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LEARNING OBJECTIVES
Upon completion of the chapter, the reader will be able to:
Describe the pathophysiology of acute pancreatitis and chronic pancreatitis.
Differentiate acute pancreatitis from chronic pancreatitis.
Formulate care plans for managing acute and chronic pancreatitis.
Choose appropriate pancreatic enzyme supplementation for patients with chronic pancreatitis.
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The pancreas is a glandular organ in the abdominal cavity lying below the liver and behind the stomach. It is primarily an exocrine gland but also has endocrine functions. The endocrine cells are the islets of Langerhans, which secrete regulatory hormones such as insulin and glucagon directly into the bloodstream.1 The exocrine cells of the pancreas are called acinar cells that produce and secrete digestive enzymes that mix with a bicarbonate-rich solution released from ductular cells to produce pancreatic juice. This alkaline solution is released through the ampulla of Vater into the duodenum to aid in digestion and buffer acidic fluid released from the stomach (Figure 24–1).2
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Pancreatic enzymes are responsible for breaking down proteins (protease), lipids (lipase), and carbohydrates (amylase) in the small intestine. Normally, these enzymes are produced and stored as inactive proenzymes within zymogen granules to prevent autolysis and digestion of the pancreas. 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. Pancreatitis is inflammation of the pancreas causing exocrine and endocrine dysfunction and can be acute or chronic in nature.
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EPIDEMIOLOGY AND ETIOLOGY
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Acute pancreatitis (AP) is one of the most common inpatient gastrointestinal (GI) diagnoses in the United States and places a significant burden on healthcare costs and resources.3 
In the Western Hemisphere, AP is caused mainly by ethanol use/abuse and gallstones (cholelithiasis), accounting for 80% to 90% of cases in the United States.4,5 Less common causes include hypertriglyceridemia, endoscopic retrograde cholangiopancreatography (ERCP), trauma, and autodigestion due to the early activation of pancreatic enzymes. Numerous medications have been implicated as causes of AP (Table 24–1), but other etiologies should be ruled out before diagnosing drug-induced pancreatitis.3,6,7
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