Chronic obstructive pulmonary disease (COPD)

Chronic obstructive pulmonary disease (COPD) is a commonly-used clinical term for a group of diseases in which there is chronic, partial or complete, obstruction to the airflow at any level from trachea to the smallest airways resulting in functional disability of the lungs.

The following diseases are included in COPD:

1) Chronic bronchitis;

2) Emphysema;

3) Bronchial asthma;

4) Bronchiectasis;

5) Chronic abscess;

6) Pneumosclerosis;

7) Idiopathic pulmonary fibrosis.

Chronic bronchitis

Chronic bronchitis is chronic inflammation of the bronchial mucous membranes.

Pathology. Macroscopic ally, there may be hyperemia, swelling, and bogginess of the mucous membranes, frequently accompanied by excessive mucinous to mucopurulent secretions layering the epithelial surfaces. Sometimes, heavy casts of secretions and pus fill the bronchi and bronchioles. The characteristic histologic feature of chronic bronchitis is enlargement of the mucus-secreting

panels of the trachea and bronchi. Although the numbers of goblet cells increase slightly, the major increase is in the size of the mucous glands. This increase can be assessed by the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage. The bronchial epithelium may exhibit squamous metaplasia and dysplasia. There is marked narrowing of bronchioles caused by goblet cell metaplasia, mucous plugging, inflammation, and fibrosis. In the most severe cases there may be obliteration of lumina.


According to the WHO, pulmonary emphysema is a combination of permanent dilatation of air spaces distal to the terminal bronchioles and the destruction of the walls of dilated air spaces. Frequently there is combination of chronic bronchitis and pulmonary emphysema.

Classification. According to the WHO pulmonary emphysema is classified into 5 types (according to the portion of the acinus involved):

1) centriacinar, 2) panacinar, 3) paraceptal, 4) irregular, 5) mixed.

These types of emphysema are called «True emphysema». There are several types of «Overin-flation». They are:

1) Compensatory overinflation (compensatory emphysema);

2) Senile hyperinflation (senile emphysema);

3) Obstructive overinflation;

4) Unilateral emphysema;

5) Surgical (interstitial) emphysema. Centriacinar emphysema.The distinctive

feature of this type of emphysema is the pattern of involvement of the lobules; the central or proximal parts of the acini, formed by respiratory bronchioles, are affected, whereas distal alveoli are spared. Thus, both emphysematous and normal airspaces exist within the same acinus and lobule. The lesions are more common and usually more severe in the upper lobes, particularly in the apical segments. The walls of the emphysematous spaces often contain large amounts of black pigment. Inflammation around bronchi and bronchioles and in the septa is common. In severe centriacinar emphysema, the distal acinus may be involved, and differentiation from panacinar emphysema becomes difficult.

Panacinar emphysema.In this type the acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli. It is important to emphasize that the prefix pan-refers to the entire acinus but not to the entire lung. In contrast to centriacinar emphysema, panacinar emphysema tends to occur more commonly in the lower zones and in the anterior margins of the lung, and it is usually most severe at the bases.

Paraceptal emphysema.In this type the proximal portion of the acinus is normal, but the distal part is dominantly involved. The emphysema is more striking adjacent to the pleura, along the lobular connective tissue septa, and at the margins of the lobules. It occurs adjacent to areas of fibrosis, scarring, or atelectasis and is usually more severe in the upper half of the lungs. The characteristic findings are of multiple, continuous, enlarged airspaces from less than 0.5 mm to more than 2.0 cm in diameter, sometimes forming cyst-like structures. This type of emphysema probably underlies many of the cases of spontaneous pneumothorax in young adults.

Irregular emphysema.Irregular emphysema, so termed because the acinus is irregularly involved, is almost invariably associated with scarring. Thus it may be the most common form of emphysema, as careful search of most lungs at autopsy shows one or more scars from a healed inflammatory process. In most instances, these foci of irregular emphysema are asymptomatic.

Pathology. The diagnosis and classification of the emphysemas are based on naked eye (or hand lens) examination of lungs fixed in a state of inflation. Panacinar emphysema, when well developed, produces voluminous lungs, often overlapping the heart and hiding it when the anterior chest wall is removed. The macroscopic signs of centriacinar emphysema are less impressive. The lungs may not appear particularly pale or voluminous unless the disease is well advanced.

Generally, the upper two-thirds of the lungs are more severely affected. Large apical blebs or bullae are more characteristic of irregular emphysema secondary to scarring. Microscopic examination is necessary to visualize the abnormal fenestrations in the walls of the alveoli, the complete destruction of septal walls, and the distribution of damage within the pulmonary lobule. With advance of the disease, adjacent alveoli fuse, producing even larger abnormal airspaces and possibly blebs or bullae. Often the respiratory bronchioles and vasculature of the lung are deformed and compressed by the emphysematous distortion of the airspaces, and, as mentioned, there may or may not be evidence of bronchitis or bronchiolitis.


In bronchial asthma there is wide-spread bronchial obstruction due to muscular spasm and plugging by thick mucus. Bronchial asthma is an episodic disease manifested clinically by paroxysm of dyspnoea, cough and wheezing. A severe and unremitting type of the disease termed status asth-maticus may prove fatal.

Etiology. According to the stimuli initiating bronchial asthma 3 etiological types are described:

• extrinsic (allergic, atopic);

• intrinsic (idiosyncratic, non-atopic);

• mixed pattern.

Extrinsic asthma usually begins in childhood or in early adult life. Most patients of this type of asthma have personal and/or family history of precursor allergic diseases such as rhinitis or eczema.

Intrinsic asthma develops later in adult life with negative personal or family history of allergy.

Pathology. The pathologic changes are similar in both major types of asthma.

Morphology. The morphologic changes in asthma have been described principally in patients dying of status asthmaticus, but it appears that the pathology in nonfatal cases is similar. Macroscopically, the lungs are overdistended because of overinflation, and there may be small areas of atelectasis. The most striking macroscopic finding is occlusion of bronchi and bronchioles by thick, tenacious mucous plugs. Microscopically, the mucous plugs contain whorls of shed epithelium, which give rise to the well-known Curschmann's spirals. Numerous eosinophils and Charcot-Leyden crystals are present; the latter are collections of crystalloid made up of eosinophil membrane protein. The other characteristic histologic findings of asthma include thickening of the basement membrane of the bronchial epithelium; edema and an inflammatory infiltrate in the bronchial walls, with a prominence of eosinophils, which form 5 to 50% of the cellular infiltrate; an increase in size of the submucosal glands; and hypertrophy of the bronchial wall muscle, a reflection of prolonged broncho-constriction.


Is defined as abnormal and irreversible dilatation of the bronchi and bronchioles developing secondary to inflammatory weakening of the bronchial walls.

The most characteristic clinical sign of bronchiectasis is persistent cough with expectoration of copious amounts of foul-smelling purulent sputum.

Etiology. The origin of inflammatory distinctive process of bronchial walls is nearly always a result of two basic mechanisms: obstruction and infection as well as secondary complication (e.g. due to narcotizing pneumonias and tuberculosis).

Pathology. Bronchiectasis usually affects the lower lobes bilaterally, particularly those air passages that are most vertical, and is most severe in the more distal bronchi and bronchioles. When tumors or aspiration of foreign bodies leads to bronchiectasis, the involvement may be sharply localized to a single segment of the lungs. The disease characteristically affects distal bronchi and bronchioles beyond the segmental bronchi. Macroscopically bilateral involvement of lover lobes occurs most frequently. The pleura are usually fibrotic and thickened with adhesions to the chest wall. Cut surface has honeycombed appearance. The walls of bronchi are thickened and the lumens are filled with mucus. The dilated airways, depending on their macroscopic picture have been subclassified into the following

different types: cylindrical; fusiform; saccular; varicose. The histologic findings vary with the activity and chronicity of the disease. In the full-blown, active case, there is an intense acute and chronic inflammatory exudation within the walls of the bronchi and bronchioles, associated with desquamation of the lining epithelium and extensive areas of narcotizing ulceration. There may be pseudostratification of the columnar cells or squamous metaplasia of the remaining epithelium. In some instances, the necrosis completely destroys the bronchial or bronchiolar walls and forms a lung abscess. Fibrosis of the bronchial and bronchiolar walls and peribronchiolar fibrosis develops in the more chronic cases.

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