Pancreatitis

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pancreatitis

[‚pan·krē·ə′tīd·əs]
(medicine)
Inflammation of the pancreas.

Pancreatitis

 

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.

REFERENCE

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

O. S. RADBIL’

References in periodicals archive ?
No significant difference in terms of polymorphism between alcoholic pancreatitis and alcohol abuse without organ damage could be found.
The frequency of the usual (wild-type) gene was significantly diminished in patients with alcoholic pancreatitis compared with the other groups, including alcoholic subjects without organ damage.
In summary, current data fail to establish an unequivocal link between any polymorphism of ethanol-oxidizing enzymes and the risk of alcoholic pancreatitis.
Stellate cell activation in alcoholic pancreatitis.
The role of acetaldehyde in the pathogenesis of acute alcoholic pancreatitis.
In all cases of chronic alcoholic pancreatitis, fibrosis was patchily distributed in the interlobular or perilobular areas with the "nodular pancreatitis" pattern[3] (Figure 3), and in some advanced cases, in which protein plugs and pancreatic stones were also found, fibrosis extended into the intralobular areas (Figure 4).
Anti-[Alpha]-SMA immunoreactivity was found in interlobular fibrosis in patients with chronic alcoholic pancreatitis.
In this study, fibrosis in chronic alcoholic pancreatitis was patchily distributed in the interlobular or perilobular areas with anti-[Alpha]-SMA immunoreactivity and nodular lobular patterns.
These findings were similar to those of chronic alcoholic pancreatitis cases.
Pancreatic fibrosis in patients with chronic alcoholic abuse: correlation with alcoholic pancreatitis.