Causing edema, (2) necrosis of fat by lipolytic enzymes, (3) an acute inflammatory reaction, (4) proteolytic destruction of pancreatic parenchyma, and (5) destruction of blood

vessels with subsequent interstitial hemorrhage.The extent and predominance of each of these alterations depend on the duration and severity of the process.

In the milder form, acute interstitial pancreatitis, histologic alterations are limited to interstitial edema and focal areas of fat necrosis in the pancreatic substance and peripancreatic fat ( Fig.

19-4 ). Fat necrosis, as we have seen, results from enzymatic destruction of fat cells. The released fatty acids combine with calcium to form insoluble salts that precipitate in situ ( Chapter

1 ).

In the more severe form, acute necrotizing pancreatitis, necrosis of pancreatic tissue affects acinar and

Figure 19-4Acute pancreatitis. The microscopic field shows a region of fat necrosis on the right and focal pancreatic parenchymal necrosis (center).

Figure 19-5Acute pancreatitis. The pancreas has been sectioned across to reveal dark areas of hemorrhage in the head of the pancreas and a focal area of pale fat necrosis in the

peripancreatic fat (upper left).

Figure 19-6Three proposed pathways in the pathogenesis of acute pancreatitis.

Figure 19-7Comparison of the sequelae of acute and chronic pancreatitis. (ARDS = acute respiratory distress syndrome)

Figure 19-8Chronic pancreatitis. A, Extensive fibrosis and atrophy has left only residual islets (left) and ducts (right), with a sprinkling of chronic inflammatory cells and acinar tissue. B,

A higher-power view demonstrating dilated ducts with inspissated eosinophilic ductal concretions in a patient with alcoholic chronic pancreatitis.

Figure 19-9Pancreatic pseudocyst. A, Cross-section through this previously bisected lesion revealing a poorly defined cyst with a necrotic brown-black wall. B, Histologically, the cyst

lacks a true epithelial lining and instead is lined by fibrin and granulation tissue.

Figure 19-10Serous cystadenoma. A, Cross-section through a serous cystadenoma. Only a thin rim of normal pancreatic parenchyma remains. The cysts are relatively small and contain

clear, straw-colored fluid. B, The cysts are lined by cuboidal epithelium without atypia.

Figure 19-11Pancreatic mucinous cystadenoma. A, Cross-section through a mucinous multiloculated cyst in the tail of the pancreas. The cysts are large and filled with tenacious mucin. B,

The cysts are lined by columnar mucinous epithelium, and a dense "ovarian" stroma is noted.

Figure 19-12Intraductal papillary mucinous neoplasm. A, Cross-section through the head of the pancreas showing a prominent papillary neoplasm distending the main pancreatic duct. B,

The papillary mucinous neoplasm involved the main pancreatic duct (left) and extending down into the smaller ducts and ductules (right).

Figure 19-13Progression model for the development of pancreatic cancer. It is postulated that telomere-shortening, and mutations of the oncogene K-RAS occur at early stages, that

inactivation of the p16 tumor suppressor gene occurs at intermediate stages, and the inactivation of the p53, SMAD4 (DPC4), and BRCA2 tumor suppressor genes occur at late stages. It is

important to note that while there is a general temporal sequence of changes, the accumulation of multiple mutations is more important than their occurrence in a specific order. (Adapted

from Wilentz RE, lacobuzio-Donahue CA, et al: Loss of expression of DPC4 in pancreatic intraepithelial neoplasia: evidence that DPC4 inactivation occurs late in neoplastic progression.

Cancer Res 2000; 60:2002.)

TABLE 19-2-- Molecular Alterations in Invasive Pancreatic Adenocarcinoma

Date: 2016-04-22; view: 644