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VeterinaryClinicalPathology兽医临床病理学Prof.ZhaoxinTangCollegeofVeterinaryMedicine,SouthChinaAgriculturalUniversity,Guangzhou,China,5106422021/02/241Pref

aceVeterinaryClinicalPathology:VeterinaryLaboratoryMedicineInclude:1ClinicalHematology2Clinicalbiochemistry3Clinicalcytology4

Clinicalmicrobiology5Clinicalparasitology6Clinicaltoxicology2021/02/242PrefaceGeneralLaboratoryconceptsVeterinarianshavemanychoicesregardi

nglaboratorytesting.Importantfactorsinclude:--Needandusefulness--Practicality--Cost-effectiveness--Accuracy--Turnaroundtime2021/02/243Com

pleteBloodCountandBoneMarrowExamination:generalcommentsandselectedtechniques•Completebloodcount•Quantitati

ontechniques•Bloodsmearanalysis•Otherdeterminations•Bonemarrowexamination•Bonemarrowbiopsyandaspirate2021/02/244Completebloodco

unt(CBC)•CBCisaprotestsusedtodescribethequantityandqualityofthecellularelementsinbloodandafewsubstancesinplasma.•CBCisacost-e

ffectivescreenthedetectsmanyabnormalitiesanddiseaseconditions.•Bonemarrowexaminationisusedinselectedinst

ancestoanswerquestionsthemorereadilyavailableCBCcannot.2021/02/245QuantitationTechniques•Samplesubmission•Microhemotcrit•Hemo

globinconcentration•Cellcounts•AbsolutenucleatedRBCcount•Automatedhematologycellcounters2021/02/246BloodSmearAnalysis•Makingthesmear•Sta

ins•Evaluatingbloodsmears--plateletmorphology--leukocytemorphology--leukocyteestimation--leukocytedifferentialcount--e

rythrocytemorphology2021/02/247BoneMarrowExamination•BonemarrowisusuallyexaminedtoanswercertainquestionthatarosefromevaluatingtheCBC.•Indic

ationsforbonemarrowexaminationinclude:--nonregenerativeanemia--Persistentneutropenia--Persistentthrombocytopenia--Unexplainedpoly

cythemiaorthrombocytosis--Atypicalcellsinblood2021/02/248Erythrocytes•Basicconceptsoferythrocytefunction,metabolism

,productionandbreakdown•Hemesynthesis•Globinsynthesis•Ironmetabolism2021/02/249Erythrocytemetabolism•Embden-meyerhofpathway--Glycolysis

generatesATPandNADH•Pentosephosphatepathway--ThispathwayproducesNADPH•Methemoblobinreductasepathway--Methemoglobin(Fe3+)cannottransportoxygen•

Rapoport-lueberingpathway--2,3diphosphoglycerate(2,3DPG)2021/02/2410RedbloodcellsThefundamentalstimulusforproductionofredbloodcells(e

rythropoiesis)iserythropoietin(红细胞生成素）,aglycoproteinproducedbythekidneysinresponsetorenaltissuehypoxia.Otherhormones,su

chascorticosteroids,thyroidhormoneandandrogens,stimulatetheproductionorreleaseoferythropoietinbuthavenointrinsicerythropoieticactivity.Theaveragelife

spanofacirculatingerythrocyteis110-120daysinthedogand68daysinthecat.Agedordamagedredcellsareremovedprimarilybymacrophagesin

theliver,spleenandbonemarrow.2021/02/2411NeutrophilsTheproductionofneutrophils,eosinophilsandbasophilsistermedgranulop

oiesis.Theneutrophilsinthebloodstreameithercirculatefreely(thecirculatingpool)oradheretothevascularendothelium(themarginalpool).Inthed

ogthemarginalpoolandthecirculatingpoolareapproximatelyequalinsize,whilstinthecatthemarginalpoolistwotothreetimeslargerthanthecircul

atingpool.Thereisacontinualexchangeofcellsbetweenthesetwopools.Thehalf-lifeofcirculatingneutrophilsisonly6-14hours,afterwhichti

metheyleavethecirculationandpassintothetissuepool.Thecirculatingtimeisshortenedduringacuteinfectionsasneutrophilspasstothesiteofinfectioninthetiss

ues.Themainfunctionoftheneutrophilisthephagocytosisofpyogenicbacteria.2021/02/2412LymphocytesLymphoidprimitive

stemcellsdivideanddifferentiateintopre-Blymphocytesandpre-Tlymphocytesinthebonemarrow.Pre-Tlymphocytesmatureandproliferat

eintoTcellsinthethymus.Pre-Bcellsproliferateinthebonemarrowandmigratetoperipherallymphoidorgans(spleenandlymph

nodes)wherefurtherproliferationtakesplace.PlateletsPlateletsareproducedfromthecytoplasmofmegakaryocytesOnceinthecirculation,plateletssurvivefor8

-12days.Upto20-30%ofcirculatingplateletscanbesequesteredinthespleen;thefiguremaybeahighas90%ifthereissplenomegaly.Oldordamagedplatel

etsareremovedfromthecirculationbythespleen,liverandbonemarrow.2021/02/2413ROUTINEHAEMATOLOGYThecomplet

ebloodcountisanintegralpartofthediagnosticinvestigationofanysystemicdiseaseprocess.Itconsistsoftwocomponents:Aquantitativeexaminationofthecel

ls,including:packedcellvolume(PCV)totalredcellcount(RBC)totalwhitecellcount(WBC)differentialwhitecellcountplateletcountmeancorpuscularvolume(MCV),mea

ncorpuscularhaemoglobin(MCH),meancorpuscularhaemoglobinconcentration(MCHC),totalplasmaproteinconcent

ration.Aqualitativeexaminationofbloodsmearsforchangesincellularmorphology.2021/02/2414Table1ReferencevaluesforredcellindicesDogsCatsTo

talredbloodcells(x1012/L)5.5~8.55.0~10.0Haemoglobin(g/dl)12.0~18.08.0~15.0PCV(L/L)0.37~0.550.26~0.45MCV(fl)60.0~77.039.0~55.0MCH(pg)19.5~24.512.5

~17.5MCHC(g/dl)32.0~37.030.0~36.0ROUTINEHAEMATOLOGY2021/02/2415REDBLOODCELLINDICESMCV(fl飞升)=PCV(L/L)×1000/totalredc

ells(×1012/L)MCH(pg皮克)=totalhaemoglobin(g/dl)×10/totalredbloodcells(×1012/L)MCHC(g/dl)=totalhaemoglobin(g/dl)/PCV(L/L)RBCindicesarehelpfulintheclassi

ficationofcertainanemias.ROUTINEHAEMATOLOGY2021/02/2416DifferentialwhitecellcountsThedifferentialwhitecellcountisperformedbycounting200leuco

cytesinabloodsmear.Thecellsarecountedalongthelongedgeofthesmear,usingthebattlementmeandermethod:fourhigh-powerfieldsarecountedinonedirection,thenfou

rmoreinadirectionatrightanglestothefirst,andsoon,followingtheshapeofabattlement.Thepercentageofeachtype

ofcellisdetermined.Thispercentageisthenmultipliedbythetotalwhitecellcounttoobtainanabsolutecountforeachcelltype.

ROUTINEHAEMATOLOGY2021/02/2417Plasmaproteinconcentration(Referencerange:60-80g/1forthedogandcat)Totalplasma

protein(TPP)andPCVshouldbeinterpretedtogether.QualitativeexaminationofabloodsmearAbloodsmearshouldalwaysbeevaluatedwhenautomatedcellcountsaremadeo

rwhenin-practiceinstrumentationislimitedtoacentrifugeforPCVPreparationofabloodsmearAsmalldropofbloodisplacedononeendofag

lassslide,usingacapillarytube.Aspreaderslide(madebybreakingoffthecomerofanotherslide,afterscoringitwithaglasscutterordi

amondwriter)isplacedontotheslideholdingtheblooddrop,infrontofthedropandatanangleof20-40°.ROUTINEHAEMATOLO

GY2021/02/2418ANAEMIAAnaemiaischaracterizedbyanabsolutedecreaseinredcellcount,haemoglobinconcentrationandPCV.AcutehaemorrhageAcutehaemorrhage

maybeduetotraumaorsurgery,bleedinggastrointestinalulcersortumours,ruptureofavasculartumour(e.g.splenic

haemangiosarcoma),oracoagulopathy(e.g.warfarintoxicity).Immediatelyfollowingacutehaemorrhagetheredcellparameters,includingPCV,

arenormalbecausebothredcellsandplasmahavebeenlostinproportion.Compensatorymechanismssuchasspleniccontractionmayfurtheroffse

tanyfallinPCV.ThePCVfallswhenbloodvolumeisreplacedbyinterstitialfluidandsodoesnotindicatethefullmagnitudeofbloodlossforatleast24hoursafter

theonsetofhaemorrhage.ROUTINEHAEMATOLOGY2021/02/2419ChronichaemorrhageChronicexternalbloodloss(e.g.chronicgastrointestinal

haemorrhage,renalorbladderneoplasia)initiallyresultsinaregenerativeanaemiabutgraduallytheanaemiabecomesnon-regenerat

iveastheironstoresbecomedepleted.Younganimalsbecomeiron-deficientmorebonemarrowisalreadyveryactiveproducingredcellsquicklythanadultsfollo

wingbloodloss,partlybecausetheyhavelowironstoresandpartlybecausetheirtomatchtheirgrowthrateandsohaslesscapacitytoincreaseitsrateofhaemopoiesis.Haemo

lyticanaemiasMostcasesofhaemolyticanaemiaareimmune-mediated.Inthedogmostcasesofimmune-mediatedishaemolyti

canaemia(IHA)areprimary(idiopathic)andaretermedautoimmunehaemolyticanaemia(AIHA).IHAmayoccurinassociationwith:drugs(e.g.potentiatedsulphona

mides);lymphoreticulardiseases(e.g.lymphoidleukaemia);systemiclupuserythematosus;orinfections(e.g.Babesia,bacterialendoc

arditis).ROUTINEHAEMATOLOGY2021/02/2420DISORDERSOFWHITECELLNUMBERNeutrophiliaFigure3.20CausesofneutrophiliaPhysiologicalresponse

(fear,excitement,exercise)Stress/corticosteroid-inducedAcuteinflammatoryresponse:bacterialinfection(localizedorgeneralized),immun

e-mediateddisease,necrosis,e.g.pancreatitis,neoplasia,especiallywithtumornecrosis.Chronicgranulocyticleukaemi

aNeutrophildysfunctionParaneoplasticsyndromes2021/02/2421NeutropeniaThethreemaincausesofneutropeniaare:•Anoverwhelmingdemandforne

utrophils•Reducedproductionofneutrophilsinthebonemarrow•Defectiveneutrophilmaturationinthebonemarrow.Anoverwhelmingdemandforneutrophilsmayoccurwithp

eracutebacterialinfections,especiallyGram-negativesepsisandendotoxaemia.Otherpossiblecausesincludeperitoni

tis,pyometra（子宫蓄脓）,aspirationpneumoniaandcanineparvovirusinfection.DISORDERSOFWHITECELLNUMBER2021/02/2422EosinophiliaEosinophilsaredistributedinthe

bodyamongvariouspoolsinasimilarwaytoneutrophils,althoughthebonemarrowstoragepoolisminimal.Eosinophilscirculateinthebloodstr

eamforonlyafewhoursbeforeenteringthetissues,wheretheymayliveforseveraldays.Theirtwomainfunctionsaretokillparasitesandtoregulateallergicandinflamm

atoryreactions.EosinopeniaEosinopeniaincombinationwithlymphopeniaoccursfollowingstress,administrationofcorticos

teroidsandinspontaneoushyperadrenocorticism(Cushing'ssyndrome).BasophiliaBasophilscontaininflammatorymediatorssuchashistamineandheparinandfunction

inasimilarmannertomastcellsinhypersensitivityreactions.DISORDERSOFWHITECELLNUMBER2021/02/2423LymphocytosisCauses

oflymphocytosis1.Physiologicallymphocytosis,withconcomitantneutrophilia,inresponsetoexcitement(espec

iallycats)2.Strongimmunestimulation(e.g.inchronicinfection,viraemiaorimmune-mediateddisease)3.Chroniclymphocyticleukaemia4.Hyp

oadrenocortiscism(lymphocytosismaybeassociatedwithaneosinophilia)5.Increasednumbersoflargereactivelymp

hocytesmayoccurtransientlyfollowingvaccination6.YounganimalshaveahigherlymphocytecountthanadultanimalsDISORDERSOFWHITECELLNUMBER2021/

02/2424LymphopeniaCausesoflymphopeniaarelisted.StressGlucocorticoidtherapyHyperadrenocorticismChylothorax(lossoflymphocytesin

tothepleuralspace)Lymphangiectasia(lossoflymphocytesintothegut)Acutephaseofmostviralinfections(e.g.caninedistemper,parvovirus,FeL

V)Septicaemia/endotoxaemiaDISORDERSOFWHITECELLNUMBER2021/02/2425DogsCatspercentageAbsolutevaluepercentageAbsolutevalue(10/TotalWBCN/a6~17N/a5.5

~19.5Bandneutropils0~30~0.30~30~0.3Neutropils60~773~11.535~372.5~12.5Lymphocytes12~301~4.820~551.5~7Monocytes3~100.2~1.51~40~1.5Eosinopils2~100.1

~1.32~120~1.5basopilsrarerarerareRareReferencerangesfortotalanddifferentialwhitebloodcellcounts2021/02/2426Table2show

sthealterationsinsomeofparametersinvariousdiseases.LaboratoryassessmentTeststoassessprimaryhaemostasisinclude:PlateletcountBleedingtimeClotretr

action.Teststoassesssecondaryhaemostasisinclude:Wholebloodclottingtime(WBCT)Activatedclottingtime(ACT)Activatedpa

rtialthromboplastintime(APPT)One-stageprothrombintime(OSPT)Thrombintime(TT)DISORDERSOFWHITECELLNUMBER2021/02/2427Disseminatedintravascularcoagul

ation(DIC):Thismaybetriggeredbyawidevarietyofdiseases,includingendotoxaemianeoplasia(especiallyhaemangiosarcoma血管肉瘤)acuteinfections(e.g.infectio

uscaninehepatitis)haemolyticanaemiapancreatitisheatstroke.TheclinicopathologicalfeaturesofDICare:•Thrombocytopenia

•IncreasedOSPT/APTT•ElevatedFDPs•Lowfibrinogen•Schistocytesinthebloodfilm.DISORDERSOFWHITECELLNUMBER2021/02/2428兽医临床病理学CollegeofVeterinaryMedicin

e,SCAU,Guangzhou,China5106422021/02/2429ClinicalbiochemistryIntroductionSerumproteinsTotalproteinandalbuminGlobulinsIndicatorsofrenalf

unctionUreanitrogenCreatinineMarkersofhepaticdiseaseAlanineaminotransferaseAspartateaminotransferaseAlkalinephos

phataseGamma-glutamyitransferaseBilirubinBileacidsAmmoniaPancreaticdiseaseAmylaseLipaseElectrolytesSodium;Potassium;Chloride

Magnesium;Calcium;PhosphorusMuscleenzymesCreatinekinaseAspartateaminotransferaseCarbohydratemetabolismGlucoseFructosamineLipidmetabolismCholeste

rolTriglyceridesMiscellaneoustestsIronLeadZincCopperChemicalprofilesandtestselection2021/02/2430SERUMPROTEINSTotalproteinandal

buminPhysiologyThecirculatingproteinsaresynthesizedpredominantlyintheliver,althoughplasmacellsalsocontributetotheirproduction.Quantitativelythesingl

emostimportantproteinisalbumin(35-50%ofthetotalserumproteinconcentration).Theotherproteinsarecollectivelyknownasglobulins.Thef

unctionsofproteinsaremanyandvariedbutincludemaintenanceofplasmaosmoticpressure,transportofsubstancesaroundthebody(e.g.ferriti

n铁蛋白,ceruloplasmin血浆铜蓝蛋白),humoralimmunity,bufferingandenzymeregulation.IndicationsforassayThemeasurementofproteinsisgenerallyincludedinan

initialhealthscreeninallpatientsbutespeciallywhereintestinal,renalorhepaticdiseaseorhaemorrhageissuspected.AnalysisProtei

nconcentrationscanbeestimatedinserum,plasma,urineorbodyfluidswitharefractometerorbyspectrophotometry.Serumalbum

inlevelsaremeasuredbybromocresolgreendye溴甲酚绿bindingandtheserumglobuliniscalculatedbysubtractionofthealbuminconc

entrationfromthetotalproteinconcentration.2021/02/2431ReferencerangesNeonatesandveryyounganimalshavelowerconcentrati

onsofalbuminandglobulins(duetominimalquantitiesofimmunoglobulins).Astheanimalgainsimmunocompetencetheproteinconcentrationsrisetoreac

hadultvalues.Physiologicaldecreasesinalbuminmaybenotedduringpregnancy.CriticalvaluesMarkedhypoalbuminaemia(

<15g/L)isassociatedwiththedevelopmentofascitesandtissueoedema.Accumulationofperitonealfluidmayoccurathigheralbuminconcen

trationsifthereisconcurrentportalveinhypertension,e.g.inchronicliverdisease.InterferingphenomenaLipaemia,h

aemolysisandhyperbilirubinaemiaproducefalseincreasesintotalproteinconcentrations.DrugeffectsHormoneshaveamarginaleffectonplasmaprote

inconcentrations.Corticosteroidsandanabolicsteroidsmayincreasetheproteinconcentrationduetotheiranaboliceffectswhilethecataboliceff

ectsofthyroxinecancauseadecrease.SERUMPROTEINS2021/02/2432Figure4.3:Causesofhypoalbuminaemia.IncreasedlossGlomerularproteinlossProtei

n-losingenteropathyCutaneouslesions,e.g.bumsExternalhaemorrhageDecreasedproductionHepaticinsufficienc

yMalnutritionMaldigestionMalabsorptionSequestrationBodycavityeffusionSERUMPROTEINS2021/02/2433GlobulinsAnalysisSerumproteinelectrophoresi

s(SPE)oncelluloseacetategelsallowsfractionationoftheproteins,dependingpredominantlyontheirchargeandsize.Afterstaini

ngforprotein,thecelluloseacetatestripisscannedbyadensitometerwhichconvertstherelativeintensitiesoftheproteinbandstopercentagesandgeneratesagraphth

atdemonstratestheproteinfractions(albumin,α1-globulin,α2-globulin,β1-globulin,β2-globulin,γ-globulin).CausesofhypoglobulinaemiaThemost

commonpathologicalcausesarehaemorrhageandprotein-losingenteropathies.SERUMPROTEINS2021/02/2434Figure4.4:Causes

ofhyperglobulinaemia.PolyclonalgammopathyInfections:BacterialdiseaseViraldisease(e.g.FIP)Immune-media

teddiseases:SystemiclupuserythematosusRneumatoidartnntisImmune-mediatedhaemolyticanaemiaImmune-mediatedthrombocytopemaNeoplasia,especiallylymphosarc

omaMonoclonalgammopathyNeoplasia:MultiplemyelomaMacroglobulinaemiaLymphosarcomaFelineinfectiousperitonitis(rare)S

ERUMPROTEINS2021/02/2435UreanitrogenPhysiology★Dietaryproteinsarehydrolysedintheintestinestotheirconstitue

ntaminoacidswhichmay,inturn,bedegradedtoammoniabytheactionofgutbacteria.★Theammoniaandaminoacidsaretransport

edtotheliverviatheportalcirculationwheretheyareutilizedintheureacycle.★Theureaformedinthehepatocytesisexcretedviathekidneytubules.★Ureapla

ysanimportantroleinconcentratingtheurine;thepresenceofhighconcentrationsofureaandsodiumchlorideintherenalmedul

laryinterstitiumcreatesanosmoticgradientforreabsorptionofwater.INDICATORSOFRENALFUNCTION2021/02/2436IndicationsforassayTheurean

itrogen(urea)concentrationisoneofthetestsusedwhenscreeningrenalfunction.Itisoftenmeasuredwhentheclinicalsignsincludevomiting,anorexia,weig

htloss,polydipsiaanddehydration.AnalysisUreacanbemeasuredinserum,plasmaandurinebyspectrophotometry.Sticktestsforwholebloodareals

oavailable.ReferencerangesDogs3.0-9.0mmol/LCats5.0-10.0mmol/LInterferingphenomenalipaemiainterfereswiththeanalysisandproducesvariabl

eeffectsdependingonthemethodology.INDICATORSOFRENALFUNCTION2021/02/2437Causesofreducedbloodurea☆Reduceddietar

yproteinintakeisassociatedwithalowbloodurea.☆Inaddition,patientswithdiffuseliverdiseasehaveanimpairedcapacitytosy

nthesizeureaandreducedhepaticproduction.Wherehepaticdiseaseissuspected,acompletebiochemistryproabileaci

dstimulationtestareindicated.☆Themarkeddiuresis（多尿）associatedwithsomeconditions,especiallyhyperadrenocorticismanddiabetes,resultsinincrease

durinarylossofureawhich,inturn,causesareductionofthebloodurea.INDICATORSOFRENALFUNCTION2021/02/2438Causesofincreasedb

loodurea☆Increaseddietaryproteinintakeproducesahighlevelofureaintheblood.Amoderateincreaseindietarypro

teinisnotcommonlyassociatedwithanotableriseinureaabovethereferencerange,buthigh-proteindietscancausesignificantincreases.☆

A12-hourfastisrecommendedbeforesamplingformeasurementofurea.☆Intestinalhaemorrhagealsoresultsinaninc

reasedconcentrationwhichisreportedtocorrelatewiththeseverityofbloodloss.☆Ureaisfreelyfilteredattheglomerulusandreabsorbedintherenaltubules.T

herateofreabsorptionishigheratslowerurinaryflowrates,e.g.indehydratedpatients.☆Bloodureaisthereforenotareliableestimateoftheglomerul

arfiltrationrate(GFR).Increasedureaconcentrationsareassociatedwithconditionsotherthanparenchymalrenaldisease.☆Thepres

enceofaconcentratedurinesample(urineSG>1.030indogs,>1.035incats)supportsthediagnosisofaprerenalazotaemia.INDICATORSOFRENALF

UNCTION2021/02/2439CreatininePhysiology◤Creatinineisformedfromcreatineinthemusclesinanirreversiblereaction.Thequa

ntityofcreatinineproduceddependsupondiet(smallcontribution)andthemusclemass.Diseaseaffectingthemusclemassmayaffectthedailycre

atinineproduction.◤Bothureaandcreatininearefreelyfilteredattherenalglomerulusbutureaissubjecttotubularreabsorptionandthuscreatinineissaid

tobeabetterindicatorofGFR.Analysis◤Creatininecanbemeasuredinserum,plasmaorabdominalfluidbyspectrophotometricmethods

.ReferencerangesDogs20-110umol/LCats40-150umol/LINDICATORSOFRENALFUNCTION2021/02/2440Causesoflowserumcreatinine◤Sincethedailyproductionofcreatininei

sdependentuponthemusclemassoftheanimal,thebodyconditionshouldbeconsideredwheninterpretingserumcreatinineconcentrations.Apoorbodycondi

tionmaybeassociatedwithlowconcentrationswhileminorrisesinsuchcasesmaybemoresignificantthaninotherindividuals.Causesofincreasedserumcreatinine◤De

creasedglomerularfiltrationisthemajorcauseofraisedserumcreatinine.However,approximately75%ofnephronfunctionmustbeimp

airedbeforeserumcreatinine(andurea)isincreased.CreatinineisconsideredamorereliableindicatorofGFRthanisureanitrogen,s

incetherearefewerfactorswhichinfluencetheserumconcentrationofcreatinine.INDICATORSOFRENALFUNCTION2021/02

/2441►Thebiochemicalparametersusedtoassessliverpathologymaybedividedintotwoclasses:thehepaticenzymesthatreflect

liverdamageandcholestasis,andtheendogenousindicatorsofliverfunction.►Alanineaminotransferase(ALT)isthemostusefulenzymeforidentifyinghepatocell

ulardamageindogsandcatsbutshouldnotbeusedaloneasascreeningtestforliverdisease.►Theproductionofotherenzymes,i.

e.alkalinephosphatase(ALP)andgamma-glutamyltransferase(GGT),isincreasedsecondarytointra-andextrahepaticchol

estasis.►Theseenzymesaremarkersofcholestaticdisease.►Bilirubin,serumalbuminandserumbileacidsareconsideredtobeindicatorsofhepaticfunction.►Itiscommon

forextrahepaticdisease(e.g.pancreatitis,diabetesmellitus,hyperadrenocorticismandinflammatoryboweldisease)tocauseabnorm

alitiesofthesebiochemicalparameters.MARKERSOFHEPATICDISEASE2021/02/2442Alanineaminotransferase(ALT)PhysiologyALTisfoundinthecytos

olofhepatocytesandinmuscletissueinthedogandcat.Activitiesintheserumareelevatedbyleakageoftheenzymesecondarytoanincrease

inhepatocytemembranepermeabilityorcellnecrosis.Theformermaysimplybeaconsequenceofhypoxiaandneednotreflectcelldeath.IncreasedserumALTmaybenotedw

ithin12hoursofanacutehepaticinsultbutcantake3-4daystoreachpeaklevelsafterexperimentalcholestasis（胆汁阻塞）.Thedegreeofincreaseinenzymeactivitycorrelat

esapproximatelywiththenumberofhepatocytesaffectedbutdoesnotindicatethenature,severityorreversibilityofthepathologic

alprocess.ALTactivityisnotanindicatorofhepaticfunction.IndicationsforassaySerumALTisausefulaidinthediagnosisofhepaticdiseaseandism

easuredwheretheclinicalsignsmightsuggestahepatopathy,e.g.weightloss,anorexia,polydipsia,vomiting,diarrhoea,ascitesandjaundice.Analysi

sTheactivityoftheenzyme(ininternationalunits)ismeasuredinserumorplasmabyspectrophotometricmethodsunderspecifi

edconditions.ReferencerangesDogs<100units/LCats<75units/LMARKERSOFHEPATICDISEASE2021/02/2443CausesofraisedALTac

tivityGuidelinesfortheinterpretationofraisedliverenzymeactivitiesinrelationtoliverdiseasesaregiveninChapte

rliver.ThemajorityofdiseasesthataffectthelivercouldpotentiallycauseanincreaseinserumALTactivitybutthosepa

thologicalprocessesthatmightcauseamarkedincreaseincludeparenchymaldisease/damage,cholangitis,cholangiohepatitis,chronichepat

itis,anoxia,cirrhosisanddiffuseneoplasia,e.g.lymphoma(lymphosarcoma).However,insomecasesthesediseases

maybeaccompaniedbyanegligibleincreaseornoincreaseinserumALTactivity.CausesofreducedALTactivityAnartefactua

lreductioninserumenzymeactivitiesmayresultfromsubstratedepletion.Dilutionandrepeatassayofthesamplearenecessarytoex

cludethisphenomenon.ReducedALTactivities(belowthereferencerange)aregenerallynotconsideredtobeofclinicalsignificance,butthepossi

bilityofchronicliverdiseaseandnutritionaldeficiencies(zincorvitaminB6)shouldbeconsidered.MARKERSOFHEPATICDISEASE2021/02/2444A

spartateaminotransferase(AST)(seealsoMuscleenzymes)PhysiologyASTislocatedinthemitochondriaofthecellandispresentinsignificantquantitiesinhep

atocytes,erythrocytesandinmuscle.ASTisthereforenotliver-specificbut,likeALT,itsactivityintheserumiselevatedbyleakageoftheenzymefromthecell.I

ndicationsforassayASTisincludedindiagnosticprofilesforinvestigationofsuspectedliverdiseaseormuscledisease.AnalysisT

heenzymeactivityismeasuredinserumandheparinizedplasmabyspectrophotometry.ReferencerangesDogs7-50units/LCats7-60units/LCausesofrais

edASTThemostcommoncausesofincreasedASTarehepaticdisease,muscledisease(trauma,inflammation)andhaemolysis.Concurrentmeasurementofotherhepaticenzymes

(ALT,ALP,GGT)andhepaticfunctionindicators(albumin,urea,bilirubin,bileacids)areessentialtoestablishtheoriginoftheincreasedserumA

STandtoprovidefurtherinformationregardingliverdamageandfunction(seeChapter9).Withrespecttoliverdamage,theserumactivityofASTtendstoparallelthatofALT

.MARKERSOFHEPATICDISEASE2021/02/2445Alkalinephosphatase(ALP,SAP)PhysiologyIndogsandcatsthereareisoformsofALPl

ocatedinbrushbordersintheliver,placenta,intestine,kidneyandbone.Inthedogthereisalsoasteroid-inducedisoen

zyme(SIALP),theoriginofwhichhasnotbeenfullydetermined.TheproductionofSIALPisincreasedbytheadministrationofglucocorticoids(

oral,parenteralortopical),byexcessiveproductionofendogenousglucocorticoids(hyperadrenocorticism)andinassociationwi

thchronicdisease(e.g.renalorhepatic).Theliverisoenzymeisresponsiblefortheserumactivityinthenormaladultdogandc

at.IndicationsforassaySerumALPisoneofthetestscommonlyincludedinscreeningprofilesforhepaticdisease(cholestasis)andhyperadrenocorticism.Itisthe

reforeusefulwheretheclinicalsignssuggesteitherofthesediagnoses,e.g.weightloss,anorexia,polydipsia,vomiting,diarrhoea,ascitesandjau

ndice.AnalysisSerumALPactivityismeasuredinserumorheparinizedplasmabyspectrophotometry.ReferencerangesDogs<200units/LCats<1

00units/LMARKERSOFHEPATICDISEASE2021/02/2446CausesofraisedALPFromadiagnosticviewpointthemostimportantisoenzymesinsmallanimalsarethebone,hepatic

andsteroid-inducedforms.IncreasesinboneALPcausesraisedserumactivitiesinyounggrowinganimals,butvaluesarerarelymorethantwo-foldgreaterthantheuppe

rlimitoftheadultreferencerange.ThisphysiologicalincreaseinserumALPshouldbeconsidered.Increasesinthehepaticisoenzymearecommo

nlyassociatedwithcholestaticdisease.Includepancreatitis,pancreaticneoplasiaandcholelithiasis.Cholelithsareveryrarei

nthedog.Theenzymeisgenerallyincludedinprofileswhereitcontributestothediagnosisofhepaticdisease.ALPshouldnotb

eusedalonewhenscreeningpatientsforevidenceofliverdisease.Indogs,theincreaseinALPassociatedwithsteroidadministrationvar

iesdependingonthepatient,thedrugusedandtherouteofadministration.ALPinthecathasaveryshorthalf-lifeandthemagnitud

eofincreasenotedinhepaticdiseaseisgenerallylessthanthatrecordedindogs.AnyincreaseinALPisprobablysignificantinacat.MARKERSOFHEPAT

ICDISEASE2021/02/2447.Gamma-glutamyltransferase(GGT)PhysiologyGGTisacytosolicandmembrane-boundenzymef

oundinhighestconcentrationsinthebrushbordersoftherenalandbileductepithelium.Cholestasisandenzymeinductionduetoglucocortic

oidtherapycauseincreasedserumactivities.IndicationsforassayGGTisusedinconjunctionwithALPandotherlivertestsinthediagnosi

sandmonitoringofhepaticdisease.ItisthoughttobemoreusefulthanALPinthecatandtheserumactivityindogsdoesnotappea

rtobeaffectedbytheadministrationofanticonvulsants.Dogs0-8.0units/LCats0-8.0units/LCausesofincreasedGGTS

erumGGTisamarkerforcholestaticdiseaseinthedogandcat.InthecatitmaybemoreusefulthanALPinthediagnosisofcholestatichepaticdiseaseMARKERSOFHEPAT

ICDISEASE2021/02/2448BilirubinPhysiologyBilirubin（胆红素）isderivedfromthecatabolismofhaemoproteinsinthecellsofthereticuloendothelialsyst

em.Thenewlyformedlipid-solublebilirubin(indirect-reactingbilirubin)isthenboundtoalbumin,whichfacilitatesitstransferthroughtheaqueousp

haseoftheplasmatotheliver.Inthehepatocytethebilirubinisconjugatedwithglucuronicacid（葡糖醛酸）,creatingawater-solublemolecule(d

irect-reactingbilirubin).IndicationsforassayMeasurementofbilirubinisindicatedwherethereisjaundice（黄疸

）onclinicalexamination,visibleicterus（黄疸）oftheserumorplasma,orsuspectedhepaticdisease.Clinicaljaundiceinthed

ogisdetectedwhenthebilirubinisatleast25-35umol/L.AnalysisThetotalserumbilirubinconcentration(conjugatedandunconjugated)is

measuredinserumorplasmabyspectrophotometry.ReferencerangesDogs0-6.8umol/LCats0-6.8umol/LMARKERSOFHEPATICDISEASE2021/02/2449

CausesofhyperbilirubinaemiaJaundicemaybeclassifiedaccordingtotheunderlyingpathologicalprocess:prehepaticjaundice(increasedproductionofb

ilirubin,e.g.haemolyticanaemia,andinternalhaemorrhage);hepaticjaundice(failureofuptakeorconjugationofbilirubin);posthepaticja

undice(obstructionofthebiliarysystem).Afullhaematologicalproindicatedinalljaundicedpatientstoexcludethepossibilityofprehepaticcauses.Characteri

sticfindingsthatmaybenotedinhaemolyticanaemiaincludemarkedreticulocytosis(网状细胞过多症，indicativeoferythrocyteregenerat

ion),autoagglutinationoftheredcellsandtheformationofspherocytes.Theplateletcountandserumproteinsarecommonlywithinthereferencerangeforthespecie

s.Theabnormalitiesofbilirubinassociatedwithhepaticdiseaseandcholestaticdiseasearediscussedmorefully.Previouslyitwasbeliev

edthatthemeasurementofdirectandindirect-reactingbilirubinwouldhelptodeterminethecauseofthejaundice.However,itisnowclearthatthisisnotthecaseinthedogan

dcatandthathepatic,haemolyticandbiliarytractdiseasesproducevariableincreasesinthesefractions.Differentiationofprehepatic,hepaticandposthepat

icjaundicerequiresafullhaematologicalandbiochemicalinvestigation(includingmeasurementofredcellmass,examinationofabloodsmearandliverfun

ctiontests)andmayrequireexaminationofthebiliarytract.Hepaticbiopsymayalsobenecessaryinsomecases.MARKERSOFHEPATIC

DISEASE2021/02/2450BileacidsPhysiologyTheprimarybileacidsareproducedintheliverfromcholesterolandarethenconjugatedtotaurine（氨基乙磺酸）orglyci

ne（氨基乙酸）.Theyareexcretedintothebiliarytreeandstoredinthegallbladder.Gallbladdercontraction(stimulatedbyingestio

noffood)releasesthebileacidsintotheintestineswheretheyfacilitatethedigestionandabsorptionofdietarylipid.Thebileacidsare

efficientlyreabsorbedintheileum,resultinginverysmallfaecalloss.Thetotalpoolofbileacidsmayundergoenterohepaticcirculationt

wotofivetimesduringasinglemeal.IndicationsforassayInclusionofbileacidsinaproindicatedwherethereissuspicionofhepaticdisease.Clinicalsignsinsuchpatient

smightincludehepatomegaly（肝大）,microhepatica（小肝）andabnormalcentralnervoussystemsigns.Thesensitivityofthebileacidassaymaybeincrea

sedbyusingabileacidstimulationtest.Referenceranges(fasted)Dogs0-15umol/LCats0-15umol/LMARKERSOFHEPATICDISEASE2021/02/2451

CausesofincreasedbileacidsThefastingserumbileacidconcentrationmayberaisedinassociationwithprimaryorsec

ondaryhepaticdisease.Theassayfacilitatesidentificationofhepaticdysfunctionbutgivesnoindicationastothenature

orreversibilityoftheliverpathology.Valuesexceeding30umol/Larecommonlyassociatedwithhistologicallesionsandbiopsymaybehelpfulinthesecases.

Itisimportanttorememberthatthehistologicalchangescouldstillbeassociatedwithsecondaryhepaticdiseaseeventhoughthefastingbileacidconcen

trationis>30umol/L,forexampleinhyperadrenocorticism.Theuseofthebileacidstimulationtestmayimprovethesen

sitivityoftesting.Forthis,serumbileacidconcentrationsaremeasuredinasamplecollectedaftera12-hourfast(fastingbileacidconcentration)

and2hoursafterafattymeal(postprandial（餐后）bileacidconcentration).Inonestudyof108cats,thepostprandialbileacidconcentrationwa

sfoundtohavethehighestsensitivityofanysingletestforthediagnosisoffelineliverdisease.MARKERSOFHEPATICDISEASE2021/02/2452AmmoniaPhysiologyDie

taryproteinsarehydrolysedintheguttoaminoacidswhich,inturn,maybedegradedbyintestinalbacteria,producingammon

ia.Ammoniaistransportedtotheliverwhereitisusedasaprecursorinthesynthesisofurea.Increasedbloodammoniaconcentr

ationsareobservedinsomepatientswithdiffuseliverdisease(withareducedcapacityforureasynthesis)andinindividualswithportosystemicshunts.Indica

tionsforassayAmmoniaisusedintheevaluationofhepaticfunction;theindicationsformeasurementarethesameasforbi

leacids.AnalysisAmmoniaismeasuredinblood,serumorplasmabydryreagentandenzymaticmethods.Samplesshouldbecollectedintoa

chilledsampletubeandstoredoniceuntilanalysis,whichmustbecarriedoutwithin20minutesofcollection.Referenceran

gesDogs0-60umol/LCats0-60umol/LMARKERSOFHEPATICDISEASE2021/02/2453CausesofincreasedammoniaIncreasedammoniaconc

entrationsareassociatedwithfeedinghigh-proteindietsandwithintestinalhaemorrhage(duetotheincreaseddeliveryofaminoacidstotheintestinalbacteria)

.Diffusehepaticdisease,resultinginthefailureofconversionofammoniatourea,andportosystemicshunts(congenitalandacquired)willalsoproducei

ncreasedserumammoniaconcentrations.MARKERSOFHEPATICDISEASE2021/02/2454PANCREATICDISEASEAmylasePhysiologyAmylase（淀粉酶）isacalcium-dep

endentenzyme,producedbythepancreaticacinarcells,whichhydrolysescomplexcarbohydrates.Theenzymepassesdirectlyfromthepancreasinto

thecirculationwhereitisfilteredbytherenaltubules;theinactivatedenzymeisreabsorbedbythetubularepithelium.Amylaseactivityinth

etissuesofthedogandcatishighestinthepancreasbutisalsofoundintheintestinesandliver.IndicationsforassayAmyl

aseshouldbemeasuredwhenthepresentingsignsmightsuggestpancreatitis（胰腺炎）,e.g.vomiting,abdominalpainoricterus,orwh

enthereisfreeperitonealfluid.AnalysisAmylaseactivitiesmaybemeasuredinserum,heparinizedplasmaandabdominalflui

dusingspectrophotometricmethods.ReferencerangesDogs400-2000units/LCats400-2000units/L2021/02/2455CausesofincreasedamylaseThet

issuedistributionofamylaseisnotrestrictedtothepancreasandthereforeraisedserumactivitiesarenotspecificforpancreatitis.Reducedglomerularfiltratio

n(prerenal,renal,postrenal)isoftenassociatedwithanincreasedserumamylaseactivitybutthisiscommonlyless

thantwotothreetimesgreaterthantheupperlimitofthereferencerange.Serumactivitiesabovethislevelaresuggestiveofpancreatitisbutthedegreeofin

creasedoesnotcorrelatewellwiththeseverityofpancreatitis.Ifanazotaemic（氮血症）patienthasanamylaseactivitytwotothreetimestheupperlimitoftherefer

encerangethenpancreaticdiseasemustbeconsidered.Thesimultaneousmeasurementofamylaseandlipaseincasesofsuspectedpancreatitisisadvisab

lewhileadditionaltestsofrenalandhepaticfunctionshouldalsobeincludedinthebiochemicalprofile.Amylaseisnotareliableindicatorofpancreatitisincats.I

ncasesthatpresentwithfreeperitonealfluid,fullanalysisofthefluid(proteinconcentration,cellcountsandcytologicalexamination)andmeasurementofth

eserumandfluidamylaseactivitiesmaybeuseful.Thepresenceofanon-septicexudatewithgreateramylaseactivitythantheserummaybeassociatedwit

hpancreatitisorbowelrupture.PANCREATICDISEASE2021/02/2456LipasePhysiologyLipaseisadigestiveenzyme,producedbyt

hepancreaticacinarcells,thathydrolysestriglycerides.Theenzymeisclearedfromthecirculationbyrenalinactivation.Aswithamylase,lipasema

yoriginatefrompancreaticorextrapancreaticsources.Pancreaticdamageandinflammationresultsinthereleaseoflipaseintothe

surroundingglandandperitonealtissuewhichmaycausethedevelopmentofnecrosisintheperipancreaticperitonealfat.IndicationsforassayIndi

cationsforthemeasurementoflipasearethesameasforamylase.Amylaseandlipaseassaysshouldbeperformedsimultaneouslyincasesinwhichpancr

eatitisissuspected,buttheincreasesinenzymeactivitiesareoftennotparallel(markedincreasesinoneenzymemaybeassociatedwith

minimalincreasesintheother).AnalysisLipaseactivitiesaremeasuredinserum,heparinizedplasmaandbodyfluidsusingturbidimetricmethods.ReferencerangesDogs

0-500units/LCats0-700units/LPANCREATICDISEASE2021/02/2457CausesofraisedserumlipaseSincelipaseoriginates

frombothpancreaticandextrapancreatictissue,anincreaseinserumactivityisnotdiagnosticofpancreatitis.Increasedserumacti

vityisalsonotedinazotaemicpatients,althoughthevaluesgenerallydonotexceedtwotothreetimestheupperlimitofthereferencerange.I

naddition,moderateelevationsoflipase(upto5-foldincreases)havebeenreportedinassociationwithadministrationofdex

amethasonewithoutevidenceofhistologicalchangesinthepancreas.Anormallipaseactivitydoesnotprecludepancreaticdisease.Lipasehasbe

enreportedtobepersistentlyelevatedincatswithexperimentallyinducedpancreatitisbutthisisnotaconsistentfindinginnaturallyoccurringdiseas

e.PANCREATICDISEASE2021/02/2458CARBOHYDRATEMETABOLISMPhysiologyGlucoseistheprincipalsourceofenergyformammaliantissuesandisderived

fromthedietandhepaticgluconeogenesis.Thebloodconcentrationiscontrolledbyhormoneswhichregulateitsentryin

to,andremovalfrom,thecirculation(insulin,glucagon,adrenaline,cortisol).Inthekidneyofthedogandcat,glucoseenteringtheglomerularultrafiltrateisreabsorbe

dbytherenaltubules.However,therenalreabsorptionofglucoseisoverwhelmedinthepresenceofbloodglucoseconcentrationsgreat

erthan10-12mmol/1,resultinginglucosuria.IndicationsforassayMeasurementofbloodglucoseisessentialwherepresentingclin

icalsignscouldsuggest：diabetesmellitus(polydipsia,polyuria,weightloss,cataractformation),diabeticket

oacidosis(vomiting,diarrhoea,anorexia)hypoglycaemia(weakness,collapse,seizures,disorientation,depression,b

lindness).Inaddition,theassayisincludedingeneralhealthscreenswhereitmayprovidesupportiveevidenceforotherdiseas

eprocesses(hyperadrenocorticism,hepaticdisease).Measurementofthebloodglucoseconcentrationistheidealmethodofmonitorin

gthestabilizationofdiabeticpatientsoninsulintherapyandallowsoptimizationofthetherapeuticregimen.Insuchcases,

glucoseismeasuredinsamplescollectedat2-hourlyintervals,allowingcalculationofthedurationofactionandpeaktimeofactionoftheadministeredinsulin.Glucos

e2021/02/2459AnalysisReagentstrips:Rapid-analysisreagentstripsrequiretheuseofwholebloodwithnoanticoagulant.Lab

oratoryanalysis:Spectrophotometricmethods(enzymaticorchemical)arcgenerallyusedforthemeasurementofbloodglucose.Wherein-houseequipmen

tdemandstheuseofheparinizedplasma,thesamplemustbeseparatedimmediatelyaftercollection.Thispreventsdepletionoft

heplasmaglucosebytheerythrocytes.Collectionofthebloodintofluorideoxalateisthepreferredmethodofpreventi

ngerythrocyteglucoseutilizationwhenadelayinanalysisisanticipated,suchasduringtransporttoacommercialla

boratory.ReferencerangesDogs3.5-5.5mmol/LCats3.5-6.5mmol/LGlucose2021/02/2460CausesofhypoglycaemiaMar

kedhypoglycaemia(glucose<2mmol/L)mostcommonlyresultsfromoverproductionofinsulinorexcessiveutilizationofglucosebyneoplasticcells.Insulin-secretingt

umoursofthepancreas(insulinomas)producebiologicallyactivehormonewhichincreasestheuptakeofglucosebythebodytissuesandimpairshe

paticgluconeogenesis,resultinginhypoglycaemia.Inonestudyofdogswithinsulinomasthemean(+SD)plasmaglucoseconcentrationwas2.14(±0.82)mmo

l/1.Extrapancrcatictumoursoccasionallycausehypoglycaemiabysecretionofaninsulin-likesubstanceorbyincreasedutilizationofpl

asmaglucose.Glucose2021/02/2461Neoplastic:Insulin-secretingtumourofthepancreas(insulinoma)HepatocellularcarcinomaEndocrine:HypoadrenocorticismHepati

cinsufficiency:CongenitalvascularshuntsAcquiredvascularshuntsChronichepaticfibrosis(cirrhosis)Hepaticnecrosis(e.g.hepato

toxins,bacterialinfection,trauma)GlucoseFigure4.19:Causesofhypoglycaemiainthedog.Catsmayrarelybeaffectedbyinsulinoma.Substratedeficiency:Neona

talhypoglycaemiaJuvenilehypoglycaemiaHuntingdoghypoglycaemiaGlycogenstoragediseaseSepsis2021/02/2462Causesofhypergl

ycaemiaHyperglycaemiacommonlyresultsfromarelativeorabsolutelackofinsulin.Thisleadstoimpairedtissueutilizationofplasmaglucoseandanincre

aseintherateofgluconeogenesis.Mildhyperglycaemia(6.7-10mmol/L)inthedogmaybenotedaspartofanadrenalinestressresponseorsecondarytoexcessives

ecretionoradministrationofotherdiabetogenichormones,inparticularglucocorticoidsandprogesterone.Themildhyperglycaemiaisaresultofthehormonala

ntagonismoftheactionsofinsulin.Inaddition,mildhyperglycaemiamaybenotedinthepostprandialperiodindogsfedasug

ar-richdietsuchassemi-moistfoods.Apersistent,moderatetomarkedhyperglycaemiainthedogisconsistentwithdiabetesmellit

us.Suchcasesdonotpresentwithclinicalsigns(polyuriaandpolydipsia)untiltherenalthresholdforglucoseisexceeded,resultinginosmoticdiures

is.Inthecat,anadrenaline-inducedstressresponsemayproduceamoderateormarkedincreaseinglucoseconcentration.Thediagnosisofdia

betesmellitusisoftendifficultincatsandconfirmationrequiresdocumentationofpersistenthyperglycaemiawithcompatibleclinicals

igns.Glucose2021/02/2463Figure4.20:Causesofhyperglycaemia.Adrenalinestressresponse(especiallymarkedincats)PostprandialDiabetesmellitusHyperad

renocorticism(dogsandrarelycats)Acromegaly(cats)Acutepancreatitis(dogsandcats)RenalinsufficiencyGlucose2021/02/2464FructosaminePhysiologyFructosa

mineisaglycatedserumproteinwhichisformedbythenon-enzymaticreactionbetweenasugarandanaminoacid.Thetotalamountoffructosamineformedisproportiona

ltotheserumglucoseconcentrationduringthelifespanoftheproteins.Indogsandcats,fructosaminehasbeenfoundtobeause

fulparameterinthediagnosisandmanagementofdiabetesmellitus.IndicationsforassaySerumfructosamineconcentrati

onsareusefulinthediagnosisofdiabetesmellitusandinidentifyingpersistenthyperglycaemiaduringtherapy.Measurementoffructosamine

mayalsobehelpfulinconfirmingthepresenceofpersistenthypoglycaemia.AnalysisFructosamineismeasuredusingam

ethodbasedonthereducingabilityoffructosamineinalkalinesolution.ReferencerangesDogs250-350umol/LCats150-

270umol/L2021/02/2465CausesoflowserumfructosamineAlowserumfructosamineconcentrationhasbeenrecordedinadogwithaninsulin-secretingtumourofthepancreas

(insulinoma).Ithasbeensuggestedthatthemeasurementofserumfructosamineinadditiontoglucoseandinsulinmaybehelpfulinconfirmingthepresenceofins

ulinomas.CausesofraisedfructosamineRaisedserumconcentrationsoffructosaminereflectpersistenthyperglycaemiaovertheprecedin

g2-3weeks.Indogswithdiabetestheserumfructosamineconcentrationissignificantlygreaterthanindogswithotherdiseas

es.Fructosamineisalsousefulforconfirmingdiabetesmellitusinthecatandcanbehelpfulinidentifyingpersistenthyperglycaemiaafterini

tialstabilizationoninsulintherapy.Fructosamine2021/02/2466LIPIDMETABOLISMPhysiologyCholesterolisthemostcommonsteroidinthebodytiss

uesandactsasaprecursorcompoundforsteroidhormoneandbilesaltsynthesis.Themajorityofthebody'scholesterolissynthesizedbytheli

ver,buttheremainderoriginatesfromdietarysources.Excesscholesterolisexcretedinthebile.IndicationsforassayHypercho

lesterolaemiaisoftenassociatedwithendocrinediseaseinthedogandcatandisfrequentlymeasuredaspartofageneralhealthprothesespecies.Raisedplasmacholes

terolaloneisnotcommonlyresponsibleforthedevelopmentofclinicaldiseaseinthedogandcat.However,markedhypercholesterolaemiaandhypert

riglyceridaemiasecondarytothyroiddysfunctionindogshavebeenassociatedwiththedevelopmentofperipheralvasculardisease.Analysis

Cholesterolconcentrationsareassayedinserum,heparinizedplasmaorEDTAplasmausingspectrophotometric,automateddirectandenzymaticmethods.Cholestero

l2021/02/2467Figure4Causesofalterationsinplasmacholesterolconcentrations.HypocholesterolaemiaProtein-losingenteropathyMa

ldigestion/malabsorptionHepatopathy(portocavalshunt,cirrhosis)HypercholesterolaemiaPostprandialhyperlipidaemiaSec

ondaryhyperlipidaemia:HypothyroidismDiabetesmellitusHyperadrenocorticismCholestaticdiseaseNephroticsyndrome2021/02/2468Causeso

fhypercholesterolaemiaAmarginalincreaseinthecholesterolconcentrationmaybenotedinsamplescollectedinthepostprandialperi

odversusafastedsample.Thisincreasedlevelgenerallydoesnotexceedthereferencerangeforthespecies.Hypercholesterolaemiai

nthedogandcatismostcommonlyassociatedwithendocrinedisease(diabetesmellitus,hypothyroidism,hyperadrenocorticism).Ineachoftheseend

ocrinedisorderstheremaybeaconcurrentincreaseinserumtriglycerideconcentration.Hypercholesterolaemiamayalsobeno

tedincholestaticdiseaseandglomerulonephritis(肾小球性肾炎）.Furtherspecialistinvestigation(e.g.lipoproteinele

ctrophoresis)maybenecessaryifnounderlyingsystemicorendocrinediseasecanbeidentifiedandthehypercholesterolaemiaismarkedandpe

rsistent.2021/02/2469TriglyceridesPhysiologyThetriglyceridesarethemostabundantlipidsinthebodyandtheirstorageinadiposetissueprovidesanessentialr

eserveofchemicalenergyfortissuerequirements.Theyarederivedfromthedietandalsosynthesizeddenovo（重新）intheliver.Indications

forassayFastinghypertriglyceridaemiainthedogandcatisapathologicalfinding.Thepresenceoflargetriglyceride

-richlipoproteinsimpartsaturbiditytotheplasmaorserum(lipaemia).Triglyceridesshouldthereforebemeasuredinallfastingbloodsamplesthatappe

artobelipaemic.Clinicalmanifestationsofhypertriglyceridaemiainclude：recurrentabdominalpain,alimentarysigns,seizures.2021/02/2470Causesofhypotrigly

ceridaemiaHypotriglyceridaemiahasnotbeenconsistentlyassociatedwithanyspecificdiseaseprocessalthoughithasbeenreportedinseveralcasesofacuteandc

hronichepaticdisease.CausesofhypertriglyceridaemiaThemostcommoncauseofapparenthypertriglyceridaemiainthedog

andcatisafailuretoobtainafastingsample(postprandialhyperlipidaemia).Ifhypertriglyceridaemiaisdocumentedi

nasamplecollectedaftera12-hourfast,endocrineandsystemicdiseaseshouldbeexcluded(diabetesmellitus,hypothyroidism,hyp

eradrencorticism,glomerulonephritis).Manydogswithspontaneousacutepancreatitishaveincreasedserumtriglycerideconcentrations.Therelationshipbetweenpanc

reatitisandhyperlipidaemiahasnotbeenfullyelucidatedbutitappearsthattheincreasedtriglycerideconcentrationmaypr

edisposepatientstopancreaticpathology.2021/02/2471Figure5CausesofhypertriglyceridaemiainthedogandcatPostprandialhyperlipidaemiaSecondaryh

yperlipidaemia:HypothyroidismDiabetesmellitusHyperadrenocorticismAcutepancreatitisPrimaryhyperlipidaemia:Idiopathichyperchylomicro

naemiaoftheMiniatureSchnauzerFamilialhyperchylomicronaemia（乳糜微粒血症）inthecatIdiopathichypertriglyceridaemia2021/02/2472CHEMICALPROFI

LESANDTESTSELECTIONOntheinitialpresentationofanillpatient,aclinicianformulatesalistofdifferentialdiagno

sesbasedonthehistoryandclinicalfindings.Wheretheclinicalfindingsarespecific,e.g.pallorofthemucousmembranessuggestiveo

fanaemia,thenstepsaretakentoconfirmthissuspicionandtoelucidatethepossiblecause.Awider,morecomprehensiveinvestigationisnecessarywhenclinicalsignsm

aybecausedbymanymetabolicdisorders;forexample,polydipsiainthedogcouldbetheresultofendocrinedisease,renaldiseaseorhepaticdisease.Theselectionofte

stsdependsuponthedifferentialdiagnoses,therangeofconditionsthatmustbeexcluded,theavailabilityofthete

sts,andthecostoftests.Inthecaseofthepolydipsicdog,acost-effectiveprorequiredtocoverthepossibilityoforganfai

lure(renal,hepatic),endocrinedisease(diabetesmellitus,hyperadrenocorticism)andhypercalcaemia.2021/02/2473Someofthesedifferentialsmaybe

excludedorconfirmedonthebasisofindividualtests(e.g.ureaandcreatinineforrenaldisease)butinclusioninamorec

omprehensiveprothesimultaneousassessmentandcost-effectiveexclusionofmanyothercausesofpolydipsia.Whentheclinicalsignsarevagueanda'

generalhealthscreen'isrequired,thenitisnecessarytoselectabroadrangeofanalyteswhichwillreflectanumberofcommondiseasesorpath

ologicalstates.Theinclusionofteststhatarenotorgan-specificbutwhichprovidegeneralinformationregardingthehydrationandessentialhomeosta

ticmechanismsisworthwhile,e.g.totalproteins,albumin,electrolytes,glucose.CHEMICALPROFILESANDTESTSELECTION2021/02/2474Pro

fileHealthPre-anaestheticscreen*Extended*healthscreenPolydipsiaprofileSeizureprofileRenalprofileHepaticprofile

TestsFBC,TP,albumin,globulin,ALT,ALP,GGT,bilirubin,amylase,urea,creatinine,glucose,urinalysisFBC，TP,albumi

n,globulin,ALT,ALP,bilirubin,urea,creatinine,glucoseAshealthscreenplusbileacids,electrolytes,cholesterol,CK,calcium,phosphorusFBC,TP,albumi

n,globulin,ALT,ALP,bilirubin,bileacids,CK,cholesterol,urea,creatinine,glucose,calcium,phosphorus,electro

lytescreen,urinalysis(SG,dipstickandsedimentexamination).FBC,TP,albumin,globulin,ALT,ALP,bileacids,urea,creatinine,glucose,calciu

m,CK,phosphorus,magnesium,electrolytescreenPCV,TP,albumin,globulin,urea,creatinine,sodium,potassium,calcium,phosphorus,urinalysis(SGdip

stickandsedimentexamination)TP,albumin,globulin,ALT,ALP,AST,GGT,bilirubin,bileacids,cholesterolIndicationsRouti

nescreeningScreenforexistingdiseasepriortoroutinesurgeryGastrointestinai.endocrinediseaseandnonlocaliz

ingsignsPolydipsiaSeizures,weakness,episodiccollapseMonitoringhepatotoxicity2021/02/24752021/02/2476GastrointestinalSystemFecalanalysisExamination

ofvomitusBloodtestsImagingtechniquesEndoscopy2021/02/2477Dysphagiaandregurgitation•Collectahistoryandconductathoroughphysicalexam

ination•Completeaneurologicalexamination•Observethepatienteating,toassessthelikelystageoftheswallowingprocessaffec

ted•Plainradiographyofpharynxandoesophagus•Possiblecontraststudies-bariumswallowandfluoroscopy•Examinationoforalcavityandpharynxundergen

eralanaesthesia•EndoscopicexaminationofpharynxandoesophagusPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2478Vomitin

g*Collectahistoryandconductathoroughphysicalexamination*Characterizethevomitusproduced*Isthevomitingprimaryorsecondary?PRIMARYSE

CONDARYHaematologyandbiochemistryHaematologyandbiochemistryPlainradiographyUrinalysisContraststudiesSpecifictestsofEndoscopy/exploratoryorg

anfunctionlaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2479Diarrhoea•Collectahistoryandconductat

horoughphysicalexamination•Physicalexaminationofthefaecesproduced•Isthediarrhoeaprimaryorsecondary?•Ifprimary,isth

ediarrhoeaofsmallorlargeintestinalorigin?PRIMARYSECONDARYSmallintestinalLargeintestinalUrinalysisHaematology/biochemistryFaecalcultureSpec

ifictestsoforganfunctionFaecalcultureWormeggcountWormeggcountRectalexaminationUndigestedfoodanalysisPlainradiograp

hySerumfolate/cobalaminEndoscopy/biopsyTrypsin-likeimmunoreactivityBreathhydrogenassaySugarpermeabilitytestUltrasoundsca

nEndoscopy/exploratorylaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2480Constipation*Collectahistor

yandconductathoroughphysicalexamination*Rectalexamination*Neurologicalexamination*Orthopaedicassessm

ent*PlainradiographyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2481Faecaltenesmus(里急后重）•Collectahistoryan

dconductathoroughphysicalexamination•Rectalexamination•Faecalcultureandwormeggcount•Plainradiography•Contraststudies•Ultrasoundscan•Endos

copy/biopsyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2482Acuteabdomen•Collectahistoryandconductathoroughphysicale

xamination•Carefulabdominalpalpation•Haematologyandbiochemistry•Plainradiography•Possiblycontraststudies•Paracentesis•Ultrasoundscan•Exploratorylapa

rotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2483Abdominalenlargement•Collectahistoryandconductathoroughphysicalexa

mination•Carefulabdominalpalpation•Haematologyandbiochemistry•Plainradiography•Paracentesis（腹腔穿刺）•Ultrasoundscan

•ExploratorylaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2484FAECALANALYSISPhysicalappearanceIniti

alexaminationofafreshfecalsampleshouldconcentrateonitsphysicalappearance.Inmanycasesofdiarrhoeaitispossibletodecidewhetheritisas

sociatedwithasmallorlargeintestinalproblemusingthecriteriashowninTable8.1.Suchadifferentiationnotonlygivestheclinicianvaluableinformationreg

ardingthelocationofthelesionbutconsequentlyassistsintheselectionoffurtherappropriatediagnostictests.Unfortunately,notalldi

arrhoeasmaybereadilyclassified,andfeaturesofbothsmallandlargeintestinaldiseasemaybepresent.Thismayreflectasmallintes

tinalproblemwhichresultsintheabnormalpresenceofnutrientsorotheragentsinthelargeintestine,therebycausingsign

soflargeintestinaldisease.Alternatively,itmayreflectaconditionthataffectsboththesmallandthelargeintestinee

qually.2021/02/2485Table8.1:Characteristicsoffaecespassedinsmallandlargeintestinaldiarrhoea.Symptom/SignSmallintestineLargeintestineFaecalvolum

eIncreasedReducedFaecaltenesmusNonePresentFaecalbloodNoneorchangedOftenpresentFaecalmucusNoneOftenpresentUrgency（尿急）RareOftenpresentDys

chezia（排便困难）AbsentOftenpresentSteatorrhoea（脂肪痢）OftenpresentAbsentVomitingMayoccurOccursin30%ofcasesWeightlossP

resentAbsentFlatus/borborygmi(肠鸣)PresentRareCoat/skinconditionPoorNormalAppetiteIncreasedNormalorreduced2021/0

2/2486Figure8.2Majorcausesofacutediarrhoeaindogsandcats.Endoparasitism:Hookworms钩虫Whipworms鞭虫Giardiasis贾第鞭毛虫病Dietaryindiscretions:Soi

ledfoodsScavengingOver-eatingViralinfections:Felinepanleucopenia猫瘟Canineparvovirus犬细小病毒Coronavirus冠状病毒Bacteriali

nfection:SalmonellosisCampylobacterinfection弯曲菌Intussusception肠套叠Haemorrhagicgastroenteritis2021/02/2487Figure8.3:Majorcauseofc

hronicdiarrhoeaindogsandcats.Smallintestinaldisease:Lymphocytic-plasmacyticenteritis淋巴细胞-浆细胞性肠炎Eosinophilicente

ritisLymphangiectasia淋巴管扩张Lymphosarcoma淋巴肉瘤GiardiasisExocrinepancreaticinsufficiency(EPI)Colitis:Lymphocytic-plasmacyticEosinophilicHistiocyticGranul

omatousLymphosarcomaSystemicdisease:Hyperthyroidism(cats)HypoadrenocorticalismHypothyroidism(dogs)Chronic

renalfailureHepaticdiseaseFeLV,FIVandFIP2021/02/2488Melaena（黑粪症）canbedefinedasthepresenceofchangedbloodinthefaeces.Theappearanceofmelaenawilldep

endontheextentofbleedinganditslocation,butmalaenicfaecesnormallyappearblackandtarryinconsistency.Thisappearanceisnormallyassociatedwit

hbleedingintothesmallintestine,althoughmelaenamayoriginatefromthestomachorfromtheoesophagus,pharynx,mouthorrespir

atorysystem.Inthelattercasesbloodisswallowedandpassesthroughthealimentarytracttoappearasmelaena,givingtheimpressionofalimentarydisease.Patientswi

thclottingdisordersmaypresentwithmelaena,butagaincarefulclinicalexaminationshouldrevealbleedingfromotherloc

ations,confirmingageneralizeddisorder.Occultblood（潜血）referstothepresenceofmicroscopicamountsofbloodthatcanonlybedetect

edbylaboratoryanalysis.Greatcareisrequiredininterpretingapositiveresultindogsandcatsastheyareoftenfedmeat-baseddiets

.Thepresenceofhaemoglobinormyoglobininthedietwillgivefalsepositiveresults.Itisthereforeimportanttoplacethepatientonameat-freedietforaminimumo

f3dayspriortotestingforoccultblood.Atruestrongpositiveresultindicatesonlythatbleedingisoccurringsomewherealongthealimentarytrac

t.2021/02/2489CultureforbacteriaNormalfloraThesmallintestineliesbetweenthealmoststerilestomach(duetogastricacid)andthelargebacterialpopulati

onlocatedinthecolon.Bacterialnumbersintheproximalsmallintestinearelowbutnumbersincreaseintheileum.Theactu

alnumberspresentinanyindividualwillvarydependingonvariousinternalandexternalfactors.Manyofthe'normal'floraarebeneficialtotheanimal

byproducingvitaminK,biotin,folateandshort-chainfattyacids(SCFAs).Ifthenumbersofbacteriapresentinthesmallinte

stineincrease,smallintestinalbacterialovergrowth(SIBO)develops.Suchaproliferationofbacteriacanseriouslydamaget

heintestinalmucosa.ThepointatwhichbacterialpopulationsinduceclinicalsignsofSIBOwillvarywitheachindividualandthegenusofbacteriapresent.2021/

02/2490PathogenicbacteriaPathogenicbacteriamayestablishwhenthereisinterferencewiththenormalphysiologicalre

gulationoftheresidentflora.Bacterialpropertiesthatpermitpathogenstoestablishinclude:thepresenceofflagellae;productionofenzymessucha

sproteases;theabilityofbacteriatoadheretothemucosa;andproductionoffactorsthatinterferewithintestinalmotili

ty.Theabilitiestoproduceenterotoxinandtoinvadeenterocytessignificantlyincreasepathogenicity.PotentialpathogensincludeSalmonella,Ca

mpylobacter,YersiniaandClostridiumspeciesandEscherichiacoli.2021/02/2491AnalysisforvirusesCanineparvovirus(CPV-2)i

nfectionusuallyresultsinanacuteenteritiswithsecondarybacterialinfection,involvingespeciallySalmonellaa

ndCampylobacterspp.Adefinitivediagnosisofparvovirusinfectionrequirescollectionofafreshfaecalsampleforviralantigendetec

tion.Ideally,samplesshouldbecollectedwithinthefirst2daysofinfectionwhenthelargestnumberofvirusparticlesarepresent.AcommercialELIS

Atestkitisavailableforthedetectionofparvovirusantigeninfaeces.Serologycanalsobecarriedoutinordertodetectarisingtitr

eofantibodyindicatingrecentparvovirusinfection.2021/02/2492EndoparasitesEndoparasiticinfectionwithroundworms(ToxocaracanisTox

ocaracati,Toxascarisleonina)andtapeworms(Dipylidiumcaninum,Taeniaspp.andEchmococcus)are,intheauthor'sexperience,v

eryrarecausesofdiarrhoeaindogsandcats.However,EchinococcusandToxocarabothcarryasignificantpublichealthriskandshouldbeidentif

iedandtreatedwheneverpossible.2021/02/2493FaecalsmearsFreshfaecalsmearsprovideaquickandcheapmethodofexaminingfaecalsamples

.However,asthereisnoconcentrationofovaitiseasytomissparasiteeggsorcyststhatarepresentinsmallnumbers.Afreshfe

calsampleshouldbemixedwithasmallvolumeofphysiologicalsalineonamicroscopeslide.Ifprotozoansaresuspected,onedropofLugol'siodinewillhighlightthesepa

rasitesbutwillreducetheirmotility.Anegativeresultmaybeaccurateormayreflectthesmallnumbersofparasitice

ggspresent,intermittentexcretion,ortheeffectsofagentssuchasbariumsulphate,kaolin,pectinorenemas.2021/02/2494FaecalflotationFaecalflotat

ionisamoresensitivemethodthanthefaecalsmearforthedetectionofparasiteeggsandcyslbecausethetechniqueconcentratestheirnumbersi

nasmallvolumeofsolution.Severalmethodshavebeedeveloped,butforthepurposesofthischapterontwomethodswillbedescribed.Faecalsamplesfordetectiono

fparasiteeggsorcystsmaybepreservedbrefrigerationat+4Cforupto2dayspriortoexamination,butshouldnotbefrozen.Preservationoffaecalsamplesmayalsobecarri

edoutusing1partfaecel3partspreservative(1.5gsodiumacetate,2mlglacialaceticacid,4ml40%formalinplus92.5mlwater).202

1/02/2495HepatobiliarySystemIntroductionDiseasesoftheliverfrequentlypresentthesmallanimalclinicianwithadiagnosticchallenge;signsareoftenvarie

dandvagueand,despiteawidearrayofdiagnostictestsofbothhepaticdamageandfunction,thereisrarelyasingletestthatidentifiestheproblemdefinitively

.Forexample,jaundiceisoftenconsideredacardinalsignofliverdisease,yetcanbecausedbynon-hepaticconditions(e.g.haemolysis,extrahepaticbiledu

ctobstruction)aswellasarangeofdifferentliverdiseases.Conversely,significantliverdiseasecanexistintheabsenceofjaundice.Nevertheless,followi

ngathoroughhistory-takingandcarefulphysicalexamination,astuteinterpretationofapaneloflaboratorytestsinconjunctionwithradiographicandultrasonog

raphicimagingofthehepatobiliarysystemwilloftenpermitapresumptivediagnosistobemade.Inmostcases,however,withtheex

ceptionofcongenitalportosystemicshunts(PSS),definitivediagnosisofprimaryliverdiseasewillrequirehistopathologicalexaminationoflivertissue.2021/02/

2496Figure9.1:Someofthemorecommonextrahepaticdisordersthatcancauseabnormallivertestresults.AcutepancreatitisD

iabetesmellitusExocrinepancreaticinsufficiencyExtrahepaticbacterialinfectionHyperadrenocortisolismHyperthyroidismHypoadreno

corticismHypothyroidismImmune-mediatedhaemolyticanaemiaInflammatoryboweldiseaseProtein-losingenteropathyRight-sidedheartfailureSepticaemiaS

hock2021/02/2497Table9.1:Clinicopathologicalabnormalitiesassociatedwithdisturbancesofhepatobiliaryfunction.FunctionAbnormallaboratoryt

estresultassociatedwithliverdysfunctionCarbohydratemetabolism:GlucosehomeostasisHyper-orhypoglycaemiaLipidmetabol

ism:CholesterolFattyacidsLipoproteinsBileacidsHypo-orhypercholesterolaemiaHypertriglyceridaemiaLipaemiaElev

atedbileacidsProteinmetabolism:AlbuminGlobulinsCoagulationproteinsHypoalbuminaemiaIncreasedacutephaseproteins,

immunoglobulinsCoagulopathiesVitaminmetabolism?Decreasedfolate,cobalaminVitaminE,vitaminKmaybereduceddependingont

hediseaseImmunologicalfunctionsHyperglobulinaemiaIncreasedacutephaseproteinsDetoxificationHyperammonaemiaDec

reasedureaHyperbilimbinaemia2021/02/2498CLINICOPATHOLOGICALCHANGESINLIVERDISEASEConsequencesofhepatobiliarydysfunctionThedi

versefunctionsofthehepatobiliarysystemarereflectedinthediverseclinicopathologicalchangesthatcanbefoundinliverdise

ase(Figure9.3).Thedefectivemetabolismandexcretionofbilirubin,causingaccumulationofcirculatingbilirubinan

dthedevelopmentofjaundice,isoftenconsideredthehallmarkofliverdisease,butitisonlyoneofmanyabnormallaboratory

teststhatmayfoundinliverdisease.Indeed,evenhyperbilirubinaemiafrombiliaryobstructionisusuallyassociatedwithhypercholesterolaemia

andelevationsofcholestaticmarkerenzymes.2021/02/2499Figure9.3:Clinicalsignsofhepatobiliarydisease.Depression,decreasedappetiteandl

ethargyStuntingandweightlossVomiting,diarrhoea,andgreyacholicfaecesPolydipsiaandpolyuriaAscitesIcterusAlteredliversizeBleedingtendencyAbdominal

pain(rare)Encephalopathy(脑病)2021/02/24100CorrelationwithclinicalsignsTheclinicalsignsofliverdiseaseareman

yandvaried(Figure9.3)andmayberelatedtospecificlaboratoryabnormalities.Signsareoftenvagueandnotapparentuntilthereiss

ignificanthepaticdysfunction,whichiswhylaboratorytestingishelpfulindetectingandcharacterizingearlyliverdisease.Howe

ver,itmustalwaysberememberedthatequallyabnormaltestsmaybesecondarytoaprimarysystemicdisease.Forexample,fattyinfiltrationoftheliverindiabetes

mellituscancauseincreasesinserumactivitiesofliverspecificenzymesinbothdogsandcats,andcanresultinjaundiceinc

ats.2021/02/24101DepressionanddiminishedappetiteThesesignsarereflectionsofdisturbedmetabolisminliverdisease,butaren

otassociatedwithspecificlaboratorytestabnormalities.Anaemiaofchronicdiseasemaybepresent.Abnormallipoproteinandcholesterolmet

abolismmayoccur.Hypoglycaemiaisseeninend-stagediseaseandmaybeoneofmanyfactorsproducingthesignsofliverfailureusually

attributedtoaccumulationofmetabolictoxins.StuntingandweightlossCongenitalPSSandjuvenilehepatopathiesareassoc

iatedwithstunting,butthebiochemicaldisturbancesresponsiblearemultifarious.Hypoproteinaemiaisoftenassociatedwithmusclewasting.G

astrointestinalsignsGrey,acholicfaecesareseeninbiliaryobstruction,andarethereforeassociatedwithjaundice.Diarrhoeamaybeareflectionofhy

poproteinaemiacausingboweloedema,althoughlackofluminalbilesaltsandportalhypertensionaremorelikelycauses.2021/02/24102Polydipsiaand

polyuriaThesesignsmaybeassociatedwithlowlevelsofserumurea,althoughothermechanisms,e.g.hypercortisolism,areinvolvedintheirpath

ogenesis.AscitesHypoproteinaemiaisarecognizedcauseoftissuefluidaccumulation.However,ascitesismorecommonthangeneralizedoedem

ainliverdisease,suggestingportalhypertensioninacquiredliverdiseaseisalsoanimportantfactor.IcterusHyperbiliru

binaemiacausesjaundice,andmaybeduetoprehepatic(haemolysis)orposthepatic(biliaryobstruction,biliaryleakage)diseaseaswellaspr

imaryintrahepaticcauses.2021/02/24103LiversizeDiseasescausingalteredliversizearelistedinFigure9.4,buttherearenospecificlabora

torymarkersofliversizeandmanydiseasesarenotassociatedwithabnormalliversize.Lipaemiamaycorrelatewithfattyinfiltrationof

theliver.BleedingtendencyCoagulationtimesareusuallyabnormalifsevereliverdysfunctioncausesbleeding.Gen

eralizedbleedingandhaemorrhagefromhepaticpeliosis(cats)andvasculartumours,suchasmetastatichaemangi-osarcoma,mayresultin

regenerativeanaemia.HepatoencephalopathyThissyndromeiscausedbyaccumulationoftoxinsbecauseofseverehepaticd

ysfunctionand/orporto-systemicshuntingofblood.Hyperammonaemiaisasensitiveandspecificmarkerforthesyndrome,alt

houghothermetabolicdisturbancesareinvolved.2021/02/24104DIAGNOSTICAPPROACHTOLIVERDISEASEInmostcases,atentat

ivediagnosiscanbededucedfromtheresultsoflaboratorytestsinconjunctionwithimagingtechniques.However,thedefinitivediag

nosisofprimaryliverdiseaseusuallydependsultimatelyonhistologicalexaminationofliverbiopsyspecimens.Primary

extrahepaticcausesofsecondaryliverdiseasewillhopefullybeidentifiedbeforebiopsyisundertaken.2021/02/24105Thusadiagnos

ticapproachtoliverdiseaseincludes:•Clinicalhistory•Physicalexamination•Laboratorytests•Examinationofasciticflu

id•Imaging:RadiographyUltrasonographyAngiographyScintigraphy•Liverbiopsy.2021/02/24106Theaimsoflaboratorytestingare:•Toidentifyand

characterizeanyhepaticdysfunction•Toidentifypossibleprimarycausesofsecondaryliverdisease•Todifferentia

tecausesoficterus•Toevaluatepotentialanaestheticrisks•Toidentifycausesofanaemiaofunknownorigin•Toassessprognosis•Toassesstheresp

onsetoxenobiotics•Tomonitorresponsetotherapy.2021/02/24107Thereisawiderangeoflaboratorytestsavailableforassessingliverstatus,but

theycanbeconvenientlydividedintofourclasses:•Generalscreeningtests•Markersofliverdamage•Liverfunction

tests•Prognosticindices.Thetestsroutinelyavailabletothepractisingveterinarysurgeonandindicationsfortheirusewillbediscussedindetail,

andmorespecializedtestsmentionedonlybriefly.2021/02/24108UrinarySystemTHEROLEOFCLINICALPATHOLOGYClinic

alpathologytestsintheevaluationofapatientforthepresenceofrenaland/orurinarytractdiseaseshouldbeperformedunde

rthefollowingcircumstances:•Whenprimaryorsecondaryurinarysystemdiseaseissuspectedfromthepresentingsigns,clinicalhistoryorphysicalexamination•Wh

enapatienthasadiseaseinanotherorgansystemthatisknowntobepotentiallyassociatedwithconcurrentorsecondaryrenalorurinar

ytractdisease•Whenscreening'atrisk'patientsaspartofageneralhealthcheck(e.g.aspartofageriatricscreeningprogramme,beforegene

ralanaesthesia,orbeforeadministrationofdrugsthatareknowntobepotentiallynephrotoxic,suchasnon-steroidalanti-inflammato

rydrugs,aminoglycosidesoroxytetracycline).2021/02/24109Theaccuratediagnosisofrenalandurinarytractdiseasesrequiresinvestigationbyanyo

rallofthefollowing:•Fullhistory•Fullphysicalexamination•Imaging:Radiography-plainandcontraststudies;sometim

esdynamicstudies,Ultrasonography•Urinalysis•Bloodchemistry•Haematology•Microbiologicalcultureandsensitivitytesting•Tissuebiopsy•S

urgicalexaminationatlaparoscopyorlaparotomy•Post-mortemexamination2021/02/24110Urineshouldbeanalysedwhen:•Thereisachangeinitsphysicalappearance,e.

g.discoloration•Ananimalpassesfrankbloodinitsurine•Ananimalexhibitspolydipsia•Ananimalexhibitspolyuria•Ananimalexhi

bitsurinarytenesmus•Ananimallicksitsexternalgenitaliaexcessively•Ananimalexhibitsincreasedurinaryfrequency•Ananimalisdehydrated•Ananimalisvom

iting•Ananimalhassignsoffluidaccumulationintheabdomen(i.e.ascites)orperipherally(subcutaneousoedema)•Primaryorseco

ndaryrenalorurinarytractdiseaseissuspected•Aurolithhasbeenpassed•Ananimalexhibitspyrexiaofunknownorigin•Itispartofaroutinescreeningtest-juvenile,g

eriatricorbeforeanaesthesia.2021/02/24111Urinalysisincludesoneormoreofthefollowing:•Physicalexamination:color,smell,turb

idity,content,volume,specificgravity•Chemicalexamination:pH,proteinuria,acetone,glucose,urea•Examinat

ionofsediment•Bacterialculture•Viralexamination.2021/02/24112ClinicalpathologypanelforurinarysystemdiseasePlasmaureaBloodureanitroge

nPlasmacreatinineUrea:creatinineratioTotalplasmaproteinPlasmaalbuminBlasmasodiumPalsmapotassiumPlasmachloridePlasmacalciumPlasmaphosphate202

1/02/24113GlomerularfunctiontestsindogsandcatsEndogenouscreatinineclearanceExogenouscreatinineclearan

ceInulin（菊酚）clearanceIothalanate(碘酞酸盐）clearanceFiltrationfraction24hoururineproteinexcretionUrinephosphate:urinecr

eatinine2021/02/24114THANKSFORWATCHING谢谢大家观看为了方便教学与学习使用，本文档内容可以在下载后随意修改，调整。欢迎下载！时间：20XX.XX.XX汇报人：XXX2021/02/24115