INFLAMMATION OF THE PANCREAS
Acute pancreatitis is acute inflammation caused by injury to the exocrine portion of the pancreas. The etiology is diverse:
• Scorpion stings
Pancreatic acinar cell injury results in activation of pancreatic enzymes and enzy-matic destruction of the pancreatic parenchyma.
Symptoms include stabbing epigastric abdominal pain radiating to the back. Severe acute pancreatitis can also cause shock. Lab studies show elevated serum amylase and lipase. Complications include acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), pancreatic pseudocyst; pancreatic calcifications, and hypocalcemia. Severe cases have a 30% mortality rate.
• Gross pathologic examination shows focal hemorrhage and liquefication in the pancreas, accompanied by chalky, white-yellow fat necrosis of adjacent adipose tissue.
• Microscopically there is liquefactive necrosis of the pancreatic parenchyma with acute inflammation and enzymatic fat necrosis.
• Necrosis of blood vessels causes hemorrhage.
Chronic pancreatitis refers to irreversible changes in pancreatic function with accom-panying chronic inflammation, atrophy, and fibrosis of the pancreas secondary to repeated bouts of pancreatitis. Manifestations include abdominal pain, pancreatic insufficiency and malabsorption, pancreatic calcifications, pseudocyst, and second-ary diabetes mellitus (late complication).
It is common in middle-aged male alcoholics. Pathology shows grossly firm, white, and fibrotic pancreas. Microscopically there is extensive fibrosis with parenchymal atrophy and chronic inflammation.
Autoimmune pancreatitis can occur in association with IgG4-associated fibrosing disorders; this variant responds to steroid therapy.
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