalers.

      Steroid inhalers

      A steroid inhaler may help in addition to a bronchodilator inhaler if you have more severe COPD or regular flare-ups (exacerbations) of symptoms. Steroids reduce inflammation. Steroid inhalers are only used in combination with a long-acting beta-agonist inhaler. (This can be with two separate inhalers or with a single inhaler containing two medicines).The main inhaled steroid medications are:

      Beclometasone. Brands include Asmabec®, Beclazone®, Becodisks®, Clenil Modulite®, Pulvinal Beclometasone® and Qvar®. These inhalers are usually brown and sometimes red in colour.

      Budesonide. Brands include Easyhaler Budesonide®, Novolizer Budesonide® and Pulmicort®.

      Ciclesonide. Brand name Alvesco®.

      Fluticasone. Brand name Flixotide®. This is a yellow-coloured or orange-coloured inhaler.

      Mometasone. Brand name Asmanex Twisthaler®.

      A steroid inhaler may not have much effect on your usual symptoms, but may help to prevent flare-ups. In the treatment of asthma, these medicines are often referred to as preventers. Side-effects of steroid inhalers include oral (in the mouth) thrush, sore throats and a hoarse voice. These effects can be reduced by rinsing your mouth with water after using these inhalers, and spitting out.

      Combination inhalers are available, usually containing a steroid medication and either a short-acting or long-acting beta-agonist.

      Examples of combination inhalers are:

      Fostair® (formoterol and beclometasone).

      Seretide® (salmeterol and fluticasone). This is a purple-coloured inhaler.

      Symbicort® (formoterol and budesonide).

      Combination inhalers are useful if people have severe symptoms or frequent flare-ups. Sometimes is is more convenient to use just one inhaler device.

      Because there are lots of different coloured inhalers available, it is helpful to remember their names, as well as the colour of the device. This might be important if you need to see a doctor who does not have your medical records (such as in A+E, if you are on holiday, or outside the normal opening hours of your GP surgery).

    • profile image

      Universitätsklinikum Magdeburg 

      10 years ago

      What are the treatments for chronic obstructive pulmonary disease?

      Stopping smoking is the most important treatment. No other treatment may be needed if the disease is in the early stage and symptoms are mild.

      If symptoms become troublesome, one or more of the following treatments may be advised. (Note: treatments do not cure COPD. Treatments aim to ease symptoms. Some treatments may prevent some flare-ups of symptoms.)

      As a general rule, a trial of 1-3 months of a treatment will give an idea if it helps or not. A treatment may be continued after a trial if it helps, but may be stopped if it does not improve symptoms).

      It can be helpful to consider treatments for three separate problems.

      Treatments for stable COPD

      Treatments for exacerbations of COPD

      Treatments for end-stage COPD


    • profile image

      Sligo General Hospital 

      10 years ago

      How can the course of the disease be altered?

      Stop smoking. This is the single most important piece of advice. If you stop smoking in the early stages of COPD it will make a huge difference. Damage already done to your airways cannot be reversed, but stopping smoking prevents the disease from worsening. It is never too late to stop smoking, at any stage of the disease. Even if you have fairly advanced COPD, you are likely to benefit and prevent further progression of the disease.

      Your cough may get worse for a while when you give up smoking. This often happens as the lining of the airways 'comes back to life'. Resist the temptation to start smoking again to ease the cough. An increase in cough after you stop smoking usually settles in a few weeks.

      The NHS provides free help and advice for people having difficulty in stopping smoking. Medication (such as varenicline, brand name Champix® and bupropion, brand name Zyban®) and nicotine replacement therapy (such as patches and chewing gum) can be prescribed, and counselling offered. You could see your GP or practice nurse for further advice, or visit the NHS website:

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      Sarasota Memorial Hospital 

      10 years ago

      What is the progression and outlook?

      Symptoms of COPD typically begin in people aged over 40 who have smoked for 20 years or more. A 'smoker's cough' tends to develop at first. Once symptoms start, if you continue to smoke, there is usually a gradual decline over several years. You tend to become more and more breathless. In time your mobility and general quality of life may become poor due to increasing breathing difficulties.

      Chest infections tend to become more frequent as time goes by. Flare-ups of symptoms (exacerbations) occur from time to time, typically during a chest infection.

      As the disease becomes more severe, not enough oxygen reaches the lungs through the narrowed airways. As a result, the amount of oxygen that gets into the bloodstream is less than normal. This can cause a type of heart failure as the heart muscle needs oxygen to work and pump normally. Heart failure causes fluid retention (oedema).

      (Note: heart failure does not mean the heart stops beating (that is called cardiac arrest). Heart failure is when the heart does not pump blood very well.

      Respiratory failure is the final stage of COPD. At this point the lungs are so damaged that the levels of oxygen in the blood are low. The waste product of breathing called carbon dioxide (CO2) builds up in the blood stream. People with end-stage COPD need palliative care to make them more comfortable and ease any symptoms.

      At least 25,000 people die each year in the UK from the end stages of COPD. Many of these people have several years of ill health and poor quality of life before they die. About 8 in 10 men with mild COPD will survive for five years or more after diagnosis, compared with 7 in 10 women. The survival rate is lower in severe COPD. About 3 in 10 men and just over 2 in 10 women with severe disease will survive five years from diagnosis.

      Depression and/or anxiety affect at least 6 in 10 people with COPD, and can be treated if recognised.


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      Fairview Health Services 

      10 years ago

      Other tests

      A chest X-ray may show signs of COPD and can be used to help exclude other serious conditions (including lung cancer). Occasionally, a special CT scan of the chest - high-resolution CT (HRCT) - is needed. A blood test to make sure you are not anaemic is often helpful. (Anaemia can lead to breathlessness.) Sometimes a blood test can show changes (called polycythaemia) that suggest you have chronically low levels of oxygen (hypoxia).

      A pulse oximeter is a device can be clipped on to your finger to measure your heart rate (pulse) and measure the amount of oxygen in your circulation (oxygen saturation). Lower levels than normal tend to be found in people who have COPD, especially if you have an exacerbation of your symptoms.

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      Shands Healthcare 

      10 years ago


      The most common test used in helping to diagnose the condition is called spirometry. This test estimates lung volumes by measuring how much air you can blow out into a machine. Two results are important: the amount of air you can blow out in one second (called forced expiratory volume in 1 second - FEV1) and the total amount you can blow out in one breath (called forced vital capacity - FVC). Your age, height and sex affect your lung volumes. So, your results are compared to the average predicted for your age, height and sex.

      A value is calculated from the amount of air that you can blow out in one second divided by the total amount of air that you blow out in one breath (called FEV1/FVC ratio). A low value indicates that you have narrowed airways. A ratio less than 70% suggests COPD. The FEV1 compared with the predicted value shows how bad the COPD is.

      COPD is divided into mild, moderate and severe groups, depending on the level of airflow obstruction. The airflow obstruction is the FEV1, measured with spirometry.

      Mild (stage 1) COPD is an FEV1 at least 80% of predicted value.

      Moderate (stage 2) COPD is an FEV1 between 50% and 79% of predicted value.

      Severe (stage 3) COPD is an FEV1 between 30% and 49% of predicted value.

      Very severe (stage 4) COPD is an FEV1 less than 30% of predicted value.

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      Tabriz University Hospitals 

      10 years ago

      Do I need any tests?

      COPD may be suspected by your doctor because of your symptoms. Examination of your chest can be normal in mild or early COPD. Using a stethoscope, your doctor may hear wheezes in your chest, or find signs of a chest infection. Your chest may show signs of being overinflated (hyperinflation). This is because the airways are obstructed and, as well as it being difficult for air to get into your lungs, it is also difficult for it to escape. Your history (symptoms) and physical examination will help your GP decide if COPD is likely.

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      Medical University of South Carolina 

      10 years ago

      What's the difference between chronic obstructive pulmonary disease and asthma?

      Asthma and COPD cause similar symptoms. However, they are different diseases. Briefly:

      In COPD there is permanent damage to the airways. The narrowed airways are fixed, and so symptoms are chronic (persistent). Treatment to open up the airways

      is therefore limited.

      In asthma there is inflammation in the airways which makes the muscles in the airways constrict. This causes the airways to narrow. The symptoms tend to come and go, and vary in severity from time to time. Treatment to reduce inflammation and to open up the airways usually works well.

      COPD is more likely than asthma to cause a chronic (ongoing) cough with phlegm.

      Night time waking with breathlessness or wheeze is common in asthma and uncommon in COPD.

      COPD is rare before the age of 35 whilst asthma is common in under-35s.

      There is more likely to be a history of asthma, allergies, eczema and hayfever (so-called atopy) in people with asthma.

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      Great Ormond Street Hospital for Children and UCL Institute of Child Health  

      10 years ago

      Chest pain and coughing up blood (haemoptysis) are not common features of COPD. It is possible to have slightly blood-streaked sputum when you have a chest infection. However, chest pain, blood in the sputum or coughing up just blood, should always be reported to a doctor. This is because other conditions need to be excluded (like angina, heart attack or lung cancer).

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      Sihtasutus Tartu Ülikooli Kliinikum  

      10 years ago

      What are the symptoms of chronic obstructive pulmonary disease?

      Cough is usually the first symptom to develop. It is productive with sputum (phlegm). It tends to come and go at first, and then gradually becomes more persistent (chronic). You may think of your cough as a 'smokers cough' in the early stages of the disease. It is when the breathlessness begins that people often become concerned.

      Breathlessness (shortness of breath) and wheeze may occur only when you exert yourself at first. For example, when you climb stairs. These symptoms tend to become gradually worse over the years if you continue to smoke. Difficulty with breathing may eventually become quite distressing.

      Sputum - the damaged airways make a lot more mucus than normal. This forms sputum (phlegm). You tend to cough up a lot of sputum each day.

      Chest infections are more common if you have COPD. A sudden worsening of symptoms (such as when you have an infection) is called an exacerbation. Wheezing with cough and breathlessness may become worse than usual if you have a chest infection and you may cough more sputum. Sputum usually turns yellow or green during a chest infection. Chest infections can be caused by bacteria or viruses. Bacteria (which can be killed using antibiotics) cause about 1 in 2 or 3 exacerbations of COPD. Viruses (not killed with antibiotics) are a common cause of exacerbations too, particularly in the winter months. The common cold virus may be responsible for up to 1 in 3 exacerbations.

      Other symptoms of COPD can be more vague. Examples are weight loss, tiredness and ankle swelling.

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      Norrbottens Lans Landsting 

      10 years ago

      What causes chronic obstructive pulmonary disease?

      Smoking is the cause in the vast majority of cases. There is no doubt about this. The lining of the airways becomes inflamed and damaged by smoking. About 3 in 20 people who smoke one packet of cigarettes (20 cigarettes) per day, and 1 in 4 40-per-day smokers, develop COPD if they continue to smoke. For all smokers, the chances of developing COPD is between 1 in 10 and 1 in 4.

      Air pollution and polluted work conditions may cause some cases of COPD, or make the disease worse. The combination effect of occupational exposure to air pollutants and smoking increases the chances of developing COPD.

      A small number of people have a genetic (hereditary) risk of COPD due to very rare protein deficiencies that can lead to lung, liver and blood disorders. (The condition is called alpha-1-antitrypsin deficiency). Less than 1 in 100 cases of COPD are due to this.

      However, people who have never smoked rarely develop COPD. (Passive smoking remains, however, a potential cause.)

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      Lucile Packard Children's Hospital Stanford 

      10 years ago

      How common is chronic obstructive pulmonary disease?

      COPD is common. About three million people in the UK have COPD. It is estimated that another half million people have the condition but have not been diagnosed with COPD. COPD mainly affects people over the age of 40 and becomes more common with increasing age. The average age of diagnosis is around 67 years. It is more common in men than women.

      COPD accounts for more time off work than any other illness. A flare-up (exacerbation) of COPD is one of the most common reasons for admission to hospital (1 in 8 admissions is due to COPD).

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      Universitätsklinikum Freiburg 

      10 years ago

      What is chronic obstructive pulmonary disease?

      Chronic obstructive pulmonary disease (COPD) is a general term which includes the conditions chronic bronchitis and emphysema. COPD is the preferred term, but you may still hear it called chronic obstructive airways disease (COAD).

      Chronic means persistent.

      Bronchitis is inflammation of the bronchi (the airways of the lungs).

      Emphysema is damage to the smaller airways and air sacs (alveoli) of the lungs.

      Pulmonary means 'affecting the lungs'.

      Chronic bronchitis or emphysema can cause obstruction (narrowing) of the airways. Chronic bronchitis and emphysema commonly occur together. The term COPD is used to describe airflow obstruction due to chronic bronchitis, emphysema, or both.

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      Ohio State University Medical Center Columbus 

      10 years ago

      Chronic obstructive pulmonary disease (COPD) is an umbrella term for people with chronic bronchitis, emphysema, or both. With COPD the airflow to the lungs is restricted (obstructed). COPD is usually caused by smoking. Symptoms include cough and breathlessness. The most important treatment is to stop smoking. Inhalers are commonly used to ease symptoms. Other treatments such as steroids, antibiotics, oxygen, and mucolytic (mucus-thinning) medicines are sometimes prescribed in more severe cases, or during a flare-up (exacerbation) of symptoms.

      taken from

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      Landstinget I Uppsala Lan 

      10 years ago

      What is chronic obstructive pulmonary disease (COPD)?

      COPD is a lung disease that makes it hard to breathe. It is caused by damage to the lungs over many years, usually from smoking.

      COPD is often a mix of two diseases:

      Chronic bronchitis (say "bron-KY-tus"). In chronic bronchitis, the airways that carry air to the lungs (bronchial tubes ) get inflamed and make a lot of mucus. This can narrow or block the airways, making it hard for you to breathe.

      Emphysema (say "em-fuh-ZEE-muh"). In a healthy person, the tiny air sacs in the lungs are like balloons. As you breathe in and out, they get bigger and smaller to move air through your lungs. But with emphysema, these air sacs are damaged and lose their stretch. Less air gets in and out of the lungs, which makes you feel short of breath.

      COPD gets worse over time. You can't undo the damage to your lungs. But you can take steps to prevent more damage and to feel better.

      What causes COPD?

      COPD is almost always caused by smoking. Over time, breathing tobacco smoke irritates the airways and destroys the stretchy fibers in the lungs.

      Other things that may put you at risk include breathing chemical fumes, dust, or air pollution over a long period of time. Secondhand smoke is also bad.

      It usually takes many years for the lung damage to start causing symptoms, so COPD is most common in people who are older than 60.

      You may be more likely to get COPD if you had a lot of serious lung infections when you were a child. People who get emphysema in their 30s or 40s may have a disorder that runs in families, called alpha-1 antitrypsin deficiency. But this is rare.

      What are the symptoms?

      The main symptoms are:

      A long-lasting (chronic) cough.

      Mucus that comes up when you cough.

      Shortness of breath that gets worse when you exercise.

      As COPD gets worse, you may be short of breath even when you do simple things like get dressed or fix a meal. It gets harder to eat or exercise, and breathing takes much more energy. People often lose weight and get weaker.

      At times, your symptoms may suddenly flare up and get much worse. This is called a COPD exacerbation (say "egg-ZASS-er-BAY-shun"). An exacerbation can range from mild to life-threatening. The longer you have COPD, the more severe these flare-ups will be.

      How is COPD diagnosed?

      To find out if you have COPD, a doctor will:

      Do a physical exam and listen to your lungs.

      Ask you questions about your past health and whether you smoke or have been exposed to other things that can irritate your lungs.

      Have you do breathing tests, including spirometry, to find out how well your lungs work.

      Do chest X-rays and other tests to help rule out other problems that could be causing your symptoms.

      taken from

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      National Cancer Institute Center for Cancer Research 

      10 years ago


      COPD has probably always existed but has been called by different names in the past. Bonet described a condition of “voluminous lungs” in 1679. In 1769, Giovanni Morgagni described 19 cases where the lungs were “turgid” particularly from air.[65] The first description and illustration of the enlarged airspaces in emphysema was provided by Ruysh in 1721."History of pathologic descriptions of COPD" (PDF). Matthew Baillie illustrated an emphysematous lung in 1789 and described the destructive character of the condition.[65] Badham used the word "catarrh" to describe the cough and mucus hypersecretion of chronic bronchitis in 1814. He recognised that chronic bronchitis was a disabling disorder.

      René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus.[65]

      In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could only measure volume, not airflow.[66] Tiffeneau in 1947 and Gaensler in 1950 and 1951 described the principles of measuring airflow.

      The terms chronic bronchitis and emphysema were formally defined at the CIBA guest symposium of physicians in 1959. The term COPD was first used by William Briscoe in 1965 and has gradually overtaken other terms to become established today as the preferred name for this disease.

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      Graz University Hospital 

      10 years ago


      Disability-adjusted life year for chronic obstructive pulmonary disease per 100,000 inhabitants in 2004.[61]

      no data

      less than 110











      more than 1350

      COPD occurs in 34 out of 1000 greater than 65 years old.[62] In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; translating into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas.[3] In the United States, the prevalence of COPD is approximately 1 in 20 or 5%, totalling approximately 13.5 million people in USA,[63] or possibly approximately 25 million people if undiagnosed cases are included.

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      University of Utah Health Care 

      10 years ago


      COPD usually gradually gets worse over time and can lead to death. The rate at which it gets worse varies between individuals. The factors that predict a poorer prognosis are:[4]

      Severe airflow obstruction (low FEV1)

      Poor exercise capacity

      Shortness of breath

      Significantly underweight or overweight

      Complications like respiratory failure or cor pulmonale

      Continued smoking

      Frequent acute exacerbations

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      National Cancer Center Hospital 

      10 years ago

      Surgery is sometimes helpful for COPD in selected cases. A bullectomy is the surgical removal of a bulla, a large air-filled space that can squash the surrounding, more normal lung. Lung volume reduction surgery is similar; parts of the lung that are particularly damaged by emphysema are removed allowing the remaining, relatively good lung to expand and work better. Lung transplantation is sometimes performed for severe COPD, particularly in younger individuals.

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      Landstinget I Östergötland 

      10 years ago

      Pulmonary rehabilitation

      Pulmonary rehabilitation is a program of exercise, disease management and counselling coordinated to benefit the individual.[59] Pulmonary rehabilitation has been shown to improve shortness of breath and exercise capacity. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.[60]


      Being either underweight or overweight can affect the symptoms, degree of disability and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake.[4] When combined with regular exercise or a pulmonary rehabilitation programme, this can lead to improvements in COPD symptoms.

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      University Hospitals of Cleveland, Ohio 

      10 years ago

      Supplemental oxygen

      Oxygen can be delivered in different forms: in large containers, in smaller containers with liquid oxygen, or with the use of an oxygen concentrator (shown here) which derives oxygen from room air. The latter two options improve mobility of people requiring long-term oxygen therapy.

      Supplemental oxygen can be given to people with COPD who have low oxygen levels in the body. Oxygen is provided from an oxygen cylinder or an oxygen concentrator and delivered to a person through tubing via a nasal cannula or oxygen mask. Supplemental oxygen does not greatly improve shortness of breath but can allow people with COPD and low oxygen levels to do more exercise and household activity. Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD and arterial hypoxemia or with complications of hypoxemia such as pulmonary hypertension, cor pulmonale, or secondary erythrocytosis.[58] High concentrations of supplemental oxygen can lead to the accumulation of carbon dioxide and respiratory acidosis for some people with severe COPD; lower oxygen flow rates are generally safer for these individuals.

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      Children's Hospital of Philadelphia 

      10 years ago

      Other medication

      Theophylline is a bronchodilator and phosphodiesterase inhibitor that in high doses can reduce symptoms for some people who have COPD. More often, side effects such as nausea and stimulation of the heart limit its use.[4] In lower doses, it may slightly reduce the number of COPD exacerbations.[56] The investigative phosphodiesterase-4 antagonists, roflumilast and cilomilast have completed Phase-2 clinical trials. Tumor necrosis factor antagonists such as infliximab suppress the immune system and reduce inflammation. Infliximab has been trialled in COPD but there was no evidence of benefit with the possibility of harm

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      Boston Medical Center 

      10 years ago


      Corticosteroids act to reduce the inflammation in the airways, in theory reducing lung damage and airway narrowing caused by inflammation.[54] Unlike bronchodilators, they do not act directly on the airway smooth muscle and do not provide immediate relief of symptoms. Some of the more common corticosteroids in use are prednisone, fluticasone, budesonide, mometasone, and beclomethasone. Corticosteroids are used in tablet or inhaled form to treat and prevent acute exacerbations of COPD. Well-inhaled corticosteroids (ICS) have not been shown to be of benefit for people with mild COPD, however, they have been shown to decrease acute exacerbations in those with either moderate or severe COPD. They however have no effect on overall one-year mortality and are associated with increased rates of pneumonia.

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      University of Missouri Health Care 

      10 years ago


      Anticholinergic drugs cause airway smooth muscles to relax by blocking stimulation from cholinergic nerves. Ipratropium is the most widely prescribed short acting anticholinergic drug. Like short-acting ?2 agonists, short-acting anticholinergics provide rapid relief of COPD symptoms and a combination of the two is commonly used for a greater bronchodilator effect. Tiotropium is the most commonly prescribed long-acting anticholinergic drug in COPD. It has more specificity for M3 muscarinic receptors so may have fewer side-effects than other anticholinergic drugs. Regular use is associated with improvements in airflow, exercise capacity, quality of life and possibly a longer life. [50][51] In January 2010, new research showed that ipratropium used to treat COPD increased cardiovascular morbidity.[52] At the same time Tiotropium was shown to be effective in eliminating the risk of all cause mortality, cardiovascular mortality and cardiovascular events.

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      University of Mississippi Medical Center 

      10 years ago

      ?2 agonists

      ?2 agonists stimulate ?2 receptors on airway smooth muscles, causing them to relax. There are several ?2 agonists available. Albuterol (common brand name: Ventolin) and terbutaline are widely used short acting ?2 agonists and provide rapid relief of COPD symptoms. Long acting ?2 agonists (LABAs) such as salmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life.

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      Salud Universitaria Catolica  

      10 years ago


      Bronchodilators are medicines that relax smooth muscle around the airways, increasing the calibre of the airways and improving air flow. They can reduce the symptoms of shortness of breath, wheeze and exercise limitation, resulting in an improved quality of life for people with COPD.[47] They do not slow down the rate of progression of the underlying disease.[4] Bronchodilators are usually administered with an inhaler or via a nebulizer.

      There are two major types of bronchodilator, ?2 agonists and anticholinergics. Anticholinergics appear to be superior to ?2 agonists in COPD. Anticholinergics reduce respiratory deaths while ?2 agonists have no effect on respiratory deaths.[48] Each type may be either long-acting (with an effect lasting 12 hours or more) or short-acting (with a rapid onset of effect that does not last as long).

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      Royal Children's Hospital 

      10 years ago

      Air pollution

      Air quality can be improved by pollution reduction efforts which should lead to health gains for people with COPD. A person who has COPD may experience fewer symptoms if they stay indoors on days when air quality is poor.

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      St. Jude Children's Research Hospital 

      10 years ago

      Occupational health

      Measures can be taken to reduce the likelihood that workers in at-risk industries such as coal mining will develop COPD. Some examples of these measures are: education of workers and management about the risks, promoting smoking cessation, surveillance of workers for early signs of COPD, the use of personal dust monitors, the use of respirators and dust control.[46] Dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation. If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role.

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      Universitätsklinikum Gießen und Marburg * 

      10 years ago

      Smoking cessation is one of the most important factors in slowing down the progression of COPD. Once COPD has been diagnosed, stopping smoking slows down the rate of progression of the disease. Even at a late stage of the disease it can significantly reduce the rate of deterioration in lung function and delay the onset of disability and death.[14] It is the only standard intervention that can improve the rate of progression of COPD.[43]

      Smoking cessation starts with an individual decision to stop smoking that leads to an attempt at quitting. Often several attempts are required before long-term smoking cessation is achieved.[44] Some smokers can achieve long-term smoking cessation through "willpower" alone. However smoking is highly addictive[45] and many smokers need further support to quit. The chance of successfully stopping smoking can be greatly improved through social support, engagement in a smoking cessation programme and the use of drugs such as nicotine replacement therapy, bupropion and varenicline.[44]

      The policies of governments, public health agencies and anti-smoking organizations can reduce smoking rates by encouraging smoking cessation and discouraging people from starting smoking.[44] These policies are important strategies in the prevention of COPD

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      Hopitaux Universitaires de Geneve 

      10 years ago


      There is currently no cure for COPD; however, COPD is both a preventable and treatable disease. Clinical practice guidelines for the management of COPD are available from the Global Initiative for Chronic Obstructive Lung Disease (GOLD),[42] a collaboration that includes the World Health Organization and the U.S. National Heart, Lung, and Blood Institute. The major current directions of COPD management are to assess and monitor the disease, reduce the risk factors, manage stable COPD, prevent and treat acute exacerbations and manage comorbidity.[4]

      The only measures that have been shown to reduce mortality is smoking cessation and supplemental oxygen

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      Buddhist Tzu Chi General Hospital 

      10 years ago

      Other tests

      On chest x-ray the classic signs of COPD are over-expanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae.[41] It can be useful to help exclude other lung diseases such as pneumonia, pulmonary edema or a pneumothorax.[41] Complete pulmonary function tests with measurements of lung volumes and gas transfer may also show hyperinflation and can discriminate between COPD with emphysema and COPD without emphysema. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases.

      A blood sample taken from an artery can be tested for blood gas levels which may show low oxygen levels (hypoxemia) and/or high carbon dioxide levels (respiratory acidosis). A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia.

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      Seattle Children's Hospital and Medical Center 

      10 years ago


      The diagnosis of COPD is confirmed by spirometry,[4] a test that measures breathing. Spirometry measures the forced expiratory volume in one second (FEV1) which is the greatest volume of air that can be breathed out in the first second of a large breath. Spirometry also measures the forced vital capacity (FVC) which is the greatest volume of air that can be breathed out in a whole large breath. Normally at least 70% of the FVC comes out in the first second (i.e. the FEV1/FVC ratio is >70%). A ratio of less than normal defines the patient as having COPD. More specifically, the diagnosis of COPD is made when the FEV1/FVC ratio is

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      Dartmouth Hitchcock Medical Center Lebanon, NH  

      10 years ago


      A chest X-ray demonstrating severe COPD. Note the small size of the heart in comparison to the lungs.

      The diagnosis of COPD should be considered in anyone who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease such as regular tobacco smoking.[4][38] No single symptom or sign can adequately confirm or exclude the diagnosis of COPD[39] although COPD is uncommon under the age of 40 years.

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      New York Presbyterian Hospital 

      10 years ago

      An acute exacerbation of COPD is a sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacteria can roughly be found in 25% of cases, viruses in another 25%, and both viruses and bacteria in another 25%. Pulmonary Embolism can also cause exacerbations of COPD. Airway inflammation is increased during the exacerbation resulting in increased hyperinflation, reduced expiratory air flow and worsening of gas transfer. This can also lead to hypo ventilation and eventually hypoxia, thus can lead to insufficient tissue perfusion then cell necrosis.

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      Universitätsklinikum und Medizinische Fakultät Tübingen  

      10 years ago


      Enlarged view of lung tissue showing the difference between healthy lung and COPD

      It is not fully understood how tobacco smoke and other inhaled particles damage the lungs to cause COPD. The most important processes causing lung damage are:

      Oxidative stress produced by the high concentrations of free radicals in tobacco smoke.

      Cytokine release due to inflammation as the body responds to irritant particles such as tobacco smoke in the airway.

      Tobacco smoke and free radicals impair the activity of antiprotease enzymes such as alpha 1-antitrypsin, allowing protease enzymes to damage the lung.

      Potential role of Coagulation and the Complement System in COPD; a complex cascade of blood plasma proteins and platelet activation as molecular perturbations associated with patients suffering from Chronic Obstructive Pulmonary Disease.

      Narrowing of the airways reduces the rate at which air can flow to and from the air sacs (alveoli) and limits the effectiveness of the lungs. In COPD, the greatest reduction in air flow occurs when breathing out (during expiration) because the pressure in the chest tends to compress rather than expand the airways. In theory, air flow could be increased by breathing more forcefully, increasing the pressure in the chest during expiration. In COPD, there is often a limit to how much this can actually increase air flow, a situation known as expiratory flow limitation.[35]

      If the rate of airflow is too low, a person with COPD may not be able to completely finish breathing out (expiration) before he or she needs to take another breath. This is particularly common during exercise when breathing has to be faster. A little of the air of the previous breath remains within the lungs when the next breath is started. When this happens, there is an increase in the volume of air in the lungs, a process called dynamic hyperinflation.[35]

      Dynamic hyperinflation is closely linked to shortness of breath (dyspnea) in COPD.[36] It is less comfortable to breathe with hyperinflation because it takes more effort to move the lungs and chest wall when they are already stretched by hyperinflation.

      Another factor contributing to shortness of breath in COPD is the loss of the surface area available for the exchange of oxygen and carbon dioxide with emphysema. This reduces the rate of transfer of these gasses between the body and the atmosphere and can lead to low oxygen and high carbon dioxide levels in the body. A person with emphysema may have to breathe faster or more deeply to compensate, which can be difficult to do if there is also flow limitation or hyperinflation.

      Some people with advanced COPD do manage to breathe fast to compensate, but usually have dyspnea as a result. Others, who may be less short of breath, tolerate low oxygen and high carbon dioxide levels in their bodies but this can eventually lead to headaches, drowsiness and heart failure.

      Advanced COPD can lead to complications beyond the lungs such as weight loss (cachexia), pulmonary hypertension and right-sided heart failure (cor pulmonale). Osteoporosis, heart disease, muscle wasting and depression are all more common in people with COPD.[4]

      Several molecular signatures associated to lung function decline and corollaries of disease severity have been proposed, a majority of which are characterized in easily accessible surrogate tissue, including blood derivatives such as serum and plasma. A recent 2010 clinical study proposes alpha 1B-glycoprotein precursor/A1BG, Alpha 2-antiplasmin, apolipoprotein A-IV precursor/APOA4, and complement component 3 precursor, among other coagulation and complement system proteins as corrollaries of lung function decline, although ambiguity between cause and effect is unresolved

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      University of North Carolina Healthcare 

      10 years ago

      There is mounting evidence that there may be an autoimmune component to COPD, triggered by lifelong smoking. Many individuals with COPD who have stopped smoking have active inflammation in the lungs. The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.This sustained inflammation is thought to be mediated by autoantibodies and autoreactive T cells.

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      Wpmc Wright Patterson Medical Center 

      10 years ago

      Other risk factors

      A tendency to sudden airway constriction in response to inhaled irritants, bronchial hyperresponsiveness, is a characteristic of asthma. Many people with COPD also have this tendency. In COPD, the presence of bronchial hyperresponsiveness predicts a worse course of the disease.[26] It is not known if bronchial hyperresponsiveness is a cause or a consequence of COPD. Other risk factors such as repeated lung infection and possibly a diet high in cured meats (possibly due to the preservative sodium nitrite) may be related to the development of COPD.

    • profile image

      University of Pittsburgh Medical Center 

      10 years ago


      Some factor in addition to heavy smoke exposure is required for a person to develop COPD. This factor is probably a genetic susceptibility. COPD is more common among relatives of COPD patients who smoke than unrelated smokers.[29] The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In this condition, the body does not make enough of a protein, alpha 1-antitrypsin. Alpha 1-antitrypsin protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke

    • profile image

      Faculty of Medicine Siriraj Hospital 

      10 years ago

      Occupational exposures

      Intense and prolonged exposure to workplace dusts found in coal mining, gold mining, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstruction, even in nonsmokers.[24] Workers who smoke and are exposed to these particles and gases are even more likely to develop COPD. Intense silica dust exposure causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[25] The effect of occupational pollutants on the lungs appears to be substantially less important than the effect of cigarette smoking

    • profile image

      Universitätsklinikum Medizinische Fakultat der Martin Luther Universitat Halle Wittenberg 

      10 years ago


      The primary risk factor for COPD is chronic tobacco smoking. In the United States, 80 to 90% of cases of COPD are due to smoking.[20][21] Exposure to cigarette smoke is measured in pack-years[22], the average number of packages of cigarettes smoked daily multiplied by the number of years of smoking. The likelihood of developing COPD increases with age and cumulative smoke exposure, and almost all life-long smokers will develop COPD, provided that smoking-related, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand

    • profile image

      INCA Instituto Nacional de Câncer 

      10 years ago

      Signs and symptoms


      The sound of wheezing as heard with a stethoscope.

      Problems listening to this file? See media help.

      Essentials of diagnosis include:

      History of cigarette smoking.

      Chronic cough and sputum production (in chronic bronchitis)

      Dyspnea (in emphysema)

      Rhonchi, decreased intensity of breath sounds, and prolonged expiration on physical examination

      Airflow limitation on pulmonary function testing that is not fully reversible and most often progressive

      One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: "My breathing requires effort," "I feel out of breath," or "I can't get enough air in".[16] People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is constantly present.

      Other symptoms of COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness.[17][18]

      People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs.[19] Symptoms of cor pulmonale are peripheral edema, seen as swelling of the ankles, and dyspnea.

      There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. Some people have COPD and have none of these signs. Common signs are:

      tachypnea, a rapid breathing rate

      wheezing sounds or crackles in the lungs heard through a stethoscope

      breathing out taking a longer time than breathing in

      enlargement of the chest, particularly the front-to-back distance (hyperaeration)

      active use of muscles in the neck to help with breathing

      breathing through pursed lips

      increased anteroposterior to lateral ratio of the chest (i.e. barrel chest).

    • profile image

      Institute of Cancer Research Royal Cancer Hospital 

      10 years ago

      Lung damage and inflammation of the air sacs (alveoli) results in emphysema. Emphysema is defined as enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls.[13] The destruction of air space walls reduces the surface area available for the exchange of oxygen and carbon dioxide during breathing. It also reduces the elasticity of the lung itself, which results in a loss of support for the airways that are embedded in the lung. These airways are more likely to collapse causing further limitation to airflow. The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, "pink puffers".

    • profile image

      Maharaj Nakorn Chiang Mai Hospital & Faculty of Medicine 

      10 years ago

      Lung damage and inflammation in the large airways results in 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.[13] In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow.[14]

      Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as "blue bloaters" because of the bluish color of the skin and lips (cyanosis) seen in them.[15] The hypoxia and fluid retention leads to them being called "Blue Bloaters

    • profile image

      Partners Healthcare System 

      10 years ago

      The twofold nature of the pathology has been studied in the past.[9] Furthermore, also in recent studies, many authors found that each patient could be classified as presenting a predominantly bronchial or emphysematous phenotype simply analyzing clinical, functional, and radiological findings or studying interesting biomarkers.[10][11][12] A statistical model reflecting the specific predominant mechanism of airflow limitation for a specific patient has been developed and trained over a database of hundreds of patients. The model is available here ( as a free on-line application.

    • profile image

      University of Iowa Hospitals and Clinics 

      10 years ago

      Chronic Obstructive Pulmonary Disease (COPD) makes it hard for you to breathe. Coughing up mucus is often the first sign of COPD. Chronic bronchitis and emphysema are common COPDs.

      Your airways branch out inside your lungs like an upside-down tree. At the end of each branch are small, balloon-like air sacs. In healthy people, both the airways and air sacs are springy and elastic. When you breathe in, each air sac fills with air like a small balloon. The balloon deflates when you exhale. In COPD, your airways and air sacs lose their shape and become floppy, like a stretched-out rubber band.

      Cigarette smoking is the most common cause of COPD. Breathing in other kinds of irritants, like pollution, dust or chemicals, may also cause or contribute to COPD. Quitting smoking is the best way to avoid developing COPD.

      Treatment can make you more comfortable, but there is no cure.

      NIH: National Heart, Lung, and Blood Institute

      taken from

    • profile image

      Centre Hospitalier Universitaire Vaudois Lausanne  

      10 years ago

      the term "COPD" includes two main conditions—emphysema (em-fi-SE-ma) and chronic bronchitis (bron-KI-tis). (Note: The Diseases and Conditions Index article about bronchitis discusses both acute and chronic bronchitis.)

      In emphysema, the walls between many of the air sacs are damaged, causing them to lose their shape and become floppy. This damage also can destroy the walls of the air sacs, leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of gas exchange in the lungs is reduced.

      In chronic bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.

      Most people who have COPD have both emphysema and chronic obstructive bronchitis. Thus, the general term "COPD" is more accurate.


      COPD is a major cause of disability, and it's the fourth leading cause of death in the United States. More than 12 million people are currently diagnosed with COPD. Many more people may have the disease and not even know it.

      COPD develops slowly. Symptoms often worsen over time and can limit your ability to do routine activities. Severe COPD may prevent you from doing even basic activities like walking, cooking, or taking care of yourself.

      Most of the time, COPD is diagnosed in middle-aged or older people. The disease isn't passed from person to person—you can't catch it from someone else.

      COPD has no cure yet, and doctors don't know how to reverse the damage to the airways and lungs. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.

      taken from

    • profile image

      Stanford Hospital & Clinics, CA 

      10 years ago

      What Is COPD?

      COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes it hard to breathe. "Progressive" means the disease gets worse over time.

      COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing, shortness of breath, chest tightness, and other symptoms.

      Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. Long-term exposure to other lung irritants, such as air pollution, chemical fumes, or dust, also may contribute to COPD.


      To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial tubes or airways.

      Within the lungs, your bronchial tubes branch into thousands of smaller, thinner tubes called bronchioles. These tubes end in bunches of tiny round air sacs called alveoli (al-VEE-uhl-eye).

      Small blood vessels called capillaries run through the walls of the air sacs. When air reaches the air sacs, the oxygen in the air passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide (a waste gas) moves from the capillaries into the air sacs. This process is called gas exchange.

      The airways and air sacs are elastic (stretchy). When you breathe in, each air sac fills up with air like a small balloon. When you breathe out, the air sacs deflate and the air goes out.

      In COPD, less air flows in and out of the airways because of one or more of the following:

      The airways and air sacs lose their elastic quality.

      The walls between many of the air sacs are destroyed.

      The walls of the airways become thick and inflamed.

      The airways make more mucus than usual, which tends to clog them.


    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      10 years ago from Europe

      It is an aided attempt to a smoker to quit smoking. Its just a big language. Sometimes programs are usually available to aid the smoker to quit

      Robert West and Saul Shiffman have authored works on smoking cessation. They believe that, used together, "behavioral support" and "medication" can quadruple the chances that a quit attempt will be successful. Both, however, disclosed that they are paid researchers or consultants to pharmaceutical companies or manufacturers of smoking cessation medications

    • profile image


      10 years ago

      I quote from this hub "Management of Chronic Obstructive Pulmonary Diseases in all severity involves; avoidance of risk factors (smoking cessation, reduction of indoor pollution, reduction of occupational exposure etc) and also influenza vaccination."

      My question now is.... WHat is smoking cessation? Thanks and you are doing a great Job D.Virtual.Doctor. Dchosen_01 wrote DVD and I was trying to figure out, I think I now know what he means

    • profile image


      10 years ago

      Great job! Weldone. Now you have 12 hubs... You are really moving DVD. Please, I still want to know the forums you post your hubs for groups, universities and hospitals to paste lots of comments like this....

    • D.Virtual.Doctor profile imageAUTHOR

      Funom Theophilus Makama 

      10 years ago from Europe

      Hello everyone! Some have personally e-mailed me about writing COPD (Chronic Obstructive Pulmonary Disease) in details, just as I have done with the other hubs, congrats! Now here it is. It has not been easy doing this compilation and write up, but finally we are here. Enjoy reading it and most importantly, ask your questions, leave your comments and send in your contributions. I will be here waiting for you so that we can all solve these ailments together. As always......



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