The article "The pancreas--hermit of the abdomen" is the basis for this AORN Journal independent study. The behavioral objectives and examination for this program were prepared by Rebecca Holm, RN, MSN, CNOR, clinical editor, with consultation from Susan Bakewell, RN, MS, education program professional, Center for Perioperative Education.
A minimum score of 70% on the multiple-choice examination is necessary to earn 3 contact hours for this independent study. Participants receive feedback on incorrect answers. Each applicant who successfully completes this study will receive a certificate of completion. The deadline for submitting this study is June 30, 2005.
Send the completed application form, multiple-choice examination, learner evaluation, and appropriate fee to
or fax the information with a credit card number to (303) 750-3212.
After reading and studying the article on the pancreas, the nurse will be able to
(1) describe the historical background of pancreatic research in regard to the role of the pancreas,
(2) identify the stages of pancreatic development,
(3) explain the link between the pancreas and cystic fibrosis,
(4) discuss pancreatitis, and
(5) define pancreatic cancer.
This program meets criteria for CNOR and CRNFA recertification, as well as other continuing education requirements.
The Pancreas--Hermit of the Abdomen
The word pancreas comes from the Greek word meaning "all flesh." It is a long racemose (ie, resembling a cluster of grapes) gland situated behind the stomach, stretching from the duodenum to the spleen. (1) The pancreas has been described as the hermit or hidden organ of the abdomen because it is located in the retroperitoneal space behind the peritoneum. (2) Its location makes it virtually impossible to palpate; therefore, life-threatening lesions often are not detected until they begin to encroach on other structures, such as the intestines or vertebral column. Additionally, the pancreas has a large endocrine and exocrine reserve so signs and symptoms of disease may not become apparent until they are very advanced. (3)
The existence of the pancreas first was noted in the Talmud (ie, writings on Jewish law and traditions) between 200 BC and 200 AD, where it was described as the "finger of the liver." The following famous anatomists identified and described pancreatic anatomy and physiology.
* Johann Wirsung of Italy identified the pancreatic duct in 1642.
* In 1720, Abraham Vater of Germany described the papilla of Vater, a small nipple-like protuberance, commonly but inaccurately called the ampulla, where the pancreatic and common bile ducts enter the duodenum.
* Giovanni Santorini of Italy described the pancreatic accessory duct in 1724.
* In 1850, Claude Bernard of France suggested the pancreas may have a role in digestion.
* Rugerio Oddi of Italy described the sphincter bearing his name in 1869.
* Paul Langerhans of Germany established the pancreas' connection with diabetes in 1890.
Allan O. Whipple, MD, was a professor of surgery at Columbia University, New York, when he pioneered pancreatic surgery in the 1930s. In the 1970s, endoscopic retrograde cholangiopancreatography (ERCP), angiography, computed tomography (CT) scans, ultrasound, and magnetic resonance imaging clearly identified the pancreas, negating the long-held nickname "hermit of the abdomen." (4)
EMBRYOLOGY AND ANOMALIES OF THE PANCREAS
The pancreas begins to sprout from the ventral and dorsal buds at approximately the fifth week of gestation. The ventral and dorsal buds emerge from the beginning of the duodenum or foregut, which is the embryonic organ from which the pharynx, esophagus, stomach, duodenum, liver, pancreas, biliary apparatus, and lower respiratory system arise. (5) Each bud has its own duct. At approximately the seventh week of gestation, the ventral and dorsal buds fuse. (6) The dorsal bud forms the superior part of the pancreas' head, body, and tail. The ventral bud gives rise to the inferior part of the pancreas' head. As the buds fuse, their ducts anastomose. The ventral duct and distal dorsal duct become the main pancreatic duct (ie, the duct of Wirsung), which drains into the duodenum at the papilla of Vater. The proximal part of the dorsal duct may atrophy or persist as an accessory duct (ie, the duct of Santorini), which drains into the duodenum slightly above the main duct. Failure to recognize such aberrant ductal anatomy may lead to potential ligation of ducts during surgery. (7) Figure 1 shows the stages of pancreatic embryonic development.
[FIGURE 1 OMITTED]
In approximately 6% of people, the ducts fail to fuse, giving rise to pancreas divisum (ie, functional division of the pancreas). With pancreas divisum, the duct of Wirsung is short and drains only a small portion of the pancreas, and the duct of Santorini drains the majority of the pancreas. This anatomic variant is associated with recurrent pancreatitis. (8) During an ERCP, patients suffering from pancreas divisum may complain of severe pain when the dye enters the short duct of Wirsung. (9) Prescribed pain medications should be administered promptly.
In approximately two-thirds of people with pancreas divisum, the duct of Wirsung empties into the common bile duct, resulting in a common channel. Gall stones may lodge at the intersection, causing obstruction to the flow of pancreatic juices or bile. Obstruction of the common channel may cause reflux of pancreatic juices or bile into the duct of Wirsung. Reflux may cause potential premature activation of pancreatic enzymes, leading to pancreatitis. (10)
Improper fusion of the pancreatic buds may cause a ring-like portion of the pancreas to encircle the duodenum. This anomaly, known as an anulur pancreas, may cause duodenal obstruction at birth or later in life and also may be associated with pancreatitis, peptic ulcers, or malignant disease in adults. (11)
Accessory or ectopic pancreatic tissue may locate in the wall of the stomach, the duodenum, or an ileal (ie, Meckel's) diverticulum. Accessory pancreatic tissue may cause pain from localized inflammation or bleeding. Two percent of islet tumors arise in ectopic pancreatic tissue. (12)
The pancreas may be absent (ie, agenesis). This usually is associated with additional severe malformations that are incompatible with life. (13)
Histogenesis (ie, germ layer tissue differentiation). The endoderm (ie, inner germ layer) of the pancreatic buds forms a network of tubules (ie, primitive ducts) from which the parenchyma (ie, functional element of an organ as contrasted with its framework) develops. Acini (ie, secretory cells resembling grape clusters) develop at the ends of the tubules early in the fetal period. The islets of Langherhan develop from cells that separate from the tubules and lie between the acini. The islets begin to secrete insulin at approximately 10 weeks gestation. Glucagon secretion has been detected as early as 15 weeks. When maternal diabetes exists, the insulin secreting beta cells of the fetus are chronically exposed to high levels of glucose, which causes them to hypertrophy to produce needed insulin. (14) Exposure to hyperglycemia and hyperinsulinemia may accelerate growth in the fetus. Such neonates often are large for their gestational age, creating delivery problems. They also may have multiple body system abnormalities. Hypoglycemia must be anticipated after birth because the maternal source of glucose is removed, and the pancreas continues to produce excess insulin. (15)
Histology (ie, microanatomy) of the pancreas. The pancreas actually is two organs in one. It functions as an endocrine and exocrine organ. (16) The endocrine cells reside in the islets of Langherhan, and the main cells are named alpha, beta, delta, and F cells. (17) Two other minor endocrine cell types (ie, DI, enterochromaffin) also exist. (18) The exocrine secretions are produced by the acini cells.
Alpha cells. Alpha cells produce glucagon, which maintains normoglycemia through the processes of glycogenolysis (ie, breakdown of glycogen) and gluconeogenesis (ie, formation of glycogen from noncarbohydrates such as fats and proteins). (19) Hyperglycemia lowers plasma glucagon levels, and hypoglycemia elevates plasma glucagon levels. Hyperglycemia also is stimulated by ingestion of proteins and stressors, such as infection, burns, tissue infarction, and major surgery. (20) Alpha cell tumors (ie, glucagonomas) produce high levels of glucagon. Such tumors are characterized by mild diabetes mellitus, migratory necrotizing skin erythemia, and anemia. They occur most often in perimenopausal and postmenopausal women. (21)
Beta cells. Beta cells produce insulin, which affects carbohydrate, protein, and fat metabolism. Insulin binds with cell receptors, increasing the cell receptors' permeability to glucose, amino acids, potassium, magnesium, and phosphate ions. (22) Insulin does not enhance glucose transport in the brain, erythrocytes, leukocytes, intestinal mucosa, or epithelium of the kidneys. (23) Insulin assists in the formation of new proteins and in the activity of intracellular enzymes. Diabetic patients who lack sufficient insulin suffer from depleted protein, decreased glucose in muscle cells, hyperglycemia, and abnormal release of stored body fat as the body shifts from carbohydrate to fat metabolism. Fat is deposited in arterial walls causing arterial disease. Fat metabolism also results in ketone formation, which if untreated, results in ketoacidosis and acidotic coma. (24)
Insulin has an antilipolytic effect on adipose cells, which contributes to fat storage. (25) Hyperinsulinemia is responsible for upper body obesity, glucose intolerance, hypertriglyceridemia, and hypertension, better known as the "deadly quartet." Upper body obesity (ie, android obesity) is a predictor of cardiovascular disease. Lower body obesity (ie, gynecoid obesity), though an overall health risk, is not considered a cardiovascular risk factor. This theory is based on android fat being more metabolically active than gynecoid fat. This increase in metabolism produces an increase in free fatty acids (FFA), which prevents hepatic clearance of insulin resulting in hyperinsulinemia. (26) Beta cell tumors (ie, insulinomas) produce a clinical triad of
* hypoglycemia with blood sugar levels below 50 mg per dL;
* central nervous system manifestations, such as confusion, stupor, and loss of consciousness related to fasting and exercise; and
* attacks relieved by feeding the patient or administering glucose.
Five percent of insulinomas are malignant. (27)
Delta cells. The delta cells secrete somatostatin, which performs many inhibitory functions, such as inhibition of growth hormone, thyroid stimulating hormone, insulin, glucagon, and various gastrointestinal (GI) hormones. It also inhibits secretion of somatostatin from acinar cells. (28) Nurses often administer octreotide acetate (ie, synthetic analogue of somatostatin) to treat the severe diarrhea and flushing that occurs in patients with GI endocrine tumors, such as the vasoactive intestinal polypeptide (VIP) tumor (ie, vipoma). Octreotide also is given to decrease growth hormone secretion in acromegaly. (29) Delta cell tumors (ie, somatostatinomas) produce high levels of somatostatin. These tumors are associated with diabetes mellitus, cholelithiasis, steatorrhea, and hypochlorhydria. (30)
F cells. The F cells secrete pancreatic polypeptide, which is released after meals in response to vagal and cholecystokinin-pancreozymin (CCK-PZ) stimulation. (31) Pancreatic polypeptide is believed to be involved in exocrine pancreatic secretion and gall-bladder emptying. (32) Elevated levels of pancreatic polypeptide serve as markers for islet cell tumors and as a measure of the tumor's response to treatment. (33)
DI cells. The DI cells produce VIP, which induces glycogenolysis and hyperglycemia. Additionally, VIP stimulates GI fluid secretion resulting in watery diarrhea. (34)
Enterochromaffin cells. Enterochromaffin cells synthesize serotonin, which results in carcinoid syndrome. (35) The features of carcinoid syndrome include
* asthmatic attacks;
* intestinal hypermotility (ie, diarrhea, vomiting, cramps);
* tachycardia; and
* vasomotor disturbances, such as skin flushes.
Hypoproteinemia and pellagra are caused when tryptophan (ie, an essential amino acid) is used for serotonin production instead of for protein and niacin synthesis. A high protein diet, niacinamide, and a serotonin-antagonist medication are recommended therapies. (36)
Other islet cells. Zollinger-Ellison syndrome (ie, gastrinoma) is a noninsulin secreting islet-cell tumor of the pancreas. (37) It produces excessive gastrin, resulting in disproportionate amounts of hydrochloric acid and pepsin leading to severe peptic ulcer disease. Islet cell tumors also may produce adrenocorticotrophin hormone, melanocyte-stimulating hormone, antidiuretic hormone, norepinephrine, and serotonin. (38) More than one-half of all gastrinomas are malignant with multiple lesions, making their discovery difficult during surgical exploration. Treatment is a total gastrectomy and removal of the islet tumor. (39)
Acini. Acini cells produce the exocrine secretions of the pancreas (Figure 2). Acini cells are organized in lobules separated by thin septa. Clusters of acini cells are drained by intercalated (ie, inserted between) ducts that empty into intralobular ducts. The intralobular ducts drain to extralobular ducts that ultimately drain into the main pancreatic duct entering the duodenum along with the common bile duct (Figure 3). (40)
[FIGURE 2-3 OMITTED]
Pancreatic juice, an exocrine secretion, is vital for digestion. Pancreatic juice consists of aqueous and enzyme components. (41) The aqueous component consists of a daily output of 1,500 mL to 3,000 mL of clear, colorless fluid with a pH of 8.3. Its ionic composition is sodium, potassium, bicarbonate, chloride, and small amounts of phosphate, sulfate, zinc, and calcium. Its main function is to adjust the pH of the duodenal contents to provide optimal activity of pancreatic enzymes. (42) The enzyme component of pancreatic juice consists of proteases, amylases, and lipases that break down proteins, starches, and fats respectively. The proteases are secreted in forms of zymogen (ie, inactive precursor to enzyme), such as trypsinogen, chymotrypsinogen, and procarboxypeptidase. A trypsin inhibitor present in pancreatic juice keeps the proteases inactive to prevent hydrolysis of pancreatic tissue. As trypsinogen is secreted into the duodenum, it is changed into trypsin by enterokinase. Trypsin then activates chymotrypsinogen and procarboxypeptidase. (43) Protein breakdown normally begins in the duodenum when the protein encounters these activated enzymes. Pancreatic juice secretion occurs in three phases: cephalic, gastric, and intestinal.
Cephalic phase. The cephalic phase of pancreatic juice secretion is stimulated by the sight, smell, taste, or thought of food. The greater the person's appetite, the more intense the stimulation. (44) This phase is called cephalic because the nerve impulses initiating it are located in the head. These nerve impulses stimulate branches of the vagus (ie, parasympathetic) nerve, which promotes secretion of gastrin from the gastric antrum. Gastrin causes the parietal cells to produce stomach acid and initiates enzyme secretion in the pancreas. (45) Based on this information, nurses ensure that patients receive appetizing food that is arranged attractively to enhance the cephalic phase of pancreatic secretion. (46)
Gastric phase. During the gastric phase of pancreatic juice secretion, gastrin continues to be released in response to stomach distension and the presence of amino acids in the stomach. This continues to stimulate pancreatic juice secretion. Distension of the gastric antrum and fundus causes vagal stimulation, which results in the release of small amounts of pancreatic juice high in enzyme content. (47)
Intestinal phase. The intestinal phase of pancreatic juice secretion begins with the arrival of acid chyme (ie, partially digested food from stomach) into the duodenum. The acid chyme stimulates the release of secretin and CCK-PZ in the small intestine. Secretin stimulates the pancreas to release copious amounts of bicarbonate and water. In response to the presence of fats and partially digested proteins in the duodenum, CCK-PZ is released to stimulate a large increase in pancreatic enzyme secretion. (48) Secretory activity also is controlled by substances released from nerve terminals. Stimulation of vagal branches enhances the release of enzymes and aqueous components. Activation of sympathetic fibers inhibits pancreatic secretion. (49) Nurses must understand the mechanisms underlying pancreatic juice secretion if they are to understand the factors that may cause pancreatic disease or increase pain when the pancreas is damaged. Figure 4 summarizes the events that trigger pancreatic juice secretion.
[FIGURE 4 OMITTED]
DISORDERS OF THE EXOCRINE PANCREAS
There are several disorders of the exocrine pancreas. These include cystic fibrosis, pancreatitis, and pancreatic cancer.
Cystic fibrosis. Cystic fibrosis (CF), formerly referred to as mucoviscidosis or fibrocystic disease of the pancreas, is a multisystem disorder prevalent in infants, adolescents, and young adults. It is characterized by alterations in exocrine glands (eg, mucus-producing glands, sweat glands). These alterations result in pulmonary disease, pancreatic insufficiency, and elevated sweat electrolytes. Historical notes recount midwives licking the foreheads of newborns to detect a salty taste as an indicator of the disease. The pilocarpine iontophoresis sweat test is the simplest and most reliable method to confirm the diagnosis. Cystic fibrosis results when a gene on chromosome 7q31 mutates. (50) This causes a defect in chloride transport, which leads to decreased reabsorption of sodium chloride (NaCl) in sweat glands and thus increased NaCl in sweat. There also is decreased chloride secretion into the airways and increased sodium and water reabsorption from the airway lumens. Both of these ion changes result in water reabsorption from the airways and dehydration of mucus membranes. Dehydrated mucus membranes cause defective mucociliary action and viscous secretions that obstruct airway passages and predispose patients to recurrent pulmonary infections. Depending on the severity of the mutation, pancreatic and salivary ducts and bile canaliculi (ie, tiny ducts) may become obstructed with mucus. In the past, most people with CF died young. With improved control of infections, many people with CF now survive into adulthood. Currently, the median life expectancy of a person with CF is approximately 26 years. (51)
Pancreatitis. Pancreatitis is an acute or chronic inflammation of the pancreas characterized by varying degrees of edema, hemorrhage, and necrosis of the acini. Progressive destruction of the gland may occur with fibrosis, stricture, and calcification. (52) Pancreatitis affects all age groups with unpredictable severity. Most afflicted people have mild to moderate abdominal pain, which subsides in a few days. In 20% to 30% of people, attacks are very severe with multiple organ failure and significant morbidity and mortality. There is almost universal agreement that the pathological mechanism in pancreatitis is autodigestion (ie, self-digestion). (53) How this process occurs is unclear; however, it is believed that something activates the zymogens while they are still in the pancreas. Trypsinogen is converted to trypsin, which then activates other enzymes prematurely, leading to autodigestion. Two other enzymes believed to be directly responsible for autodigestion are elastase and phospholipase A. Elastase digests the elastic tissue of blood vessel walls, leading to hemorrhage. Phospholipase A digests the phospholipids of cell membranes. Trypsin also activates kallikrein, which causes vasodilation, increased vascular permeability, invasion of white blood cells, and pain. (54)
Cause of pancreatitis. The cause of pancreatitis is multifactorial. The two most common theories of causation are alcoholism in men and biliary tract disease in women.
Alcoholic pancreatitis is believed to result from the inflammatory effects of alcohol on the pancreas and its ducts. Supporting this belief is the "aftershave lotion theory." This theory is named such because aftershave, which contains alcohol, smarts when it enters the eye. Alcohol, therefore, can be expected to have a similar irritating effect on the sphincter of Oddi, potentially causing spasm of that muscle and obstructing the flow of secretions. (55)
The inflammatory effects of alcohol damage acini, which changes secretory function and increases enzyme and protein production. (56) Secretions become viscous and inspissated (ie, glutinous and thickened by evaporation or absorption), and calcium carbonate precipitates, which results in ductal stone formation. (57) This leads to obstruction of secretions and degeneration and fibrosis of acini cells. (58) Alcohol also may decrease sphincter of Oddi tone, causing duodenal reflux and premature activation of enzymes. (59) There is no evidence, however, that a single drinking bout in an otherwise abstemious person will lead to pancreatitis. (60) Researchers believe that it takes five to 10 years of drinking several pints of whiskey or equivalent alcoholic beverages per day to cause pancreatitis. (61) Acinar cell injury also can be caused by viruses, endotoxins, ischemia, and trauma. These agents are thought to activate pancreatic enzymes prematurely, thus initiating pancreatic autodigestion. (62)
Obstruction of biliary ducts, as with gallstones, can lead to increased pressure and rupture of the pancreatic duct or reflux of bile and duodenal contents into the pancreas, leading to premature activation of enzymes and autodigestion. (63) This could occur in a person who has a common channel as in pancreas divisum. (64) The same concept of bile activating the enzymes prematurely occurs in women with gallbladder disease. A stone leaves the gallbladder, travels down the common bile duct (CBD), and becomes lodged in the main pancreatic duct outlet. The bile backs up in the CBD and enters the duct of Wirsung, activating the proteases, which then start to digest the pancreas.
Hyperlipidemia and hypercalcemia are additional causes of pancreatitis. Hyperlipidemia, resulting from lipolysis of triglycerides by pancreatic lipase, leads to high concentrations of FFA, which can initiate pancreatic injury. Hypercalcemia occurs with parathyroid adenomas and carcinomas. Hypercalcemia increases calcium, which is believed to activate trypsinogen.
Acute pancreatitis is a recognized complication of sphincter of Oddi manometry, as well as diagnostic and therapeutic ERCP. (65) Pancreatitis may be inherited as an autosomal dominant trait. Patients with hereditary pancreatitis are advised to refrain from smoking or drinking alcohol because these behaviors put them at risk for pancreatic cancer. (66) Table 1 lists conditions associated with acute pancreatitis.
Manifestations of pancreatitis. Manifestations vary greatly depending on the severity of the attack. Some patients may be almost asymptomatic, and others may be in extreme distress with multiple organ failure and death ensuing. (67) Alcohol-related pancreatitis (ie, abdominal pain after an episode of inebriation) or gallstone-related pancreatitis (ie, abdominal pain after eating a heavy meal) often occurs. (68) Steady epigastrum or upper left quadrant pain is common. This pain is the result of edema of the pancreas, obstruction of the biliary tree, and release of pancreatic enzymes into surrounding tissue. (69) Acute pancreatitis is characterized as a severe chemical burn of the peritoneal cavity. (70) Pain may radiate to the patient's back and flank because the pancreas is located in the retroperitoneal space. Many patients mistake the sensation for orthopedic pain. (71) Patients often assume a position of comfort (eg, sitting with the spine flexed in a fetal position). Eating exacerbates the pain by stimulating secretion of prematurely activated enzymes, which promote autodigestion of the gland. Nausea and vomiting caused by hypermotility or paralytic ileus secondary to pancreatitis often occurs. After emesis there is an increase, not a decrease, in pain because retching increases intraductal pressure thus obstructing outflow of pancreatic secretions and producing further organ damage. (72)
Fever often is present and may be caused by peritonitis, cholangitis (ie, inflammation of the bile ducts), or intra-abdominal abscesses. (73) Pancreatic infection may occur via
* the biliary duct system,
* the circulatory system,
* lymphatics, and
* transmural migration of gram negative organisms from the GI tract through the colonic wall. (74)
Cardiovascular complications, such as hypotension and tachycardia, result from exudation of plasma into the retroperitoneal space, pancreatic hemorrhage, vasodilation from the release of kallikrein, and accumulation of fluid in the small bowel. These complications may lead to systemic hypotension and shock, resulting in acute tubular necrosis and myocardial and cerebral ischemia. Pulmonary complications, such as pleural effusion, result from retroperitoneal transudation of fluid from the swollen pancreas.
Hematocrit levels may elevate as a result of dehydration, or they may decrease as a result of pancreatic hemorrhage. (75) Lactic acidosis may result from hypovolemia or the ketosis that may occur with destruction of the pancreas (ie, loss of beta cells, lack of insulin). Release of necrotic tissue and enzymes into the blood stream results in altered coagulation processes. Hypercoagulation defects occur because of elevations of platelets, fibrinogen, and factor VIII. Disseminated intravascular coagulation (DIC) with consumption of clotting factors and formation of microthrombi may occur. Jaundice may be present because the swollen pancreatic head impinges on the common bile duct or it may be compressed by pseudocysts or stones. (76) Turner's sign (ie, discoloration of the flanks) or Cullen's sign (ie, blue-red discoloration around the umbilicus) represents extravasation (ie, leakage) of pancreatic exudate and destruction of hemoglobin. (77) In chronic pancreatitis, all the previously mentioned manifestations may be present in addition to greasy foul smelling stool caused by steatorrhea (ie, excess fat in the stool) and azotorrhea (ie, excess nitrogenous products in the stool). Poor absorption of nutrients, especially fat-soluble vitamins (ie, A, D, E, K), may lead to coagulopathy, night vision problems, and weight loss. (78) Prothrombin levels may be decreased due to trypsin activity or from decreased synthesis of vitamin K in the bowel, which is related to malabsorption of fats. (79)
Laboratory findings. Elevated serum lipase and amylase levels are instrumental in diagnosing acute pancreatitis. Lipase is more specific to the pancreas and may remain elevated for up to 14 days. Normal levels range from 32 U [dagger] per L to 80 U [dagger] per L. Amylase rises within 24 hours after the onset of symptoms, peaks in 20 to 30 hours, and returns to normal in three to five days. Normal levels are 35 U [dagger] per L to t 15 U [dagger] per L; however, levels can be misleading. Levels may be normal or decreased in the presence of pancreatitis if patients have diuresed after fluid challenges or diuretics because amylase is excreted by the kidneys. Similarly, they may be increased after administration of opiates and diagnostic dyes. (80) In addition to the pancreas, amylase is found in the salivary glands, fallopian tubes, small intestine, and lungs; therefore, increased amylase levels may suggest trauma, inflammation, or tumors in any of these areas. (81) Liver function tests, such as lactate dehydrogenase and aspartate aminotransferase, may be elevated in alcoholic liver disease and pancreatitis associated with cholelithiasis. Leukocytosis occurs in 80% of patients with pancreatitis as a result of the inflammatory process. (82) Hyperglycemia may occur as a result of decreased insulin from damaged beta cells and increased glucocorticoids and catecholamines. (83)
Hypocalcemia may occur from lipolysis of tissues with the release of FFA. These fatty acids combine with calcium to form soaps in the retroperitoneal space. The parathyroid glands do not respond to decreasing calcium levels caused by the mechanism of soap formation, so hypocalcemia (ie, tetany) may occur. (84) Hypocalcemia also may be caused by hypoalbuminemia. (85) Most calcium is bound to albumin, so hypoalbuminemia occurs with third spacing of fluid in the retroperitoneal space. Albumin also may be decreased due to increased capillary permeability and leakage in surrounding tissues. (86)
Hypomagnesemia is common in patients with alcoholic pancreatitis. Magnesium is sequestered in the retroperitoneal space during fat necrosis.
Hyperkalemia may occur and is related to tissue necrosis, metabolic acidosis, and renal failure. Tissue necrosis results in potassium leaving the cell. Metabolic acidosis occurs as hydrogen ions move into the cell and potassium moves into the blood as the body attempts to compensate. Renal failure occurs as the kidneys fail to excrete the excess potassium. (87)
Imaging studies. Plain abdominal radiographs may reveal an ileus pattern or sentinel loop (ie, distended loop of small bowel in the area of the pancreas). An ultrasound displays the gallbladder, pancreas, common bile duct, and other abdominal structures. The pancreas, along with edema, cysts, and abscesses, is shown in detail by CT scan. (88) An ERCP can reveal dilated pancreatic ducts with areas of stricture, often referred to as the "chain of lakes" or "string of pearls" appearance. This is found in patients with chronic pancreatitis. (89)
Prognosis. Grading systems have been developed to predict the outcome of patients with severe pancreatitis. These systems use clinical assessments and biochemical measurements to determine severity. Based on severity, as determined by a large number of risk factors, certain patients may warrant monitoring in an intensive care setting. (90) Two commonly used grading systems are the acute physiology and chronic health evaluation (APACHE) scoring system and Ranson's Early prognostic signs. (91)
The APACHE uses the worst of 12 physiological variables plus age and previous health status to provide a measure of disease severity. The physiological variables of the APACHE scoring system include
* arterial oxygenation,
* arterial pH,
* heart rate,
* mean arterial pressure,
* respiratory rate,
* serum sodium,
* the Glascow coma scale, and
* white blood cells.
Each physiological variable is assigned a weighted score of zero to four. Points also are assigned for age on a scale of zero to six. Additionally, chronic health points are assigned for severe organ system (ie, hepatic, cardiovascular, pulmonary, renal, immune) dysfunction. Five points are allotted for organ system dysfunction in nonsurgical or emergency postoperative patients and two points for elective postoperative patients. The higher the total computed score (ie, zero to 71), the more ill the patient. The APACHE provides a good indication of illness severity and has an excellent correlation with outcome. (92)
Ranson's early prognostic signs are the most widely used and provide an excellent yardstick for grading severity (Table 2). Mortality is related to the number of signs present. Patients with fewer than three signs have a 1% mortality rate, patients with three to four signs have a 15% to 20% mortality rate, and patients with five to six signs have a 40% mortality rate. Patients with more than six signs have a 100% mortality rate. (93)
Obesity is a negative prognostic indicator for acute pancreatitis. Fat deposits in the pancreas and retroperitoneal spaces increase the risk of fat necrosis and early and extra pancreatic complications. Truncal adiposity is related to the worst clinical course of pancreatitis. (94)
Medical and nursing collaborative management. Management of pancreatitis consists of removing the cause, if possible, supporting patients, and preventing and treating complications. Nurses perform an assessment to explore the patient's family history of pancreatitis and history of
* abdominal trauma,
* alcohol intake,
* connective tissue and parathyroid disease,
* diagnostic procedures,
* diseases of the biliary tract,
* exposure to drugs and medications and toxic substances (eg, organophosphorus insecticides that cause cholinergic overstimulation of the pancreas),
* infections (eg, mumps), and
* peptic ulcers. (95)
Nurses also assess for possible precipitating factors (eg, food intake) as well as observing for behaviors that lessen pain (eg, fetal position).
A cholecystectomy may be necessary if the cause is biliary tract disease, otherwise medical treatment is indicated. (96) Nursing interventions and care concentrate on relief of pain. Nurses assess the severity of the patient's pain on a zero to 10 pain scale and ensure that all prescribed medications are administered in a timely fashion.
Fentanyl citrate is preferred to morphine because morphine can cause spasm of the sphincter of Oddi, which increases bile obstruction and stasis. (97) Meperidine or pentazocine are recommended by some physicians. (98) Others view meperidine as inappropriate because the metabolite if meperidine, normeperidine, causes analeptic activity (ie, central nervous system stimulation). (99)
Shock is the leading cause of death in patients with pancreatitis; therefore, nursing interventions focus on shock prevention. (100) Nurses frequently measure the patient's vital signs, central venous pressure, urine output, and intravascular volume replacement (eg, crystalloid solutions, blood, albumin). Some authorities favor fresh frozen plasma, which contains trypsin inhibitors, to correct the hypoalbuminemia. (101)
Nurses monitor and report abnormalities in the patient's electrolyte profiles, particularly potassium, magnesium, and calcium levels, and watch for electrocardiogram abnormalities. They also monitor closely for signs of tetany, including
* a positive Trousseau's sign (ie, spasm of hand after inflation of blood pressure cuff),
* carpopedal (ie, hands and feet) spasm,
* Chvostek's sign (ie, tapping of cheek evokes a spasm), and
* paresthesias (ie, numbness and tingling) of fingers and around the oral cavity. (102)
Nurses administer potassium, magnesium, and calcium gluconate if serum levels are low. Sodium bicarbonate may be ordered if metabolic acidosis occurs. Nurses monitor blood sugar levels according to facility protocol and administer insulin, if needed, to control hyperglycemia.
Nurses assess for abnormal lung sounds, such as crackles, wheezes, or decreased breath sounds. Pulse oximetry and arterial blood gases are monitored, and respiratory support, such as oxygen, is provided if necessary. Patients may experience acute respiratory distress syndrome (ARDS), which is an acute form of pulmonary edema caused by disruption of the alveolar-capillary membrane and is a severe complication of pancreatitis. (103) If ARDS occurs, intubation and mechanical ventilation with positive end expiratory pressure may be ordered. (104) Physicians may require that patients remain NPO ,if oral feedings are tolerated poorly. An acute pancreatitis attack may produce a hypermetabolic state, which necessitates total parenteral nutrition. Gastrointestinal decompression by nasogastric (NG) tube reduces vomiting and decreases pancreatic inflammation and secretions by preventing antral distension and limiting duodenal acidification. (105) Nurses frequently check the patient's nares for any indication of pressure from the NG tube, which may cause necrosis.
Anticholinergics, such as atropine or propantheline, may be ordered to decrease vagal stimulation, pancreatic secretion, and ampullary spasm. Histamine receptor antagonists, such as cimetidine, may be ordered to decrease hydrochloric acid production and thus decrease pancreatic secretions. Aluminum-magnesium antacids, such as magaldrate, also may be ordered. (106) Octreotide acetate may be ordered to suppress GI hormones that stimulate pancreatic secretion. It also acts on acinar receptors to inhibit their secretions. (107)
Controversy exists regarding the value of administering prophylactic antibiotics because the pancreas has a barrier similar to the blood-brain barrier. This barrier allows selective uptake of certain antibiotics, although antibiotics will be administered if secondary infections develop, for example, the fluoroquinolones (eg, ciprofloxcin) and imipenem/cilastatin have high pancreatic concentrations, but the aminoglycosides are unable to penetrate the pancreatic barrier in bacteriocidal concentrations. (108) Most pathogens responsible for pancreatic infections are gastrointestinal gram-negative because of the possible pathways for pancreatic infections. A meta analysis of data from a number of studies shows that mortality was significantly reduced in patients given broad spectrum antibiotics, such as ciprofloxin and imipenem/cilastin; thus, current evidence suggests that antibiotics should be administered to patients with severe pancreatitis. (109)
Nurses monitor the patient closely for bruising and bleeding because of the risk for bleeding and DIC. Stools are examined for melena (ie, dark tarry stools) and occult blood. Nurses also observe for hematuria and monitor the patient's platelet count, prothrombin time, and activated partial thromboplastin time. (110) They perform all injections, whether for administering medications or drawing blood samples, with a small bore needle and apply extra pressure, as needed, to control bleeding.
Pancrelipase may be ordered to replace enzymes if the patient suffers from pancreatic insufficiency. Pancrelipase has lipolytic, amylolytic, and proteolytic activity, which improves the digestion of fats, carbohydrates, and proteins respectively in the GI tract. (111)
Development of a pseudocyst is a very severe complication of pancreatitis. A pseudocyst is an encapsulated sac-like structure that forms on or around the pancreas and lacks the epithelial lining of a true cyst. It may contain several liters of pancreatic enzymatic exudate (ie, straw-colored or dark-brown viscous fluid). It may present as an epigastric mass, epigastric pain radiating to the back, abdominal fullness, nausea, vomiting, or jaundice. A pseudocyst may resolve spontaneously, or it may rupture and hemorrhage. (112) A large pseudocyst that ruptures, becomes infected, or hemorrhages requires drainage of the cyst cavity. A soft sump tube with multiple openings is inserted through a stab wound. The sump tube contains three lumens--one to vent air, one for infusion of irrigating solution, and one for drainage of debris. The cyst is first drained and then irrigated with normal saline or lactated Ringer's solution approximately 12 hours later. The amount of fluid drained should equal or exceed the amount instilled. The irrigation continues until a CT scan reveals pancreatic healing. (113) Figure 5 shows a pancreatic sump tube in place.
[FIGURE 5 OMITTED]
Pancreatic cancer. Cancer of the pancreas is one of the major cancers of the industrial world and the fifth leading cause of cancer death. (114) The occurrence of pancreatic cancer is high in the United States, Europe, and Polynesia. The highest incidence occurs in New Zealand Maoris, native Hawaiians, and African Americans. The lowest incidences are found in India and Nigeria. Pancreatic cancer occurs most often in the seventh and eighth decades of life, with a slightly higher incidence in males. African American men have one of the highest risks in the world for pancreatic cancer. The most significant risk factor is cigarette smoking. Other risk factors include use of alcohol, use of coffee, and poor diet. (115) There is a positive correlation between mortality from pancreatic cancer and per capita consumption of fats and meat. (116)
The role of the p53 suppressor gene in the development of pancreatic cancer is being explored. Suppressor genes exist in normal cells and function to control cell growth. When suppressor genes mutate, the normal constraints on cell growth are removed, and uncontrolled growth results. (117) One-half of all people with pancreatic cancer harbor p53 mutations. (118) Pancreatic cancer has a deceptively silent growth habit so that by the time it is diagnosed, the cure rate is extremely low. (119) The major symptoms are weight loss, abdominal pain, back pain, vomiting, malaise, and weakness. Jaundice also may be present. Migratory thrombophlebitis (eg, Trousseau's syndrome) occurs in 10% of people with pancreatic cancer. Trousseau diagnosed his own fatal tumor as cancer of the pancreas when he developed spontaneously appearing and disappearing thromboses. This phenomenon is attributed to platelet-aggregating factors and procoagulants from the tumor or its necrotic products. (120) Pancreaticoduodenectomy (ie, Whipple procedure) is a radical pancreatic cancer procedure (Figure 6). It consists of resecting the proximal head of the pancreas, the adjoining duodenum, the distal portion of the stomach, and the distal segment of the common bile duct. This is followed by an anastomosis of the jejunum to the pancreatic duct, common bile duct, and stomach. Even with such radical surgery, the five-year survival rate is low. (121)
[FIGURE 6 OMITTED]
The pancreas really is two organs in one, and it functions as both an endocrine and exocrine organ. Its endocrine function is performed by the Islets of Langerhans, and its exocrine function occurs in the acini cells. The various forms of neoplasia that occur in the islets produce some interesting and often difficult to diagnose endocrinopathies. The most significant disorders of the exocrine pancreas are cystic fibrosis, pancreatitis, and tumors. Although, cancer of the pancreas is one of the major cancers of the world, its cure rate is very low even with radical surgery because it is often far advanced when diagnosed.
THE PANCREAS--HERMIT OF THE ABDOMEN
1. The word pancreas comes from the Greek word meaning
a. cluster of grapes.
c. all flesh.
d. hidden organ.
2. The pancreas is described as the hermit of the abdomen because
a. little is known about how it functions and how to treat pancreatic disease.
b. it is located in the retroperitoneal space behind the peritoneum.
c. the kidneys hide it from radiographic view.
d. its grape cluster-like shape makes it difficult to view on computer tomography (CT) scan.
3. Signs and symptoms of disease may not become apparent until it is very advanced because
a. of the large endocrine and exocrine reserve.
b. the pancreas only affects glucose metabolism.
c. the spleen takes over the functional responsibilities of the pancreas.
d. the pituitary gland functions as a backup during early pancreatic disease.
4. The existence of the pancreas was first noted in the Talmud between--, where it was described as the "finger of the liver."
a. 200 BC and 200 AD
b. 300 BC and 100 AD
c. 200 BC and 100 AD
d. 100 BC and 100 AD
5. --, MD, was a professor of surgery at Columbia University, New York, when he pioneered pancreatic surgery in the 1930s.
a. Paul Langherhans
b. Claude Bernard
c. Johann Wirsung
d. Allan O. Whipple
6. The ventral bud forms the superior part of the pancreas' head, body, and tail.
7. The ventral duct and distal dorsal duct become the main pancreatic duct (ie, the duct of--), which drains into the duodenum.
8. Failure to recognize aberrant ductal anatomy may lead to
a. misdiagnosis of the specific type of pancreatic pathology.
b. false negative intraoperative cholangiogram results.
c. successful malpractice litigation.
d. potential ligation of ducts during surgery.
9. Pancreas divisum is associated with
a. recurrent pancreatitis.
b. cystic fibrosis.
c. multiple sclerosis.
d. pancreatic cancer.
10. Obstruction of the common channel may cause reflux of pancreatic juices or bile into the duct of Wirsung, resulting in
a. hematemesis and dysphagia.
b. potential premature activation of pancreatic enzymes.
c. heartburn and odynaphagia.
d. peptic ulcers.
11. Pancreatic--usually is associated with additional severe malformations that are incompatible with life.
12. -- (ie, secretory cells resembling grape clusters) develop at the ends of the tubules early in the fetal period.
13. The islets begin to secrete insulin at approximately--weeks gestation.
14. The endocrine cells reside in the
a. acini cells.
b. enterochromaffin cells.
c. islets of Langherhan.
d. pituitary gland.
15. Beta cells produce--, which affects carbohydrate, protein, and fat metabolism.
c. adrenocorticotrophin hormone
16. All of the following make up a clinical triad produced by beta cell tumors (ie, insulinomas) except
a. hypoglycemia with blood sugar levels below 50 mg per dL.
b. central nervous system manifestations, such as confusion, stupor, and loss of consciousness related to fasting and exercise.
c. musculoskeletal manifestations, such as tetany.
d. attacks relieved by feeding the patient or administering glucose.
17. Nurses often administer--(ie, synthetic analogue of somatostatin) to treat the severe diarrhea and flushing that occurs in patients with gastrointestinal endocrine tumors
a. octreotide acetate
c. ondansetron hydrochloride
18. Vasoactive intestinal polypeptide stimulates GI fluid secretion resulting in
c. watery diarrhea.
19. The features of carcinoid syndrome include all of the following except
a. asthmatic attacks.
c. intestinal hypermotility.
d. vasomotor disturbances.
20. Treatment of gastrinomas is
a. noninvasive, such as dietary modifications.
c. radiation therapy.
d. a total gastrectomy and removal of the islet tumor.
21. The enzyme component of pancreatic juice consists of proteases, amylases, and lipases that breakdown --, --, and --, respectively.
22. The--phase of pancreatic juice secretion begins with the arrival of acid chyme into the duodenum.
23. Cystic fibrosis is characterized by alterations in exocrine glands that result in
a. pulmonary disease, pancreatic insufficiency, and elevated sweat electrolytes.
b. cardiac disease, decreased sweat electrolytes, and pancreatic insufficiency.
c. renal disease, elevated pancreatic activity, and elevated sweat electrolytes.
d. pulmonary disease, pancreatic insufficiency, and elevated pancreatic activity.
24. There is almost universal agreement that the pathological mechanism in pancreatitis is
d. uncontrolled neoplastic growth.
25. The two most common theories for causation of pancreatitis are--in men and--in women.
b. biliary tract/hypercalcemia
d. alcoholism/biliary tract disease
26.Patients often assume a position of comfort (eg,--) to ease the symptoms of pancreatitis.
a. lying supine with pillow under knees
b. reclining with small pillow at base of spine.
c. sitting with the spine flexed in a fetal position
d. lying prone with pillows under hip and chest
27. Pancreatic infection may occur via all of the following routes except
a. the pulmonary system.
b. the biliary duct system.
c. transmural migration through the colonic wall.
d. the circulatory system.
28. Pulmonary complications of pancreatitis, such as pleural effusion, result from
b. vasodilation from the release of kallikrein.
c. retroperitoneal transudation of fluid from the swollen pancreas.
d. release of necrotic tissue and enzymes into the blood stream.
29. Ranson's early prognostic signs use the worst of 12 physiological variables plus age and previous health status to provide a measure of disease severity.
30. Patients with three to four Ranson signs have a--mortality rate.
b. 15% to 20%
31. Obesity is a negative prognostic indicator for acute pancreatitis because
a. obesity dramatically increases perioperative risk.
b. reduced activity in obese patients increases the pulmonary complications of pancreatitis.
c. the cardiac complications related to obesity adversely affect postoperative recovery.
d. fat deposits in the pancreas and retroperitoneal spaces increase the risk of fat necrosis.
32. -- is preferred to morphine for treatment of pancreatitis pain because morphine can cause spasm of the sphincter of Oddi.
a. Pentazocine lactate
b. Fentanyl citrate
c. Hydromorphone hydrochloride
d. Ocycodone hydrochloride
33. Some authorities favor fresh frozen plasma, which contains trypsin inhibitors, to correct the hypoalbuminemia.
34. All of the following are signs of tetany except
a. a negative Trousseau's sign.
b. carpopedal spasm.
c. Chvostek's sign.
d. paresthesias of fingers and around oral cavity.
35. -- reduces vomiting and decreases pancreatic inflammation and secretions by preventing antral distension and limiting duodenal acidification.
a. Administering intravascular volume replacement
b. Gastrointestinal decompression
c. Administering narcotic pain medication
d. Initiating nasogastric feedings
36. Anticholinergic medications may be ordered to decrease
a. pancreatic secretion, hydrochloric acid production, and enzyme consumption.
b. vagal stimulation, enzyme consumption, and pseudocyst formation.
c. ampullary spasm, hydrochloric acid production, and pseudocyst formation.
d. vagal stimulation, pancreatic secretion, and ampullary spasm.
37. All injections (drawing blood samples, administering medications) are performed with a small bore needle to minimize the risk of infection.
38. Risk factors for pancreatic cancer include all of the following except
a. poor diet.
b. use of alcohol and coffee.
c. cigarette smoking.
d. vegetarian diet.
39. There is a positive correlation between mortality from pancreatic cancer and per capita consumption of
a. high fiber foods.
b. carbonated beverages.
c. fats and meat.
d. refined sugar products.
40. All of the following are steps in the pancreaticoduodenectomy except
a. resecting the proximal head of the pancreas and the adjoining duodenum.
b. resecting the distal portion of the stomach and the distal segment of the common bile duct.
c. incising the distal portion of the ileum in preparation for anastomosis.
d. anastomosis of the jejunum to the pancreatic duct, common bile duct, and stomach.
THE PANCREAS--HERMIT OF THE ABDOMEN
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(1) Describe the historical background of pancreatic research in regard to the role of the pancreas.
(2) Identify the stages of pancreatic development.
(3) Explain the link between the pancreas and cystic fibrosis.
(4) Discuss pancreatitis.
(5) Define pancreatic cancer.
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CONDITIONS OF FACTORS ASSOCIATED WITH ACUTE PANCREATITIS
End-stage renal failure
Injection into the pancreatic duct (eg, endoscopic retrograde cholangiopancreatography)
Infectious agents and toxins (eg, mycoplasma pneumoniae infection, viral infections, scorpion bite)
* Organ transplantation
* Accessory pancreatic duct
* Bile ducts
* Duodenum/ampullary region
* Main pancreatic duct
* Outflow obstruction
* Pancreas divisum
* Sphincter of Oddi dysfunction
Vascular disease (eg, hypoperfusion)
RANSON'S EARLY PROGNOSTIC SIGNS
Objective signs on admission
Age older than 55 years
White blood cell count > 16,000 per [mm.sup.3]
Serum glucose > 200 mg per dL
Serum lactate dehydrogenase level > 350 U [dagger] per L
Serum aspartate aminotransferase (ie, formerly serum glutamic oxalsacetic transaminase) level > 250 U [dagger] per L
Signs during first 48 hours
Hematocrit decreases more than 10%
Blood urea nitrogen rises more than 5 mg per dL
Serum calcium < 8 mg per dL
Arterial oxygen pressure < 60 mm Hg
Base deficit > 4 mEq per L
Estimated fluid sequestration > 6 L
(1.) W A Dorland, Dorland's Illustrated Medical Dictionary, 28th ed (Philadelphia: W B Saunders Co, 1994) 1218, 1402.
(2.) R M Gore, "Normal anatomy and examination techniques," in Textbook of Gastrointestinal Radiology, first ed, R M Gore, M S Levine, I Laufer, eds (Philadelphia: W B Saunders Co, 1994) 2096-2111.
(3.) J M Crawford, R S Cotran, "The pancreas: The exocrine pancreas," in Robbins Pathologic Basis of Disease, fifth ed, R S Cotran, V Kumar, S L Robbins, eds (Philadelphia: W B Saunders Co, 1994) 897.
(4.) Gore, "Normal anatomy and examination techniques," first ed, 2096-2111.
(5.) K L Moore, T V N Persaud, The Developing Human: Clinically Oriented Embryology, fifth ed (Philadelphia: W B Saunders Co, 1993) 237, 264.
(6.) T Brown, "Alterations in function of the gallbladder and exocrine pancreas," in Perspectives on Pathophysiology, first ed, L E Copstead, ed (Philadelphia: W B Saunders Co, 1995) 748.
(7.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 899.
(8.) F Naffah, "Acute pancreatitis," in Clinical Gastroenterology, second ed, E Achker, R G Farmer, B Fleshier, eds (Philadelphia: Lea & Febiger, 1992) 463-473.
(9.) P P Toskes, "Recurrent acute pancreatitis," Hospital Practice 20 (July 15, 1985) 85-92.
(10.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 900; Brown, "Alterations in function of the gallbladder and exocrine pancreas," first ed, 751.
(11.) Moore, Persaud, The Developing Human: Clinically Oriented Embryology, fifth ed, 245.
(12.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 899.
(14.) Moore, Persaud, The Developing Human: Clinically Oriented Embryology, fifth ed, 245.
(15.) S M Gomberg, V Prout, "Neonatal conditions," in Nursing Care of the Childbearing Family, eds L N Sherwen, M A Scoloveno, C Tousie-Weingarten (Norwalk, Conn: Appleton & Lange, 1995) 1192-1232.
(16.) Brown, "Alterations in function of the gallbladder and exocrine pancreas," first ed, 746.
(17.) G J Tortora, S R Grabowski, Principles of Anatomy and Physiology, seventh ed (New York: Harper Collins College Publishers, 1993) 549.
(18.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 909.
(19.) R M Berne, M N Levy, "Hormones of the pancreatic islets," in Physiology, third ed, R M Berne, M N Levy, eds (St Louis: Mosby Year Book, 1993) 869.
(20.) Ibid, 868.
(21.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 924.
(22.) M J Kirkhorn, "Frontiers of research: Diabetes mellitus," in Perspectives on Pathophysiology, ed L E Copstead (Philadelphia: W B Saunders Co, 1995) 777.
(23.) D Heaman, B L Bullock, "Normal and altered functions of the pancreas," in Pathophysiology: Adaptations and Alterations in Function, fourth ed (Philadelphia: Lippincott, 1996) 730.
(24.) Kirkhorn, "Frontiers of research: Diabetes mellitus," 777.
(25.) Heaman, Bullock, "Normal and altered functions of the pancreas," fourth ed, 732.
(26.) R HAnding, B L Bullock, "Normal and altered nutritional balance," in Pathophysiology: Adaptations and Alterations in Function, fourth ed (Philadelphia: Lippincott, 1996) 242.
(27.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 924.
(28.) E Amirata, D H Livingston, J Elcavage, "Octreotide acetate decreases pancreatic complications after pancreatic trauma," American Journal of Surgery 168 (October 1994) 345-347; K M Venable, N G Walters, L O Burrell, "Disorders of the endocrine pancreas: Diabetes mellitus," in Adult Nursing in Hospital and Community Settings (Norwalk, Conn: Appleton & Lange, 1992) 1148.
(29.) J H Deglin, A H Vallerand, "Octreotide," in Davis's Drug Guide for Nurses, sixth ed (Philadelphia: F A Davis Co, 1999) 740.
(30.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 924.
(31.) Tortora, Grabowski, Principles of Anatomy and Physiology, seventh ed, 549.
(32.) B L Bullock, "Normal hepatobiliary and pancreatic exocrine function," in Pathophysiology: Adaptations and Alterations in Function (Philadelphia: Lippincott, 1996) 814.
(33.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 872.
(34.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 909.
(36.) C W Taber, C L Thomas, Taber's Cyclopedic Medical Dictionary, 16th ed (Philadelphia: F A Davis Co, 1989) 310.
(37.) Ibid, 2178.
(38.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 924.
(39.) Taber, Thomas, Taber's Cyclopedic Medical Dictionary, 16th ed, 2178.
(40.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 669; R R Seeley, T D Stephens, P Tate, Anatomy and Physiology, second ed (St Louis: Mosby Year Book, 1992) 788.
(41.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 669.
(42.) Ibid, 672; T J Palmer, "Hepatobiliary and gastrointestinal disturbances," in Nurse Anesthesia, eds J J Nagelhout, K L Zaglaniczny (Philadelphia: W B Saunders Co, 1997) 166.
(43.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 672.
(44.) A C Guyton, Textbook of Medical Physiology, eighth ed (Philadelphia: WB Saunders Co, 1991) 716.
(45.) E E Chaffee, E M Greisheimer, Basic Physiology and Anatomy, second ed (Philadelphia: Lippincott, 1969) 485.
(47.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 674.
(48.) Palmer, "Hepatobiliary and gastrointestinal disturbances," 166.
(49.) Berne, Levy, "Hormones of the pancreatic islets," third ed, 673.
(50.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 755.
(51.) D Schofield, R S Cotran, "Diseases of infancy and childhood," in Robbins Pathologic Basis of Disease, fifth ed, R S Cotran, V Kumar, S L Robins, eds (Philadelphia: W B Saunders Co, 1994) 451-454.
(52.) L M Wilson, G N Lindseth, "Disorders of the liver, gallbladder, and pancreas," in Pathophysiology: Clinical Concepts of Disease Processes, fifth ed, S A Price, L M Wilson, eds (St Louis: Mosby, 1997) 398-399.
(53.) N Agarwal, C S Pitchumoni, "Assessment of severity in acute pancreatitis," American Journal of Gastroenterology 86 (October 1991) 1385-1391.
(54.) Wilson, Lindseth, "Disorders of the liver, gallbladder, and pancreas," fifth ed, 398.
(55.) F Gorelick, H M Spiro, "Pancreatic disorders," in Clinical Gastroenterology, fourth ed (New York: McGraw-Hill, 1993) 937-1041.
(56.) S Holt, "Chronic pancreatitis," Southern Medical Journal 86 (February 1993) 201-207.
(57.) H I Hertan, C S Pitchumoni, "Chronic calcific pancreatitis in a patient with Waldenstrom's macro-globulinemia," American Journal of Gastroenterology 86 (May 1991) 633-634.
(58.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 751.
(59.) Ibid; C M Hudak, B M Gallo, J J Benz, eds, Critical Care Nursing: A Holistic Approach, sixth ed (Philadelphia: Lippincott, 1994) 859-869.
(60.) Gorelick, Spiro, "Pancreatic disorders," fourth ed, 959.
(61.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 751.
(62.) Toskes, "Recurrent acute pancreatitis," 85-92.
(63.) Hudak, Gallo, Benz, Critical Care Nursing: A Holistic Approach, sixth ed, 861.
(64.) Wilson, Lindseth, "Disorders of the liver, gallbladder, and pancreas," fifth ed, 398.
(65.) M E Maldonado et al, "Incidence of pancreatitis in patients undergoing sphincter of Oddi manometry (SOM)," American Journal of Gastroenterology 94 (February 1999) 387-390.
(66.) D C Whitcomb, "The first international symposium on hereditary pancreatitis," Pancreas 18 (January 1999) 1-12.
(67.) Agarwal, Pitchumoni, "Assessment of severity in acme pancreatitis," 1385-1391.
(68.) J M Black, E Matassarin-Jacobs, eds, Luckmann and Sorensen's Medical-Surgical Nursing: A Psychophysiologic Approach, fourth ed (Philadelphia: W B Saunders Co, 1993) 1745.
(69.) M S Ambrose, H M Dreher, "Pancreatitis: Managing a flare-up," Nursing 26 (April 1996) 33-39.
(70.) Palmer, "Hepatobiliary and gastrointestinal disturbances," 167.
(71.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(72.) Ibid; L Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," in Adult Health Nursing, third ed, P G Beare, J L Myers, eds (St Louis: Mosby, 1998) 1603; S Simmons, B Given, "Acute pancreatitis," American Journal of Nursing 71 (May 1971) 934-939.
(73.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(74.) S W Schmid et al, "The role of infection in acute pancreatitis," Gut 45 (August 1999) 311-315.
(75.) L O Burrell, "Fluid, electrolyte, and acid-base balances and imbalances and related nursing management," in Adult Nursing in Hospital and Community Settings, sixth ed (Norwalk, Conn: Appleton & Lange, 1992) 135; L O Burrell, "Disorders of the biliary tract and exocrine pancreas," in Adult Nursing in Hospital and Community Settings, sixth ed (Norwalk, Conn: Appleton & Lange, 1992) 1529.
(76.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 751-752; D D Ignatavicius, M L Workman, M A Mishler, eds, Medical-Surgical Nursing Across the Health Care Continuum, third ed (Philadelphia: W B Saunders Co, 1999) 1506-1507.
(77.) Burrell, "Disorders of the Biliary Tract and Exocrine Pancreas," 1506-1507; L O Banks, "Acute and chronic pancreatitis," in Adult Nursing in Hospital and Community Settings, sixth ed (Norwalk, Conn: Appleton & Lange, 1992) 809-862.
(78.) Brown, "Alterations in function of the gallbladder and exocrine pancreas," first ed, 754; Heaman, "Normal and altered functions of the pancreas," fourth ed, 753.
(79.) Simmons, Given, "Acute pancreatitis," 73.
(80.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(81.) J H Ranson, "Risk factors in acute pancreatitis," Hospital Practice 20 (April 15, 1985) 69-73.
(82.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(83.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 752.
(85.) J H Ranson, "The current management of acute pancreatitis," Advances in Surgery 28 (1995) 93-112.
(86.) Heaman, "Normal and altered functions of the pancreas," fourth ed, 752.
(87.) Burrell, "Fluid, electrolyte, and acid-base balances and imbalances and related nursing management," 135; Burrell, "Disorders of the Biliary Tract and Exocrine Pancreas," 1529.
(88.) Brown, "Alterations in function of the gallbladder and exocrine pancreas," first ed, 752.
(89.) M L Steer, "Cyclosporin and chronic pancreatitis: A supermodel?" Gut 45 (August 1999) 167-168.
(90.) Brown, "Alterations in function of the gallbladder and exocrine pancreas," first ed, 752.
(91.) Agarwal, Pitchumoni, "Assessment of severity in acute pancreatitis," 1385-1391.
(93.) Ranson, "The current management of acute pancreatitis," 93-112.
(94.) J Martinez et al, "Obesity: A prognostic factor of severity in acute pancreatitis," Pancreas 19 (July 1999) 15-20.
(95.) W M Steinberg, "Acute drug and toxin induced pancreatitis," Hospital Practice 20 (May 15, 1985) 95-102.
(96.) Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," 1604.
(97.) Palmer, "Hepatobiliary and gastrointestinal disturbances," 168.
(98.) Ranson, "The current management of acute pancreatitis," 93-112.
(99.) Palmer, "Hepatobiliary and gastrointestinal disturbances," 168.
(100.) Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," 1604.
(101.) Ranson, "The current management of acute pancreatitis," 93-112.
(102.) Burrell, "Fluid, Electrolyte, and Acid-Base Balances and Imbalances and Related Nursing Management," 124.
(103.) Ignavaticius, Workman, Mischler, Medical Surgical Nursing Across the Health Care Continuum, third ed, 1506.
(104.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(105.) Ibid; Naffah, "Acute pancreatitis," second ed, 463-473.
(106.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(107.) Amirata, Livingston, Elcavage, "Octreotide acetate decreases pancreatic complications after pancreatic trauma," 345-347.
(108.) Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," 1604.
(109.) Schmid et al, "The role of infection in acute pancreatitis," 311-315.
(110.) Ambrose, Dreher, "Pancreatitis: Managing a flare-up," 33-39.
(111.) Deglin, Vallerand, Davis's Drug Guide for Nurses, 764.
(112.) Ignavaticius, Workman, Mischler, Medical Surgical Nursing Across the Health Care Continuum, third ed, 1514.
(113.) Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," 1604.
(114.) D Campani et al, "Over expression in lymph node metastases predicts clinical outcome in ductal pancreatic cancer," Pancreas 19 (July 1999) 26-32.
(115.) J D Ahlgren, "Epidemiology and risk factors in pancreatic cancer," Seminars in Oncology 23 (April 1996) 241-250.
(116.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 905.
(117.) D L Volker, "Neoplasia," in Adult Health Nursing, third ed, P G Beare, J L Myers, eds (St Louis: Mosby, 1998) 93.
(118.) H T Lynch et al, "Familial pancreatic cancer: A review," Seminars in Oncology 23 (April 1996) 251-275.
(119.) Crawford, Cotran, "The pancreas: The exocrine pancreas," fifth ed, 905.
(120.) Ibid, 907.
(121.) Haycraft, "Nursing management of adults with disorders of the liver, biliary tract, or exocrine pancreas," 1607.
Mary Gavaghan, RN, MSN, EdD, was an associate professor at Bloomsburg University, Bloomsburg, Pa, at the time this article was written. Dr Gavaghan currently is retired.
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