Lung برای بزرگنمایی عکسها کلیک را روی ان نگه دارید Figure 10.1 Gross appearance of cut surface of normal lung showing pulmonary lobules separated by connective tissue septa Figure 10.2 Gross appearance of congenital cystic adenomatoid mal- formation of lung Figure 10.3 Microscopic appearance of large cyst (Stocker type 1) congenital cystic adenomatoid transformation. A large cystic air spaces is lined by ciliated respiratory epithelium and mucinous gastric-like epi- thelium is scattered throughout the adjacent lung parenchyma Figure 10.4 Microscopic appearance of small cyst (Stocker type 2) congenital cystic adenomatoid malformation. Microcystic air spaces lined by cuboidal epithelium are associated with tubular bronchiole-like structures lined by columnar respiratory epithelium Figure 10.5 Microscopic appearance of placental transmogrification in which connective tissue papillae persist in a giant bulla resulting in an unusual histology that is reminiscent of chorionic villi Figure 10.6 Extralobar type of pulmonary sequestration. The lung has a spongy appearance and is covered by normal pleura Figure 10.7 Intralobar type of pulmonary sequestration. As is often the case with this variety, there are extensive secondary inflammatory changes. (Courtesy of Dr. J Costa, New Haven, CT.) Figure 10.8 Localized bronchiectasis involving the lower lobe in a lung resected from a patient with a centrally obstructing endobronchial neoplasm Figure 10.9 Diffuse bronchiectasis in lung resected from a patient with cystic fibrosis Figure 10.10 Bronchopneumonia with abscess formation in a 2-year-old boy secondary to aspiration of a foreign body (timothy grass inflorescence). The first recorded case of this condition seems to be that recorded in a book entitled Some account of Lord Boringdon's accident on July 21st, 1817, and its consequences as follows: 'In 1662, Armand de Boutree, son of the Compte de Nogent, was seized with a violent fever, accompanied by a great difficulty in breathing, a dry cough, afterwards spotting of blood, sleeplessness, and great pain in the right side. A tumor at length appeared on that side, and a surgeon extracted from it an ear of barley almost entire which was quite green and had undergone no change.' (From Kissane JIM. Pathology of Infancy and Childhood. 2nd ed. St Louis, MO: Mosby; 1975.) Figure 10.11 Large lung abscess Figure 10.12 Massive destruction of lung parenchyma by tuberculosis Figure 10.13 Tuberculoma that presented as asymptomatic 3-cm solitary lung nodule Figure 10.14 Tuberculosis. An area of caseous necrosis is bounded by a mixed inflammatory infiltrate that includes epithelioid and multinucleated histiocytes. A sarcoidal non-necrotizing granuloma accompanied the necrotizing granuloma Figure 10.15 Tuberculosis. Ziehl-Neelsen stain demonstrating two acid-fast bacilli Figure 10.16 Atypical mycobacteriosis due to MAC. An area of necrosis showing 'infarct-like' features is surrounded by an inflammatory infiltrate that includes epithelioid and multinucleated histiocytes. Loose clusters of epithelioid and multinucleated giant cells also form non-necrotizing granulomas at the periphery. These histologic features are indistinguishable from those seen with other infectious granulomatous diseases including tuberculosis. Cultures from this case grew M. avium complex Figure 10.17 Coccidioidomycotic granuloma. The necrotic center is surrounded by fibrous tissue showing concentric lamination Figure 10.18 Pulmonary histoplasmosis. The organisms are demonstrated with the Grocott stain and are relatively small (1-5 μm) with a characteristic oval or teardrop shape Figure 10.19 Pulmonary blastomycosis. Microscopic appearance of B. dermatitidis in a hematoxylin and eosin stain. The organisms are large (8-15 μm) with a doubly refractile wall and basophilic nucleus Figure 10.20 Pulmonary cryptococcosis. Microscopic appearance of C. neoformans in a hematoxylin and eosin stain. Variably sized, round, and occasionally fractured yeast are intermediate in size (4-7 μm) and have pale staining, thin walls with associated halos Figure 10.21 Microscopic appearance of cryptococcosis in a Grocott stain. Note the clear halo around the organisms Figure 10.22 Microscopic appearance of C. immitis in a hematoxylin and eosin stain. Large (30-60 μm) intact and ruptured spherules contain much smaller (2-5 μm) endospores. In this example there are also mycelia (upper right) which is an uncommon finding Figure 10.23 Disseminated histoplasmosis. Sheets of histiocytes demonstrate numerous organisms within their cytoplasm Figure 10.24 Sharply outlined lung infarct resulting from Dirofilaria infestation Figure 10.25 Microscopic appearance of D. immitis within the necrotic center of a dirofilarial nodule Figure 10.26 Sarcoidosis. Well-formed granuloma characteristic of sarcoidosis with characteristic collaret of coarse collagen bundles Figure 10.27 Sarcoidosis. Numerous granulomas with associated fibrosis form conglomerate nodules that expand visceral pleura, interlobular septa, and bronchovascular bundles in a characteristic 'lymphangitic' pattern Figure 10.28 Necrotizing sarcoid granulomatosis. There is extensive involvement of large vessels by the inflammatory infiltrate, which has a necrotizing quality. Most authorities consider this a variant of nodular sarcoidosis Figure 10.29 Granulomatosis with polyangiitis (Wegener's). The lesion is well circumscribed, with a granulomatous and partially necrotic appearance Figure 10.30 Granulomatosis with polyangiitis (Wegener's) demonstrating characteristic 'geographic' pattern of necrosis Figure 10.31 Bronchocentric variant of granulomatosis with polyangiitis (Wegener's) in which the necrosis is centered an airway lumen and the airway wall partially replaced by a granulomatous infiltrate comprising palisaded histiocytes Figure 10.32 Granulomatous microabscess characteristic of granulo- matosis with polyangiitis (Wegener's) Figure 10.33 Granulomatosis with polyangiitis (Wegener's) showing characteristic pattern of patchy vessel wall inflammation and necrosis Figure 10.34 Capillaritis and alveolar hemorrhage in a patient with granulomatosis with polyangiitis (Wegener's) Figure 10.35 Bronchocentric granulomatosis in a patient with allergic bronchopulmonary aspergillosis. The bronchial wall is partially replaced by epithelioid histiocytes with associated eosinophilia Figure 10.36 Mucoid impaction of bronchi in a patient with allergic bronchopulmonary aspergillosis. Thick, tenacious secretions expand ectatic bronchi and in this patient formed a hilar mass for which clinical concerns included carcinoma Figure 10.37 Mucoid impaction of bronchi showing the 'allergic mucin' typical of allergic bronchopulmonary aspergillosis including numerous Charcot-Leyden crystals Figure 10.38 Drug abuser's lung in which perivascular granulomas include foreign body giant cells containing birefringent particulates, in this case a combination of talc and cellulose Figure 10.39 Usual interstitial pneumonia. Patchwork pattern of fibrosis with scarring and honeycomb change is characteristic Figure 10.40 Usual interstitial pneumonia. Characteristic appearance of honeycomb change Figure 10.41 Usual interstitial pneumonia with prominent fibroblast foci. Fibroblast foci resemble organizing pneumonia except for their interstitial location Figure 10.42 Nonspecific interstitial pneumonia demonstrating the diffuse uniform interstitial widening without the patchwork fibrosis or honeycomb change typical of UIP Figure 10.43 Cellular NSIP. Alveolar septa are uniformly expanded by cellular infiltrate with minimal fibrosis Figure 10.44 Respiratory bronchiolitis. Pigmented (smoker's) macro- phages are clustered in the lumens of distal airways and peribronchiolar air spaces. The smoking-associated pigment is positive with Prussian-blue iron stains and should not be confused with hemosiderin Figure 10.45 Smoking-related interstitial fibrosis. Subpleural septa are expanded by deeply eosinophilic collagen but without the patchwork distribution or honeycomb change characteristic of UIP. There is associated emphysema and respiratory bronchiolitis Figure 10.46 Desquamative interstitial pneumonia, an increasingly anachronistic term that should be abandoned in favor of the more modern alternatives NSIP, RBILD, or SRIF with considerable overlap between the latter two. Pigmented ('smoker's') macrophages identical to those illustrated in RBILD are more extensively distributed within alveolar spaces Figure 10.47 Diffuse alveolar damage in the acute phase with well-formed hyaline membranes Figure 10.48 Diffuse alveolar damage in the organizing phase accom- panied by alveolar collapse Figure 10.49 Hilar mass that was considered radiographically to be carcinoma but proved pathologically to be organized pneumonia Figure 10.50 Cryptogenic organizing pneumonia showing characteristic intraluminal plugs of organizing fibroblasts and myofibroblasts. The central portion of some of the plugs show an infiltrate of chronic inflammatory cells, a nonspecific finding of no special significance Figure 10.51 Lymphoid interstitial pneumonia in a patient with Sjögren syndrome Figure 10.52 Pleuroparenchymal fibroelastosis Figure 10.53 Hypersensitivity pneumonia showing patchy interstitial infiltrate of lymphocytes distributed in an exquisitely bronchiolocentric fashion Figure 10.54 Hypersensitivity pneumonia with characteristic loose cluster of multinucleated giant cells in peribronchiolar interstitium Figure 10.55 Langerhans cell histiocytosis Figure 10.56 Prominent longitudinal grooves in the nuclei of Langerhans cells in a case of pulmonary Langerhans cell histiocytosis Figure 10.57 Fibrotic Langerhans cell histiocytosis showing characteristic stellate configuration and associated peripheral 'scar emphysema' (paracicatricial air space enlargement) Figure 10.58 Erdheim-Chester disease Figure 10.59 Erdheim-Chester disease involving the lung showing histiocyte-rich infiltrate Figure 10.60 Simple silicosis showing classic, uncomplicated silicotic module Figure 10.61 Asbestosis showing a pattern of fibrosis resembling UIP Figure 10.62 Asbestos body in a patient with asbestosis showing characteristic beaded appearance with central translucent core Figure 10.63 Exogenous lipoid pneumonia in a transbronchial biopsy from a patient suspected of having a malignancy Figure 10.64 Aspiration pneumonia showing a combination of organizing pneumonia with granulomatous inflammation (A) and degenerated organic particulates typical of food (B) Figure 10.65 Aspiration pneumonia with organizing pneumonia and granulomatous inflammation in which a multinucleated giant cell contains crospovidone, an inorganic filler used in oral medications Figure 10.66 Eosinophilic pneumonia. Numerous mature eosinophils are admixed with histiocytes and granular pneumocytes Figure 10.67 Filling of alveolar spaces by amorphous grumous material in alveolar proteinosis Figure 10.68 Diffuse alveolar hemorrhage with capillaritis in a patient with granulomatosis with polyangiitis (Wegener's) Figure 10.69 Frothy alveolar exudate in P. jirovecii pneumonia Figure 10.70 GMS stain showing P. jirovecii in frothy alveolar exudate Figure 10.71 Cytomegalovirus infection with characteristic viral cytopathic changes in infected pneumocytes Figure 10.72 Intranuclear inclusions in herpes simplex pneumonia Figure 10.73 Adenovirus showing characteristic smudge cells Figure 10.74 Gross appearance of hydatidosis of lung. (Courtesy of Dr. RA Cooke, Brisbane, Australia. From Cooke RA, Stewart B. Colour Atlas of Anatomical Pathology. Edinburgh: Churchill Livingstone; 2004.) Figure 10.75 Microscopic appearance of pulmonary hydatidosis Figure 10.76 Angiogram of a 28-year-old man with multiple arteriovenous malformations. The patient had Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). After left lower lobectomy, oxygen saturation rose from 86% to 95% Figure 10.77 Gross appearance of pulmonary arteriovenous malformation Figure 10.78 Typical wedge-shaped appearance of pleural-based pulmonary infarct. A large occluding thrombus is evident in the vessel leading to the area of the infarct Figure 10.79 Pulmonary hyalinizing granuloma showing circumscribed nodule (A) with characteristic pattern of collagen fibrosis and inflammation (B) Figure 10.80 Typical peripheral location of pulmonary adenocarcinoma, in this case puckering and retracting visceral pleura. (Courtesy of Dr. J. Carvalho, Minneapolis, MN.) Figure 10.81 A and B, Outer aspect and cut section of two pulmonary adenocarcinomas showing pleural retraction Figure 10.82 Peripheral adenocarcinoma of lung spreading diffusely to pleural surfaces and closely simulating the gross appearance of malignant mesothelioma. Note metastases in intrapulmonary peribronchiolar lymph nodes Figure 10.83 Endobronchial polypoid adenocarcinoma with post- obstructive bronchiectasis and obstructive 'golden' (endogenous lipid) pneumonia. (Courtesy of Dr. J. Carvalho, Minneapolis, MN.) Figure 10.84 Lepidic (bronchioloalveolar) growth pattern that predominated in this minimally invasive adenocarcinoma. Overall architecture is preserved (A) with neoplastic nonmucinous columnar cells distributed along interstitial surfaces (B) Figure 10.85 Micropapillary adenocarcinoma Figure 10.86 Solid adenocarcinoma indistinguishable from large cel carcinoma except for focal positivity with a mucin stain and an immunostain for TTF-1 Figure 10.87 Acinar adenocarcinoma with desmoplastic stromal response Figure 10.88 Papillary adenocarcinoma Figure 10.89 Invasive mucinous adenocarcinoma Figure 10.90 TTF-1- and mucin-positive primary pulmonary adenocar- cinoma with signet ring cells Figure 10.91 Intraluminal bronchial growth of squamous cell carcinoma. (Courtesy of Dr. J. Carvalho, Minneapolis, MN.) Figure 10.92 Large squamous cell carcinoma associated with central cavitation Figure 10.93 Microscopic appearance of squamous cell carcinoma with keratinization and necrosis Figure 10.94 Microscopic appearance of squamous cell carcinoma with intercellular bridges Figure 10.95 Basaloid squamous cell carcinoma with characteristic lobulated growth pattern (A) and diffusely positive staining for p63 (B) Figure 10.96 Squamous cell carcinoma of lung. Neoplastic cells with numerous tonofilaments, some of them attached to desmosomes. This is characteristic of squamous differentiation (x16,850) Figure 10.97 Small cell carcinoma of the lung. The tumor is growing diffusely along the wall of a lobar bronchus and its branches Figure 10.98 Small cell carcinoma showing cells with darkly staining oval to spindle nuclei and extremely scanty cytoplasm Figure 10.99 Small cell carcinoma in bronchial biopsy with extensive crush artifact making diagnosis all but impossible in this field Figure 10.100 Small cell carcinoma smear from endobronchial ultrasound- guided fine-needle aspiration of subcarinal lymph node Figure 10.101 Small cell carcinoma with extensive necrosis associated with hematoxyphilic staining of the vessel walls (so-called 'Azzopardi effect') Figure 10.102 Combined small cell-squamous cell carcinoma Figure 10.103 Large cell neuroendocrine carcinoma with a nested ('organoid') growth pattern, characteristic pattern of necrosis and numerous mitoses Figure 10.104 Central carcinoid tumor showing well-circumscribed quality situated within a large bronchus. (Courtesy of Dr. J. Carvalho, Minneapolis, MN.) Figure 10.105 Whole mount of central carcinoid tumor showing polypoid endobronchial growth Figure 10.106 Peripheral carcinoid tumor showing characteristic sub- pleural location and well-circumscribed configuration Figure 10.107 Carcinoid tumor showing characteristic architecture and cytology Figure 10.108 Spindle cell appearance of peripheral carcinoid tumor, which may simulate a mesenchymal neoplasm Figure 10.109 Central carcinoid tumor with paraganglioma-like pattern of growth Figure 10.110 Oncocytic variant of carcinoid tumor Figure 10.111 Atypical carcinoid tumor Figure 10.112 So-called pulmonary tumorlet Figure 10.113 Diffuse idiopathic pulmonary neuroendocrine cell hyper- plasia in a patient with multiple carcinoid tumorlets Figure 10.114 Large cell carcinoma Figure 10.115 Adenosquamous carcinoma of lung showing an admixture of glandular (A) and squamous (B) components in the same tumor Figure 10.116 Prominent neoplastic giant cells in a sarcomatoid ('giant cell') carcinoma Figure 10.117 Prominent spindle cells in a sarcomatoid ('spindle cell') carcinoma Figure 10.118 Sarcomatoid carcinoma with extensive necrosis Figure 10.119 Sarcomatoid ('pleomorphic') squamous cell carcinoma showing a spindle cell component and an epithelial component with squamous differentiation demonstrating clear cell change (A); staining for p63 was limited to the squamous component (B) Figure 10.120 Pulmonary blastoma forming a large well-circumscribed necrotic mass Figure 10.121 Pulmonary blastoma showing typical biphasic pattern of growth and 'fetal' appearance of the epithelial component Figure 10.122 Fetal adenocarcinoma (pulmonary endodermal tumor resembling fetal lung). In contrast to pulmonary blastoma, a mesenchymal component is absent Figure 10.123 Carcinoma in situ of bronchial mucosa Figure 10.124 Early invasive squamous cell carcinoma of bronchial mucosa Figure 10.125 Low (A) and high (B) magnification view of atypical adenomatous hyperplasia Figure 10.126 A, Squamous cell carcinoma of lung resected by Dr. Evarts A. Graham in 1933. Note extension into surrounding lung and involvement of two regional lymph nodes. The patient died in 1962 without evidence of cancer. B, Poorly differentiated squamous cell carcinoma shown in A Figure 10.127 Lobulated shape and shiny cut surface of pulmonary hamartoma. (Courtesy of Dr. RA Cooke, Brisbane, Australia. From Cooke RA, Stewart B. Colour Atlas of Anatomical Pathology. Edinburgh: Churchill Livingstone; 2004.) Figure 10.128 Endobronchial hamartoma Figure 10.129 Pulmonary hamartoma showing intermingling of hyaline cartilage, fat, myxoid stroma, and non-neoplastic respiratory epithelium Figure 10.130 Pulmonary chondroma Figure 10.131 Incidentally discovered meningothelial-like nodule Figure 10.132 Sclerosing pneumocytoma. Yellow solid areas alternate with foci of fresh hemorrhage and fibrosis. (Courtesy of Dr. J. Carvalho, Minneapolis, MN.) Figure 10.133 Sclerosing pneumocytoma. A variety of growth patterns is appreciated on low-power examination resulting in a characteristic variegated appearance Figure 10.134 Sclerosing pneumocytoma. Higher-magnification views of tumor illustrated in Fig. 10.133 show solid (A), papillary (B), sclerotic (C), and hemorrhagic (D) areas. Areas of solid growth (A) show neoplastic round cells while papillary areas (B) show non-neoplastic bronchiolar epithelium lining papillary surfaces Figure 10.135 Inflammatory myofibroblastic tumor. Elongated myoid cells are heavily infiltrated by plasma cells. Incorporated non-neoplastic respiratory epithelium results in a 'pseudobiphasic' appearance Figure 10.136 Capillary hemangioma presenting as solitary mass in a child Figure 10.137 Endobronchial glomus tumor Figure 10.138 Epithelioid hemangioendothelioma. Nodular intra-alveolar aggregates of tumor cells are seen enclosing an amorphous eosinophilic material Figure 10.139 Prominent intracytoplasmic lumen formation and cytoplas- mic intranuclear pseudoinclusions in epithelioid hemangioendothelioma Figure 10.140 Strong immunoreactivity for CD31 in epithelioid hemangioendothelioma Figure 10.141 Gross appearance of a MALT lymphoma in a surgical lung biopsy Figure 10.142 MALT lymphoma of lung showing a tumefactive and vaguely nodular configuration on the left with extension along lymphatic pathways on the right Figure 10.143 A, Intravascular lymphoma in a patient with unexplained breathlessness. B, An immunostain for CD20 shows neoplastic large B cell exquisitely localized to alveolar septal capillaries Figure 10.144 Lymphomatoid granulomatosis showing polymorphic infiltrate forming centrally necrotic nodule (A) and characteristic angio- invasive growth pattern (B) Figure 10.145 Adenoid cystic carcinoma presenting as an endobronchial mass invading adjacent lung parenchyma Figure 10.146 Endobronchial growth of mucoepidermoid carcinoma Figure 10.147 Endobronchial mucoepidermoid carcinoma showing characteristic low-grade histology Figure 10.148 Myoepithelioma of lung. This particular tumor had arisen from a typical hamartoma Figure 10.149 Clear cell tumor (PEComa) of lung. Medium-sized clear cells grow in a solid pattern, separated by a prominent vasculature Figure 10.150 Explanted lung showing lymphangioleiomyomatosis in a woman whose pretransplant diagnosis was emphysema Figure 10.151 Lymphangioleiomyomatosis in which cystic space (A) is associated with loose interstitial aggregates of lesional smooth muscle-like (LAM) cells (B) Figure 10.152 Benign metastasizing leiomyoma Figure 10.153 Primary monophasic synovial sarcoma of lung. Some areas have a fibroblastic appearance, whereas in others the cells are slightly plumper, although still lacking an identifiable epithelial organization. There was focal immunoreactivity for keratin Figure 10.154 Primary pulmonary myxoid sarcoma with a EWSR1-CREB1 fusion Figure 10.155 Metastatic renal cell carcinoma to lung. The lesion is well circumscribed, multinodular, and golden yellow Figure 10.156 Renal cell carcinoma of clear cell type metastatic to lung Figure 10.157 Well-differentiated colonic adenocarcinoma metastatic to lung, diagnosed in a bronchial biopsy Figure 10.158 Malignant melanoma metastatic to lung be especially helpful in supporting pulmonary origin, while staining Figure 10.159 Metastatic prostatic adenocarcinoma simulating the appearance of a well differentiated lepidic-predominant adenocarcinoma of the lung Figure 10.160 Metastatic cellular fibrous histiocytoma of cutaneous origin (cystic fibrohistiocytic tumors) forming multiple bilateral cystic masses in a young woman with a preoperative diagnosis of lymphangioleiomyomatosis
