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Chronic obstructive pulmonary disease (COPD)


Reviewers: Elliot Weisenberg, M.D.(see Reviewers page)
Revised: 31 August 2011, last major update August 2011
Copyright: (c) 2003-2011, PathologyOutlines.com, Inc.


● Abnormal permanent enlargement of air spaces distal to terminal bronchiole with wall destruction but without fibrosis (eMedicine)
● Differs from overinflation, which is not due to wall destruction (example: due to loss of opposite lung)

Clinical features

● Acinar and airspace enlargement is usually due to tobacco related wall destruction, due to alteration in balance between proteases and antiproteases
● No symptoms until 1/3 of functional capacity is lost; get shortness of breath, coughing, wheezing, weight loss, barrel chest; breath through pursed lips (pink-puffer), which causes slowing of forced expiration
● May cause secondary pulmonary vascular hypertension, cor pulmonale, congestive heart failure, pneumothorax, death due to respiratory acidosis and coma
● Best to assess based on morphometry, not lung function data; most informative techniques are intrabronchial formalin instillation or inflation fixation with freeze drying (Dail and Hammarís Pulmonary Pathology, 3rd edition, Mod Pathol 2003;16:1)


Bullous emphysema: Sometimes incorrectly used as a synonym for paraseptal emphysema; any form that produces blebs >1 cm, often subpleural, near apex, associated with tuberculosis scarring; may rupture and cause pneumothorax or hemorrhage; called placental transmogrification if it resembles chorionic villi; bullae are found within lung parenchma, in contrast to blebs, located within visceral pleura
Centroacinar (centrilobular or proximal acinar): 85% of emphysema cases, causes significant airflow obstruction, affects central part of acini sparing distal alveoli; worse in upper lobes, particularly apices; walls are anthracotic, parabronchial inflammation; may have adjacent normal alveolar architecture; seen in heavy smokers (age 40+), coal worker pneumoconiosis
Compensatory emphysema: response to loss of lung elsewhere, such as post-lobectomy; generally more hyperinflation, as opposed to true emphysema with destruction of lung tissue
Interstitial emphysema: air within connective tissue stroma of lung, mediastinum or subcutaneous tissue, due to alveolar tears, chest wounds, coughing or whooping cough
Irregular (paracicatricial): minor clinically, invariably associated with scarring; irregular involvement of acini, associated with remote granulomatous disease, healed infarction, organized pneumonia, pneumoconiosis
Obstructive emphysema: due to tumor, foreign body or congenital lobar overinflation (infants, perhaps due to hypoplasia of bronchial cartilage; associated with other cardiopulmonary anomalies); due to ball-valve effect with inhalation via collaterals (pores of Kohn, canals of Lambert), may compress normal lung, may be life-threatening
Panacinar (panlobular): 5% of cases, causes significant airflow obstruction, acini are uniformly enlarged from respiratory bronchiole to terminal alveoli (central to peripheral); usually affects lower lungs, associated with alpha-1-antitrypsin deficiency; lungs are usually voluminous
Paraseptal (distal acinar or localized): 5% of cases, minor clinically, only distal acini affected, emphysema is next to pleura, near areas of fibrosis, scarring or atelectasis; multiple continuous airspaces are affected, may be source of spontaneous pneumothorax in young adults
Senile emphysema: due to age-related alterations in internal geometry of alveoli, leading to larger alveolar ducts, smaller alveoli, but no loss of elastic tissue or destruction of lung substance, thus not true emphysema

Gross images

Various images

Micro images

Dilated air spaces and loss of alveolar walls

Virtual slides


End of Lung-nontumor > Chronic obstructive pulmonary disease (COPD) > Emphysema

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