This case study involves a 53-year-old white male seen in his primary care physician's office for a sudden onset of acute chest pain. The patient was admitted to a local hospital for diagnostic studies related to the pain. Cardiac enzymes, stress test, and a heart catheterization study were all normal. The pain subsided and the patient was discharged. The patient continued to see his primary care physician with recurrent episodes of acute chest pain and was eventually referred to a gastroenterologist for evaluation. The patient is a non-smoker and a non-drinker.
The gastroenterologist ordered an amylase and lipase. The amylase was and has remained normal over the years except for one acute exacerbation of pain when it elevated to 4 times the upper limit of normal. The lipase was and has remained elevated over the years ranging from just slightly abnormal to 30 times the upper limit of normal.
The initial diagnosis was that the pancreatitis was due to acute gallbladder disease though there were no stones. The gall bladder was removed and the pain subsided for a period of time. Pain once again began to occur. An endoscopic retrograde cholangiopancreatogram (ERCP) was performed and indicated a thickening of the pancreatic duct. A stent was inserted and brought about temporary relief. Pain recurred. Another ERCP was performed and a sphincterotomy successfully completed.
The patient continues to suffer intermittent bouts of pancreatitis indicated by elevations of serum lipase levels and has been diagnosed with idiopathic chronic pancreatitis which the patient has learned to live with and control the pain of with over-the-counter analgesics, Nexium, and hydrocodone as needed when pain becomes severe enough.
The pancreas is a large, flat gland located in the abdomen behind the stomach and close to the duodenum. The pancreas plays an important role in both digestion (exocrine) and metabolism (endocrine). The part of the pancreas with endocrine function (secretes hormones in blood stream to travel to other sites in the body for activity) is made up of the islets of Langerhans which are composed of four different types of cells: alpha cells secrete glucagon; beta cells secrete insulin; delta cells secrete somatostatin; and, gamma cells secrete pancreatic polypeptide. Glucagon acts to increase blood glucose levels while insulin acts to decrease blood glucose levels. Somatostatin regulates the activity of both the alpha and beta cells. Pancreatic polypeptide functions to regulate both endocrine and exocrine pancreatic secretion activities (http:// www.mayoclinic.com/health/pancreatitis/DS00371).
The acinar cells of the pancreas produce and transport a variety of chemical compounds called proenzymes which are stored in zymogen granules that exit the body via the digestive system where the proenzymes are converted into active enzymes and assist in the digestion of fats, proteins, and carbohydrates. When food enters the mouth, the digestive process begins with mastication and the addition of salivary amylase. This food leaves the mouth via the esophagus and empties into the stomach where acids are mixed with the food to continue the digestive process. The food passes directly from the stomach into the first part of the small intestine called the duodenum where bile, bicarbonate, and pancreatic fluids are added to the digestive system via the pancreatic duct. Bile is a greenish-yellow fluid produced in the liver that is secreted via the bile ducts which combine with the cystic duct which runs to the gallbladder where bile is stored. The common bile duct enters the head of the pancreas and joins the pancreatic duct to form the ampulla of Vater which empties into the duodenum. The pancreatic duct carries the pancreatic fluid produced by the acinar cells of the pancreas. The ductal cells of the pancreas produce bicarbonate which acts to neutralize the acidity of the contents from the stomach. Food, bile, bicarbonate, and pancreatic fluid travel through the remaining portion of the duodenum, jejunum, and ileum (small intestine) then through the cecum, large intestine, rectum, and anal canal (http://pathology. jhu.edu/pc/BasicOverview3.php?area=ba; http://teachmeanatomy.info/abdomen/physiology/ pancreas/).
There are many different pancreatic enzymes that are secreted as a part of the pancreatic fluid including: amylase (carbohydrates), lipase (triglycerides), carboxypeptidase (proteins), chymotrypsin (proteins), trypsin (proteins), phospholipase (fats), elastases (protein), nucleases (nucleic acids) , and various proteases (protein). These enzymes are generally secreted into the duodenum in an inactive form (zymogen or proenzyme). Once released into the intestine, enteropeptidase in the intestinal mucosal cells cleaves trypsinogen into the active form trypsin. The free trypsin cleaves the remaining trypsinogen and chymotrypsinogen to its active form chymotrypsin. These active enzymes then act to degrade their specific substrates from the ingested food. If these enzymes become active inside the pancreas, the process of autodigestion occurs leading to pancreatitis (http://teachmeanatomy.info/abdomen/ physiology/pancreas/; http://en.wikipedia.org/ wiki/Pancreas).
Pancreatitis is the inflammation and autodigestion of the pancreas in which pancreatic enzymes destroy the tissues of the pancreas itself and leads to inflammation which may be sudden (acute) or ongoing (chronic); in addition, there are also hereditary (genetic) forms of pancreatitis. Both acute and chronic pancreatitis are marked by mild to severe abdominal pain, often with nausea, vomiting, and fever; and, both can lead to severe complications (http://www.healthsystem.virginia.edu/UVAHealth/ adult_liver/pancrea.cfm).
The primary causes of pancreatitis are heavy alcohol use and gallstones (cholelithiasis), but other factors can also cause pancreatitis (Table 1 below); however, sometimes the cause is never identified (idiopathic). If alcohol abuse and gallstones can be ruled out, other possible causes should be investigated so that appropriate treatment can be initiated. Table 1 below lists some of the risk factors (causes) of pancreatitis found in a review of the literature (http://healthsystem. virginioa.edu/UVAHealth/adult_liver/pancreas.cfm; http://medic.med.uth.tmc.edu/path/00001214.HTM; http://188.8.131.52/search?q=cache:VTEj77AREB4J:www.ddw.org /user-assets/document).
Acute pancreatitis, as the name suggests, often occurs suddenly, with mild to severe constant pain in the upper abdomen that usually radiates to the back and sometimes to the chest. The pain may be almost constant for hours or days and is likely to become worse when alcohol is imbibed or food is ingested. Bending forward into the fetal position may provide temporary alleviation of the pain. Other signs and symptoms shown in Table 2 include: nausea and vomiting; fever; rapid pulse; swollen and tender abdomen; ascites; jaundice; and, can progress to dehydration, hypotension, internal bleeding, and shock. These symptoms are not specific for pancreatitis and may mimic other medical conditions; therefore, a physician should always be consulted (http://digestive.niddk.nih. gov/ddiseases/pubs/pancreatitis/; http://healthsystem.virginia.edu/UVAHealth/adult_liver/pandrea.cfm).
In cases of chronic pancreatitis, most patients will have abdominal pain though some complain of no pain at all. In some cases, the pain will go away as the condition advances, probably due to the fact that the pancreas is no longer producing pancreatic enzymes. Patients often lose weight even though appetite and eating habits are normal. This occurs because the body is not producing enough pancreatic enzymes to break food down so that nutrients can be absorbed. Poor digestion often leads to excretion of fat, protein, and glucose in the feces leading to malodorous stool production. Diabetes may also develop if the islets of Langerhans have been damaged in the process of the disease (http:// www.mayoclinic.com/health/pancreatitis/DS00371).
Diagnosis of pancreatitis begins with a medical history, physical examination, and appropriate diagnostic tests. The medical history of a patient is obtained via discussion of the physician with the patient or individuals with knowledge of the patient. However, the physician should ask specific questions and not general questions related to the patients current and past medical issues. Answers to these specific questions can help to obtain information that allows the physician to make a provisional diagnosis and provide appropriate and targeted medical care to the patient. This process should elicit the symptoms or complaints including the chief complaint, history of present illness, past medical history, review of symptoms, family illnesses, childhood diseases, social history, medication history, allergies, and other questions as appropriate to the specific patient. Evaluation of the medical history allows the physician to come to a provisional diagnosis or diagnoses (http://en.wikipedia.org/wiki/Medical_history).
Once the history is completed, the physician will perform a physical examination to ascertain the clinical signs associated with the patient's medical problem. The physical examination will involve a determination of vital signs and a systematic head-to-toe assessment of all parts of the body. This examination involves the use of inspection, palpation, percussion, and auscultation. The physical examination often reveals clues that the physician can use to formulate a differential diagnosis. The physical examination usually reveals abdominal distension or muscle spasms with epigastric pain and left upper-quadrant tenderness (See Table 2 above) (http://en.wikipedia.org/wiki/Physical_examination; http://my.clevelandclinic.org/heart/diagnostics-testing/physical-examination.aspx).
Diagnosis is not always straight forward because the signs and symptoms overlap many other conditions leading to the need for a differential diagnosis that includes the use of various blood tests including a complete blood count (CBC), electrolytes, urea, creatinine, liver function tests, pregnancy test, amylase and lipase. Chest and abdominal radiographs may also aid in the diagnosis. An EKG may be used to rule out an acute myocardial infarction which can present as abdominal pain. If the diagnosis is still not clear, more advanced procedures may be used to reveal the diagnosis: computed tomography of the abdomen/pelvis (CT or CAT scan); abdominal magnetic resonance imaging (MRI), abdominal or pelvic ultrasound; endoscopic retrograde cholangiopancreatography (ERCP), and endoscopy and colonoscopy (http:// healthsystem.virginia.edu/UVAHealth/adult_liver/ pandrea.cfm; http://www.aafp.org/ afp/20000701/164.html).
While plain abdominal radiography was once used for evaluating abdominal disease, newer imaging modalities such as ultrasound, CT, MRI, and nuclear medicine are in more common use today; however, physicians still frequently order this examination and abdominal radiography is still a useful tool in many instances today. There are no absolute contraindications to abdominal radiography; but, if diagnostically appropriate, ultrasound, CT scan, or MRI should be considered as an alternative imaging modality (ACR-SPR Practice Guidelines for the Performance of Abdominal Radiography, 2011).
Ultrasound procedures use reflected sound waves to produce an image of structures in various areas of the body. An abdominal ultrasound can be used to evaluate the abdominal aorta, liver, gallbladder, spleen, pancreas, and kidneys. The ultrasound procedure may detect gallstones, inflammation of the gallbladder, blocked bile ducts, or abnormalities in the pancreas (www.webmd.com/ digestive-disorders/abdominal-ultrasound?print=true).
Endoscopic retrograde cholangiopancreatography (ERCP)
An ERCP uses a flexible, lighted scope (endoscope) that is inserted through the mouth to the duodenum until it reaches the point where the pancreatic and bile ducts drain into the duodenum. A tube is then passed through the scope and a radiographic contrast media is injected to allow the internal organs to be observed on an x-ray. This procedure is sometimes used to enable endoscopic sphincterotomy or to remove impacted stones. The ERCP may be performed on patients with persistent pain or jaundice to locate gallstones, remove gallstones, open a narrowed bile duct, insert a drainage tube, collect a tissue sample for further testing, or to measure the pressure inside the bile ducts. Thus, the ERCP is not only used for diagnosis but also for treatment of certain problems that are identified during the test (www.webmd.com/digestive-disorders/ endoscopic-retrograde-cholangiopancreatogram?print=true). The risks of ERCP with sphincterotomy include precipitating an acute episode of pancreatitis, introducing infection, causing hemorrhage, and perforation of the bowel (www.aafp.org/afp/20000701/164.html).
Computed tomography (CT or CAT scan)
A CT scan uses x-rays to make detailed pictures of structures inside the body. Each rotation of the scanner provides an image of a thin slice of the area scanned. A CT scan of the abdomen can find cysts, abscesses, infection, tumors, an aneurysm, enlarged lymph nodes, foreign objects, bleeding, diverticulitis, inflammatory bowel disease, and appendicitis. Radiographic contrast media may be used during CT scans to delineate some structures more clearly (www.webmd.com/a-to-z-guides/ computed-tomography-ct-scan-of-thebody?print=true).
Magnetic resonance imaging (MRI)
MRI uses a magnetic field and pulses of radio waves to make pictures of structures inside the body. MRI often shows problems that cannot be seen with other imaging studies. The MRI can locate tumors, bleeding, infection, and blockages which may be causes of acute and/or chronic pancreatitis. Radiographic contrast media may be used during MRI to define certain structures more clearly (www.webmd.com/a-to-z-guides/magnetic -resonance-imaging-mri?print=true).
Clinical Laboratory Tests
Amylase is an enzyme produced by the salivary glands and pancreas that catalyzes the hydrolysis of starch into disaccharides and trisaccharides (sugars) and can be measured for purposes of medical diagnosis. An elevated level may reflect one of several medical conditions including: pancreatitis; perforated peptic ulcer; torsion of an ovarian cyst; strangulation of the ileus; mesenteric ischemia; macroamylasemia; appendicitis; ascites; pancreatic pseudocysts; acute cholecystitis; ruptured ectopic pregnancy; peritonitis; burns; diabetic ketoacidosis; cancer of the lung , esophagus, or ovary; alcohol use; prostate tumors; bulimia and anorexia nervosa; mumps; and, cystic fibrosis. There are also a number of medications that can elevate serum amylase levels including aspirin, some birth control pills, corticosteroids, cholinergic drugs, methyldopa, thiazide and loop diuretics, simvastatin, opiates (codeine and morphine), and some chemotherapy agents (www.healthline.com/health/amylase-and-lipase-tests; www.urmc.rochester.edu/encyclopedia /content.aspx?ContentTypeID=167&Contentl...).
Amylase may be measured in serum, plasma, urine, and peritoneal fluid. Serum amylase values in patients with pancreatitis vary depending upon the severity of the disease. Amylase levels start to rise between two to 12 hours following onset of symptoms, peaks at 12-72 hours, and returns to normal within one week. Though the test lacks sensitivity (75-92 percent) and specificity (20-60 percent), amylase is the most widely used test for diagnosing pancreatitis www.aafp.org/ afp/20000701/164.html).
Amylase clearance testing may be used to differentiate between macroamylasemia and pancreatitis. Macroamylase is a complex of amylase and serum immunoglobulins that render the particles too large to be filtered by the kidneys resulting in a high serum amylase level. The condition requires no treatment and is often transient and once diagnosed can negate the need for other expensive imaging modalities. The normal ratio for amylase clearance is 2-5%. In macroamylasemia, the ratio is often less than 1% and in acute pancreatitis the ratio is greater than 5% (http://medic.med.uth.tmc.edu/ path/000011214.htm).
Lipase is another enzyme produced by the pancreas utilized in the diagnosis of pancreatitis, often in conjunction with amylase. Lipase levels begin to rise about 4-8 hours after onset of pancreatitis, peak about 24 hours, and may remain elevated up to 14 days. The specificity (50-99 percent) and sensitivity (86-100 percent) of lipase is significantly higher than amylase levels for detecting pancreatitis. Elevated lipase values may be associated with bowel obstruction, celiac disease, duodenal ulcer, pancreatic cancer, and pancreatitis. Birth control pills, codeine, morphine, and thiazide diuretics are common medications that may elevate lipase results. Since analgesic medications may tend to elevate amylase and lipase levels, samples for testing should be collected prior to administration of these analgesics. Low levels of lipase may be associated with cystic fibrosis and familial lipoprotein lipase deficiency www.aafp.org/afp/20000701/164.html; www.healthline.com/health/lipase-test).
An elevated trypsin level is a better indicator for acute pancreatitis than amylase since it is more sensitive and specific. However, trypsin levels are not widely available and therefore not routinely used in the workup of acute pancreatitis (www. aafp.org/afp/20000701/164.html).
The presence of free fat in a fecal sample may be indicative of chronic pancreatitis since the fat is not digested and absorbed normally by the small intestine and produces a greasy/oily, foul-smelling feces (www.mayoclinic.com/print/pancreatitis/DS00371/ METHOD=print&DSECTION=all).
Treatment of pancreatitis depends upon severity of the attack and is initiated to support bodily functions and prevent complications. The patient is usually admitted to the hospital for observation. Pancreatitis usually improves without intervention except for intravenous replacement of fluids while being maintained in a fasting state until the amylase and lipase values return to normal; however, one should also note that replacement of fluids will also dilute the serum amylase and lipase which may elevate again once the intravenous fluids are discontinued. Fasting is instituted since eating stimulates the pancreas to produce additional amounts of enzymes. In severe cases, the patient may require total parenteral nutrition over a period of weeks until the pancreas heals and may require admission to the intensive care unit. If diabetes develops as a consequence of pancreatitis, insulin administration may be necessary for a period of time (http://digestive.niddk.nih.gov /ddiseases/pubs/pancreatitis/).
The analgesic of choice for pancreatitis is morphine even though there are reports in the literature where morphine has caused a spasm of the sphincter of Oddi and worsened the pain. Meperidine is also used in less severe cases. Long-term use of opioid analgesics is not recommended due to the potential for addiction. Antibiotics may also be administered to reduce the likelihood of pancreatic sepsis. Various other analgesics, both prescription and over-the-counter, may be prescribed to control ongoing pain. Over-the-counter medications such as acetaminophen, aspirin, or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen may help to relieve pain. Tricyclic anti-depressants such as amitriptyline or imipramine may help people sleep and cope with pain and depression (http://sanfordhealth.org/HealthInformation/Healthwise /Topic?uf4370).
If gallstones are causing the pancreatitis, an endoscopic retrograde cholangiopancreatogram (ERCP) to remove stones from the common bile duct may be a part of the treatment. The ERCP may be followed with a cholecystectomy to remove the gallbladder and stones to prevent future attacks. In some instances when it is determined that the pancreatic duct is narrowed, surgery may be performed to widen the duct by inserting a stent or a sphincterotomy or to remove tissue that may be blocking the duct or to drain a pseudocyst (http://webmd.com/ digestive-disorders/tc/pancreatitis-treatment-overview).
Once the crisis has passed, patients are instructed to eat small low fat, high protein meals. The more an individual eats at one time, the more digestive juices the pancreas produces. Limiting fat in the diet will reduce loose and oily stools. Patients are also advised to drink plenty of fluids to prevent dehydration which can further irritate the pancreas and to use over-the-counter or prescription analgesics as prescribed by the physician. When these over-the-counter pain killers are ineffective in controlling pain, opiate-based painkillers may be prescribed (www.aafp.org/ afp/20000701/164.html; http://wwwnhs.uk/Conditions /Pancreatitis-chronic/Pages/Treatment.aspx).
The intraduodenal pH is acidic due to increased production of gastric acid and impaired secretion of bicarbonate; thus the physician may also prescribe acid-reducing medication to enhance the effectiveness of some pancreatic enzyme products. H2-blockers such as Pepsid, Tagamet, and Zantac decrease gastric acid production in the stomach. Proton pump inhibitors such a Nexium or Prilosec may also be prescribed. Anticholinergics have been used to decrease gastric secretions and increase pH ((www.aafp.org/afp/20000701/164.html; http://ncbi.nlm.nih.gov/pmc/articles/ PMC210383/).).
Enzyme supplements such as Pancrease, Creon, Violiase, or Viokase can help to eliminate malabsorption problems and restore normal digestive function and improve steatorrhea. These medications, taken before meals and snacks, may lead to weight gain and a feeling of well-being. These pancreatic enzymes function by increasing the levels of pancreatic enzymes in the duodenum which decreases the secretion of enzymes by the pancreas. The most common side effect of these supplements is constipation but may also cause nausea, abdominal cramps, and diarrhea. These pancreatic supplements should not be taken at the same time as calcium or magnesium containing antacids such as Maalox, Mylanta, Tums, and Rolaids. (http:// mayoclinic.com/print/pancreatitis?DS00371 /METHOD-pring&DSECTION=all; http://www.pancan.org /section_facing_pancreatic_cancer/learn_about_pan_cancer/).
Most complications of acute pancreatitis and subsequent deaths occur within two weeks of onset with secondary pancreatic infection being the most common cause of death. Other potential complications of acute pancreatitis include: hypovolemia, pancreatic necrosis, extrapancreatic necrosis, acute respiratory distress syndrome (ARDS), acute renal failure, adynamic ileus, circulatory shock, and sepsis. Later occurring complications include pseudocysts and abscess formation (www.aafp.org/ afp/20000701/164.html).
Chronic pancreatitis is caused by repeated episodes of acute pancreatitis that leads to scarring of the pancreas over a long period of time and may be associated with life-threatening complications. These episodes of acute pancreatitis may lead to a failure to produce enough enzymes to digest food products and a lack of insulin production leading to diabetes. Most individuals with chronic pancreatitis suffer with abdominal pain that is either constant or episodic; however, a few individuals with chronic pancreatitis never experience discomfort (http://jama.ama-assn.org/cgi/content/ full/299/13/1630).
This inherited form of pancreatitis is marked by recurrent attacks of pain, nausea, vomiting, and fever lasting anywhere from two days to two weeks and usually progress to chronic pancreatitis. Although the genetic defect that causes the condition is present at birth, pancreatitis symptoms do not appear until the first or second decade of life. Hereditary pancreatitis has been linked to an increased risk for developing pancreatic cancer. There are three areas of genetic mutations associated with recurrent acute and chronic pancreatitis: Cystic fibrosis which is linked to CFTR gene mutations; and Hereditary Pancreatitis which is linked to PRSS1 and SPINK1 (PRSI) gene mutations (http:// dcmsonline.org/jax-medicine/2002journals/june-july2002 /pancreatic.htm; http://pancreasfoundation.org /cgi/csNews/csNews.cgi?database=learn _genetics.db&c; http://www.ucpancreas.org /hereditarypancreatitis.htm).
This patient was diagnosed with chronic pancreatitis at age 53, and has been treated with: cholecystectomy, pancreatic duct stent, sphincterotomy, dietary modification, and Nissen fundoplication for gastroesophageal reflux disease (GERD) which can exacerbate chronic pancreatitis to the acute form, NSAIDs, Tylenol, hydrocodone, and Nexium. This patient also developed nodules in the thyroid/parathyroids along with hypercalcemia. A needle biopsy of the thyroid/parathyroid could not confirm whether or not the nodules were malignant; therefore the patient underwent a total thyroidectomy along with the removal of one parathyroid gland. This thyroid was not malignant and the calcium levels returned to normal within two weeks. Seventeen years later the patient continues to exhibit periodic episodes of chronic abdominal pain in spite of all therapies including 80 mg of Nexium on a daily basis and has suffered additional episodes of acute pancreatitis requiring hospitalization. No specific cause for the continued episodes has been identified and thus is classified as idiopathic. It seems that chronic pancreatitis is a disease that goes on and on and has no end.
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1. Which of the following is NOT a diagnostic form of pancreatitis?
2. According to this article, which of the following pancreatic enzymes is NOT used in the diagnosis of pancreatitis?
3. Which of the following amylase clearance ratio values would be indicative of macroamylasemia?
4. Of the following, which risk factor is MOST commonly associated with pancreatitis?
5. Which of the following will provide the definitive diagnosis in a patient with abdominal pain and a provisional diagnosis of pancreatitis?
A. Medical history
B. Laboratory testing
C. Abdominal imaging
D. Physical examination
6. Which of the following procedures could be used as an aid in the diagnosis and in the treatment of a patient with acute pancreatitis?
A. Computed tomography
B. Abdominal ultrasonography
C. Magnetic resonance imaging
D. Endoscopic retrograde cholangiopancreatography
7. A patient presented to the Emergency Department complaining of severe epigastric pain. Due to the apparent distress the patient was in, the attending physician ordered a morphine injection to help the patient relax before proceeding with his examination and blood collection for laboratory testing. Which of the following laboratory results would be most suspect for this patient?
A. Normal liver enzymes
B. Lipase within normal limits
C. WBC elevated at 14,000/cumm
D. Amylase level two times the upper limit
8. Which of the following is least likely to be recommended as a part of the long-term treatment plan for patients with chronic pancreatitis?
A. Morphine for pain
B. Enzyme supplements
C. Dietary modifications
D. Acid-reducing medications
9. Pancreatic enzyme supplements act to:
A. Decrease secretion of bile acids
B. Increase secretion of bicarbonate
C. Decrease production of gastric acids
D. Increase levels of pancreatic enzymes
10. Which of the following is NOT a gene mutation associated with recurrent acute and chronic pancreatitis?
George H. Roberts, EdD, MT(AMT), MLS(ASCP), Dean School of Health Sciences, Natural Sciences, and Math, Louisiana Delta Community College, Monroe, LA
TABLE 1: Risk Factors for Pancreatitis Alcohol abuse Blocked Autoimmune disease pancreatic duct Gallstones Heredity Vascular disease Abdominal trauma Idiopathic Crohn's disease Major surgery Medications ERCP and pancreatic biopsy Inherited pancreatic Viral infections Kidney failure disease Hypercalcemia Bacterial infections Lupus erythematosus Hypertriglyceridemia Pancreatic cancer Reye's syndrome Venomous stings Snake bites in children TABLE 2: Pancreatitis Symptoms Severe upper abdominal pain Nausea and vomiting Fever Tachycardia Swollen and tender abdomen Ascites Jaundice Dehydration Hypotension Internal bleeding Shock
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|Author:||Roberts, George H.|
|Publication:||Journal of Continuing Education Topics & Issues|
|Article Type:||Case study|
|Date:||Jan 1, 2015|
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