Clinical Term Anatomic Site Major Pathologic Changes Etiology Signs/Symptoms

Chronic bronchitis Bronchus Mucous gland hyperplasia, hypersecretion Tobacco smoke, air pollutants Cough, sputum production

Bronchiectasis Bronchus Airway dilation and scarring Persistent or severe infections Cough, purulent sputum, fever

Asthma Bronchus Smooth muscle hyperplasia, excess mucus,

inflammation

Immunologic or undefined causes Episodic wheezing, cough, dyspnea

Emphysema Acinus Airspace enlargement; wall destruction Tobacco smoke Dyspnea

Small airway disease, *

bronchiolitis

Bronchiole Inflammatory scarring/obliteration Tobacco smoke, air pollutants,

miscellaneous

Cough, dyspnea

*A feature of chronic bronchitis (see text).

Of these, only the first two cause clinically significant airflow obstruction ( Fig. 15-5 ). Centriacinar emphysema is far more common than the panacinar form, constituting more than 95%

of cases. Clinical management does not rely on precise anatomic diagnosis and classification, which, however, do provide important clues to pathogenesis.

Centriacinar (Centrilobular) 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 ( Fig. 15-6B ). Thus, both emphysematous and normal airspaces exist within the same acinus and lobule. The lesions are more common and usually more

severe in the

Figure 15-5 A, Diagram of normal structures within the acinus, the fundamental unit of the lung. A terminal bronchiole (not shown) is immediately proximal to the respiratory bronchiole.

B, Centriacinar emphysema with dilation that initially affects the respiratory bronchioles. C, Panacinar emphysema with initial distention of the peripheral structures (i.e., the alveolus and

alveolar duct); the disease later extends to affect the respiratory bronchioles.

Figure 15-6 A, Centriacinar emphysema. Central areas show marked emphysematous damage (E), surrounded by relatively spared alveolar spaces. B, Panacinar emphysema involving the

entire pulmonary architecture.

Figure 15-7Pathogenesis of emphysema. The protease-antiprotease imbalance and oxidant-antioxidant imbalance are additive in their effects and contribute to tissue damage. a1 -

antitrypsin (a1 -AT) deficiency can be either congenital or "functional" as a result of oxidative inactivation. See text for details. IL-8, interleukin 8; LTB4 , leukotriene B4 ; TNF, tumor

necrosis factor.

TABLE 15-4-- Emphysema and Chronic Bronchitis

Predominant Bronchitis Predominant Emphysema

Age (yr) 40–45 50–75

Dyspnea Mild; late Severe; early

Cough Early; copious sputum Late; scanty sputum

Infections Common Occasional

Respiratory insufficiency Repeated Terminal

Cor pulmonale Common Rare; terminal

Airway resistance Increased Normal or slightly increased

Elastic recoil Normal Low

Chest radiograph Prominent vessels; large heart Hyperinflation; small heart

Appearance Blue bloater Pink puffer

Date: 2016-04-22; view: 852