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Canine and Feline Pancreatitis

Canine and Feline Pancreatitis

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P
ancreatitis is the result of inappropriaterelease of digestive enzymes within thepancreas.The inciting cause of canineand feline pancreatitis is not commonly identi-fied,perhaps because of the complex nature of the disease or the subacute to chronic nature of many cases.Although an underlying cause iscommonly not identified,risk factors includebreed,age,concurrent endocrine disease,obe-sity,drugs,and trauma.
PHYSIOLOGY
 The exocrine pancreas produces zymogens,pancreatic secretory trypsin inhibitor (PSTI),and active enzymes (i.e.,lipase,amylase,andthe procoenzyme procolipase).
1,2
 The zymogensinclude trypsinogen,chymotrypsinogens,kallikreinogen,proelastases,procarboxypepti-dases,and prophospholipase A
2
.
2
 Trypsin,theactive form of protrypsinogen,is the only acti- vated zymogen capable of activating itself or the otherzymogens.This activation iscontrolled in large measure by local calcium concentration.
3
Interestingly,calcium hasboth inhibitory and activating
Article #
3
ABSTRACT:
CE
Pancreatitis is a multifactorial disease with a variable clinical course and outcome.Anunderlying cause is not commonly identified,but risk factors include breed,age,concurrentendocrine disease,obesity,drugs,and trauma.The clinical signs of the disease range frommild lethargy to severe vomiting,multiple-organ failure,and death.The diagnosis is oftenchallenging and relies on a constellation of history,physical examination,and diagnosticfindings.Treatment generally includes supportive care,pain control,nutritional support,and treatment of concurrent diseases.The outcome is variable,and the disease mayrecur without warning.
effects on trypsinogen,depending on its con-centration.At a low concentration,as is found within acinar cells,calcium binding protects thetrypsinogen activation peptide from exposure.Increased calcium concentration,as is found inthe ducts and intestine,increases the sensitivity of trypsinogen to activation by trypsin.
3
Ductu-lar PSTI,also known as
serine protease inhibitor Kazal-type 1(SPINK1)
,protects the pancreasby binding to the active site on trypsin in acinarcells and pancreatic ducts to prevent furtherzymogen activation and is packaged withinzymogen granules.
3
Like most cells,exocrinepancreatic cells contain lysosomal granulesimportant for cellular function;these containproteases,including cathepsin B,that can acti- vate zymogens on contact.Protective mechanisms that decrease the risk of zymogen activation include the inclusion of PSTI with zymogens,the segregation of zymo-gens within lipid structures,and the maintenanceof high alkaline ductular flushing.Alkalinity ismaintained by bicarbonate secretion through thecystic fibrosis transmembrane conductance regu-lator (CFTR).
3
 The association of pancreatitis with CFTR mutations in humans emphasizesthe importance of ductular bicarbonate secretion
COMPENDIUM
766
October 2005
Canine and Feline Pancreatitis
 Jacqueline C.Whittemore,DVM,DACVIM (SAIM)Vicki L.Campbell,DVM,DACVA,DACVECC
Colorado State University 
Now Online:CE Test Answersat CompendiumVet.com
Send comments/questions via email
editor@CompendiumVet.com
or fax
800-556-3288
.Visit
CompendiumVet.com
forfull-text articles,CE testing,and CEtest answers.
 
October 2005COMPENDIUMCanine and Feline Pancreatitis
767
CE
as a protective mechanism.
3
Zymogen granulesecretion is the result of both neural and humoralmechanisms.The humoral mediators secretin andcholecystokinin are believed to be most importantin stimulating zymogen secretion in dogs and cats.Duodenal brush border cells produce enteroki-nase,a strong protease responsible for zymogenactivation within the intestinal lumen (Figure 1).Enterokinase is unique in that it is 2,000 timesmore effective at activating trypsinogen thantrypsin itself.
4
Production of enterokinase in theintestine instead of the pancreas helps ensure effi-cient and effective activation of zymogens in theintestine while limiting the risk of zymogen acti- vation within the pancreas.Enterokinase is notinactivated by PSTI and does not form complexes with antiproteases.Muscle sphincters in the pan-creatic ducts help prevent reflux of enterokinaseand duodenal contents into the pancreas.Low levels of circulating exocrine pancreaticenzymes are commonly present in plasma,probably due to direct leakage into the bloodstream.They are commonly cleared through the kidneys.Circu-lating zymogens are bound by circulating enzymeinhibitors (i.e.,
α
1
-antitrypsin,
α
2
-macroglobulin)that decrease their activity and increase mono-cyte–macrophage clearance,respectively.
PATHOPHYSIOLOGY
Pancreatitis is a multifactorial and complexprocess that eventually culminates in inappropriateactivation of zymogens within the pancreaticparenchyma.In most patients,this is likely theresult of abnormal fusion of lysosomal and zymo-gen granules within the acinar cell.
1,2
A small sub-set of veterinary cases,like a large percentage ohuman cases,may be due to inappropriate duode-nal reflux into the pancreas.
5
 The activation of trypsino-gen to trypsin furthers pancreatic damage by activatingthe other zymogens and trypsinogen.Once zymogenactivation has occurred,damage is amplified by free rad-ical–associated damage (e.g.,lipid peroxidation) andincreased capillary permeability due to endothelialmembrane damage.This increase in permeability canlead to pancreatic edema,decreased microvascular circu-lation,increased free radical stasis,and local ischemia. The accumulation of free radicals and presence of localischemia may lead to worsening inflammation andparenchymal damage (Figure 1).As proteolytic enzymes propagate,they may overwhelmthe circulating antiproteases.Activation of inflammatory cascades,including complement,kinin,and coagulationsystems,by proteases then occurs.This may lead to severerefractory hypotensive and vasoactive shock,disseminatedintravascular coagulopathy (DIC),multiple organ dys-function syndrome (MODS),and death.
2,6,7
Pancreatitis can be acute or chronic and mild or severe.Acute pancreatitis may occur singly or recurrently.It canbe mild or self-limiting.Severe cases may be associated with complications,including pancreatic abscessation orpseudocysts,hypotensive shock,acute renal failure,
Figure 1.
Normal pancreatic function and consequences of abnormal zymogen release.
(Reprinted with permission,© AmericanGastroenterological Association,Bethesda,MD)Normal zymogen release into the duodenum with activation byenterokinase.Local and systemic sequelae of pancreatic inflammation.
Site of zymogenaAcute pancreatitis: mechanisms
 
COMPENDIUMOctober 2005Canine and Feline Pancreatitis
768
CE
MODS,DIC,and death.
2,6,7
Pancreatic pseudocysts arecollections of pancreatic secretions that form secondary to fibrosis or inflammation.
8,9
Pancreatic abscessationmay also occur.
10,11
Although usually sterile,both pancre-atic pseudocysts and abscesses may require surgical inter- vention for successful outcomes.Chronic pancreatitismay also be mild or severe.Mild cases are associated with minimal clinical signs and minimal morphologic orfunctional changes.Severe disease may lead to markedhistologic abnormalities and may rarely be associated with development of exocrine pancreatic insufficiency orendocrine insufficiency (i.e.,diabetes mellitus [DM]).In humans,defects in the trypsinogen,SPINK1,andCFTR genes are associated with hereditary pancreatitis.
3
Itis currently unknown whether there are specific hereditary causes of pancreatitis in dogs or cats,although terriers,miniature schnauzers,and Siamese cats are overrepre-sented.
12,13
RISK FACTORS,CLINICAL SIGNS,ANDPHYSICAL EXAMINATION FINDINGS
Known or suspected risk factors for canine pancreati-tis include breed (i.e.,terriers,miniature schnauzers),age (i.e.,older than 5 years),concurrent endocrine dis-ease (i.e.,DM,hyperadrenocorticism,hypothyroidism,hypertriglyceridemia),hypercalcemia,obesity,gastroin-testinal (GI) disease,drugs (i.e.,sulfonamides,azathio-prine),epilepsy,infection,and blunt abdominaltrauma.
2,12,14–16
Glucocorticoids are no longer considereda risk factor for development of pancreatitis in humans.In addition,research does not support an association with pancreatitis in dogs or cats.
16
Risk factors in catsinclude breed (i.e.,Siamese),age (i.e.,older than 7 years),trauma,and concurrent disease (i.e.,triaditis,hepatic lipidosis,DM).
5,17–20
 The term
triaditis
is used by some veterinary gastroenterologists to refer to concur-rent inflammatory bowel disease (IBD),cholangiohep-atitis,and pancreatitis.Feline cases may be caused bFIP,toxoplasmosis,liver flukes,or pancreatic flukes.
5,21–24
Clinical signs in dogs include anorexia,vomiting,diarrhea,abdominal pain,and fever.
2,16,25
Signs in catsinclude lethargy (100%),anorexia (97%),dehydration(92%),and jaundice (64%).
18,26
Vomiting (35%) anddiarrhea (15%) are uncommonly associated with felinepancreatitis;mild weight loss or atypical behavior may be the only clinical sign.
18
Physical examination findings
Figure 2.
Ultrasonographic findings associated with pancreatitis.
Mixed echogenicity of a pancreas
(Panc)
in a hyperechoicmesentery visualized via ultrasonography.Hypoechoic focus in the pancreas consistent with a pancreaticabscess
(Pan Ab)
visualized using ultrasonography.

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