acute pancreatitis

18 Nursing made Incredibly Easy! September/October 2006

Acutepancreatitis

Inflammationgone wild

2.5ANCC/AACN

CONTACT HOURS

EVER CARE FOR a patient with pancreatitis who died despitegiving him every antibiotic in the book? When nothing worked,I’ll bet you wondered just what had happened. And even ifyour patient survived, you were probably pretty alarmed byjust how serious this condition can be.

Pancreatitis can be frightening—for you and for the patient—because so much can be going wrong and you may feel power-less to stop it. But not every patient with acute pancreatitis dies,and there’s a lot you can do to help patients recover. In this arti-cle, I’ll get into the details on this potentially deadly condition,including signs and symptoms of pancreatitis, risk factors for thedisease, its diagnosis and treatment, and nursing considerationsyou should know.

Let’s start with a brief review of the anatomy and physiologyof the pancreas.

Two organs in oneThe pancreas is both an endocrine and an exocrine gland. Theorgan is divided into a head, body, and tail. The head joins thecommon bile duct where it drops down behind and into the de-scending duodenum. The body of the pancreas forms a shelfwhere the stomach rests; it’s also where veins and arteries forthe duodenum separate. The tail forms a shelf for the spleen torest on. The pancreatic duct runs transversely left to right

September/October 2006 Nursing made Incredibly Easy! 19

An attack of acute pancreatitis can leaveyour patient seriously ill; it can even kill him.In this article, we’ll help you understand whathappens inside the body when the pancreasis attacked, how pancreatitis is diagnosed,and what you can do to help your patient. REBECCA A. PHILLIPS, RN, PHDAssistant Professor • College of Nursing • University of OklahomaOklahoma City, Okla.

The author has disclosed that she has no significant relationships with or financial interest in anycommercial companies that pertain to this educational activity.

This isserious—can

you help preventit from being

fatal?

though the gland, joining with the commonbile duct to carry pancreatic juices to be se-creted into the duodenum.

The functional components of the pan-creas include the islets of Langerhans,

which produce insulin, glucagon, andsomatostatin to keep blood glucose in

balance, and the acinar cells, which pro-duce pancreatic juices and bicarbonate

needed for digestion.Pancreatic juices contain the inactive

protease form of trypsinogenand chymotrypsinogen. Theseactivate in the duodenum tobecome trypsin and chy-motrypsin, which help

digest protein. Pancreatic lipaseis also released to digest triglyc-erides, and amylase is added to the

mix to digest starches. This combi-nation turns the food we eat into substances

the body can use for energy.Now that you know what goes on when

everything’s working, let’s look at what hap-pens when things start going wrong.

WildfireAcute pancreatitis can take two forms: edem-atous (or interstitial) pancreatitis or necro-tizing pancreatitis.

n Edematous pancreatitis causes fluid ac-cumulation and swelling. It’s usually mildand self-limiting.n Necrotizing pancreatitis is more severe,as its name suggests. It causes cell deathand tissue damage, with serious systemiccomplications.

No matter which form it takes, at its core,pancreatitis is an inflammatory process thatbegins within the acinar cells. If not checked,it can affect multiple systems and causethem to fail. The severe form of pancreatitisis an aggressive hyperinflammatory reaction;it’s caused by release of chemical mediators,called cytokines, that are associated withinflammation (see At the cellular level). Theseverity of acute pancreatitis and the risk ofmortality are predicted by using Ranson’scriteria (see How bad is it?).

The patient’s response determineswhether pancreatitis becomes chronic.Chronic pancreatitis is diagnosed when pro-gressive, recurring episodes of inflammationcause structural changes within the pancreas(see What about chronic pancreatitis?).

Stones, toxins, and whoknows?The wide-angle view of the causes of acutepancreatitis includes obstruction, genetic


If we don’t halt the

inflammatoryprocess, the

patient’s headedfor trouble.

At the cellular levelThe inflammatory process is in full swing in a patient with pancreatitis, regardless of what causedthe condition. The process begins in the acinar cells of the pancreas when they secrete, amongother things, platelet-activating factor (PAF), cytokines, and acute phase proteins (APPs) in responseto various triggers.

PAF stimulates the hyperinflammatory response that can result in multiorgan failure. It’s releasedby the polymorphonuclear white cells, which are usually mildly to moderately elevated at first. PAFalso signals for the release of histamine, which causes the cells of the blood vessel walls to begin toloosen their hold on each other and creates a tiny gap for fluid to leak through and out into the tis-sues.

Cytokines are released from monocytes and signal the liver, which is already releasing cytokinesfrom its Kupffer cells, to synthesize and release APPs. Release of APPs triggers the coagulation, fib-rinolytic, kallikrein-kinin, and complement cascades. The end point for the kallikrein-kinin and com-plement cascades is further production and release of cytokines. And so the cycle continues.

predisposition, toxic metabolic processes,hypertriglyceridemia, infectious agents, andidiopathic origin.

Obstruction can be caused by gallstones,stenosis of the sphincter of Oddi, neoplasms,pancreatic divisum, and trauma. Obstructionmost commonly occurs from gallstones thatmigrate into the lower bile duct, where theyblock passage of bile into the duodenum.They may also settle in the pancreatic ductbefore it joins the common bile duct, block-ing the bile passage higher up in the drain-age system.

Repeated exposure to stones may causestenosis of the sphincter of Oddi. The sphinc-ter’s job is to regulate the forward flow ofbile and pancreatic juices into the duodenumwhile preventing reflux. So it’s easy to seehow obstruction could lead to an attack ofacute pancreatitis.

Any lesion, such as a neoplasm, that occu-pies space in the pancreatic parenchyma will

obstruct the outflow of juices and causeobstructive autodigestion and pancreatitis.

Pancreatic divisum is a congenital anom-aly occurring when the dorsal and lateralducts of the pancreas fail to fuse during thesecond month of gestation. This causes upto 95% of the pancreatic juice to flowthrough the dorsal duct, which happens tobe the one with the small, minor papillaryorifice. Although this rarely causes prob-lems, you can see how it could create anobstruction that would lead to an acutepancreatitis.

Trauma may be caused by injury duringendoscopic retrograde cholangiopancre-atography related to multiple contrastinjections, high injection pressures, contrastshot into the acinar cell cluster, or an inex-perienced operator performing the proce-dure. Patients who’ve had upper abdomi-nal, renal, or cardiovascular surgeries maydevelop pancreatitis because of injury to


Pyloricsphincter

Common bileductDuodenal papilla

Duodenum

Circular fold

Accessorypancreaticduct

Pancreaticduct

Pancreas

Necrotizingpancreatitis is

characterized by cell death and

tissue damage.

A view of acute pancreatitis


the pancreas or obstruction ofthe bile pathway during the pro-cedure. And any episode of pro-

longed ischemia could lead topancreatitis.

Genetic predispositionrelates to the genes for cationic

trypsinogen and serine proteaseinhibitor. Mutation of these

genes allows trypsinogen to convertto trypsin in the pancreas instead of theduodenum, setting the stage for autodiges-tion and pancreatitis.

Toxic metabolic processes include ethanolabuse and certain drug regimens. Ethanolabuse is classified as a chronic, daily intakeof 100 to 150 grams/dL. Ethanol sets up atransient but severe drop in blood flow tothe pancreas, triggering a vicious cycle ofrepeated ischemic episodes resulting in cel-lular damage. The more cells destroyed bythe ischemic event, the sooner pancreatitiswill occur and the more severe the attackwill be.

Immunosuppressant drug regimens,including azathioprine (Imuran), mercapto-purine (Purinethol), and didanosine (Videx),may also cause acute pancreatitis. Why’sthat? Suppression of the immune systemincreases the risk of infection, which is one ofthe causes of acute pancreatitis.

Hypertriglyceridemia occurs when largeamounts of cytotoxic free fatty acids arereleased into the pancreatic circulation.

When the triglyceride level exceeds 1,000mg/dL, lipase in the pancreas binds triglyc-erides to albumin. Once albumin is saturat-ed, the pancreas releases triglycerides as freefatty acids that are toxic to the acinar cells. Inaddition, red blood cells become sluggishand plug capillaries. Capillary plugging andstasis of blood flow result in vascularendothelial damage, pancreatic ischemia,acidosis, activation of trypsinogen, and theflare-up of acute pancreatitis.

The patient’s blood becomes so lipemicthat serum amylase can’t be used to measurepancreatic dysfunction. Urine amylase mustbe checked to find out how the pancreas isdoing.

Infectious agents that can cause acute pan-creatitis include viruses, bacteria, and para-sites. Most of the viruses you know fall intothis category: measles, mumps, rubella, cox-sackie B, Epstein-Barr, cytomegalovirus, andthe viruses that cause the different types ofhepatitis. Bacterial sources include Legionella,Mycoplasma pneumoniae, Mycobacterium tuber-culosis, and Campylobacter jejuni, to name afew. Parasites that can cause acute pancreati-tis include Ascaris and Clonorchis.

How bad is it?The severity of acute pancreatitis is deter-mined by the existence of certain criteria,called Ranson’s criteria. The more criteriamet by the patient, the more severe theepisode of pancreatitis—which increases therisk of mortality.

Mortality is less than 1% among patientswho meet fewer than three of the criteria. Itrises to 16% when three to four criteria aremet and to 40% with five or six criteria.Mortality is 100% when the patient meetsseven or eight criteria.

The health care provider establishes theseverity of the disease on admission and dur-ing the first 48 hours after admission by eval-uating the patient for the following criteria:On admission• patient older than age 55 years• white blood cell count > 16,000/mcL • serum glucose level > 200 mg/dL• serum lactate dehydrogenase level > 350

units/liter• aspartate aminotransferase level > 250

units/literAfter admission• 10% decrease in hematocrit• blood urea nitrogen level increase > 5 to 8

mg/dL within 48 hours of admission• serum calcium level < 8 mg/dL• base deficit > 4 mEq/liter• partial pressure of arterial oxygen < 60 mm

Hg• estimated fluid sequestration > 6 liters.

Am I at theroot of your

patient’sproblem?


What about chronic pancreatitis?Structural changes within the pancreas, resulting from progressive, recurring episodes of inflamma-tion, are at the root of chronic pancreatitis. Damage to the functional capabilities of the organ usual-ly starts with the exocrine side, causing weight loss from an inability to digest and absorb nutritionfrom the intestinal tract.

If pancreatitis causes damage to the organ’s islets of Langerhans, the patient typically developsdiabetes mellitus. This is usually a late symptom of chronic pancreatitis. As a complication of theinflammatory process, calculi develop within the pancreas in up to 60% of the cases. These calculican cause stenosis of the common bile duct and portal hypertension.

The causes of chronic pancreatitis differ from those that trigger an acute attack and include thefollowing: • Ethanol intake creates a progressive, calcifying form of pancreatitis and causes 80% of cases ofchronic pancreatitis. It occurs with a daily intake of 80 grams/dL or more for a period of 35 years orlonger. Ethanol-induced attacks of acute pancreatitis are likely to end up in chronic pancreatitis, butthis outcome depends on how much the ethanol has destroyed the underlying parenchyma.• Protein and trace element malnutrition is referred to as tropical chronic pancreatitis, or kwash-iorkor, and it’s associated with toxin uptake that causes calcifications in the pancreas.• Hereditary chronic pancreatitis is an autosomal disorder described in over 100 cases to date. • A lowered trypsinogen level due to a mutation in the activation peptide can lead to chronicepisodes of pancreatitis.• Juvenile idiopathic chronic pancreatitis is caused by an imbalance of proteases and antiproteasesin the early decades of life. • Idiopathic causes remain unclear, but may be related to inflammation and fibrosis of the pan-creas.• Recurrent acute episodes can lead to a chronic state because of the underlying calcification ofthe pancreas in acute episodes.

Patients with chronic pancreatitis aren’t immune to acute pancreatitis. How can you tell if yourpatient’s having an acute attack? Generally, not by the pain that’s typical of acute pancreatitis: Upto half of patients with chronic pancreatitis won’t experience that pain during an acute episode. Itseems that the longer pancreatitis exists, the more the gland is destroyed and the less likely thepatient is to have severe pain—or any pain—related to an attack. If your patientwith chronic pancreatitis does have pain, expect to see a complicating fac-tor, such as pseudocysts or cholestasis.

Other acute symptoms, however, do occur in patients with chronicpancreatitis, such as nausea and vomiting, along with fever, bloating, oilymalodorous stool, and weight loss.

Because ethanol abuse is the number one cause, expect chemicaldependency therapy to be offered to your patient with chronic pancreatitis.Also, give enzymes to aid digestion and encourage absorption, andrecommend dietary changes that will help decrease the pain that canbe associated with early chronic pancreatitis, such as reducingfat intake and consuming smaller, more frequent meals.

As with all chronic illnesses, depression is a common prob-lem that will need to be treated to bring the chemical disrup-tion back into balance and provide emotional stability for thepatient.

A heavy drinkercan damage

more than hisliver.


Why do theseinfectious agentscause acute pancre-atitis? Here’s onetheory: Pathogenicorganisms arethought to triggerproteolytic enzymes(trypsinogen, chy-motrypsinogen, pro-tease) to become acti-vated within thepancreas instead ofwithin the intestine.The enzymes digestpancreatic tissue,resulting in pancre-atitis.

Idiopathic is list-ed far more fre-quently than itprobably should beas the reason forpancreatitis. It’s thecatchall for “I don’t know what causedthis.” As many as one-quarter of pancreati-tis episodes are labeled idiopathic follow-ing a workup that includes a thorough his-tory; routine lab studies such as liver func-tion tests, calcium level, triglycerides, glob-ulin level, and serum amylase and serumlipase levels; and noninvasive studies suchas ultrasound.

When these studies fail to identify thecause, most health care providers stoplooking and call the etiology idiopathic.However, health care providers shouldtake advantage of the diagnostic technolo-gies available before labeling an episodeidiopathic. These include abdominal andchest X-rays (which show bowel dilationand ileus, as well as pleural effusion), com-puted tomography scan (which can visual-ize pancreatic abscesses, pseudocysts, andan enlarged pancreas with fluid collection),cholangiopancreatography (which visual-izes bile duct stones), and special lab stud-ies such as gene analysis.

Knowing the cause of the disease increas-es the likelihood that patients will receive themost appropriate treatment—which meansthey’ll be less likely to suffer a recurrence.

Detecting pancreatitisThe patient with acute pancreatitis willcomplain of nausea, vomiting, and upperabdominal pain, usually with an abruptonset and a characteristically steady, boringpain located in the periumbilical area andepigastrium. This pain may radiate to theback and may be more intense when thepatient is walking or lying supine. It maybe relieved by sitting up and leaning for-ward.

Other signs and symptoms of acute pan-creatitis may include tachycardia, tachypnea,hypotension, abdominal distension, abdomi-nal rigidity, mild jaundice, diminishedbowel sounds, and occasional musclespasms due to hypocalcemia. In more severecases, you may see the Grey Turner sign(discoloration of the flank area) or the Cullensign (discoloration of the periumbilical arearelated to hemorrhagic pancreatitis).

The trick is to be sure the symptoms aren’tcaused by some other abdominal disorder.The health care provider will order serumamylase and lipase levels, as well as a urineamylase level. If you see a serum amylaselevel four times the top of the reference scale,you can be sure your patient has acute pan-creatitis. Elevated lipase and urine amylaselevels seal the diagnosis.

Rest, drains, and drugsTreatment goals for patients with acutepancreatitis include resting the pancreasand bowel, relieving pain, replacing fluidsand electrolytes, providing nutritionalsupport, and, in some cases, reducing hy-pertriglyceridemia and administering an-tibiotics. Some patients may even needsurgery. n Rest and relief of pain. If no other organsystems are involved and if there’s no signof necrosis or infection, keep the patient

did youknow?Why do you some-times see fever inpatients with acutepancreatitis eventhough they don’thave an infection?Pancreatic ascitesfluid, obtained froma swollen andboggy pancreas, isrich in the cytokinesinterleukin-1β‚ andtumor necrosis fac-tor-α, powerfulpyrogenic inflamma-tory mediators. Theycause the hypothal-amus to raise bodytemperature, result-ing in a fever.


N.P.O. so pancreatic juices are suppressedand the pancreas can take a rest. A nasogas-tric tube may be placed to relieve nauseaand vomiting, keep the stomach empty, andreduce pain. Administering medications forpain relief is a nursing priority for patientswith acute pancreatitis. Opioids are thedrug of choice in this situation. n Fluid and electrolyte replacement. Mostpatients with acute pancreatitis need intra-venous (I.V.) replacement of fluid, protein,and electrolytes. You’ll generally give I.V.fluids like 0.9% sodium chloride and lac-tated Ringer’s solution to increase intravas-cular volume. Electrolyte replacements areused to treat hyocalcemia, hypermagne-semia, and hypokalemia based on serumlab values. Monitor the patient’s hemody-namic status, fluid balance status, and elec-trolyte values.n Nutritional support. If your patient withacute pancreatitis has to remain N.P.O. for a

long period of time, or if he developscomplications from pancreatitis, you canexpect to administer total parenteral nu-trition. You won’t usually give lipids,though; they can raise the triglyceridelevel, which can exacerbate the inflam-matory process in acute pancreatitis.n Hypertriglyceridemia. The health

care provider may order fibric acid de-rivatives like gemfibrozil (Lopid) as a firstattempt to reduce the patient’s triglyc-eride level. These drugs have three ac-tions: reduce the liver’s ability to producetriglycerides through fatty acid uptake,reduce exchange between very low-density lipoproteins and high-densitylipoproteins, and stimulate reverse choles-terol transport.

However, fibric acid derivatives aren’twithout adverse effects. Patients may experi-ence elevated liver enzymes (aspartateaminotransferase and alanine aminotrans-

ferase), myalgia, gallstones, or, in rarecases, rhabdomyolysis. Closely monitor-

ing hepatic function during acute pancre-atitis is important anyway; it’s even more so

with these types ofdrugs.

Plasma exchangehas also been usedto reduce triglyc-eride level, but onlylipoprotein aphaere-sis should be used.This form of ex-change removes the large molecules from the plasmawhile retainingimmunoglobulins,

albumin, and clotting factors. It significantlylessens the adverse effects of aphaeresis ther-apy by lowering the potential for bleedingand infection.n Antibiotics. Many health care providersfeel that prophylactic antibiotic therapywith imipenem-cilastatin (Primaxin) is thebest way to avoid infection-related mortal-ity during pancreatitis. Imipenem is one ofthe third-generation cyclosporine antibioticsthat effectively diffuse into the pancreatictissues, giving it the best chance of killingany invading organism.n Surgery. When surgery is needed, theaim is to debride the necrotic tissue of thepancreas and provide adequate drainagefor any remaining debris. If the patientalso has organ failure, the mortality raterises. Postoperative management includeshigh-volume retroperitoneal lavage and re-peat debridement as needed.n Easing the tension. While you’re busygiving treatments and monitoring the situa-tion, don’t forget to take time to providepsychological support to patients and theirfamilies.

A shocking developmentLocal and systemic complications can occurwith pancreatitis. The major complication ofacute pancreatitis is systemic inflammatoryresponse syndrome, a hyperinflammatorystate that the body creates to help defend it-self against an invasion of some type. This

A little R&R willhelp calm things

down for thestressedpancreas.

patientpointerInstruct a patientbeing treated foracute pancreatitisto avoid high-fatfoods and alcoholafter he’s dis-charged. They cantrigger anotheracute attack.


defense attempt goes awry, leading to com-plications such as acute respiratory failure,acute respiratory distress syndrome, andshock.

Lung injury during an attack of acute pan-creatitis is caused by the rapid infiltration ofneutrophils as soon as 3 hours after the ill-ness is triggered. As the blood travelsthrough the portal circulation and the liver,alveolar macrophages leap into action. Butthey end up making the lung injury worseby helping to create pleural effusions, atelec-tasis, and pneumonia, all of which reduceoxygen uptake and carbon dioxide releasewithin the capillaries.

The hypoperfusion of shock furtherinjures the sick pancreas as blood flowthrough the capillary bed slows. The pan-creas reacts by releasing a substanceknown as myocardial depressant factor,which further adds to the systemic compli-cations by reducing cardiac contractility,cardiac output, and perfusion pressure.During this low-flow state, stasis in thecapillary beds leads to pancreatic ischemiaand necrosis, as well as pooling ofcytokines. Once perfusion pressure israised, the cytokine pool is free to circu-late, dumping a fresh load of chemicalmediators within the circulating systemand causing the cycle to continue.

Shock needs to be aggressively treatedwith volume replacement, vasopressors, andcontractility agents as indicated by thepatients’ hemodynamic state. LactatedRinger’s solution or albumin is used to cor-rect for loss of fluids. Blood and clotting fac-tors should also be replaced as needed.

Once volume has been replaced, you maybe adding vasopressors to help supportblood pressure. Contractility agents are usedwhen it becomes apparent that the cardiacoutput is falling because the heart is nolonger beating strongly enough.

The development of pancreatic necrosis,and the probable infection that follows, is themost significant variable for patient mortali-ty and relates to the progressive advance of

multiorgan dysfunction. Once infectionoccurs in the face of necrotic tissue, the mor-tality rate ranges from 40% to 70%.

You’ll primarily provide supportive carefor a patient with multiorgan dysfunction.That includes monitoring vitalsigns, oxygen saturation,and hemodynamicparameters. Providesupplemental oxygenand prepare for endo-tracheal intubationand mechanical ven-tilation as necessary.Monitor the patient’sfluid balance status and serum labvalues.

Bowel rest is ordered, but in the face of thehyperinflammatory reaction, an inactivebowel allows for translocation of intestinalflora and pancreatic infection. Usual organ-isms cultured are Escherichia coli, Klebsiella,Enterococcus, Staphylococcus, and Pseudo-monas. When the fungus Candida albicans iscultured, the outcome is grim.

Outcome optionsThe goal of treating an attack of pancreatitisis complete recovery. To get to that goal, it’simportant to correct the cause of the attack.If the patient has gallstones, for instance, acholecystectomy will be needed to removethe stones. If hypertriglyceridemia causedthe problem, working to control the triglyc-erides will help reduce the number and per-haps the severity of attacks, although mostof these patients will develop chronic pan-creatitis.

Severe attacks, with prolonged periods ofhypoperfusion and pancreatic necrosis andinfection, will end in death 70% of the time.Little can be done when the hyperinflamma-tory state leaves the patient profoundlyhypoperfused and refractory to therapy.

Stay positiveDon’t be discouraged after reading the lastsection. Yes, some patients with acute pan-

Shocked by howfast things cango bad when I’munder attack?


creatitis die, but others live and can leadproductive, happy lives. Give your pa-tients the best chance for survival by beingalert to the possibility of pancreatitis, re-acting quickly when it occurs, and watch-ing closely for complications. You justmay save someone’s life. n

Learn more about itAhmed SA, et al. Chronic pancreatitis: Recent advancesand ongoing challenges. Current Problems in Surgery.43(3):127-238, March 2006.

Connor S, Neoptolemos JP. Surgery for pancreatic necro-sis: “Whom, when and what.” World Journal of Gastroen-terology. 10(12):1697-1698, June 2004.

Khoury G, Deeba SS. Pancreatitis. http://www.emedicine.com/EMERG/topic354.htm. Accessed June 16, 2006.

Kim H, et al. Idiopathic acute pancreatitis. Journal of Clini-cal Gastroenterology. 37(3):238-250, September 2003.

Porth CM. Essentials of Pathophysiology: Concepts of AlteredHealth States. Philadelphia, Pa., Lippincott Williams &Wilkins, 2006.

Smeltzer SC, Bare B. Brunner & Suddarth’s Textbook ofMedical-Surgical Nursing, 10th edition. Philadelphia, Pa.,Lippincott Williams & Wilkins, 2003.

Society for Surgery of the Alimentary Tract. Treatment ofAcute Pancreatitis. Manchester, Mass., Society for Surgeryof the Alimentary Tract, 2004. http://www.guideline.gov/summary/summary.aspx?ss=15&doc_id=5512&nbr=3755.Accessed June 16, 2006.

Straight A’s in Pathophysiology. Philadelphia, Pa., Lippin-cott Williams & Wilkins, 2005.

Tierney LM, et al. (eds). Current Medical Diagnosis &Treatment, 45th edition. New York, N.Y., McGraw-Hill,2006.

Whitcomb DC. Clinical practice. Acute pancreatitis. TheNew England Journal of Medicine. 354(20):2142-2150, May18, 2006.

Yadav D, Pitchumoni C. Issues in hyperlipidemic pancre-atitis. Journal of Clinical Gastroenterology. 36(1):54-62, Janu-ary 2003.

INSTRUCTIONS

Acute pancreatitis: Inflammation gone wildTEST INSTRUCTIONS• To take the test online, go to our secure Web site at www.nursingcenter.com/ce/nmie.• On the print form, record your answers in the test answer sectionof the CE enrollment form on page 55. Each question has only onecorrect answer. You may make copies of these forms.• Complete the registration information and course evaluation. Mailthe completed form and registration fee of $22.95 to: LippincottWilliams & Wilkins, CE Group, 2710 Yorktowne Blvd., Brick, NJ08723. We will mail your certificate in 4 to 6 weeks. For faster service,include a fax number and we will fax your certificate within 2 businessdays of receiving your enrollment form. Deadline is October 31, 2008.• You will receive your CE certificate of earned contact hours and ananswer key to review your results. There is no minimum passinggrade.

DISCOUNTS and CUSTOMER SERVICE• Send two or more tests in any nursing journal published byLippincott Williams & Wilkins together and deduct $0.95 from the

price of each test.• We also offer CE accounts for hospitals and other health care facili-ties on nursingcenter.com. Call 1-800-787-8985 for details.

PROVIDER ACCREDITATION:Lippincott Williams & Wilkins, the publisher of Nursing madeIncredibly Easy!, will award 2.5 contact hours for this continuingnursing education activity. Lippincott Williams & Wilkins is accred-ited as a provider of continuing nursing education by theAmerican Nurses Credentialing Center’s Commission onAccreditation. This activity is also provider approved by theCalifornia Board of Registered Nursing, Provider Number CEP11749 for 2.5 contact hours. Lippincott Williams & Wilkins is alsoan approved provider by the American Association of Critical-CareNurses (AACN 00012278, CERP Category A), Alabama#ABNP0114, Florida #FBN2454, and Iowa #75. LippincottWilliams & Wilkins home study activities are classified for Texasnursing continuing education requirements as Type 1. Your certifi-cate is valid in all states.

Earn CE credit online: Go to http://www.nursingcenter.com/CE/nmie and receive a certificate within minutes.


1. Which statement about the pancreas is correct?a. It’s comprised of four lobes.b. It’s both an endocrine and exocrine gland.c. Its tail forms a shelf where the stomach rests.

2. Which statement about pancreatic juices is correct?a. Amylase helps digest protein.b. Lipase helps digest triglycerides.c. Trypsinogen helps digest starches.

3. The development of pancreatitis begins with thea. islets of Langerhans.b. pancreatic head.c. acinar cells.

4. The hyperinflammatory response that occurs with pancre-atitis is stimulated by a. chymotrypsin.b. somatostatin.c. platelet-activating factor.

5. Ethanol abuse damages the pancreas by causinga. ischemia.b. autodigestion.c. insulin resistance.

6. Which class of medication is most likely to cause acutepancreatitis?a. antidiabetic agentsb. immunosuppressantsc. lipid-lowering agents

7. A patient with acute pancreatitis is most likely to reportpain thata. has an insidious onset and is relieved by walking.b. can be relieved by sitting up and leaning forward.c. is peristaltic and felt in the mid to lower abdomen.

8. All of the following are possible signs or symptoms ofacute pancreatitis excepta. flat, soft abdomen.b. abdominal rigidity and distension.c. mild jaundice and diminished bowel sounds.

9. The Cullen sign can be recognized bya. discoloration of the periumbilical area.b. petechiae covering the abdomen. c. ecchymosis of the flank area.

10. Which laboratory test result is not consistent with acutepancreatitis? a. triglycerides level > 1,000 mg/dLb. urine amylase below normal levelsc. serum amylase level four times the top of the reference scale

11. A priority nursing intervention for a patient with acutepancreatitis isa. administering total parenteral nutrition (TPN) with lipids.b. offering small, frequent meals.c. administering opioid analgesics.

12. A patient with acute pancreatitis is most likely to receivewhich intravenous fluid? a. 5% dextrose in water b. lactated Ringer’s solutionc. 5% dextrose in 1⁄2 normal saline

13. Which drug may be ordered for hypertriglyceridemia in apatient with acute pancreatitis?a. gemfibrozil (Lopid)b. atorvastatin (Lipitor)c. pravastatin (Pravachol)

14. Which antibiotic should you expect to administer to a pa-tient with acute pancreatitis?a. ciprofloxacin (Cipro)b. imipenem-cilastatin (Primaxin)c. trimethoprim and sulfamethoxazole (Bactrim DS)

15. An initial clinical finding associated with chronic pancre-atitis isa. diabetes mellitus.b. jaundice.c. weight loss.

16. The most common cause ofchronic pancreatitis isa. kwashiorkor. b. ethanol abuse.c. elevated trypsinogen.

17. Dietary instructions for a patientwith chronic pancreatitisincludea. decreasing fat intake

and eating small,frequent meals.

b. eliminating the ingestionof liquids with meals.

c. consuming a low-carbohydrate, low-protein diet.

Acute pancreatitis: Inflammation gone wildGENERAL PURPOSE: To provide registered professional nurses with an overview of the causes, signs and symptoms, diagnosis, andnursing care for patients with acute pancreatitis. LEARNING OBJECTIVES: After reading the article and taking this test, you should beable to: 1. Describe the anatomy, physiology, and pathophysiology of the pancreas. 2. Discuss the causes, signs and symptoms, anddiagnosis of acute and chronic pancreatitis. 3. Identify appropriate nursing interventions for acute and chronic pancreatitis.

2.5 ANCC/AACN CONTACT HOURS

Turn to page 55 for the CE Enrollment Form.

Go wild—youcan ace this

test!

Date post:	30-Oct-2014
Category:	Documents
Upload:	junaid-masoodi
View:	110 times
Download:	2 times

acute pancreatitis

Documents