August/September 2024 Issue
CPE Monthly: Nutrition Interventions for Pancreatic Insufficiency
By Lauren Botelho, MS, RD, LDN
Today’s Dietitian
Vol. 26 No. 7 P. 40
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Pancreatic insufficiency is typically a secondary cause as the result of a particular disease such as: chronic pancreatitis, acute pancreatitis, cystic fibrosis (CF), and pancreatic cancer. It can also be caused by diabetes mellitus or surgical resection.1 Since the pancreas is responsible for the digestion of many nutrients, a lack of certain pancreatic enzymes can cause malabsorption, leading to malnutrition and potentially poorer health outcomes and increased mortality.1 RDNs are at the forefront of managing and treating malnutrition. Therefore, it is crucial that they understand the etiology of pancreatic insufficiency in order to help prevent/treat malnutrition and provide individualized MNT.
Pancreatic Function
The pancreas is an organ located in the posterior abdominal wall and has both endocrine and exocrine functions. It is essential to the digestion, absorption, and metabolism of various nutrients.2 It is approximately 85% exocrine gland and 2% endocrine gland. The rest of the pancreas mass is made up of an extracellular matrix, ductal cells, and blood vessels.3 The exocrine pancreas contains acinar cells and epithelial cells that line pancreatic ductal cells. The pancreatic acini produce and secrete digestive enzymes that are then delivered to the duodenum along with bile salts which allows for digestion within the small intestine.3 Ductal cells produce water and bicarbonate which guides enzyme transport through the ducts. It also provides an ideal pH for enzyme activity.3
Pancreatic islets make up the portion of the pancreas that is endocrine. This part of the pancreas produces the hormones insulin, glucagon, amylin, ghrelin, pancreatic polypeptide, and somatostatin that are secreted directly into circulation.3 When the pancreas is functioning normally, it secretes the enzymes amylase, lipase, and protease; water; and ions bicarbonate and phosphate. This occurs when secretin and cholecystokinin are released from the duodenum with the arrival of chyme (gastric juices and partially digested food).2
Pancreatic Insufficiency Etiology and Symptoms
Pancreatic insufficiency most commonly affects exocrine function. Exocrine pancreatic insufficiency (EPI) is a condition that affects normal nutrient digestion and absorption. This is the result of having low levels of digestive enzymes and there are several conditions that can cause EPI. Symptoms of EPI are nonspecific and include bloating, abdominal discomfort, steatorrhea, diarrhea, excess gas, and weight loss.4 Symptoms may not become apparent until exocrine pancreatic function is less than 10% of normal.5 Causes of EPI include decrease in production and secretion of lipase, increased lipase destruction, pancreatic duct obstruction, decreased lipase stimulation and production, and motility disorders.3
EPI can be categorized as mild, moderate, or severe. Mild insufficiency is typically the result of a reduction in one or two enzymes but preserved bicarbonate and normal fecal fat. Moderate insufficiency includes impaired bicarbonate secretion. Severe insufficiency includes steatorrhea.2 Diagnosis can be challenging as these symptoms can mimic those seen in other conditions or diseases. The prevalence of EPI is not known but it is most common in those with chronic pancreatitis, CF, pancreatic cancer, pancreatic resection, or other gastrointestinal conditions (such as inflammatory bowel disease, celiac disease, and irritable bowel syndrome).4
Diagnosing Pancreatic Insufficiency
A diagnosis for pancreatic insufficiency takes a team approach. Providers can be aided in this with the help of the RDN to assess for malnutrition and potential nutrient deficiencies. Providers ultimately diagnose a patient based on symptoms and additional laboratory testing. Getting an overall picture of the patient’s health and nutrition status is key to diagnosis.
A diagnosis of EPI is based on a patient’s symptoms, history, and physical exam, ruling out other potential diagnoses. The gold standard test for diagnosing EPI is the 72-hour fecal fat quantification to determine the coefficient for fat absorption. Despite this, its use is limited and not widely accepted.2 This is an indirect test that requires a collection of all stool over 72 hours and also requires maintaining a diet of 100 g of fat daily for five days. A positive test is > 7 g of fat over a 24-hour period.6 As this testing process is quite cumbersome, the fecal elastase-1 (FE-1) test is most widely used to help make a diagnosis.4 FE-1 is an enzyme produced by the pancreas that remains intact through intestinal transit and is highly sensitive and specific for diagnosing EPI that is advanced, but less so in milder cases and those who have had pancreatic resection or who have watery diarrhea.4
The diagnosis of EPI is primarily evaluated via determining the degree of maldigestion of nutrients or by quantifying the exocrine pancreatic secretion. Indirect tests assess the degrees of exocrine insufficiency and look for quantitative changes in pancreatic secretion. Direct tests assess secretive production but are invasive and costly. They are also not useful in monitoring a patient’s response to pancreatic enzyme replacement therapy (PERT).7 A secretin pancreatic function test can be used for diagnosis, as this hormone triggers the release of digestive enzymes, but it is very invasive.8 Another direct test involves the collection of cholecystokinin from the duodenum at certain points in time to assess this enzyme and bicarbonate concentrations.6 However, the FE-1 level is the most commonly used test for diagnosis. FE-1 is a proteolytic enzyme that the acinar cells of the pancreas produce. This enzyme binds to bile salts and then passes through the gut. It can then be detected in fecal samples. A concentration of less than 200 μg/g is considered abnormal.7
Diseases Causing Pancreatic Insufficiency
Certain diseases are most commonly associated with EPI and this condition is most common in those with chronic pancreatitis. Due to the progressive loss of acinar cells and fibrosis that follows, lipase secretion is reduced in those with chronic pancreatitis. EPI occurs in 60% to 90% of patients with chronic pancreatitis within 10 to 12 years of diagnosis.7 There is also an increased risk associated with alcohol consumption and chronic pancreatitis can be associated with genetic factors.7 Acute pancreatitis is another common cause of EPI. Recurrence of the disease, extent of pancreatic necrosis, and level of alcohol use are factors associated with this.7
Pancreatic Cancers and Surgery
Pancreatic cancers are causes of EPI. Most commonly, a type of cancer known as pancreatic ductal adenocarcinoma is responsible for EPI. It is noted that a reduced FE-1 is associated with a reduced survival rate in patients with advanced disease.7 Additionally, since pancreatic surgery alters the anatomy of the digestive tract, it can cause EPI. Surgery also alters how food, bile, and pancreatic enzymes are mixed and reduces pancreatic volume.7 Whipple procedures (which remove the head of the pancreas, the first part of the duodenum, the gallbladder, and the bile duct) performed to treat pancreatic cancer led to the highest rates of EPI at 85% to 95% of patients.7
Cystic Fibrosis
CF is another disease associated with EPI as the pancreas becomes surrounded by a thick mucus and cannot function adequately due to genetic mutations.7 It is estimated that 85% of those with CF have pancreatic insufficiency, and that even those who are considered pancreatic sufficient still have some degree of abnormal pancreatic function.6 The pancreatic function in those individuals may deteriorate over time. CF-related diabetes (CFRD) develops in 20% to 50% of CF patients.6 The level of immunoreactive trypsinogen measured in newborns is inversely correlated with later risk of CFRD and suggests that higher degrees of EPI in infants is predictive of later CFRD.6
Schwachman-Diamond syndrome is another cause of inherited EPI, and is found to have extensive fatty replacement of acinar cells and severe reduction of fecal elastase levels.7 Additionally, Zolinger-Edison syndrome can cause EPI due to the inactivation of lipase as a result of an acidic environment within the duodenal lumen.9
Diabetes and Inflammatory Bowel Disease
Insulin resistance, poor glycemic control, and long disease duration are associated with EPI in those with both type 1 and type 2 diabetes mellitus. Both insulin and glucagon are secreted from the pancreas, thus leading to EPI when blood sugar levels are not well controlled or regulated.7 EPI may also affect those with inflammatory bowel disease and celiac disease. Intestinal inflammation and atrophy can lead to impaired pancreatic signaling.7 EPI also occurs in those who have had gastrectomies or esophagectomies, due to impaired gastric relaxation and hormone signaling.7
Maldigestion and Malabsorption of Nutrients
The pancreas is responsible for the digestion of various macronutrients and micronutrients. Amylase is an enzyme that breaks down carbohydrates. Protease digests fats. Protease and elastase are both enzymes responsible for digesting protein.8 Impairment to pancreatic function therefore leads to maldigestion and malabsorption. Of particular concern is the malabsorption of fat.
Dietary Fat and Fat-Soluble Vitamin Malabsorption
Fat malabsorption is one main concern with EPI. This occurs when intraduodenal levels of lipase are under 5% to 10% of what is considered a normal enzyme output.10 This is what leads to symptoms of steatorrhea, weight loss, and decreased quality of life. In CF and chronic pancreatitis there is also a decreased level of bicarbonate which leads to a lower intestinal pH and causes bile salt acids to precipitate and impair micelle formation of fats. The maldigestion of fat is also caused by decreased pancreatic secretion of lipase and colipase.10
Since fat malabsorption is a result of EPI, patients are likely to have deficiencies in the fat-soluble vitamins A, D, E, and K. Low levels of vitamin A are associated with night blindness, xeropthalmia (dry eye and tear ducts), abnormal perinatal development, deficiencies in tissue repair, and immune deficiencies.6 Retinol-binding protein, a marker of vitamin A status, has been found to be low in those with alcohol-induced chronic pancreatitis and steatorrhea.11 Lab testing should include plasma retinol and retinal esters.6
Vitamin D may be low in individuals with EPI due to decreased absorption of calcium, leading to osteoporosis. High levels of osteoporosis and osteopenia have been associated in particular with those who have chronic pancreatitis.12 In fact, 65% of those with chronic pancreatitis have been found to have either osteopenia or osteoporosis.9 Additionally, vitamin D deficiency has been found to predict the severity of acute pancreatitis. A study of 242 patients with acute pancreatitis found that the prevalence of vitamin D deficiency was 56.2% and that 28.5% of patients met criteria for insufficiency.13 These levels were negatively correlated to severity of acute pancreatitis based on multiple scoring systems (p=0.015) and also predicted the need for ICU admission (p=0.035).13
Low levels of vitamin E have been associated with steatorrhea caused by chronic pancreatitis or CF.11 Deficiencies in vitamin E can result in neurological deficits. A prospective controlled cohort study (n=128) of 62 patients with chronic pancreatitis and 66 controls found that 24.2% of those with chronic pancreatitis were deficient in vitamin E. The study highlighted the importance of a full nutrition assessment on these patients, despite that fact that 50% were considered overweight or obese.14 Vitamin E levels should be tested as alpha-tocopherol and measured while fasting, with cholesterol and triglycerides as well as the ratio of alpha-tocopherol to total lipid, which is most accurate for reflecting vitamin E tissue stores.6 Measurements of vitamin K are not accurate as they reflect recent intake of this vitamin and testing is therefore not recommended.
PT/INR (prothrombin time/international normalized ratio) is the most accurate measurement for assessing vitamin K status.6 Additionally, fatty acid deficiencies of linoleic acid and DHA have been found in those with CF and have been found to play a role in the severity of symptoms and progression of the disease due to its effect on the liver, where essential fatty acids are metabolized.3 However, the exact pathogenesis of this deficiency in CF patients requires more research.
Malabsorption of Additional Micronutrients
In addition to macronutrient malabsorption, various micronutrient levels may be low in patients with EPI. Chronic pancreatitis is associated with deficiencies in vitamin B12, zinc, magnesium, calcium, and folic acid. If nutrients are found to be low in these individuals, it may aid in a diagnosis of EPI.15 A cross-sectional study of 50 patients who had chronic pancreatitis was compared among those who had EPI vs those who did not. Patients with EPI had higher levels of hemoglobin A1c and lower levels of magnesium and prealbumin, when compared with those without EPI.15
Micronutrient malabsorption is particularly common in acute pancreatitis due to alcohol consumption. In addition to possible malabsorption of B12, zinc, and folic acid, there may be deficiencies in vitamins A, B1, B2, B3, and C.16 Hypocalcemia related to saponification of calcium, hypomagnesemia, decreased parathyroid hormone release, and increased calcitonin levels occurs in 40% to 60% of these patients.16
Malnutrition in Pancreatic Insufficiency
The malabsorption of various nutrients as a result of EPI can lead to malnutrition. Signs and symptoms of malnutrition associated with EPI include dry skin, depression, edema, fatigue, dizziness, feeling cold often, irritability, memory/concentration issues, and muscle loss.8 Malnutrition in chronic pancreatitis is related to multiple factors, including exocrine insufficiency, endocrine insufficiency, chronic abdominal pain, alcohol use, delayed gastric emptying, and increased metabolism.17
Steatorrhea and malabsorption as a result of EPI are leading causes of malnutrition.17 One study found that patients (n=77) with chronic pancreatitis and EPI (31.5%) had a medium or higher risk for malnutrition based on the Malnutrition Universal Screening Test, scoring one or higher. This was also associated with an increased risk for osteopenia and osteoporosis.18 Patients with acute pancreatitis are also at risk for malnutrition and may need nutritional support due to increased stress and inflammation.9
Patients with advanced pancreatic cancer are especially at risk for malnutrition, in addition to decreased physical functioning.19 Many patients with pancreatic cancer have cachexia, which involves weight loss due to skeletal muscle and adipose tissue wasting. Those with malnutrition have a lower quality of life, increased morbidity and mortality, longer hospital stays, and reduced response to treatment.20 Weight loss and malnutrition in patients with pancreatic cancer also leads to low therapeutic tolerance. Up to 85% of these patients have weight loss at diagnosis and 70% develop malnutrition during chemotherapy.9 Sarcopenia, which is a loss of muscle mass and associated with poor health outcomes, has been found to be associated with EPI. One study (n=132) found this was true for both men (P<0.001) and women (P=0.012).21
Diet in Exocrine Pancreatic Insufficiency
The nutrition needs of patients with EPI depend on their diet, pancreatic exocrine and endocrine function, gastrointestinal integrity, anatomy, and gastrointestinal function. Some, but not all, deficiencies can be compensated with physiological reserves or adaptation.22 It is important for RDNs to assess dietary intake including macronutrients and micronutrients (fat-soluble vitamins, calcium, iron), cooking methods, and use of any supplements.22 Assessing the intake of B12, selenium, magnesium, zinc, and copper may be necessary as well. Both diet and lifestyle changes may help control severe EPI. These changes include consuming small, frequent meals; consuming high protein foods; avoiding alcohol and tobacco; and supplementing with PERT.22
Macronutrient Needs for Pancreatic Insufficiency
Chronic pancreatitis increases energy expenditure by 30% to 50% and requires a higher caloric diet to meet nutrient needs.12 Calorie recommendations range from 25 kcals/kg/day to 35 kcal/kg/day or closer to 35 kcal/kg/day.9,12 In acute pancreatitis that is considered moderate to severe or severe, the inflammation and complications of sepsis result in increased metabolism and energy requirements. Energy expenditure can be 139% of the Harris-Benedict equation estimate for calorie needs.9 Hypermetabolism has also been found in patients with advanced pancreatic cancer and an increase of 30% of calorie needs may be needed.19
Protein recommendations are 1 to 1.5 g/kg/day.9,12 Whitcomb et al recommend protein at 1.5 to 2 g/kg/day for mild to moderate chronic pancreatitis as these patients can typically follow an unrestricted diet.22 O’Brien and Omer also report that most patients with chronic pancreatitis do not require any dietary restrictions and can be managed with PERT.17 In acute pancreatitis, protein catabolism is increased and nitrogen loss is estimated to be 20 to 40 g/day, and authors Lakananurak and Gramlich recommend 1.2 to 1.5 g/kg/day.9,19
Carbohydrates don’t typically need to be decreased unless diabetes is present and these patients should aim for complex carbohydrates.9,22 The digestion of carbohydrates is maintained for a long period of time by salivary amylase and brush-border oligosaccharidoses.23 Although soluble fiber can help decrease inflammation and maintain colonic mucosal integrity and immune function, it can interfere with PERT.22 Fiber intake needs should be individualized.
A low-fat diet may actually decrease pancreatic secretion, which would cause decreased energy from fat, so an unrestricted fat intake is therefore recommended.9 However, those with severe steatorrhea may need to restrict fat intake to as low as 25 g/day.24 In general, it is recommended to avoid foods high in saturated fat, although a diet too low in fat may cause an essential fatty acid deficiency.24 Additionally, small, frequent meals are recommended.9,12,22
Nutrition Support in Pancreatic Insufficiency
Many patients with EPI, especially those meeting criteria for malnutrition, may require nutrition supplements. If the patient is on an oral diet, then oral nutrition supplements can be provided.
Whey protein has been found to improve the musculoskeletal system, cachexia, and increase insulinlike growth factors that could positively effect cell apoptosis (process of normal cell death).9 A study involving MCF-7, which is a breast cancer cell line, showed that whey proteins may be cytotoxic and useful in treatment). 25 L-carnitine and branched-chain amino acids could improve cachexia, but the results of these studies are low/limited. 9 If patients are unable to tolerate an oral diet, they may require enteral nutrition (EN) or parenteral nutrition (PN).
Approximately 5% of patients with chronic pancreatitis require EN tube feedings. This is typically for those who require more rapid weight gain or have significant abdominal pain with regular diet intake. Studies have shown that nasogastric tube feedings are safe and well-tolerated in most patients.9 A prospective randomized study of patients admitted to the hospital with severe acute pancreatitis (n=50) showed that complications of pancreatic infection, central venous catheter infection, and multiorgan failure were significantly lower in those who received early enteral feeding via nasogastric tube vs total PN (within 24 hours of admission). Early recovery in the enteral fed group was also significantly lower with a mean duration 6.76 days vs 10.4 days.26 Many recommend nasojejunal tube feedings. If the nutrition is expected to last over 30 days, then a jejunostomy through a gastrostomy or direct percutaneous jejunostomy is recommended.9 Elemental formulas have been shown to reduce episodes of pain in some patients with chronic pancreatitis.9 A prospective study of patients with chronic pancreatitis (n=17) in Japan showed that consuming a low-fat elemental diet for eight weeks had a significant impact on pain control, with 15 out of 17 patients reporting alleviation of pain and 10 out of 17 reporting complete disappearance of pain.27
Patients hospitalized for acute pancreatitis are initially prescribed nil per os to minimize pancreatic stimulation. However, oral nutrition or EN have not been found to significantly increase pancreatic secretion or worsen inflammation. Both oral nutrition and EN promote intestinal integrity and functionality by decreasing the inflammatory response.9 Additionally, studies have shown that patients on oral diets/EN compared with patients who are nil per os reduces complications of necrosis, organ failure, and mortality.9
The 2018 American Gastroenterological Association guidelines recommend oral feeding within the first 24 hours. If nutrition support is needed, EN is favored over total PN due to reduced rates of infection. Despite the reasoning that elemental formulas are easier to digest (and as previously stated, could possibly reduce episodes of pain), polymeric formulations of EN are typically recommended as no benefit to elemental formulas has been found overall and these formulas are cheaper.9 Authors Ramanathan and Aadam report that studies have shown no significant differences in nasogastric tube vs nasojejunal tube, but also emphasize the importance of early initiation of EN within 24 hours.28 Some randomized controlled trials in the general critical care setting have shown positive effects with the addition of immunomodulation supplements to EN. However, it is noted that most of these randomized controlled trials had low quality and were of high bias. Additionally, no clear evidence exists for its benefit to patients with EPI.28
Micronutrient Needs in Pancreatic Insufficiency
Patients who have signs of micronutrient/vitamin deficiencies, inadequate intake, or prolonged malabsorption should be assessed. This should include vitamin A, D, E, K, B12, iron, zinc, selenium, and copper.9 Authors Cañamares-Orbís, García-Rayado, and Alfaro-Almajano recommend a Mediterranean diet for patients with chronic pancreatitis for the high amount of fruits, legumes, nuts, cereals, fish, and unsaturated fats that are consumed.9 They also state the importance of polyphenols, which may help reduce inflammation and manage reactive oxygen species and immunomodulation. However, they do note that evidence for this is limited.9 Initiation of fat-soluble vitamins should begin in EPI patients when PERT is started. Monitoring of levels should be done annually and every three to six months after a change in vitamin therapy.6 Water-electrolyte and acid-base balance disturbances may occur with acute pancreatitis as well and many therefore have vitamin and micronutrient deficiencies.9
Some smaller studies have suggested a symbiotic relationship with the use of prebiotics and probiotics in those with acute pancreatitis. Development of systemic inflammatory response syndrome, organ failure, infected necrosis, and surgical interventions decreased but results were not significant. 28 There is also an increased risk of vitamin B12 and zinc deficiencies with a pancreaticoduodenectomy.9
Pancreatic Enzyme Replacement Therapy
PERT is necessary for those with EPI as it allows for the appropriate absorption of nutrients. These replacement enzymes are available in capsules and the number after the enzyme name corresponds to the number of lipase units per capsule in 1,000s.6 The FDA has approved Creon, Zenpep, Pancreaze, Pertzye, and Viokase as PERT.22 These enzymes can’t be exposed to heat as this can reduce their effectiveness. They should also be taken during or just after a meal. Dosing of PERT is based on body weight, fat content of meals, or pancreatic lipase output; it’s also based on age and weight per Whitcomb et al.6,22 PERT should begin when there are clinical signs indicating a need, such as weight loss or biochemical markers of malnutrition. FE-1 can also be used as an indication.9 PERT may be indicated in those with abnormal fecal fat excretion, steatorrhea, and/or weight loss.5 The capsules are covered enterically to resist stomach acid and microspheres are released when the pH is over 5.5 in the duodenal lumen. When PERT is taken during or after meals this allows for a better distribution of chyme in the stomach.9 The recommended dose of PERT is 40,000 to 50,000 units with each meal and 25,000 units with snacks.9 A decrease in fecal fat excretion, fecal weight, and abdominal pain with no major side effects has been shown with PERT in a meta-analysis.9 There is no maximum dose.9 Patients with chronic pancreatitis and PERT have been found to have higher levels of vitamin A and prealbumin.9 FE-1 can’t be used to determine a response to PERT because it doesn’t change the intrinsic elastase formed by the patient. However, the C-mixed-triglyceride breath test which measures pancreatic lipase through the carbon dioxide in exhaled air and coefficient fat absorption (also known as the fecal fat test) can be used but are not typically available.9
If initial response to PERT is insufficient, a proton pump inhibitor (PPI) can be added to reduce gastric acidity and to ensure that enzyme release is occurring appropriately within the duodenal lumen. However, some studies have not demonstrated any benefit to using a PPI.9 Another option is to increase the PERT dose as the physiological secretion is much higher and the dose required may be higher. PERT in pancreatic cancer patients has been associated with improved survival and nutritional status. It is also routinely recommended in patients after pancreatic resection.9 PERT has been demonstrated to be effective in treating malabsorption, improving nutritional status, and BMI in those who’ve had pancreatic resections and gastrointestinal surgeries.29 Administration of PERT in EN has not been demonstrated to be effective or safe. The only FDA-approved PERT for patients requiring EN is RELiZORB, which is a cartridge filled with lipase covalently bound to small beads. This connects with EN feeding pumps to hydrolyze fat in the formula.30
Putting It Into Practice
EPI is a complex condition that is the result of many metabolic disturbances. It is typically multifactorial and its treatment plan should be individualized. RDNs play an important role in assessing the nutrition status of patients with EPI and closely monitoring their macronutrient and micronutrient needs. Additionally, many of these patients may need nutrition support that requires the expertise of an RDN. The nutrient needs of these patients may be especially complex and RDNs can advocate for best route of administration, in addition to the appropriate nutrition prescription. RDNs can also work with providers to ensure that patients are receiving appropriate supplementation, as well as PERT as indicated. PERT administration is given surrounding meal times, so RDNs can assist with creating a plan for this as well.
— Lauren Botelho, MS, RD, LDN, is a dietitian in the Boston area. Botelho has worked in inpatient settings, outpatient settings, and long term care. She has a BFA in writing, literature, and publishing and is a freelance nutrition writer. Additionally, Botelho recently became a family nurse practitioner and plans to specialize in gastroenterology.
Learning Objectives
After completing this continuing education course, nutrition professionals should be better able to:
1. Explain the etiology and describe common disease states causing pancreatic insufficiency.
2. Identify specific macronutrients and micronutrients of concern for patients with pancreatic insufficiency.
3. Provide MNT for patients with pancreatic insufficiency, utilizing best practices and recommendations to include supplements when appropriate.
Examination
1. Which macronutrient is of most concern in terms of malabsorption in patients with exocrine pancreatic insufficiency (EPI)?
a. Fat
b. Carbohydrate
c. Protein
d. Fiber
2. Which diagnostic test is most widely used/available for diagnosing EPI?
a. Secretin quantification
b. Fecal elastase
c. Cholecystokinin quantification
d. 72-hour fecal fat test
3. What disease is EPI most commonly associated with?
a. Acute pancreatitis
b. Cystic fibrosis
c. Pancreatic cancer
d. Chronic pancreatitis
4. Which vitamin deficiency associated with EPI can lead to night blindness?
a. Vitamin B1
b. Vitamin A
c. Folic acid
d. Vitamin C
5. Which nutrient may need to be adjusted or lowered in the diets of patients on pancreatic enzyme replacement therapy (PERT)?
a. Fiber
b. Carbohydrate
c. Protein
d. Vitamin A
6. How often should levels of fat-soluble vitamins be checked in those who have EPI and require supplementation?
a. Annually and every three to six months following any change in supplementation
b. Every two years
c. Every month after a change in supplementation
d. None is indicated after initial labs are done
7. How should PERT be taken to be most effective?
a. Two hours after meals
b. At meal/snack times
c. Four hours after meals/snacks
d. Two hours before meals
8. Which type of nutrition support is typically recommended/tolerated in those with chronic/acute pancreatitis and EPI?
a. Elemental enteral nutrition
b. Semielemental enteral nutrition
c. Polymeric enteral nutrition
d. Parenteral nutrition
9. Patients with acute pancreatitis generally need a minimum of how much protein intake daily?
a. 1.2 g/kg/day
b. 2 g/kg/day
c. 1 g/kg/day
d. 0.8 g/kg/day
10. What is an additional recommendation for patients with chronic pancreatitis and EPI?
a. Increase fiber intake
b. Limit fat intake
c. Limit protein intake
d. Avoid alcohol
References
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