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Upon completion of the chapter, the reader will be able to:

  1. Describe the pathophysiology of acute and chronic pancreatitis.

  2. Differentiate acute from chronic pancreatitis.

  3. Discuss the clinical implications of pancreatic fluid collections, pancreatic abscess, and pancreatic necrosis in acute pancreatitis.

  4. Formulate care plans for managing acute pancreatitis.

  5. Identify pharmacologic and nonpharmacologic means of preventing repeat episodes of chronic pancreatitis.

  6. Choose appropriate pancreatic enzyme supplementation for patients with chronic pancreatitis.




  • Image not available. The most common causes of acute and chronic pancreatitis in adults are ethanol abuse and biliary stones.

  • Image not available. Pancreatic necrosis occurs within the first 2 weeks of acute pancreatitis and develops in 10% to 20% of patients with acute pancreatitis.

  • Image not available. Therapy of acute pancreatitis is primarily supportive unless a specific etiology is identified. Supportive therapy involves fluid repletion, nutrition support, and analgesia.

  • Image not available. Medications aimed at decreasing pancreatic enzyme release, nasogastric suction, and anticholinergic medications have not shown benefit in the treatment of acute pancreatitis.

  • Image not available. Long-term sequelae of chronic pancreatitis include dietary malabsorption, impaired glucose tolerance, cholangitis, and potential addiction to opioid analgesics.

  • Image not available. Treatment of chronic pancreatitis is aimed at removing the cause (ethanol abuse, cigarette smoking, or biliary stones), providing analgesia, supplementing with pancreatic enzyme preparations, and implementing dietary restrictions.




The pancreas is a gland in the abdomen lying in the curvature of the stomach as it empties into the duodenum. The pancreas functions primarily as an exocrine gland, although it also has endocrine function. The exocrine cells of the pancreas are called acinar cells that produce and store various digestive enzymes that mix with a bicarbonate-rich solution released from duct cells to produce pancreatic juice. This pancreatic juice is released through the ampulla of Vater into the duodenum to aid in the digestive process as well as buffer acidic fluid released from the stomach (Fig. 23–1).1

FIGURE 23–1.

Anatomical structure of the pancreas and biliary tract. (From Bolesta S, Montgomery PA. Pancreatitis. In: DiPiro JT, Talbert RL, Yee GC, et al., eds. Pharmacotherapy: A Pathophysiologic Approach, 8th ed. New York, NY: McGraw-Hill, 2011; Figure 46–1, with permission.)

Graphic Jump Location

These enzymes are produced and stored as inactive proenzymes within zymogen granules to prevent autolysis and digestion of the pancreas. The zymogen granules are also responsible for enzyme transport to the pancreatic duct. Amylase and lipase are released from the zymogen granules in the active form, whereas the proteolytic enzymes are activated in the duodenum by enterokinase. Enterokinase triggers the conversion of trypsinogen to the active protease trypsin, which then activates the other proenzymes to their active enzymes. The pancreas contains a trypsin inhibitor to prevent autolysis.






Image not available. In the Western Hemisphere, acute pancreatitis is caused ...

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