gastrointestinal disorders
Acute Pancreatitis
Etiology of Acute Pancreatitis
 70% of acute pancreatitis cases. The remaining cases result from myriad causes ( see Table: Some Causes of Acute Pancreatitis ). Gallstones are the most common etiology of acute pancreatitis. The precise mechanism of gallstone pancreatitis is unknown but likely involves increased pressure in the pancreatic duct caused by obstruction at the ampulla secondary to a stone or edema caused by the passage of a stone. Ductal hypertension results in aberrant activation of digestive enzymes from acinar cells. The toxic effects of bile acid itself on acinar cells might also be a mechanism. Gallstone pancreatitis is rare in pregnancy and occurs most commonly in the 3rd trimester. Alcohol intake is the second most common etiology of acute pancreatitis. The risk of developing pancreatitis increases with increasing doses of alcohol (≥ 4 to 7 drinks/day in men and ≥ 3 drinks/day in women); risk was once thought to increase proportionally to duration of alcohol consumption, but acute pancreatitis attacks may occur in susceptible patients after short periods of high alcohol intake. Low or moderate levels of alcohol consumption are associated with progression from acute to Chronic Pancreatitis . However, < 10% of patients with chronic alcohol consumption develop acute pancreatitis, suggesting additional triggers or cofactors are needed to precipitate pancreatitis. Pancreatic acinar cells metabolize alcohol into toxic metabolites via both oxidative and nonoxidative pathways and exhibit effects that predispose the cells to autodigestive injury and predispose the pancreas to necrosis, inflammation, and cell death. These effects include increased enzyme content, destabilization of lysosomal and zymogen granules, sustained increase in calcium overload, and activation of pancreatic stellate cells. Another theory proposes that alcohol increases the propensity of formation of protein plugs within pancreatic ducts by altering the level of lithogenic proteins and increasing the viscosity of pancreatic secretions, causing obstruction, and, eventually, acinar atrophy. A number of genetic mutations predisposing to pancreatitis have been identified. An autosomal dominant mutation of the cationic trypsinogen gene causes pancreatitis in 80% of carriers; an obvious familial pattern is present. Other mutations have lesser penetrance and are not readily apparent clinically except through genetic testing. The gene that causes Etiology increases the risk of recurrent acute pancreatitis as well as chronic pancreatitis. Acute pancreatitis is a complication that develops after Endoscopic retrograde cholangiopancreatography (ERCP) (ERCP) in about 5% of patients. 