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A Primer on Exocrine Pancreatic Insufficiency, Fat Malabsorption, and Fatty Acid Abnormalities
Samer Alkaade, MD and Ashley A. Vareedayah, MD
Options for Addressing Exocrine Pancreatic Insufficiency in Patients Receiving Enteral Nutrition Supplementation
Steven D. Freedman, MD, PhD

A Primer on Exocrine Pancreatic Insufficiency, Fat Malabsorption, and Fatty Acid Abnormalities

Samer Alkaade, MD and Ashley A. Vareedayah, MD
Exocrine pancreatic insufficiency (EPI) is characterized by a deficiency of exocrine pancreatic enzymes, resulting in deficits in digestion of all macronutrients, with deficiencies in digestion of fats being the most clinically relevant. The leading cause of EPI is chronic pancreatitis. However, many other causes and conditions may be implicated, including cystic fibrosis, pancreatic duct obstruction, gastric and pancreatic surgery, diabetes mellitus and other conditions. Physical and biochemical causes of EPI include decreased production and secretion of lipase, increased lipase destruction, pancreatic duct obstruction, decreased lipase stimulation and degradation, as well as gastrointestinal motility disorders. EPI is largely diagnosed clinically, and is often identified by symptoms such as steatorrhea, weight loss, abdominal discomfort, and abdominal bloating. Lifestyle modifications (eg, smoking cessation, limiting or avoiding alcoholic drinks, and reducing dietary fat intake) and exogenous pancreatic enzyme supplements are commonly used to help restore normal digestion and absorption of dietary nutrients in patients with EPI.
Am J Manag Care. 2017;23:-S0

Normal Pancreatic Physiology
Positioned next to the duodenum and behind the stomach, the pancreas is an essential part of the gastrointestinal system.1 The location of the pancreas and its unique cellular organization facilitate its physiological role in the digestion and absorption of nutrients. The pancreas is composed of exocrine and endocrine glands; the exocrine portion accounts for roughly 85% of the total volume of the pancreas, whereas the endocrine pancreas represents less than 2%. The remaining pancreatic mass is accounted for by extracellular matrix (10%) and ductal cells and blood vessels (4%).2 The exocrine pancreas is composed of acinar cell clusters and epithelial cells which line pancreatic ducts (ductal cells). The pancreatic acini produce and secrete digestive enzymes which are delivered to the duodenum and along with bile salts are responsible for the majority of the digestive process within the small intestine. Ductal cells produce large quantities of an alkaline mixture of water and bicarbonate, which guides enzyme transport through the pancreatic ducts for delivery to the duodenum, as well as providing the optimum pH for enzyme activity. Clusters of endocrine cells, or pancreatic islets, make up the endocrine portion of the pancreas.1 The endocrine pancreas is involved in the production of several hormones (ie, insulin, glucagon, somatostatin) that are secreted directly into circulation via the dense network of capillaries associated with pancreatic islets.1 There is no separation of exocrine and endocrine pancreatic components; pancreatic islets are scattered among the pancreatic acini and acinar cells are vascularized through the islet capillaries.1 Thus, disease states which cause malfunction or damage in one of the components of the pancreas may lead to functional defects in the other component.3

Under normal physiological conditions (Figure 11,4,5), the exocrine pancreas post-prandially produces approximately 1.5 L of an aqueous digestive solution that contains 3 main types of enzymes: amylase, protease, and lipase, which aid in digestion of carbohydrates, proteins, and fats, respectively.1,6,7 The relative quantity of these enzymes varies based on multiple factors including diet, age, and gender.6 Pancreatic enzyme synthesis begins during the cephalic phase of digestion, before food reaches the stomach. However, pancreatic enzymes are not secreted until the initiation of the intestinal phase—after food has been converted to chyme and passed into the duodenum. The intestinal phase controls the rate of gastric emptying to ensure that digestive and absorptive processes are appropriately carried out in the small intestine.1  

When chyme reaches the duodenum, pancreatic secretions are triggered exby 2 duodenal hormones: secretin and cholecystokinin (CCK).1 Entry of acidic chyme stimulates the release of secretin into the bloodstream, which in turn stimulates  pancreatic production of an aqueous buffer solution (pH 7.5 to 8.8) containing bicarbonate and phosphate ions, from pancreatic ductal cells. The secretion of this pancreatic fluid enables the activity of pH-sensitive pancreatic digestive enzymes by neutralizing acidic chyme. CCK stimulates the production and secretion of pancreatic enzymes from acini, and movement of bile from the gallbladder.1,6 Pancreatic enzymes are delivered to the duodenum through the pancreatic duct via pancreatic fluid, which merges with incoming bile from the liver and gallbladder to initiate intestinal digestion.1

Post-prandial secretions of salivary amylase in the mouth aid in the first steps of carbohydrate digestion; pancreatic amylase and enzymatic activity from the intestinal brush border continue to break down carbohydrates, and the digested products are absorbed in the duodenum. Proteins are hydrolyzed in the stomach by gastric acid and pepsin, and protein digestion continues in the duodenum via pancreatic proteases and proteolytic activity in the small intestine brush border.6,8 Lingual and gastric lipases are responsible for fat digestion in the stomach and hydrolysis continues in the duodenum through the action of pancreatic and gastric lipases. Fat molecules are emulsified by bile salts into micelles and absorbed in the jejunum.8

Postprandial fat digestion relies on three critical events facilitated by the pancreas; disruption in these processes may lead to clinical manifestations of maldigestion and malabsorption of fat (steatorrhea). Clinical symptoms of steatorrhea are prevented when pancreatic lipase output remains greater than 10% of normal physiological output.3,9 Postprandial  synchrony—the appropriate timing and delivery of gastric contents into the duodenum and discharge of pancreatic and biliary secretions for digestive action following nutrient intake—is an essential process in fat digestion and absorption.3 Additionally, the acidic contents of the stomach must be neutralized to prevent degradation and allow normal function of pancreatic enzymes.3

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