|Pancreatic Pathology Online
Pathology of Chronic Pancreatitis
Chronic pancreatitis is thought to result from recurrent bouts of acute pancreatitis, which lead to a progressive destruction of acinar cells, followed by healing and fibrosis.
As a result, exocrine and endocrine functions are lost.
Like acute pancreatitis, chronic pancreatitis is associated with alcoholism and, less commonly, with biliary tract disease, hypercalcemia, or hyperlipidemia.
About one half of cases are seen in patients without any of these risk factors.
In the acute phase, focal pancreatic necrosis is accompanied by a polymorphonuclear infiltrate, which is replaced by lymphocytes and plasma cells.
Healing is characterized by the removal of necrotic tissue by macrophages, a proliferation of capillaries and fibroblasts, and finally the collagen.
Large areas of the pancreas are replaced by fibrosis, and the exocrine and endocrine tissues become atrophic.
In advanced cases, large areas of the pancreas are replaced by fibrosis, and the exocrine and endocrine tissues become atrophic.
The most common type of chronic pancreatitis is chronic calcifying pancreatitis, a disorder most frequently associated with alcoholism.
Intraductal protein plugs eventually calcify and lead to the formation of stones in the ducts.
Acinar atrophy occuring after pancreatic duct obstruction
In chronic pancreatitis following sustained alcohol abuse, ductules and ducts are so often filled with thick proteinaceous secretion that some have concluded that such secretions may be an important mechanism of obstruction.
Since alcohol is potent secretagogue for the exocrine glands, one can visualize a situation of secretion against obstruction.
In another form of this disease, chronic obstructive pancreatitis, stenosis of the sphincter of Oddi is associated with gallbladder stones. Gallbladder Pathology Online
Although in this condition the pancreatic ducts are filled with thick proteinaceous secretions, they are rarely the focus of calcification or stone formation.
Chronic pancreatitis is more common in men, and in about 10% of cases it is associated with the pancreas divisum (incomplete fusion of the ventral and dorsal pancreatic anlage).
Diabetes mellitus, pancreatic insufficiency with its attendant steatorrhea and malabsorption, and pancreatic pseudocyst are frequent complications in the late stages of chronic pancreatitis.
A rare variant of chronic pancreatitis, familial hereditary pancreatitis, requires special mention.
It occurs with increased frequency in certain families, predominantly in girls, and become apparent in early childhood.
Its pattern of inheritance is autosomal dominant, and in some instances the disease is associated with an aminoaciduria, in which the pattern of excretion resembles that of the recessive form of cystinuria.
A second biochemical abnormality in some cases is hypercalcemia, secondary to hyperplasia or adenomas of the parathyroid glands.
Hereditary pancreatitis is not associated with alcohol abuse or chronic biliary disease.
It is noteworthy that about 20% of such patients have subsequently developed ductal adenocarcinoma of the pancreas.
In view of the rarity of this disease, these data must be interpreted with caution.
Except for the features noted previously, hereditary pancreatitis is indistinguishable from chronic relapsing pancreatitis, including its associated late complications.
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