The Pancreas

Figure 9.1

Normal pancreas, gross

The normal adult pancreas weighs 85–90 g and has indistinct regions, including a head adjacent to the duodenum (a small portion of duodenum appears here on the left ), a body, and a tail (on the right ) with a tan, lobular architecture. Adjacent adipose tissue and lymph nodes are closely apposed. Of the pancreatic mass, 99% is acinar parenchyma producing digestive enzymes and bicarbonate, with the remainder islets of Langerhans. The pancreas forms embryologically from a larger dorsal and smaller ventral endodermal bud from the duodenum; the buds fuse along with their respective developing ducts of Wirsung and Santorini. The pancreatic duct runs the length of the pancreas to empty into the duodenum at the ampulla of Vater.

Figure 9.2

Normal pancreas, CT image

This is a normal abdominal CT scan with contrast enhancement at the L1 level showing the upper abdomen with the liver ( ), gallbladder ( ), stomach ( + ) and duodenum ( ), pancreas ( ), colon ( ), spleen (×), portal vein, inferior vena cava ( ), right kidney ( ), left kidney ( ), and aorta ( ). The pancreas forms embryologically from dorsal and ventral buds that form from gut outpouchings; these fuse to form the pancreas. Failure of fusion may produce pancreas divisum, with exocrine pancreatic tissue draining into the duodenum through a larger duct of Santorini and a smaller duct of Wirsung that normally forms the papilla of Vater. Much rarer is abnormal fusion of dorsal and ventral buds to form an annular pancreas that encircles the duodenum and can produce bowel obstruction. Pancreatic ectopia in gastrointestinal tract mucosa is common (2% of the population), but it is an incidental finding because the mass of tissue is typically less than 1 cm in diameter.

Figure 9.3

Normal pancreas, microscopic

Normal exocrine pancreas is composed of acini that secrete enzymes, including the proenzymes phospholipases A and B, trypsin, chymotrypsin, and elastase, under the influence of cholecystokinin. These proenzymes require activation in the gut. Amylase and lipase are secreted as active enzymes. Secretin triggers release of bicarbonate and water from ductal cells. The pancreas produces about 2 L/day of fluid that flows into the duodenum. Interspersed within the exocrine acini are the islets of Langerhans with endocrine function, one of which is seen here in the center. Small capillaries within the islet receive the secretions of islet α cells (glucagon), β cells (insulin), and δ cells (somatostatin).

Figure 9.4

Acute pancreatitis, gross

At autopsy, the stomach (◼) is reflected superiorly, and the spleen (♦) can be seen at the far upper right. The pancreas is swollen and does not show the typical tan, lobulated architecture. Instead, hemorrhagic necrosis appears as blotchy black to red areas. Serum lipase is typically elevated. Several mechanisms are implicated in triggering intrapancreatic activation of trypsin and other proenzymes causing the inflammation. Mechanisms include pancreatic duct obstruction (the most common cause, typically from gallstone impaction), acinar cell injury (typical of viral infections), and defective intracellular transport of acinar cell proenzymes. Alcohol-induced pancreatitis can develop through all three of these.

Figure 9.5

Acute pancreatitis, CT image

This abdominal CT scan with contrast enhancement reveals decreased attenuation of a swollen pancreas (♦) from edema, hemorrhage, and fat necrosis. In this case, as a consequence of the inflammation, splenic vein thrombosis (▲) can be seen. Pancreatitis is an emergency marked by an acute abdomen. Patients have severe abdominal pain and paralytic ileus. The clinical course can be complicated by disseminated intravascular coagulation, shock, and secondary bacterial infection with sepsis. Chalky deposits of fat necrosis can involve the pancreas and adipose tissue within the abdomen and lead to hypocalcemia. An intraperitoneal fluid collection (ascites) can be present.

Figure 9.6

Acute pancreatitis, microscopic

Acute inflammation with necrosis and hemorrhage is seen here along with residual pancreatic acini (♦). The damage involves primarily the acinar cells, but the vasculature is also affected, and if severe and extensive, even the islets of Langerhans may be destroyed. Less common causes of pancreatitis include hypertriglyceridemia (typically >500 mg/dL); hypercalcemia; trauma; drugs; viral infections; and inherited gene mutations. In 10%–20% of cases, an underlying cause cannot be identified.

Figure 9.7

Fat necrosis, gross

Chalky tan foci fat necrosis (▲) are visible throughout the pancreas, seen here longitudinally sectioned in half. There is some edema, but no hemorrhage, in this case of mild acute pancreatitis. Enzymatic release from the exocrine pancreas leads to autodestruction. Trypsin activation triggers a cascade of additional proenzyme activation, including proelastase and prophospholipase, which disintegrate adipocytes and pancreatic parenchyma. Trypsin release also activates prekallikrein to bring the kinin system into play, with vascular thrombosis.

Figure 9.8

Fat necrosis, microscopic

Adjacent to the pancreas these adipocytes have lost their nuclei and their cytoplasm has a granular pink appearance, most pronounced on the right. The rare autosomal dominant condition of hereditary pancreatitis results from gain of function mutations in the PRSS1 gene that lead to abnormal activation of trypsin. Another rare inherited autosomal recessive SPINK1 gene mutation reduces inhibition of trypsin activity and leads to pancreatitis. These inherited forms of pancreatitis often have a chronic, relapsing course and increased risk for pancreatic adenocarcinoma.

Figures 9.9 and 9.10

Pancreatic phlegmon, CT images

In these abdominal CT scans without contrast enhancement, there is a phlegmon that represents a swollen, inflamed mass (♦) in the region of the pancreas. This complication may occur if acute pancreatitis persists and worsens. Laboratory markers of more severe pancreatitis include greater increases in lactate dehydrogenase (LDH), glucose, aspartate aminotransferase (AST), and white blood cell (WBC) count. Infection of a phlegmon results in a pancreatic abscess. In the right panel, a drain (♦) is in place after laparotomy with débridement of the abscess.

Only gold members can continue reading. Log In or Register to continue

Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on The Pancreas
Premium Wordpress Themes by UFO Themes
%d bloggers like this: