is (7:44).
Premature activation of pancreatic enzymes is the central event in the pathogenesis of acute pancreatitis (7:44). Once activated, trypsin can activate many other enzymes, including kallikrein, phospholipase A2, and elastase. This leads to autodigestion of pancreatic tissue as well as systemic effects from circulating enzymes causing vasodilation, increase capillary permeability with leaking of fluid, and disseminated intravascular coagulation. In the most severe cases the result is circulatory collapse, renal insufficiency, and respiratory failure. Despite extensive research, the mechanism(s) that trigger the initial sequence of enzymatic activation remain incompletely understood. Factors that can initiate this process include acute obstruction of the pancreatic duct, exposure to toxins and venoms, and ischemia.
In acute pancreatitis the structure and function of the pancreas usually return to normal. The cause of acute pancreatitis is not fully understood (2:8, 7). About half of the people who develop pancreatitis also have gallstones or common duct stones. Another common factor leading to pancreatitis is excessive drinking; 80 percent of acute pancreatitis attacks are alcohol related. Less frequent causes are stomach or duodenal ulcers, abdominal injury, and certain prescription medications (7).
The primary symptom of acute pancreatitis is pain in the middle of the upper abdomen (2:8, 7:44). Pain frequently occurs 12 to 24 hours after a large meal or heavy drinking. It radiates to the back and chest, and is eased by sitting or leaning forward. Vomiting usually occurs. In severe cases, signs of shock may occur, including restlessness, rapid heartbeat, coldness, and sweaty extremities.
Acute pancreatitis is diagnosed by taking a medical history, conducting blood tests to measure serum amylase and lipase, liver function tests, blood calcium levels, blood glucose levels, a complete blood count...