Fig.13.47B ).Atypical carcinoid tumorsdisplayahighermitoticrateandsmallfociofnecrosis.Thesetumorshaveahigherincidenceoflymphnodeanddistantmetastasisthantypicalcarcinoids.Unliketypicalcarcinoids,theatypicaltumorshaveTP53 mutationsin20%to40%ofcases.Typicalcarcinoid,atypicalcarcinoid,andlargecellneuroendocrineandsmallcellcarcinomacanbeviewedasacontinuumofincreasinghistologicaggressivenessandmalignantpotentialwithinthespectrumofpulmonaryneuroendocrineneoplasms.
Fig. 13.47 Bronchialcarcinoid.(A)Carcinoidgrowingasaspherical,palemass(arrow) protrudingintothelumenofthebronchus.(B)Histologicappearancedemonstratingsmall,rounded,uniformnucleiandmoderatecytoplasm. (Courtesy of Dr. Thomas Krausz, Department of Pathology, University of Chicago Pritzker School of Medicine, Chicago, Illinois.) http://ebooksmedicine.net
Most carcinoid tumors manifest with signs and symptoms related to their intraluminal growth, including cough, hemoptysis, and recurrent bronchial and pulmonary infections. Peripheral tumors are often asymptomatic and are discovered incidentally on chest radiographs. Only rarely do pulmonary carcinoids induce the carcinoid syndrome, characterized by intermittent attacks of diarrhea, flushing, and cyanosis. The reported 5and 10-year survival rates for typical carcinoids are above 85%, while these rates drop to 56% and 35%, respectively, for atypical carcinoids.
Disease of the pleura usually is a complication of an underlying pulmonary disease. Secondary infections and pleural adhesions are common findings at autopsy. Important primary disorders are (1) primary intrapleural bacterial infections and (2) malignant mesothelioma, a primary neoplasm of the pleura.
Pleural effusions (fluids in the pleural space) can be either transudates or exudates. When the effusion is a transudate, the condition is termed hydrothorax. Congestive heart failure is the most common cause of bilateral hydrothorax. An exudate, characterized by protein content greater than 30 g/L and, often, inflammatory cells, suggests pleuritis. The four principal causes of pleural exudate formation are microbial invasion through either direct extension of a pulmonary infection or blood-borne seeding (suppurative pleuritis or empyema); (2) cancer (lung carcinoma, metastatic neoplasms to the lung or pleural surface, mesothelioma); pulmonary infarction; and (4) viral pleuritis. Other, less common causes of exudative pleural effusions are systemic lupus erythematosus, rheumatoid arthritis, and uremia, as well as previous thoracic surgery. Malignant effusions characteristically are large and frequently bloody (hemorrhagic pleuritis). Cytologic examination may reveal the malignant cells.
Whatever the cause, transudates and serous exudates usually are resorbed without residual effects if the inciting cause is controlled or remits. By contrast, fibrinous, hemorrhagic, and suppurative exudates may lead to fibrous organization, yielding adhesions or fibrous pleural thickenings that sometimes undergo calcification.
Pneumothorax,Hemothorax,andChylothorax