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Inflammation of the pancreas.



acute or chronic inflammation of the pancreas.

Acute pancreatitis may be edematous, hemorrhagic, necrotic, or purulent. It is caused by overeating; by diseases of the stomach, duodenum, biliary tract, or liver; or by stenosis of the gland’s ducts. In acute pancreatitis the pancreas is digested by its own enzymes—trypsin, chymotrypsin, and lipase. When the gland’s tissue decomposes, kinins are released. They decrease arterial pressure and are a factor in blood circulation disorder of both organic and reflex origin in the pancreas. The kinins also cause bile to flow into the gland’s ducts, which damages their walls.

Acute pancreatitis may be marked by very severe abdominal pains, persistent vomiting, and collapse. Complications are peritonitis, abscesses, cysts of the gland, and diabetes mellitus. The disease is treated by narcotics, antibiotics, vasoconstrictors, and such antienzyme preparations as trasilol and contrical and by A. V. Vishnevskii’s paranephric novocain blockade. Serious complications are treated surgically.

In chronic pancreatitis, the gland’s external and internal secretions gradually become insufficient. The disease is treated by diet, antispasmodics, substitutes, cholegogues, antibiotics, and antienzyme preparations. During periods of remission, the patient may receive treatment at a health resort.


Shelagurov, A. A. Bolezni podzheludochnoi zhelezy. Moscow, 1970.


References in periodicals archive ?
Alcohol redirects CCK-mediated apical exocytosis to the acinar basolateral membrane in alcoholic pancreatitis.
Sex and age differences in alcoholic pancreatitis in Japan:A multicenter nationwide survey.
Pancreatic morphological changes in long-term follow-up after initial episode of acute alcoholic pancreatitis.
Effects of oxidative alcohol metabolism on the mitochondrial permeability transition pore and necrosis in a mouse model of alcoholic pancreatitis.
Given the failure of the sphincteric and ductular obstruction theories to fully explain the pathogenesis of alcoholic pancreatitis, the attention of researchers has shifted over the past 10 years toward the acinar cells, the most abundant cells in the pancreas.
Of particular interest to the pathogenesis of chronic alcoholic pancreatitis is the finding that PSCs are activated by exposure to physiologically relevant concentrations of ethanol (10 and 50 mM [i.
Such studies of potential risk factors for alcoholic pancreatitis ideally should compare alcoholics without pancreatic disease with alcoholics displaying pancreatic injury, but this has not always been the case.
The most commonly cited theory for the cause of chronic alcoholic pancreatitis suggests the deposition of protein plugs that later calcify, leading to duct obstruction with subsequent fibrotic replacement of the acinar tissue upstream from the occlusion.
In this study, we investigated the mechanism of interlobular fibrosis of the pancreas, which is categorized as chronic alcoholic pancreatitis, based on histologic changes in the pancreatic tissue in patients with ampullary carcinomas with various degrees of stricture of the main pancreatic duct.
In addition, 20 patients with clinically diagnosed chronic alcoholic pancreatitis (mean age, 52 years) at Juntendo University Hospital were included in this study.
CONCLUSION: There is a rise in the disease pattern of chronic pancreatitis in the state of Karnataka too, while our neighboring state, Kerala is known for highest prevalence of Chronic Pancreatitis in the world, which can be attributed to changing lifestyle leading to a shift in etiology from tropical to Alcoholic pancreatitis, and an older age of onset of disease.
Acute (nonprogressive) alcoholic pancreatitis: prospective longitudinal study of 144 patients with recurrent alcoholic pancreatitis.