Disorders of the pancreas | Gastrointestinal pathology | Pathology

Disorders of the pancreas

Pancreatitis: Pancreatitis is inflammation of the pancreas. It can be acute or chronic. Acute pancreatitis has a rapid onset, while chronic pancreatitis involves long-standing inflammation with recurrent symptoms.

Acute pancreatitis: The key pathologic event in acute pancreatitis is the premature activation of inactive digestive enzymes (zymogens) into their active forms inside the pancreas, leading to pancreatic injury and inflammation. Trypsin is central because it activates other digestive enzymes and also activates prekallikrein, which then triggers the clotting and complement systems. Activated enzymes and free radicals injure acinar cells, leading to the release of cytokines (IL1, IL6, IL8), tumour necrosis factor-α, and vasoactive mediators such as nitric oxide. You can see parenchymal edema and peripancreatic fat necrosis. In severe cases, necrosis and hemorrhage occur. Local inflammation can progress to a systemic inflammatory response.

The leading causes of acute pancreatitis are gallstones and alcohol. Other causes include ERCP, scorpion bites, drugs like steroids, thiazides, didanosine, azathioprine, OC pills, hypercalcemia, hypertriglyceridemia, ischemia, burns, trauma, ischemia, septicemia, post-surgery on biliary tract, viral infections like Mumps, Adenoviruses, parasitic infestations like ascariasis, Clonorchis sinensis etc. Congenital causes of acute pancreatitis include pancreas divisum, annular pancreas and sphincter of Oddi dysfunction.

Clinical features include epigastric or periumbilical abdominal pain, boring pain that radiates to the back, nausea, vomiting, diarrhea, fever, tachycardia, shock, abdominal tenderness, decreased bowel sounds, jaundice, hypocalcemia etc.

Both the Cullen and Grey-Turner signs are seen in acute, hemorrhagic or necrotizing pancreatitis due to the movement of blood along fascial planes to reach the umbilicus or flanks respectively.

Cullen sign: Bluish discoloration around the umbilicus

Grey-Turner sign: Reddish-brown discoloration in the flanks

Laboratory findings include elevated lipase (more specific) and amylase. Gallstone pancreatitis will show findings of obstructive jaundice and raised alkaline phosphatase. Ultrasound can show gallbladder stones. CT with contrast is the investigation of choice. CT scan shows an enlarged pancreas and peripancreatic fat-stranding. Severe cases show lack of attenuation of the pancreas in necrosis, fluid collections and retroperitoneal air. MRI can also be done with similar results. ERCP or MRCP can be used to evaluate gallstone pancreatitis.

Mild cases are managed by NPO, iv fluids and analgesics. Severe cases are managed in ICU with supportive treatment, antibiotics and management of complications.

Complications of acute pancreatitis include abscess, infected necrosis, pseudocysts, venous thrombosis (splenic vein and portal vein) and DIC.

Pseudocysts are fluid collections in the pancreatic or peri-pancreatic tissue, most commonly found in the pararenal space or the lesser sac. They are sequelae of acute pancreatitis. They are composed of sterile pancreatic fluid walled off by an inflammatory wall and take around 4 weeks to develop. CT is used for diagnosis. Pseudocysts <6 cm are asymptomatic and typically resolve on their own. Some may enlarge causing obstructive symptoms, undergo hemorrhage, or get infected. Treatment of symptomatic or large pseudocysts is with external or internal drainage with cystogastrostomy or cystoduodenostomy and excision.

Chronic pancreatitis: Chronic pancreatitis is characterized by long standing pancreatic inflammation with loss of pancreatic parenchyma, fibrosis and calcification, leading to loss of pancreatic function. There is typically a history of recurrent attacks of pancreatitis precipitated by alcohol, gallstones, smoking, hypercalcemia etc. It presents with abdominal pain or mid-back pain lasting a few hours, steatorrhea, weight loss and hyperglycemia.

CT scan shows characteristic calcium deposits in the pancreas and pancreatic or biliary ductal dilation. ERCP and MRCP delineate the pancreatic and biliary ducts, helping to locate fibrosis and calculi. Secretin stimulated MRCP helps to assess the exocrine function of the pancreas at the same time. Amylase and lipase may be normal or only mildly elevated.

Treatment is supportive with NPO, pain control with morphine, and pancreatic enzyme supplementation. Enzyme supplementation helps control pain by inhibiting the release of cholecystokinin. Other options include celiac ganglion block in intractable pain and surgical procedures like Whipple’s operation of pancreaticoduodenectomy (if disease is limited to the head of pancreas) or pancreaticojejunostomy. Sphincterotomy of the pancreatic duct may help patients with a tight pancreatic sphincter. Pseudocyst may form and have to be treated appropriately.

Disorders of the pancreas

Pancreatitis: Pancreatitis is inflammation of the pancreas. It can be acute or chronic. Acute pancreatitis has a rapid onset, while chronic pancreatitis involves long-standing inflammation with recurrent symptoms.

Acute pancreatitis: The key pathologic event in acute pancreatitis is the premature activation of inactive digestive enzymes (zymogens) into their active forms inside the pancreas, leading to pancreatic injury and inflammation. Trypsin is central because it activates other digestive enzymes and also activates prekallikrein, which then triggers the clotting and complement systems. Activated enzymes and free radicals injure acinar cells, leading to the release of cytokines (IL1, IL6, IL8), tumour necrosis factor-α, and vasoactive mediators such as nitric oxide. You can see parenchymal edema and peripancreatic fat necrosis. In severe cases, necrosis and hemorrhage occur. Local inflammation can progress to a systemic inflammatory response.

The leading causes of acute pancreatitis are gallstones and alcohol. Other causes include ERCP, scorpion bites, drugs like steroids, thiazides, didanosine, azathioprine, OC pills, hypercalcemia, hypertriglyceridemia, ischemia, burns, trauma, ischemia, septicemia, post-surgery on biliary tract, viral infections like Mumps, Adenoviruses, parasitic infestations like ascariasis, Clonorchis sinensis etc. Congenital causes of acute pancreatitis include pancreas divisum, annular pancreas and sphincter of Oddi dysfunction.

Clinical features include epigastric or periumbilical abdominal pain, boring pain that radiates to the back, nausea, vomiting, diarrhea, fever, tachycardia, shock, abdominal tenderness, decreased bowel sounds, jaundice, hypocalcemia etc.

Both the Cullen and Grey-Turner signs are seen in acute, hemorrhagic or necrotizing pancreatitis due to the movement of blood along fascial planes to reach the umbilicus or flanks respectively.

Cullen sign: Bluish discoloration around the umbilicus

Grey-Turner sign: Reddish-brown discoloration in the flanks

Laboratory findings include elevated lipase (more specific) and amylase. Gallstone pancreatitis will show findings of obstructive jaundice and raised alkaline phosphatase. Ultrasound can show gallbladder stones. CT with contrast is the investigation of choice. CT scan shows an enlarged pancreas and peripancreatic fat-stranding. Severe cases show lack of attenuation of the pancreas in necrosis, fluid collections and retroperitoneal air. MRI can also be done with similar results. ERCP or MRCP can be used to evaluate gallstone pancreatitis.

Mild cases are managed by NPO, iv fluids and analgesics. Severe cases are managed in ICU with supportive treatment, antibiotics and management of complications.

Complications of acute pancreatitis include abscess, infected necrosis, pseudocysts, venous thrombosis (splenic vein and portal vein) and DIC.

Pseudocysts are fluid collections in the pancreatic or peri-pancreatic tissue, most commonly found in the pararenal space or the lesser sac. They are sequelae of acute pancreatitis. They are composed of sterile pancreatic fluid walled off by an inflammatory wall and take around 4 weeks to develop. CT is used for diagnosis. Pseudocysts <6 cm are asymptomatic and typically resolve on their own. Some may enlarge causing obstructive symptoms, undergo hemorrhage, or get infected. Treatment of symptomatic or large pseudocysts is with external or internal drainage with cystogastrostomy or cystoduodenostomy and excision.

Chronic pancreatitis: Chronic pancreatitis is characterized by long standing pancreatic inflammation with loss of pancreatic parenchyma, fibrosis and calcification, leading to loss of pancreatic function. There is typically a history of recurrent attacks of pancreatitis precipitated by alcohol, gallstones, smoking, hypercalcemia etc. It presents with abdominal pain or mid-back pain lasting a few hours, steatorrhea, weight loss and hyperglycemia.

CT scan shows characteristic calcium deposits in the pancreas and pancreatic or biliary ductal dilation. ERCP and MRCP delineate the pancreatic and biliary ducts, helping to locate fibrosis and calculi. Secretin stimulated MRCP helps to assess the exocrine function of the pancreas at the same time. Amylase and lipase may be normal or only mildly elevated.

Treatment is supportive with NPO, pain control with morphine, and pancreatic enzyme supplementation. Enzyme supplementation helps control pain by inhibiting the release of cholecystokinin. Other options include celiac ganglion block in intractable pain and surgical procedures like Whipple’s operation of pancreaticoduodenectomy (if disease is limited to the head of pancreas) or pancreaticojejunostomy. Sphincterotomy of the pancreatic duct may help patients with a tight pancreatic sphincter. Pseudocyst may form and have to be treated appropriately.