the cellular injury response that is mediated by proinflammatory cytokines.
The mechanisms by which the digestive enzymes become activated within the
acinar cell are unclear. However, such inappropriate activation of pancreatic
enzymes leads to destruction of the acinar cell and surrounding fat deposits,
and it weakens the elastic fibers of the blood vessels, resulting in leakage.
Obstruction of the main pancreatic duct as a result of a gallstone lodged
in or near to the hepatopancreatic ampulla can result in acute pancreatitis. One
theory is that obstruction increases the pressure in the main pancreatic duct.
The increase in pressure causes interstitial edema, which impairs the blood
flow to the acinus. The lack of blood flow leads to ischemic injury of the aci-
nar cell, resulting in release of the digestive enzymes into the interstitial space.
How this leads to premature activation of the proenzymes stored in the acinar
cell is unclear.
a-Amylase and lipase are two digestive enzymes that are synthesized and
stored in the acinar cell as the active enzymes. Amylase is an endosaccharidase
that catalyzes the hydrolysis of the a(1^4) glycosidic bonds that form the
main polymeric backbone of the polysaccharides starch and glycogen. Present
in both saliva and pancreatic juice, it is the pancreatic form of the enzyme that
breaks down most of the dietary polysaccharides. a-Amylase hydrolyzes
dietary starch and glycogen to glucose, maltose, maltotriose, and an oligosac-
charide referred to as the a-limit dextrin.
Pancreatic lipase is the primary digestive enzyme for the breakdown of
triglycerides. It acts on triglycerides to hydrolyze the fatty acyl ester bonds.
Lipase is specific for the ester bonds in the 1'- and 3'-positions to produce free
fatty acids and P-monoacylglycerols. Pancreatic lipase is strongly inhibited by
bile acids and therefore requires the presence of colipase, a small protein that
binds to the lipase and activates it.
Since both a-amylase and lipase are stored in the pancreas as the active
enzymes, they are important blood markers to help diagnose acute pancreati-
tis. The serum level of a-amylase will increase in the first 12 hours following
the onset of acute pancreatitis. During the next 48 to 72 hours, the levels will
usually fall back to normal values. Serum lipase levels also rise, but they
remain elevated after the a-amylase levels have returned to normal and may
take 7 to 10 days to normalize.
Most cases (85 to 90 percent) of acute pancreatitis that are caused by gall-
stones will resolve on their own, and therefore conservative treatment modal-
ities are appropriate. These include pain management with analgesics,
administration of intravenous fluids to maintain the intravascular volume and
electrolyte balance, as well as removal of oral alimentation to decrease the
secretion of pancreatic juice. Nasogastric suction has also been used to
decrease gastrin release from the stomach and to eliminate gastric emptying
into the duodenum. However, controlled trials have not demonstrated the effi-
cacy of nasogastric suction in the treatment of mild to moderate acute
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