Pancreas برای بزرگنمایی عکسها کلیک را روی ان نگه دارید..... Figure 22.1 Normal pancreatic acini consist of tubular glands with round, basally located nuclei and prominent granules. A small duct is in the center of the photograph Figure 22.2 A, Compact islet with well-defined borders; note the small capillaries within the islet. Nuclei have speckled or "salt and pepper" chromatin typical of neuroendocrine cells. B, Diffuse islets have poorly defined borders and are often larger than compact islets; nuclei are typically more hyperchromatic Figure 22.3 Hypertrophic, irregular islet with closely approximated duct (ductuloinsular complex) in a case of hyperinsulinemic hypoglycemia. (Courtesy of Dr. Jessica Comstock.) Figure 22.4 A, Firm lobules of heterotopic pancreatic tissue are visible in this resection specimen from the stomach. B, Endoscopically, there is often central umbilication, corresponding to the duct that opens in the small bowel lumen. C, Low-power view of heterotopic pancreas in small bowel; both acinar tissue and ducts are easily identified. D, Higher-power view of heterotopic pancreatic acinar tissue and small ducts; the specimen was from the duodenum. (A and B, Courtesy of Dr. Rhonda Yantiss.) Figure 22.5 This case of cystic fibrosis shows fatty replacement of pancreatic parenchyma, cyst formation, and dilated ducts containing inspissated eosinophilic secretions (arrows). (Courtesy of Dr. Mari Mino-Kenudson.) Figure 22.6 Islet cell amyloidosis in a patient with type 2 diabetes Figure 22.7 A, Extensive hemorrhagic necrosis of the pancreas spreads into the surrounding mesentery. B, A higher-power photograph from another case shows hemorrhagic acute pancreatitis with numerous foci of fat necrosis (arrows). C, Hemorrhagic pancreatitis with large foci of fat necrosis extending into the mesenteric fat. D, Acute necrotizing pancreatitis with extensive hemorrhage and fat necrosis. There is no longer any recognizable pancreatic parenchyma. (B and C, Courtesy of Dr. George F. Gray Jr.) Figure 22.8 A, Alcoholic pancreatitis featuring large, irregular areas of fibrosis and calculi within dilated ducts. B, Another case shows diffuse fibrosis of the pancreas associated with stenosis and increased tortuosity of the main pancreatic duct. C, Close-up of another case of chronic pancreatitis, showing fibrosis and cystic dilation of ducts, some of which are occupied by a grumous secretory material. (A, Courtesy of Dr. George F. Gray Jr.) Figure 22.9 A, Chronic pancreatitis with fibrosis, mild chronic inflammation, and loss of acinar parenchyma. B, More extensive disease shows diffuse fibrosis, with prominent nerves, thick-walled vessels, and aggregates of islet cells. C, Residual islets may form aggregates (pseudohyperplasia) that can mimic a neuroendocrine neoplasm. D, Perineural extension of pancreatic endocrine cells (arrow) in chronic pancreatitis can mimic perineural invasion by a neoplasm Figure 22.10 A, A Whipple specimen in autoimmune pancreatitis shows dense, focally nodular fibrosis that is most prominent in the head of the pancreas. B, Lobular destruction by a dense lymphoplas- macytic infiltrate and fibrosis, with resultant parenchymal loss. C, Obliterative phlebitis is a common finding. D, Abundant stromal plasma cells in type 1 autoimmune pancreatitis, many of which were positive for IgG4. E, Granulocytic epithelial lesions are common in type 2 autoimmune pancreatitis. (E, Courtesy of Dr. Mari Mino-Kenudson.) Figure 22.11 Both the pancreatic duct (stented) and the common bile duct are dilated, and there is extensive scarring of the paraduodenal pancreas in this case of paraduodenal pancreatitis. (Courtesy of Dr. Mari Mino-Kenudson.) Figure 22.12 Numerous epithelioid, noncaseating granulomas in a case of pancreatic involvement by sarcoidosis Figure 22.13 Pseudocyst with thick, irregular, fibrotic wall and hemorrhagic contents. (Courtesy of Dr. George F. Gray Jr.) Figure 22.14 A, This large congenital cyst has a true epithelial lining and does not communicate with the pancreatic ductal system. B, Congenital cysts are lined by a single layer of flat nonmucinous epithelium Figure 22.15 A, Lymphoepithelial cysts are often multilocular and contain abundant squamous debris. B, The cyst walls contain lymphoid tissue and are lined by squamous epithelium Figure 22.16 Gross Appearance of Invasive Pancreatic Ductal Adenocarcinoma. A, A poorly defined mass obliterates the normal pancreatic architecture (arrows). B, A gritty, gelatinous poorly defined tumor surrounds common bile duct, which is markedly dilated. (A, Courtesy of Dr. George F. Gray Jr.) Figure 22.17 A, Well-differentiated ductal adenocarcinomas with infiltrating, haphazard glands and surrounding desmoplastic stroma. Well-differentiated neoplastic glands may be extremely bland at low power, and attention must be given to cytologic features such as marked nuclear pleomorphism, variation in nuclear size (B), loss of polarity, prominent nucleoli, and mitotic activity (C, arrow). D, Neoplastic glands immediately adjacent to muscular arteries are a useful diagnostic feature of malignancy. Perineural invasion (E) and vascular invasion (F) are frequent findings in ductal adenocarcinoma Figure 22.18 A, Low-grade PanIN characterized by tall columnar mucinous epithelium without nuclear atypia. B, High-grade PanIN features architectural complexity, unsupported tufts of epithelium in the lumen of the duct, and marked nuclear atypia Figure 22.19 A, Foamy gland pattern of ductal adenocarcinoma features foamy, microvesicular cytoplasm; small, often basally located nuclei; and condensation of the cytoplasm at the luminal aspect of cell resembling a brush border. B, The neoplastic glands in the large duct pattern are large and microcystic, and may be mistaken for benign dilated glands or a lower-grade noninvasive cystic neoplasm. C, Vacuolated pattern with cribriformed nests of cells with prominent large, empty vacuoles. D, Adenosquamous carcinoma consists of both glandular and squamous components. E, Some adenosquamous variants may have prominent basaloid features Figure 22.19 cont'd F, Medullary carcinoma is similar to that seen in other organs, with a solid growth pattem and numerous tumor-infiltrating lymphocytes. G, Colloid carcinoma features large pools of mucin- containing clusters of tumor cells, some of which have signet ring cell features. (F, Courtesy of Dr. Volkan Adsay.) Figure 22.20 A, This undifferentiated carcinoma is composed entirely of spindle cells and should not be misinterpreted as a sarcoma. B, This example of undifferentiated carcinoma with osteoclast-like giant cells contains areas of cartilage with ossification. C, Anaplastic carcinoma of pancreas showing immu- noreactivity for keratin. D, Some cases contain large anaplastic tumor cells as well as osteoclast-like giant cells (A, Courtesy of Dr. Volkan Adsay. D, Courtesy of Dr. Becky Wheeler.) Figure 22.21 Genetic Progression Model of Pancreatic Carcinogenesis. The progression from histologi- cally normal epithelium to low-grade pancreatic intraepithelial neoplasia (PanIN1 and PanIN2), to high-grade PanIN3, to invasive carcinoma (left to right) is associated with the accumulation of specific genetic alterations. On the basis of their temporal appearance in this progression model, the molecular abnormalities can be classified as early (KRAS2 mutation, telomere shortening), intermediate (P16/CDKN2A loss), or late (mutations of DPC4/SMAD4, TP53, BRCA2). However, those changes that specifically promote progression to metastatic disease remain unknown. (From Yachida S, lacobuzio-Donahue CA. The pathology and genetics of metastatic pancreatic cancer. Arch Pathol Lab Med. 2009;133:413-422.) Figure 22.22 A, Serous cystadenoma composed of numerous small cysts, with a central fibrous scar. B, Close-up of another case showing innumerable cystic cavities separated by a thin fibrous wall. C, Unilocular variant of serous cystadenoma features a large single cavity. D, Multiple small cysts separated by varying amounts of stroma and lined (E) by a single layer of flat or cuboidal cells with centrally located nuclei and clear cytoplasm. (A, Courtesy of Dr. George F. Gray Jr.) Figure 22.23 Mucinous Cystadenoma of Pancreas. A, This lesion is multilocular and contains abundant mucin; some of the cysts contain mural nodules. B, The lining consists of a single layer of tall columnar mucinous epithelium with small, basally located nuclei; note the underlying cellular ovarian-type stroma (B). The ovarian-type stroma is positive for progesterone receptor (C) and inhibin (D). E, High-grade dysplasia on one side of the cyst (top) and attenuated low-grade epithelium on the bottom side of the cyst. F, Carcinoma in situ featuring complex cribriforming architecture and high-grade nuclear atypia. Note the underlying ovarian-type stroma. (A, Courtesy of Dr. George F. Gray Jr.) Figure 22.24 A focus of poorly differentiated adenocarcinoma is seen within the wall of a mucinous cystic neoplasm (arrows). Note the overlying low-grade mucinous epithelium and ovarian-type stroma Figure 22.25 A, Intraductal papillary mucinous tumor showing marked dilation of the major pancreatic duct with grossly visible papillary excrescences. The duct contained a large amount of mucin in its lumen. The surrounding pancreas shows fibrosis and atrophy. B, Low-grade gastric-type IPMN with flat to papillary mucinous epithelium; note the relatively paucicellular dense fibrous stroma. C, In this low-grade IPMN, the epithelium is tall columnar with small, basally located nuclei. D, Pancreatobiliary type IPMN with high-grade dysplasia Figure 22.25 cont'd E, Intestinal-type IPMN with numerous goblet cells. F, Core needle biopsy of oncocytic type IPMN showing striking oncocytic epithelium with punched out spaces and scattered goblet cells. G, Adenocarcinoma with a tubular pattern arising from an IPMN with high-grade dysplasia. (A, Courtesy of Dr. David S. Klimstra.) Figure 22.26 A and B, Intraductal tubulopapillary neoplasm showing intraductal growth of densely packed tubular glands and papillae with mild nuclear atypia. There is no mucin production. (A and B, Courtesy of Dr. Olca Basturk.) Figure 22.27 A, The cut surface of this acinar cell carcinoma is solid and has a necrotic center. It lacks the fibrous component usually seen in ductal adenocarcinoma. B, Prominent acinar architecture with minimal stroma is characteristic. C, The nuclei are round with mild pleomorphism and a single prominent nucleolus. D, PAS-positive, diastase-resistant cytoplasmic granules are seen in some cases (PAS stain) Figure 22.28 Incidental acinar cell hyperplasia, which may be confused with hyperplastic islets of Langerhans Figure 22.29 A, Pancreatoblastomas are often lobular at low power, with prominent stroma. B, The cells are arranged in a prominent acinar pattern, and squamoid corpuscles (arrows) are prominent Figure 22.30 A, Large solid pseudopapillary tumor with hemorrhage, necrosis, and cystic degeneration. B, Pseudopapillae covered by several layers of discohesive cells, with fibrovascular cores. Cholesterol clefts are also present. C, Nuclei are ovoid, with indistinct nucleoli and occasional longitudinal grooves. D, Cytoplasmic hyaline globules may be very prominent. E, Nuclear reactivity with B-catenin is a helpful diagnostic finding Figure 22.31 Gross Appearance of Pancreatic Endocrine Tumors. The neoplasms shown in (A) and (B) are partially cystic. On cut section, tumors are firm, homogeneous, yellow-tan, and typically unencapsulated (C). D, Some may be multifocal (arrows). E, PanNET may contain grossly apparent foci of hemorrhage or necrosis. (C-E, Courtesy of Dr. George F. Gray Jr.) Figure 22.32 A, The nuclei of PanNETs are uniform and somewhat cuboidal, with speckled nuclear chromatin, indistinct nucleoli, and eosinophilic or amphophilic finely granular cytoplasm. B, Pleomorphic PanNETs have significant nuclear pleomorphism and anisocytosis, but this has no clinical significance. PanNETs can have multiple patterns, including solid (C), trabecular (D), and acinar/pseudoglandular (E) Figure 22.33 Morphologic variants of PanNET include clear cell (A) and oncocytic (B) tumors, as well as spindled variants (C). Psammoma bodies are associated with somatostatinomas (D) Figure 22.34 A, Stroma is typically not prominent in PanNETs, as seen in this relatively solid tumor with only a small amount of intervening stroma. B, Occasional tumors are stroma rich and contain compressed, infiltrative nests or cords of tumor cells within the dense fibrosis. C, Amyloid may be seen in PanNETs, especially insulinomas Figure 22.35 Poorly differentiated neuroendocrine carcinomas may have a large cell (A) or a small cell (B) phenotype. Necrosis and nuclear crush artifact are common, as in the lung. By definition these tumors are G3 (C), with a Ki-67 proliferation index of greater than 20% Figure 22.36 Primary diffuse large B-cell lymphoma extending to involve the common bile duct. The patient presented with jaundice and radiographi- cally was thought to have pancreatic ductal adenocarcinoma Figure 22.37 Intrapancreatic schwannoma with numerous Verocay bodies Figure 22.38 This intra-ampullary papillary tubular neoplasm is located entirely within the ampullary channel. (Courtesy of Dr. George F. Gray Jr.) Figure 22.39 Invasive ampullary adenocarcinoma arising from an intra- ampullary papillary-tubular neoplasm of intestinal type
