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 ?
Alcohol redirects CCK-mediated apical exocytosis to the acinar basolateral membrane in alcoholic pancreatitis. Traffic 8(5):605-617, 2007.
Corresponding risk estimates were 2.0 (1.8-2.2) observationally and 1.0 (0.8-1.1) genetically for any alcoholic liver disease, 1.4 (1.1-1.9) observationally and 1.1 (0.8-1.5) genetically for alcoholic pancreatitis, and 1.3 (1.1-1.6) observationally and 1.0 (0.8-1.3) genetically for any pancreatitis (Fig.
Pathobiology of alcoholic pancreatitis. Pancreatology 2007;7:105-114.
This article reviews past theories and current knowledge about the pathophysiology of chronic alcoholic pancreatitis, with particular emphasis on alcohol metabolism by acinar and stellate cells and on the toxic effects of alcohol and its metabolites on these cells.
Lipase/Amylase Ratio (> 4) Sensitivity for Diagnosing Alcoholic Pancreatitis Alcoholic AP Total Absent Present Test Positive 2 15 17 Test Negative 25 5 30 Total 27 20 47 Table 6.
Other studies have shown that excessive alcohol consumption is more frequent among patients with unsatisfactory surgical results and have considered patients with alcoholic pancreatitis poor candidates for surgery.[2,21,22] The lack of abstinence with subsequent acute exacerbations of pancreatitis in the residual pancreas may explain persistence of postoperative intractable pain in alcoholic CP.[2,3] It has been suggested that patients most likely to be pain free after MPR have no preoperative use of tranquilizers, little dilatation of the pancreatic duct, and no pseudocysts.[22]
Prophylactic antibiotics in treatment of severe acute alcoholic pancreatitis. pancreas 1996;13:198-201.
Unlike alcoholic pancreatitis, NADDCP is not associated with pancreatic pseudocysts or significant calcification.
Among these patients, 16 were diagnosed as having chronic alcoholic pancreatitis; the remaining 16 had other extrapancreatic gastrointestinal disorders (8 with functional gastrointestinal disorders, 3 with chronic inflammatory bowel disease, 3 with malabsorption due to sprue, and 1 each with liver cirrhosis and a secretory diarrhea).
When comparing the etiology of AP in women to those in men, women had significantly more gallstone pancreatitis (60.9% versus 33.6%), but less alcoholic pancreatitis (4.5% versus 25.7%) (Table 2).
Among these 3 patterns, the fibrosis of chronic alcoholic pancreatitis was found mainly in the perilobular or interlobular areas with a nodular lobular appearance.[2]