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VeterinaryClinicalPathology兽医临床病理学Prof.ZhaoxinTangCollegeofVeterinaryMedicine,SouthChinaAgriculturalUniversity,Guangz

hou,China,5106422021/02/241PrefaceVeterinaryClinicalPathology:VeterinaryLaboratoryMedicineInclude:1ClinicalHematology2Clinicalbi

ochemistry3Clinicalcytology4Clinicalmicrobiology5Clinicalparasitology6Clinicaltoxicology2021/02/242PrefaceGeneralLaboratoryconceptsVeterinari

anshavemanychoicesregardinglaboratorytesting.Importantfactorsinclude:--Needandusefulness--Practicality--Cost-e

ffectiveness--Accuracy--Turnaroundtime2021/02/243CompleteBloodCountandBoneMarrowExamination:generalcommentsandselectedtechni

ques•Completebloodcount•Quantitationtechniques•Bloodsmearanalysis•Otherdeterminations•Bonemarrowexamination•Bonemarrow

biopsyandaspirate2021/02/244Completebloodcount(CBC)•CBCisaprotestsusedtodescribethequantityandqualityofthecellularele

mentsinbloodandafewsubstancesinplasma.•CBCisacost-effectivescreenthedetectsmanyabnormalitiesanddiseaseconditions.•Bonemarrowexam

inationisusedinselectedinstancestoanswerquestionsthemorereadilyavailableCBCcannot.2021/02/245QuantitationTechniques•Samplesubmission•Microhemotc

rit•Hemoglobinconcentration•Cellcounts•AbsolutenucleatedRBCcount•Automatedhematologycellcounters2021/02/246Bl

oodSmearAnalysis•Makingthesmear•Stains•Evaluatingbloodsmears--plateletmorphology--leukocytemorphology--leukocyteestimation--leukocytedifferent

ialcount--erythrocytemorphology2021/02/247BoneMarrowExamination•Bonemarrowisusuallyexaminedtoanswercertainquestionthata

rosefromevaluatingtheCBC.•Indicationsforbonemarrowexaminationinclude:--nonregenerativeanemia--Persistentneutropenia--Persistentt

hrombocytopenia--Unexplainedpolycythemiaorthrombocytosis--Atypicalcellsinblood2021/02/248Erythrocytes•Basicconceptsoferythrocytefunction

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

meyerhofpathway--GlycolysisgeneratesATPandNADH•Pentosephosphatepathway--ThispathwayproducesNADPH•Methemoblobinreduct

asepathway--Methemoglobin(Fe3+)cannottransportoxygen•Rapoport-lueberingpathway--2,3diphosphoglycerate(2,3DPG)2021/02/2410RedbloodcellsThefundament

alstimulusforproductionofredbloodcells(erythropoiesis)iserythropoietin(红细胞生成素）,aglycoproteinproducedbythekidneysinresponsetorenaltissuehy

poxia.Otherhormones,suchascorticosteroids,thyroidhormoneandandrogens,stimulatetheproductionorreleaseof

erythropoietinbuthavenointrinsicerythropoieticactivity.Theaveragelifespanofacirculatingerythrocyteis110-1

20daysinthedogand68daysinthecat.Agedordamagedredcellsareremovedprimarilybymacrophagesintheliver,spleenandbonemarrow.2021/02/2411Neutrop

hilsTheproductionofneutrophils,eosinophilsandbasophilsistermedgranulopoiesis.Theneutrophilsinthebloodstreameithercircul

atefreely(thecirculatingpool)oradheretothevascularendothelium(themarginalpool).Inthedogthemarginalpoolandthecirculatingpoolareapproxima

telyequalinsize,whilstinthecatthemarginalpoolistwotothreetimeslargerthanthecirculatingpool.Thereisacontinualexchang

eofcellsbetweenthesetwopools.Thehalf-lifeofcirculatingneutrophilsisonly6-14hours,afterwhichtimetheyleav

ethecirculationandpassintothetissuepool.Thecirculatingtimeisshortenedduringacuteinfectionsasneutrophilspasstothesiteofinfectioni

nthetissues.Themainfunctionoftheneutrophilisthephagocytosisofpyogenicbacteria.2021/02/2412LymphocytesLymphoidprimitivestemcellsdiv

ideanddifferentiateintopre-Blymphocytesandpre-Tlymphocytesinthebonemarrow.Pre-TlymphocytesmatureandproliferateintoTcellsinthethymus.Pre-Bcellsproli

ferateinthebonemarrowandmigratetoperipherallymphoidorgans(spleenandlymphnodes)wherefurtherproliferationtakesplace.P

lateletsPlateletsareproducedfromthecytoplasmofmegakaryocytesOnceinthecirculation,plateletssurvivefor8-12days.Upto20-30%ofcircu

latingplateletscanbesequesteredinthespleen;thefiguremaybeahighas90%ifthereissplenomegaly.Oldordamagedpla

teletsareremovedfromthecirculationbythespleen,liverandbonemarrow.2021/02/2413ROUTINEHAEMATOLOGYThecompleteblood

countisanintegralpartofthediagnosticinvestigationofanysystemicdiseaseprocess.Itconsistsoftwocomponents:Aquantitati

veexaminationofthecells,including:packedcellvolume(PCV)totalredcellcount(RBC)totalwhitecellcount(WBC)differentialwhitecellcount

plateletcountmeancorpuscularvolume(MCV),meancorpuscularhaemoglobin(MCH),meancorpuscularhaemoglobinconcentration(MCHC),totalplasmaproteinconcentr

ation.Aqualitativeexaminationofbloodsmearsforchangesincellularmorphology.2021/02/2414Table1Referencevaluesforredcellindice

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

L/L)RBCindicesarehelpfulintheclassificationofcertainanemias.ROUTINEHAEMATOLOGY2021/02/2416Differential

whitecellcountsThedifferentialwhitecellcountisperformedbycounting200leucocytesinabloodsmear.Thecellsarecountedalongthelongedgeofthe

smear,usingthebattlementmeandermethod:fourhigh-powerfieldsarecountedinonedirection,thenfourmoreinadirectionatri

ghtanglestothefirst,andsoon,followingtheshapeofabattlement.Thepercentageofeachtypeofcellisdetermined.Thisp

ercentageisthenmultipliedbythetotalwhitecellcounttoobtainanabsolutecountforeachcelltype.ROUTINEHAEMATOLO

GY2021/02/2417Plasmaproteinconcentration(Referencerange:60-80g/1forthedogandcat)Totalplasmaprotein(TPP)andPCVsho

uldbeinterpretedtogether.QualitativeexaminationofabloodsmearAbloodsmearshouldalwaysbeevaluatedwhenautomatedcellcountsaremadeorwhenin

-practiceinstrumentationislimitedtoacentrifugeforPCVPreparationofabloodsmearAsmalldropofbloodisplacedononeendofaglas

sslide,usingacapillarytube.Aspreaderslide(madebybreakingoffthecomerofanotherslide,afterscoringitwithaglasscutterordi

amondwriter)isplacedontotheslideholdingtheblooddrop,infrontofthedropandatanangleof20-40°.ROUTINEHAEMATOLOGY2021/02/2418

ANAEMIAAnaemiaischaracterizedbyanabsolutedecreaseinredcellcount,haemoglobinconcentrationandPCV.AcutehaemorrhageAcutehaemorrha

gemaybeduetotraumaorsurgery,bleedinggastrointestinalulcersortumours,ruptureofavasculartumour(e.g.splenichaemangiosarcoma),oracoag

ulopathy(e.g.warfarintoxicity).Immediatelyfollowingacutehaemorrhagetheredcellparameters,includingPCV,arenormalbecausebothredcellsandplas

mahavebeenlostinproportion.CompensatorymechanismssuchasspleniccontractionmayfurtheroffsetanyfallinPCV.The

PCVfallswhenbloodvolumeisreplacedbyinterstitialfluidandsodoesnotindicatethefullmagnitudeofbloodlossforatleast24hoursaftertheonsetofhaemorrhage.ROUT

INEHAEMATOLOGY2021/02/2419ChronichaemorrhageChronicexternalbloodloss(e.g.chronicgastrointestinalhaemorrhage,renal

orbladderneoplasia)initiallyresultsinaregenerativeanaemiabutgraduallytheanaemiabecomesnon-regenerativeastheironstoresbecomedepleted.Younganim

alsbecomeiron-deficientmorebonemarrowisalreadyveryactiveproducingredcellsquicklythanadultsfollowingblood

loss,partlybecausetheyhavelowironstoresandpartlybecausetheirtomatchtheirgrowthrateandsohaslesscapaci

tytoincreaseitsrateofhaemopoiesis.HaemolyticanaemiasMostcasesofhaemolyticanaemiaareimmune-mediated.Inthedogmostcasesofimmune-mediatedishaemolyticana

emia(IHA)areprimary(idiopathic)andaretermedautoimmunehaemolyticanaemia(AIHA).IHAmayoccurinassociationwith:drugs(e.g.potentiatedsulphonamides);lymphor

eticulardiseases(e.g.lymphoidleukaemia);systemiclupuserythematosus;orinfections(e.g.Babesia,bacterialendocarditis).ROUTINEHAEMATOLOGY20

21/02/2420DISORDERSOFWHITECELLNUMBERNeutrophiliaFigure3.20CausesofneutrophiliaPhysiologicalresponse(fear,excitemen

t,exercise)Stress/corticosteroid-inducedAcuteinflammatoryresponse:bacterialinfection(localizedorgeneralized),

immune-mediateddisease,necrosis,e.g.pancreatitis,neoplasia,especiallywithtumornecrosis.Chronicgranul

ocyticleukaemiaNeutrophildysfunctionParaneoplasticsyndromes2021/02/2421NeutropeniaThethreemaincausesofneutropeniaare:•Anoverwhelmingdemandforneutro

phils•Reducedproductionofneutrophilsinthebonemarrow•Defectiveneutrophilmaturationinthebonemarrow.Anoverwhelmingdema

ndforneutrophilsmayoccurwithperacutebacterialinfections,especiallyGram-negativesepsisandendotoxaemia.Ot

herpossiblecausesincludeperitonitis,pyometra（子宫蓄脓）,aspirationpneumoniaandcanineparvovirusinfection.DISORDERSOFWHITECELLNUMBER2021/02/

2422EosinophiliaEosinophilsaredistributedinthebodyamongvariouspoolsinasimilarwaytoneutrophils,althoughthebonemarrowstoragepoolisminimal.Eosino

philscirculateinthebloodstreamforonlyafewhoursbeforeenteringthetissues,wheretheymayliveforseveraldays.Theirtwomainfunctionsaretokillparasitesan

dtoregulateallergicandinflammatoryreactions.EosinopeniaEosinopeniaincombinationwithlymphopeniaoccursfollowingstress,admini

strationofcorticosteroidsandinspontaneoushyperadrenocorticism(Cushing'ssyndrome).BasophiliaBasophilscontaininflammatorymediatorssuchashistamineandh

eparinandfunctioninasimilarmannertomastcellsinhypersensitivityreactions.DISORDERSOFWHITECELLNUMBER2021/02/2423LymphocytosisCausesoflymphocy

tosis1.Physiologicallymphocytosis,withconcomitantneutrophilia,inresponsetoexcitement(especiallycats)2.Strongimmu

nestimulation(e.g.inchronicinfection,viraemiaorimmune-mediateddisease)3.Chroniclymphocyticleukaemia4.Hypoadrenocortiscism(lymphocytosismaybeas

sociatedwithaneosinophilia)5.Increasednumbersoflargereactivelymphocytesmayoccurtransientlyfollowingvaccinatio

n6.YounganimalshaveahigherlymphocytecountthanadultanimalsDISORDERSOFWHITECELLNUMBER2021/02/2424Lymph

openiaCausesoflymphopeniaarelisted.StressGlucocorticoidtherapyHyperadrenocorticismChylothorax(lossoflymphocytesintothepleuralspace)

Lymphangiectasia(lossoflymphocytesintothegut)Acutephaseofmostviralinfections(e.g.caninedistemper,par

vovirus,FeLV)Septicaemia/endotoxaemiaDISORDERSOFWHITECELLNUMBER2021/02/2425DogsCatspercentageAbsolutevaluepercentageAbsol

utevalue(10/TotalWBCN/a6~17N/a5.5~19.5Bandneutropils0~30~0.30~30~0.3Neutropils60~773~11.535~372.5~12.5Lymph

ocytes12~301~4.820~551.5~7Monocytes3~100.2~1.51~40~1.5Eosinopils2~100.1~1.32~120~1.5basopilsrarerarerareRareReferencerangesfor

totalanddifferentialwhitebloodcellcounts2021/02/2426Table2showsthealterationsinsomeofparametersinvariousdiseases.LaboratoryassessmentTest

stoassessprimaryhaemostasisinclude:PlateletcountBleedingtimeClotretraction.Teststoassesssecondaryhaemost

asisinclude:Wholebloodclottingtime(WBCT)Activatedclottingtime(ACT)Activatedpartialthromboplastintime(

APPT)One-stageprothrombintime(OSPT)Thrombintime(TT)DISORDERSOFWHITECELLNUMBER2021/02/2427Disseminatedintravascularcoagulation(DIC):

Thismaybetriggeredbyawidevarietyofdiseases,includingendotoxaemianeoplasia(especiallyhaemangiosarcoma血管肉瘤)acuteinfections(e.g.infectiousc

aninehepatitis)haemolyticanaemiapancreatitisheatstroke.TheclinicopathologicalfeaturesofDICare:•Thrombocytopenia•IncreasedOSPT/APTT•Elevat

edFDPs•Lowfibrinogen•Schistocytesinthebloodfilm.DISORDERSOFWHITECELLNUMBER2021/02/2428兽医临床病理学CollegeofVeterinaryMedicine,SC

AU,Guangzhou,China5106422021/02/2429ClinicalbiochemistryIntroductionSerumproteinsTotalproteinandalbuminGlobulinsIndicatorsofrenalfunctionUrea

nitrogenCreatinineMarkersofhepaticdiseaseAlanineaminotransferaseAspartateaminotransferaseAlkalinephosphataseGamma-glutamyitransferase

BilirubinBileacidsAmmoniaPancreaticdiseaseAmylaseLipaseElectrolytesSodium;Potassium;ChlorideMagnesium;Calcium;PhosphorusMuscleenzymesCreatinek

inaseAspartateaminotransferaseCarbohydratemetabolismGlucoseFructosamineLipidmetabolismCholesterolTriglyceridesMiscellaneous

testsIronLeadZincCopperChemicalprofilesandtestselection2021/02/2430SERUMPROTEINSTotalproteinandalbuminPhysiologyThecirculatingp

roteinsaresynthesizedpredominantlyintheliver,althoughplasmacellsalsocontributetotheirproduction.Quantitat

ivelythesinglemostimportantproteinisalbumin(35-50%ofthetotalserumproteinconcentration).Theotherproteinsarecollectivelyknownasglobulins.Thefunct

ionsofproteinsaremanyandvariedbutincludemaintenanceofplasmaosmoticpressure,transportofsubstancesaroundthebody(e.g.ferritin铁蛋白,ceruloplasmin血浆铜蓝蛋白),h

umoralimmunity,bufferingandenzymeregulation.IndicationsforassayThemeasurementofproteinsisgenerallyincludedinaninitialhealthscreen

inallpatientsbutespeciallywhereintestinal,renalorhepaticdiseaseorhaemorrhageissuspected.AnalysisProteinconce

ntrationscanbeestimatedinserum,plasma,urineorbodyfluidswitharefractometerorbyspectrophotometry.Serumalbuminlevelsaremeasure

dbybromocresolgreendye溴甲酚绿bindingandtheserumglobuliniscalculatedbysubtractionofthealbuminconcentrationfromthetotalpro

teinconcentration.2021/02/2431ReferencerangesNeonatesandveryyounganimalshavelowerconcentrationsofalbuminandglobulins(duetominimalquantities

ofimmunoglobulins).Astheanimalgainsimmunocompetencetheproteinconcentrationsrisetoreachadultvalues.Physiologicalde

creasesinalbuminmaybenotedduringpregnancy.CriticalvaluesMarkedhypoalbuminaemia(<15g/L)isassociatedwiththe

developmentofascitesandtissueoedema.Accumulationofperitonealfluidmayoccurathigheralbuminconcentrationsifthereisconcurrentportalvei

nhypertension,e.g.inchronicliverdisease.InterferingphenomenaLipaemia,haemolysisandhyperbilirubinaemiaproducefalseincreasesintotalproteinconcentra

tions.DrugeffectsHormoneshaveamarginaleffectonplasmaproteinconcentrations.Corticosteroidsandanabolicsteroidsmayincreasetheprot

einconcentrationduetotheiranaboliceffectswhilethecataboliceffectsofthyroxinecancauseadecrease.SERUMPROTEINS2021/

02/2432Figure4.3:Causesofhypoalbuminaemia.IncreasedlossGlomerularproteinlossProtein-losingenteropathyCutaneouslesions,e.g.bumsExternalhaemorrhageDecr

easedproductionHepaticinsufficiencyMalnutritionMaldigestionMalabsorptionSequestrationBodycavityeffusionSERUMPROTEINS2021/02/2433GlobulinsAnaly

sisSerumproteinelectrophoresis(SPE)oncelluloseacetategelsallowsfractionationoftheproteins,dependingpredominan

tlyontheirchargeandsize.Afterstainingforprotein,thecelluloseacetatestripisscannedbyadensitometerwhichconvertstherelativeintensitie

softheproteinbandstopercentagesandgeneratesagraphthatdemonstratestheproteinfractions(albumin,α1-globulin,α2-globulin,β1-gl

obulin,β2-globulin,γ-globulin).CausesofhypoglobulinaemiaThemostcommonpathologicalcausesarehaemorrhageandprotein-losingentero

pathies.SERUMPROTEINS2021/02/2434Figure4.4:Causesofhyperglobulinaemia.PolyclonalgammopathyInfections:BacterialdiseaseVirald

isease(e.g.FIP)Immune-mediateddiseases:SystemiclupuserythematosusRneumatoidartnntisImmune-mediatedhaemolyticanaemiaImmune-med

iatedthrombocytopemaNeoplasia,especiallylymphosarcomaMonoclonalgammopathyNeoplasia:MultiplemyelomaMacroglo

bulinaemiaLymphosarcomaFelineinfectiousperitonitis(rare)SERUMPROTEINS2021/02/2435UreanitrogenPhysiology★Dietaryproteinsarehydr

olysedintheintestinestotheirconstituentaminoacidswhichmay,inturn,bedegradedtoammoniabytheactionofgutbacteria.★Theammoniaandamin

oacidsaretransportedtotheliverviatheportalcirculationwheretheyareutilizedintheureacycle.★Theureaformedinthehepatocytesisexcretedviathekidneytubul

es.★Ureaplaysanimportantroleinconcentratingtheurine;thepresenceofhighconcentrationsofureaandsodiumchlorideintherenalmedullaryinterstitiumcreates

anosmoticgradientforreabsorptionofwater.INDICATORSOFRENALFUNCTION2021/02/2436IndicationsforassayTheureanitrogen(urea)concentrationisoneofthetestsused

whenscreeningrenalfunction.Itisoftenmeasuredwhentheclinicalsignsincludevomiting,anorexia,weightloss,polydipsiaanddehydration.AnalysisUreacanbemea

suredinserum,plasmaandurinebyspectrophotometry.Sticktestsforwholebloodarealsoavailable.Referencerange

sDogs3.0-9.0mmol/LCats5.0-10.0mmol/LInterferingphenomenalipaemiainterfereswiththeanalysisandproducesva

riableeffectsdependingonthemethodology.INDICATORSOFRENALFUNCTION2021/02/2437Causesofreducedbloodurea☆Reduced

dietaryproteinintakeisassociatedwithalowbloodurea.☆Inaddition,patientswithdiffuseliverdiseasehaveanimpairedcapacitytosynthesizeureaandreducedhepati

cproduction.Wherehepaticdiseaseissuspected,acompletebiochemistryproabileacidstimulationtestareindicated.☆Themarked

diuresis（多尿）associatedwithsomeconditions,especiallyhyperadrenocorticismanddiabetes,resultsinincreasedurinarylossofureawhich,inturn,causes

areductionofthebloodurea.INDICATORSOFRENALFUNCTION2021/02/2438Causesofincreasedbloodurea☆Increaseddietaryproteinintakeproducesahighleve

lofureaintheblood.Amoderateincreaseindietaryproteinisnotcommonlyassociatedwithanotableriseinureaabovethereferencerange,buthigh-

proteindietscancausesignificantincreases.☆A12-hourfastisrecommendedbeforesamplingformeasurementofurea.☆Intestinalhaemorrhagealsoresults

inanincreasedconcentrationwhichisreportedtocorrelatewiththeseverityofbloodloss.☆Ureaisfreelyfiltered

attheglomerulusandreabsorbedintherenaltubules.Therateofreabsorptionishigheratslowerurinaryflowrates,e.g.indehydratedpatients.☆Bloodu

reaisthereforenotareliableestimateoftheglomerularfiltrationrate(GFR).Increasedureaconcentrationsareassociatedwithconditionsotherthanpar

enchymalrenaldisease.☆Thepresenceofaconcentratedurinesample(urineSG>1.030indogs,>1.035incats)supportsthediagnosisofaprerenala

zotaemia.INDICATORSOFRENALFUNCTION2021/02/2439CreatininePhysiology◤Creatinineisformedfromcreatineinthemusclesinanirreversiblerea

ction.Thequantityofcreatinineproduceddependsupondiet(smallcontribution)andthemusclemass.Diseaseaffectingt

hemusclemassmayaffectthedailycreatinineproduction.◤Bothureaandcreatininearefreelyfilteredattherenalglomerulusbutureaissubjecttotubularreabsor

ptionandthuscreatinineissaidtobeabetterindicatorofGFR.Analysis◤Creatininecanbemeasuredinserum,plasmaorabd

ominalfluidbyspectrophotometricmethods.ReferencerangesDogs20-110umol/LCats40-150umol/LINDICATORSOFRENALFUNCTION2021/02/2440Causesoflows

erumcreatinine◤Sincethedailyproductionofcreatinineisdependentuponthemusclemassoftheanimal,thebodyconditionshouldbeconsidere

dwheninterpretingserumcreatinineconcentrations.Apoorbodyconditionmaybeassociatedwithlowconcentrationswhileminorrisesins

uchcasesmaybemoresignificantthaninotherindividuals.Causesofincreasedserumcreatinine◤Decreasedglomerularfiltrationisthema

jorcauseofraisedserumcreatinine.However,approximately75%ofnephronfunctionmustbeimpairedbeforeserumcreatinine(andurea)isincreased.Creatininei

sconsideredamorereliableindicatorofGFRthanisureanitrogen,sincetherearefewerfactorswhichinfluencetheserumconcentrationofc

reatinine.INDICATORSOFRENALFUNCTION2021/02/2441►Thebiochemicalparametersusedtoassessliverpathologymaybedividedintotwoclasses:thehepaticenzymesthatre

flectliverdamageandcholestasis,andtheendogenousindicatorsofliverfunction.►Alanineaminotransferase(ALT)isthemostusefulenzymeforident

ifyinghepatocellulardamageindogsandcatsbutshouldnotbeusedaloneasascreeningtestforliverdisease.►Theproductionofotherenzymes,i.e.alkalinephosphat

ase(ALP)andgamma-glutamyltransferase(GGT),isincreasedsecondarytointra-andextrahepaticcholestasis.►Theseenzymesaremarkersofcholestaticdi

sease.►Bilirubin,serumalbuminandserumbileacidsareconsideredtobeindicatorsofhepaticfunction.►Itiscommonforextrahepaticdisease(e.g.pancreati

tis,diabetesmellitus,hyperadrenocorticismandinflammatoryboweldisease)tocauseabnormalitiesofthesebiochemical

parameters.MARKERSOFHEPATICDISEASE2021/02/2442Alanineaminotransferase(ALT)PhysiologyALTisfoundinthecytosolo

fhepatocytesandinmuscletissueinthedogandcat.Activitiesintheserumareelevatedbyleakageoftheenzymesecondarytoa

nincreaseinhepatocytemembranepermeabilityorcellnecrosis.Theformermaysimplybeaconsequenceofhypoxiaandnee

dnotreflectcelldeath.IncreasedserumALTmaybenotedwithin12hoursofanacutehepaticinsultbutcantake3-4daystoreachpeaklevelsafterexperimentalcholestasis（胆汁阻

塞）.Thedegreeofincreaseinenzymeactivitycorrelatesapproximatelywiththenumberofhepatocytesaffectedbutdoesnotindi

catethenature,severityorreversibilityofthepathologicalprocess.ALTactivityisnotanindicatorofhepaticfunction.

IndicationsforassaySerumALTisausefulaidinthediagnosisofhepaticdiseaseandismeasuredwheretheclinicalsignsmightsuggestahepatop

athy,e.g.weightloss,anorexia,polydipsia,vomiting,diarrhoea,ascitesandjaundice.AnalysisTheactivityoftheenzyme(ininternationalunits)ismeasu

redinserumorplasmabyspectrophotometricmethodsunderspecifiedconditions.ReferencerangesDogs<100units/LCats<75units/LMARKE

RSOFHEPATICDISEASE2021/02/2443CausesofraisedALTactivityGuidelinesfortheinterpretationofraisedliverenzymeactivitiesinrelationtoliverdisease

saregiveninChapterliver.ThemajorityofdiseasesthataffectthelivercouldpotentiallycauseanincreaseinserumALTactivitybutthosepathologicalprocessest

hatmightcauseamarkedincreaseincludeparenchymaldisease/damage,cholangitis,cholangiohepatitis,chronichepa

titis,anoxia,cirrhosisanddiffuseneoplasia,e.g.lymphoma(lymphosarcoma).However,insomecasesthesediseasesmaybeaccompaniedbyanegligibleincreaseo

rnoincreaseinserumALTactivity.CausesofreducedALTactivityAnartefactualreductioninserumenzymeactivitiesmayresultfromsubstrate

depletion.Dilutionandrepeatassayofthesamplearenecessarytoexcludethisphenomenon.ReducedALTactivities(belowthereferencerang

e)aregenerallynotconsideredtobeofclinicalsignificance,butthepossibilityofchronicliverdiseaseandnutritionaldeficiencies(zi

ncorvitaminB6)shouldbeconsidered.MARKERSOFHEPATICDISEASE2021/02/2444Aspartateaminotransferase(AST)(seealsoMus

cleenzymes)PhysiologyASTislocatedinthemitochondriaofthecellandispresentinsignificantquantitiesinhepa

tocytes,erythrocytesandinmuscle.ASTisthereforenotliver-specificbut,likeALT,itsactivityintheserumiselevatedbyleakageoftheenzymefromthecell

.IndicationsforassayASTisincludedindiagnosticprofilesforinvestigationofsuspectedliverdiseaseormuscledisease.AnalysisTheenzymeactivity

ismeasuredinserumandheparinizedplasmabyspectrophotometry.ReferencerangesDogs7-50units/LCats7-60units/LCausesofraisedASTThemostcommoncausesofincr

easedASTarehepaticdisease,muscledisease(trauma,inflammation)andhaemolysis.Concurrentmeasurementofotherhepaticenzymes(ALT,ALP,GGT)andhepaticfunctio

nindicators(albumin,urea,bilirubin,bileacids)areessentialtoestablishtheoriginoftheincreasedserumASTandtoprovidefurtherinformationregardi

ngliverdamageandfunction(seeChapter9).Withrespecttoliverdamage,theserumactivityofASTtendstoparallelthatofALT.MARKERSOFHEPATICDISEASE2021/0

2/2445Alkalinephosphatase(ALP,SAP)PhysiologyIndogsandcatsthereareisoformsofALPlocatedinbrushbordersintheliver,placent

a,intestine,kidneyandbone.Inthedogthereisalsoasteroid-inducedisoenzyme(SIALP),theoriginofwhichhasnotbe

enfullydetermined.TheproductionofSIALPisincreasedbytheadministrationofglucocorticoids(oral,parenteralortopical),byexcessiveproductionofendogenousg

lucocorticoids(hyperadrenocorticism)andinassociationwithchronicdisease(e.g.renalorhepatic).Theliveriso

enzymeisresponsiblefortheserumactivityinthenormaladultdogandcat.IndicationsforassaySerumALPisoneofthetestscommonlyincludedinscreenin

gprofilesforhepaticdisease(cholestasis)andhyperadrenocorticism.Itisthereforeusefulwheretheclinicalsignssuggesteitherofthesediagnos

es,e.g.weightloss,anorexia,polydipsia,vomiting,diarrhoea,ascitesandjaundice.AnalysisSerumALPactivityismeasuredinserumorhep

arinizedplasmabyspectrophotometry.ReferencerangesDogs<200units/LCats<100units/LMARKERSOFHEPATICDISEASE2021/02/2446Caus

esofraisedALPFromadiagnosticviewpointthemostimportantisoenzymesinsmallanimalsarethebone,hepaticandsteroid-inducedforms.IncreasesinboneALPc

ausesraisedserumactivitiesinyounggrowinganimals,butvaluesarerarelymorethantwo-foldgreaterthantheupperlimitoftheadultref

erencerange.ThisphysiologicalincreaseinserumALPshouldbeconsidered.Increasesinthehepaticisoenzymearecommonlyassociatedwithcholestaticdisease.Includepa

ncreatitis,pancreaticneoplasiaandcholelithiasis.Cholelithsareveryrareinthedog.Theenzymeisgenerallyincludedinprofileswhereitcontributestothedi

agnosisofhepaticdisease.ALPshouldnotbeusedalonewhenscreeningpatientsforevidenceofliverdisease.Indogs,theincrea

seinALPassociatedwithsteroidadministrationvariesdependingonthepatient,thedrugusedandtherouteofadministration.A

LPinthecathasaveryshorthalf-lifeandthemagnitudeofincreasenotedinhepaticdiseaseisgenerallylessthanthatrecordedindogs.Anyinc

reaseinALPisprobablysignificantinacat.MARKERSOFHEPATICDISEASE2021/02/2447.Gamma-glutamyltransferase(GGT)PhysiologyGGTisa

cytosolicandmembrane-boundenzymefoundinhighestconcentrationsinthebrushbordersoftherenalandbileductepithelium.Cholestasisandenzymeinductiondue

toglucocorticoidtherapycauseincreasedserumactivities.IndicationsforassayGGTisusedinconjunctionwithALPandotherlivertestsinthedi

agnosisandmonitoringofhepaticdisease.ItisthoughttobemoreusefulthanALPinthecatandtheserumactivityindogsdoesnotapp

eartobeaffectedbytheadministrationofanticonvulsants.Dogs0-8.0units/LCats0-8.0units/LCausesofincreasedGGTSerumGGTisamarkerfo

rcholestaticdiseaseinthedogandcat.InthecatitmaybemoreusefulthanALPinthediagnosisofcholestatichepaticdiseaseMARKERSOFHEP

ATICDISEASE2021/02/2448BilirubinPhysiologyBilirubin（胆红素）isderivedfromthecatabolismofhaemoproteinsinthece

llsofthereticuloendothelialsystem.Thenewlyformedlipid-solublebilirubin(indirect-reactingbilirubin)ist

henboundtoalbumin,whichfacilitatesitstransferthroughtheaqueousphaseoftheplasmatotheliver.Inthehepatocytethebilirubinisconjugat

edwithglucuronicacid（葡糖醛酸）,creatingawater-solublemolecule(direct-reactingbilirubin).IndicationsforassayMeasurementofbilirubi

nisindicatedwherethereisjaundice（黄疸）onclinicalexamination,visibleicterus（黄疸）oftheserumorplasma,orsuspectedhepa

ticdisease.Clinicaljaundiceinthedogisdetectedwhenthebilirubinisatleast25-35umol/L.AnalysisThetotalserumbilirubinconce

ntration(conjugatedandunconjugated)ismeasuredinserumorplasmabyspectrophotometry.ReferencerangesDogs0-6.8umol/LCats0-6.8umol/LMA

RKERSOFHEPATICDISEASE2021/02/2449CausesofhyperbilirubinaemiaJaundicemaybeclassifiedaccordingtotheunderlyingpathologicalprocess:prehepatic

jaundice(increasedproductionofbilirubin,e.g.haemolyticanaemia,andinternalhaemorrhage);hepaticjaundice(failureof

uptakeorconjugationofbilirubin);posthepaticjaundice(obstructionofthebiliarysystem).Afullhaematologicalproindicatedinalljaundicedpatie

ntstoexcludethepossibilityofprehepaticcauses.Characteristicfindingsthatmaybenotedinhaemolyticanaemiainclud

emarkedreticulocytosis(网状细胞过多症，indicativeoferythrocyteregeneration),autoagglutinationoftheredcellsandtheformationofsp

herocytes.Theplateletcountandserumproteinsarecommonlywithinthereferencerangeforthespecies.Theabnormalitiesofbilirubinassociatedwithhepa

ticdiseaseandcholestaticdiseasearediscussedmorefully.Previouslyitwasbelievedthatthemeasurementofdirectandindirect-reactingbilirubinwouldhel

ptodeterminethecauseofthejaundice.However,itisnowclearthatthisisnotthecaseinthedogandcatandthathepatic,haemolyticandbiliarytractdiseasesproduce

variableincreasesinthesefractions.Differentiationofprehepatic,hepaticandposthepaticjaundicerequiresafullhaematologicalandbiochemicalinvest

igation(includingmeasurementofredcellmass,examinationofabloodsmearandliverfunctiontests)andmayrequireexamin

ationofthebiliarytract.Hepaticbiopsymayalsobenecessaryinsomecases.MARKERSOFHEPATICDISEASE2021/02/2450BileacidsPhysiologyTheprim

arybileacidsareproducedintheliverfromcholesterolandarethenconjugatedtotaurine（氨基乙磺酸）orglycine（氨基乙酸）.Theyareexcretedin

tothebiliarytreeandstoredinthegallbladder.Gallbladdercontraction(stimulatedbyingestionoffood)releasesthebileacidsi

ntotheintestineswheretheyfacilitatethedigestionandabsorptionofdietarylipid.Thebileacidsareefficientlyreabsorbedintheil

eum,resultinginverysmallfaecalloss.Thetotalpoolofbileacidsmayundergoenterohepaticcirculationtwotofivetimesduringasinglemeal.Indi

cationsforassayInclusionofbileacidsinaproindicatedwherethereissuspicionofhepaticdisease.Clinicalsignsins

uchpatientsmightincludehepatomegaly（肝大）,microhepatica（小肝）andabnormalcentralnervoussystemsigns.Thesensitivityofthebile

acidassaymaybeincreasedbyusingabileacidstimulationtest.Referenceranges(fasted)Dogs0-15umol/LCats0-15u

mol/LMARKERSOFHEPATICDISEASE2021/02/2451CausesofincreasedbileacidsThefastingserumbileacidconcentrationmayberaised

inassociationwithprimaryorsecondaryhepaticdisease.Theassayfacilitatesidentificationofhepaticdysfunctionbutgive

snoindicationastothenatureorreversibilityoftheliverpathology.Valuesexceeding30umol/Larecommonlyassociatedwithhistologicallesionsandbiop

symaybehelpfulinthesecases.Itisimportanttorememberthatthehistologicalchangescouldstillbeassociatedwithsecondaryhepaticdiseaseeventh

oughthefastingbileacidconcentrationis>30umol/L,forexampleinhyperadrenocorticism.Theuseofthebileacidstimulationtestmayimprovethesensitivit

yoftesting.Forthis,serumbileacidconcentrationsaremeasuredinasamplecollectedaftera12-hourfast(fastingbileacidconcentration)and2hours

afterafattymeal(postprandial（餐后）bileacidconcentration).Inonestudyof108cats,thepostprandialbileacidconcentra

tionwasfoundtohavethehighestsensitivityofanysingletestforthediagnosisoffelineliverdisease.MARKERSOFHEPATICDISE

ASE2021/02/2452AmmoniaPhysiologyDietaryproteinsarehydrolysedintheguttoaminoacidswhich,inturn,maybedegradedbyintestinalbacteria,producingamm

onia.Ammoniaistransportedtotheliverwhereitisusedasaprecursorinthesynthesisofurea.Increasedbloodammoniaconcentrationsareobservedinsomepatientswit

hdiffuseliverdisease(withareducedcapacityforureasynthesis)andinindividualswithportosystemicshunts.IndicationsforassayAmmoniais

usedintheevaluationofhepaticfunction;theindicationsformeasurementarethesameasforbileacids.AnalysisAmmoniaismeasuredinblood,serumor

plasmabydryreagentandenzymaticmethods.Samplesshouldbecollectedintoachilledsampletubeandstoredoniceuntilanalysis,whichmustbecarriedoutw

ithin20minutesofcollection.ReferencerangesDogs0-60umol/LCats0-60umol/LMARKERSOFHEPATICDISEASE2021/02/2453CausesofincreasedammoniaIncreasedammo

niaconcentrationsareassociatedwithfeedinghigh-proteindietsandwithintestinalhaemorrhage(duetotheincreaseddeliveryofami

noacidstotheintestinalbacteria).Diffusehepaticdisease,resultinginthefailureofconversionofammoniatourea,andportosystemicshunts(con

genitalandacquired)willalsoproduceincreasedserumammoniaconcentrations.MARKERSOFHEPATICDISEASE2021/02/2454PANCREATICDISEASEAmylasePhysiologyAmylase（淀粉

酶）isacalcium-dependentenzyme,producedbythepancreaticacinarcells,whichhydrolysescomplexcarbohydrates.

Theenzymepassesdirectlyfromthepancreasintothecirculationwhereitisfilteredbytherenaltubules;theinactivatedenzyme

isreabsorbedbythetubularepithelium.Amylaseactivityinthetissuesofthedogandcatishighestinthepancreasbu

tisalsofoundintheintestinesandliver.IndicationsforassayAmylaseshouldbemeasuredwhenthepresentingsignsmightsuggestpancreatitis（胰腺炎）,e.g.vom

iting,abdominalpainoricterus,orwhenthereisfreeperitonealfluid.AnalysisAmylaseactivitiesmaybemeasuredinserum,heparinizedplasma

andabdominalfluidusingspectrophotometricmethods.ReferencerangesDogs400-2000units/LCats400-2000units/L202

1/02/2455CausesofincreasedamylaseThetissuedistributionofamylaseisnotrestrictedtothepancreasandthereforeraisedserumactivitiesarenotspeci

ficforpancreatitis.Reducedglomerularfiltration(prerenal,renal,postrenal)isoftenassociatedwithanincreasedserum

amylaseactivitybutthisiscommonlylessthantwotothreetimesgreaterthantheupperlimitofthereferencerange.Serumactivitiesabovethislevelaresugg

estiveofpancreatitisbutthedegreeofincreasedoesnotcorrelatewellwiththeseverityofpancreatitis.Ifanazotaemic（氮血症）patie

nthasanamylaseactivitytwotothreetimestheupperlimitofthereferencerangethenpancreaticdiseasemustbeconsidered.Thesimultaneousmeasureme

ntofamylaseandlipaseincasesofsuspectedpancreatitisisadvisablewhileadditionaltestsofrenalandhepaticfunctionshouldalsobeincludedinth

ebiochemicalprofile.Amylaseisnotareliableindicatorofpancreatitisincats.Incasesthatpresentwithfreeperitonealfluid,fullanalysiso

fthefluid(proteinconcentration,cellcountsandcytologicalexamination)andmeasurementoftheserumandfluidamylaseact

ivitiesmaybeuseful.Thepresenceofanon-septicexudatewithgreateramylaseactivitythantheserummaybeassociatedwit

hpancreatitisorbowelrupture.PANCREATICDISEASE2021/02/2456LipasePhysiologyLipaseisadigestiveenzyme,producedbythepancreaticacinarcells,thathy

drolysestriglycerides.Theenzymeisclearedfromthecirculationbyrenalinactivation.Aswithamylase,lipasemayorigin

atefrompancreaticorextrapancreaticsources.Pancreaticdamageandinflammationresultsinthereleaseoflipaseintothesurroundingg

landandperitonealtissuewhichmaycausethedevelopmentofnecrosisintheperipancreaticperitonealfat.IndicationsforassayIndicationsforthemeasurementoflipas

earethesameasforamylase.Amylaseandlipaseassaysshouldbeperformedsimultaneouslyincasesinwhichpancreatitisissuspected,buttheincreasesinenzymeactivities

areoftennotparallel(markedincreasesinoneenzymemaybeassociatedwithminimalincreasesintheother).AnalysisLipaseactivitiesaremeasuredinserum,hepa

rinizedplasmaandbodyfluidsusingturbidimetricmethods.ReferencerangesDogs0-500units/LCats0-700units/LPANCREATICDISEASE2021/02/2457Causesofraised

serumlipaseSincelipaseoriginatesfrombothpancreaticandextrapancreatictissue,anincreaseinserumactivityisnotdiagnosticofpancreatitis.Increasedserumacti

vityisalsonotedinazotaemicpatients,althoughthevaluesgenerallydonotexceedtwotothreetimestheupperlimitofthereferen

cerange.Inaddition,moderateelevationsoflipase(upto5-foldincreases)havebeenreportedinassociationwithadm

inistrationofdexamethasonewithoutevidenceofhistologicalchangesinthepancreas.Anormallipaseactivitydoesnotprecludepancreaticdisease.Lipasehasbee

nreportedtobepersistentlyelevatedincatswithexperimentallyinducedpancreatitisbutthisisnotaconsistentfindingin

naturallyoccurringdisease.PANCREATICDISEASE2021/02/2458CARBOHYDRATEMETABOLISMPhysiologyGlucoseistheprincipalsourceofenergyformammalian

tissuesandisderivedfromthedietandhepaticgluconeogenesis.Thebloodconcentrationiscontrolledbyhormoneswhichregulateitsent

ryinto,andremovalfrom,thecirculation(insulin,glucagon,adrenaline,cortisol).Inthekidneyofthedogandcat,glucoseenteringtheglomer

ularultrafiltrateisreabsorbedbytherenaltubules.However,therenalreabsorptionofglucoseisoverwhelmedinthepresenceofbloodglucoseconcentrationsgrea

terthan10-12mmol/1,resultinginglucosuria.IndicationsforassayMeasurementofbloodglucoseisessentialwhere

presentingclinicalsignscouldsuggest：diabetesmellitus(polydipsia,polyuria,weightloss,cataractformation

),diabeticketoacidosis(vomiting,diarrhoea,anorexia)hypoglycaemia(weakness,collapse,seizures,disorientation,depression,blindness).Inaddition,t

heassayisincludedingeneralhealthscreenswhereitmayprovidesupportiveevidenceforotherdiseaseprocesses(hyperadrenocorticism,hepa

ticdisease).Measurementofthebloodglucoseconcentrationistheidealmethodofmonitoringthestabilizationofdiabeticpatientsoninsulinther

apyandallowsoptimizationofthetherapeuticregimen.Insuchcases,glucoseismeasuredinsamplescollectedat2-hourlyinterv

als,allowingcalculationofthedurationofactionandpeaktimeofactionoftheadministeredinsulin.Glucose2021/02/2459AnalysisReag

entstrips:Rapid-analysisreagentstripsrequiretheuseofwholebloodwithnoanticoagulant.Laboratoryanalysis:Spectrophotometricmethods(enzymaticorc

hemical)arcgenerallyusedforthemeasurementofbloodglucose.Wherein-houseequipmentdemandstheuseofheparinizedplasma,thesamplemustbeseparatedimmediately

aftercollection.Thispreventsdepletionoftheplasmaglucosebytheerythrocytes.Collectionofthebloodintofluorideoxalateisthepreferredmethod

ofpreventingerythrocyteglucoseutilizationwhenadelayinanalysisisanticipated,suchasduringtransporttoacommer

ciallaboratory.ReferencerangesDogs3.5-5.5mmol/LCats3.5-6.5mmol/LGlucose2021/02/2460CausesofhypoglycaemiaMarkedhypog

lycaemia(glucose<2mmol/L)mostcommonlyresultsfromoverproductionofinsulinorexcessiveutilizationofgluco

sebyneoplasticcells.Insulin-secretingtumoursofthepancreas(insulinomas)producebiologicallyactivehormonewhichincreasestheuptakeofgluco

sebythebodytissuesandimpairshepaticgluconeogenesis,resultinginhypoglycaemia.Inonestudyofdogswithinsulinomasthemean(+SD)plasmaglucoseconcen

trationwas2.14(±0.82)mmol/1.Extrapancrcatictumoursoccasionallycausehypoglycaemiabysecretionofaninsulin-li

kesubstanceorbyincreasedutilizationofplasmaglucose.Glucose2021/02/2461Neoplastic:Insulin-secretingtumourofthepancreas(insulinoma)Hepatoce

llularcarcinomaEndocrine:HypoadrenocorticismHepaticinsufficiency:CongenitalvascularshuntsAcquiredvascularshuntsChronic

hepaticfibrosis(cirrhosis)Hepaticnecrosis(e.g.hepatotoxins,bacterialinfection,trauma)GlucoseFigure4.19:Causesofhypoglycaemiainthedo

g.Catsmayrarelybeaffectedbyinsulinoma.Substratedeficiency:NeonatalhypoglycaemiaJuvenilehypoglycaemiaHuntingdoghypoglycae

miaGlycogenstoragediseaseSepsis2021/02/2462CausesofhyperglycaemiaHyperglycaemiacommonlyresultsfromarelativeorabsolutelackofinsulin.Thisl

eadstoimpairedtissueutilizationofplasmaglucoseandanincreaseintherateofgluconeogenesis.Mildhyperglycaemia(6.7-10mmol/L)inthedogma

ybenotedaspartofanadrenalinestressresponseorsecondarytoexcessivesecretionoradministrationofotherdiabetogen

ichormones,inparticularglucocorticoidsandprogesterone.Themildhyperglycaemiaisaresultofthehormonalantagonismoftheac

tionsofinsulin.Inaddition,mildhyperglycaemiamaybenotedinthepostprandialperiodindogsfedasugar-richdietsuchassemi-moistfoods.Apersistent

,moderatetomarkedhyperglycaemiainthedogisconsistentwithdiabetesmellitus.Suchcasesdonotpresentwithclinicalsigns(polyuriaandpolydipsia)until

therenalthresholdforglucoseisexceeded,resultinginosmoticdiuresis.Inthecat,anadrenaline-inducedstressresponsemay

produceamoderateormarkedincreaseinglucoseconcentration.Thediagnosisofdiabetesmellitusisoftendifficultincatsandconfirma

tionrequiresdocumentationofpersistenthyperglycaemiawithcompatibleclinicalsigns.Glucose2021/02/2463Figure4.20:Causesofhyperglycaemia.Adrena

linestressresponse(especiallymarkedincats)PostprandialDiabetesmellitusHyperadrenocorticism(dogsandrarelycats)Acromegaly(cats)Acutepancreati

tis(dogsandcats)RenalinsufficiencyGlucose2021/02/2464FructosaminePhysiologyFructosamineisaglycatedserumproteinwh

ichisformedbythenon-enzymaticreactionbetweenasugarandanaminoacid.Thetotalamountoffructosamineformedisproportionaltotheserum

glucoseconcentrationduringthelifespanoftheproteins.Indogsandcats,fructosaminehasbeenfoundtobeausefulparame

terinthediagnosisandmanagementofdiabetesmellitus.IndicationsforassaySerumfructosamineconcentrationsareusefuli

nthediagnosisofdiabetesmellitusandinidentifyingpersistenthyperglycaemiaduringtherapy.Measurementoffructosaminemayalsobehelpfulinconf

irmingthepresenceofpersistenthypoglycaemia.AnalysisFructosamineismeasuredusingamethodbasedonthereducingabilityoffructosamineinalk

alinesolution.ReferencerangesDogs250-350umol/LCats150-270umol/L2021/02/2465CausesoflowserumfructosamineAlowserumfructosamine

concentrationhasbeenrecordedinadogwithaninsulin-secretingtumourofthepancreas(insulinoma).Ithasbeensuggestedt

hatthemeasurementofserumfructosamineinadditiontoglucoseandinsulinmaybehelpfulinconfirmingthepresenceofinsulinomas.C

ausesofraisedfructosamineRaisedserumconcentrationsoffructosaminereflectpersistenthyperglycaemiaoverthepreced

ing2-3weeks.Indogswithdiabetestheserumfructosamineconcentrationissignificantlygreaterthanindogswithotherdiseases.Fructosamineisalsousefulforcon

firmingdiabetesmellitusinthecatandcanbehelpfulinidentifyingpersistenthyperglycaemiaafterinitialstabilizationoninsulintherapy.Fructos

amine2021/02/2466LIPIDMETABOLISMPhysiologyCholesterolisthemostcommonsteroidinthebodytissuesandactsasaprecurs

orcompoundforsteroidhormoneandbilesaltsynthesis.Themajorityofthebody'scholesterolissynthesizedbytheliver,buttheremainderoriginates

fromdietarysources.Excesscholesterolisexcretedinthebile.IndicationsforassayHypercholesterolaemiaisoftenassocia

tedwithendocrinediseaseinthedogandcatandisfrequentlymeasuredaspartofageneralhealthprothesespecies.Raisedplasma

cholesterolaloneisnotcommonlyresponsibleforthedevelopmentofclinicaldiseaseinthedogandcat.However,markedhypercholesterolaemiaandhypertriglyceridaemi

asecondarytothyroiddysfunctionindogshavebeenassociatedwiththedevelopmentofperipheralvasculardisease.AnalysisCholesterolconcentrationsareass

ayedinserum,heparinizedplasmaorEDTAplasmausingspectrophotometric,automateddirectandenzymaticmethods.Chol

esterol2021/02/2467Figure4Causesofalterationsinplasmacholesterolconcentrations.HypocholesterolaemiaProtein-l

osingenteropathyMaldigestion/malabsorptionHepatopathy(portocavalshunt,cirrhosis)HypercholesterolaemiaPostprandialhyperlipidaemiaSe

condaryhyperlipidaemia:HypothyroidismDiabetesmellitusHyperadrenocorticismCholestaticdiseaseNephroticsyndrome2021/02/2468Causesofhypercholester

olaemiaAmarginalincreaseinthecholesterolconcentrationmaybenotedinsamplescollectedinthepostprandialperiodversusaf

astedsample.Thisincreasedlevelgenerallydoesnotexceedthereferencerangeforthespecies.Hypercholesterolaemiainthedogandcatismostcommonlyassociatedwi

thendocrinedisease(diabetesmellitus,hypothyroidism,hyperadrenocorticism).Ineachoftheseendocrinedisorderstheremaybeaconcurrentincreaseinse

rumtriglycerideconcentration.Hypercholesterolaemiamayalsobenotedincholestaticdiseaseandglomerulonephritis(肾小球性肾炎）.Furtherspecialistin

vestigation(e.g.lipoproteinelectrophoresis)maybenecessaryifnounderlyingsystemicorendocrinediseasecanbeidentifiedandthehypercholesterolaemiaismar

kedandpersistent.2021/02/2469TriglyceridesPhysiologyThetriglyceridesarethemostabundantlipidsinthebodyandtheirstorageinadiposetissueprovidesa

nessentialreserveofchemicalenergyfortissuerequirements.Theyarederivedfromthedietandalsosynthesizeddenovo（重新）intheliver.Indicationsforas

sayFastinghypertriglyceridaemiainthedogandcatisapathologicalfinding.Thepresenceoflargetriglyceride-richlipoprotein

simpartsaturbiditytotheplasmaorserum(lipaemia).Triglyceridesshouldthereforebemeasuredinallfastingbloodsamplesthatappeartobelipaemic.Clinicalm

anifestationsofhypertriglyceridaemiainclude：recurrentabdominalpain,alimentarysigns,seizures.2021/02/2470Causesofhypotr

iglyceridaemiaHypotriglyceridaemiahasnotbeenconsistentlyassociatedwithanyspecificdiseaseprocessalthoughithasbeenreportedinseve

ralcasesofacuteandchronichepaticdisease.CausesofhypertriglyceridaemiaThemostcommoncauseofapparenthypertriglyceridaemiainthedogandcatisafailuret

oobtainafastingsample(postprandialhyperlipidaemia).Ifhypertriglyceridaemiaisdocumentedinasamplecollect

edaftera12-hourfast,endocrineandsystemicdiseaseshouldbeexcluded(diabetesmellitus,hypothyroidism,hyperadrencorticism,glomerulonephritis

).Manydogswithspontaneousacutepancreatitishaveincreasedserumtriglycerideconcentrations.Therelationshipbetweenpancreatitisandhyperlipidae

miahasnotbeenfullyelucidatedbutitappearsthattheincreasedtriglycerideconcentrationmaypredisposepatientstopancreaticpathology.2021/02/2471

Figure5CausesofhypertriglyceridaemiainthedogandcatPostprandialhyperlipidaemiaSecondaryhyperlipidaemia:HypothyroidismDiabetesmellitus

HyperadrenocorticismAcutepancreatitisPrimaryhyperlipidaemia:IdiopathichyperchylomicronaemiaoftheMiniatureSchnauzerFamilialhyperchylomi

cronaemia（乳糜微粒血症）inthecatIdiopathichypertriglyceridaemia2021/02/2472CHEMICALPROFILESANDTESTSELECTIONOntheinitialpresen

tationofanillpatient,aclinicianformulatesalistofdifferentialdiagnosesbasedonthehistoryandclinicalfindings.Wheretheclinicalfindingsar

especific,e.g.pallorofthemucousmembranessuggestiveofanaemia,thenstepsaretakentoconfirmthissuspicionan

dtoelucidatethepossiblecause.Awider,morecomprehensiveinvestigationisnecessarywhenclinicalsignsmaybecaused

bymanymetabolicdisorders;forexample,polydipsiainthedogcouldbetheresultofendocrinedisease,renaldiseaseorhepaticdisease.

Theselectionoftestsdependsuponthedifferentialdiagnoses,therangeofconditionsthatmustbeexcluded,theavailabilityofthetes

ts,andthecostoftests.Inthecaseofthepolydipsicdog,acost-effectiveprorequiredtocoverthepossibilityoforganfailure(renal,hepatic),endoc

rinedisease(diabetesmellitus,hyperadrenocorticism)andhypercalcaemia.2021/02/2473Someofthesedifferentialsmaybeexcludedorconfirmedon

thebasisofindividualtests(e.g.ureaandcreatinineforrenaldisease)butinclusioninamorecomprehensiveprothes

imultaneousassessmentandcost-effectiveexclusionofmanyothercausesofpolydipsia.Whentheclinicalsignsarevagueanda'generalhealthscreen'isreq

uired,thenitisnecessarytoselectabroadrangeofanalyteswhichwillreflectanumberofcommondiseasesorpathologicalstates.Thei

nclusionofteststhatarenotorgan-specificbutwhichprovidegeneralinformationregardingthehydrationandessentialhome

ostaticmechanismsisworthwhile,e.g.totalproteins,albumin,electrolytes,glucose.CHEMICALPROFILESANDTESTSELECTION2021/02/2474Pr

ofileHealthPre-anaestheticscreen*Extended*healthscreenPolydipsiaprofileSeizureprofileRenalprofileHepaticprofileTestsFBC,TP,alb

umin,globulin,ALT,ALP,GGT,bilirubin,amylase,urea,creatinine,glucose,urinalysisFBC，TP,albumin,globulin,ALT,ALP,bilirubi

n,urea,creatinine,glucoseAshealthscreenplusbileacids,electrolytes,cholesterol,CK,calcium,phosphorusFBC,TP,albumin,globulin,ALT,ALP,b

ilirubin,bileacids,CK,cholesterol,urea,creatinine,glucose,calcium,phosphorus,electrolytescreen,urinalysis(SG,dipstickandsedimentexamin

ation).FBC,TP,albumin,globulin,ALT,ALP,bileacids,urea,creatinine,glucose,calcium,CK,phosphorus,magnesium,electrolytescreenPCV,TP,albumin,glob

ulin,urea,creatinine,sodium,potassium,calcium,phosphorus,urinalysis(SGdipstickandsedimentexamination)

TP,albumin,globulin,ALT,ALP,AST,GGT,bilirubin,bileacids,cholesterolIndicationsRoutinescreeningScreenfore

xistingdiseasepriortoroutinesurgeryGastrointestinai.endocrinediseaseandnonlocalizingsignsPolydipsiaSeizures,weakness,episodicco

llapseMonitoringhepatotoxicity2021/02/24752021/02/2476GastrointestinalSystemFecalanalysisExaminationofvomitusBloodtestsImagingtechn

iquesEndoscopy2021/02/2477Dysphagiaandregurgitation•Collectahistoryandconductathoroughphysicalexamination•Completeaneurologicalexamination•O

bservethepatienteating,toassessthelikelystageoftheswallowingprocessaffected•Plainradiographyofpharynxando

esophagus•Possiblecontraststudies-bariumswallowandfluoroscopy•Examinationoforalcavityandpharynxundergeneralanaesthesia•Endoscopicexaminat

ionofpharynxandoesophagusPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2478Vomiting*Collec

tahistoryandconductathoroughphysicalexamination*Characterizethevomitusproduced*Isthevomitingprimaryorsecondary?PRIMARYSECONDARYHaemato

logyandbiochemistryHaematologyandbiochemistryPlainradiographyUrinalysisContraststudiesSpecifictestsofEndoscopy/ex

ploratoryorganfunctionlaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2479Diarrhoea•Collectahist

oryandconductathoroughphysicalexamination•Physicalexaminationofthefaecesproduced•Isthediarrhoeaprimaryorse

condary?•Ifprimary,isthediarrhoeaofsmallorlargeintestinalorigin?PRIMARYSECONDARYSmallintestinalLargeintestinalUrinaly

sisHaematology/biochemistryFaecalcultureSpecifictestsoforganfunctionFaecalcultureWormeggcountWormeggcountRectalexami

nationUndigestedfoodanalysisPlainradiographySerumfolate/cobalaminEndoscopy/biopsyTrypsin-likeimmunoreactivityBre

athhydrogenassaySugarpermeabilitytestUltrasoundscanEndoscopy/exploratorylaparotomyPossiblediagnosticprocedures

forcommonalimentarysymptoms2021/02/2480Constipation*Collectahistoryandconductathoroughphysicalexamination*

Rectalexamination*Neurologicalexamination*Orthopaedicassessment*PlainradiographyPossiblediagnosticproceduresforcommonalimentarysym

ptoms2021/02/2481Faecaltenesmus(里急后重）•Collectahistoryandconductathoroughphysicalexamination•Rectalexamination•Faecalcultureandworme

ggcount•Plainradiography•Contraststudies•Ultrasoundscan•Endoscopy/biopsyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2

482Acuteabdomen•Collectahistoryandconductathoroughphysicalexamination•Carefulabdominalpalpation•Haematologyandbiochemistry•Plainradiography•Possiblyc

ontraststudies•Paracentesis•Ultrasoundscan•ExploratorylaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2483Abdominalen

largement•Collectahistoryandconductathoroughphysicalexamination•Carefulabdominalpalpation•Haematologyandbiochemistr

y•Plainradiography•Paracentesis（腹腔穿刺）•Ultrasoundscan•ExploratorylaparotomyPossiblediagnosticproceduresforcommonaliment

arysymptoms2021/02/2484FAECALANALYSISPhysicalappearanceInitialexaminationofafreshfecalsampleshouldconcentrateonits

physicalappearance.Inmanycasesofdiarrhoeaitispossibletodecidewhetheritisassociatedwithasmallorlargeintestinalproblemusingthecrite

riashowninTable8.1.Suchadifferentiationnotonlygivestheclinicianvaluableinformationregardingthelocationofthelesionbutconsequentlya

ssistsintheselectionoffurtherappropriatediagnostictests.Unfortunately,notalldiarrhoeasmaybereadilyclassified,andf

eaturesofbothsmallandlargeintestinaldiseasemaybepresent.Thismayreflectasmallintestinalproblemwhichresultsintheabnormalpresenceofnutrient

sorotheragentsinthelargeintestine,therebycausingsignsoflargeintestinaldisease.Alternatively,itmayreflect

aconditionthataffectsboththesmallandthelargeintestineequally.2021/02/2485Table8.1:Characteristicsoffaecespassedinsmal

landlargeintestinaldiarrhoea.Symptom/SignSmallintestineLargeintestineFaecalvolumeIncreasedReducedFaecaltenesmusNonePresentFaecalbl

oodNoneorchangedOftenpresentFaecalmucusNoneOftenpresentUrgency（尿急）RareOftenpresentDyschezia（排便困难）AbsentOftenpresentSteat

orrhoea（脂肪痢）OftenpresentAbsentVomitingMayoccurOccursin30%ofcasesWeightlossPresentAbsentFlatus/borborygmi(肠鸣)Presen

tRareCoat/skinconditionPoorNormalAppetiteIncreasedNormalorreduced2021/02/2486Figure8.2Majorcausesofacutediar

rhoeaindogsandcats.Endoparasitism:Hookworms钩虫Whipworms鞭虫Giardiasis贾第鞭毛虫病Dietaryindiscretions:SoiledfoodsScavengingOver-eatingViralinfections:Felin

epanleucopenia猫瘟Canineparvovirus犬细小病毒Coronavirus冠状病毒Bacterialinfection:SalmonellosisCampylobacterinfection弯曲菌Intussuscept

ion肠套叠Haemorrhagicgastroenteritis2021/02/2487Figure8.3:Majorcauseofchronicdiarrhoeaindogsandcats.Smallintestinaldisease:Lymphocytic-pla

smacyticenteritis淋巴细胞-浆细胞性肠炎EosinophilicenteritisLymphangiectasia淋巴管扩张Lymphosarcoma淋巴肉瘤GiardiasisExocrinepancreaticinsufficienc

y(EPI)Colitis:Lymphocytic-plasmacyticEosinophilicHistiocyticGranulomatousLymphosarcomaSystemicdisease:Hypert

hyroidism(cats)HypoadrenocorticalismHypothyroidism(dogs)ChronicrenalfailureHepaticdiseaseFeLV,FIVandFIP2021/02/2488Melaena（黑粪症）canbedefinedasthe

presenceofchangedbloodinthefaeces.Theappearanceofmelaenawilldependontheextentofbleedinganditslocation,butmalaenicfaecesnormallyappearb

lackandtarryinconsistency.Thisappearanceisnormallyassociatedwithbleedingintothesmallintestine,althoughmelaenamayoriginatefromthestomachorfromtheo

esophagus,pharynx,mouthorrespiratorysystem.Inthelattercasesbloodisswallowedandpassesthroughthealimentarytracttoappearasmelaena,givingtheim

pressionofalimentarydisease.Patientswithclottingdisordersmaypresentwithmelaena,butagaincarefulclinicalexaminationshouldrevealbleedingfrom

otherlocations,confirmingageneralizeddisorder.Occultblood（潜血）referstothepresenceofmicroscopicamountsofbloodthatcanonlybedetectedbylaborator

yanalysis.Greatcareisrequiredininterpretingapositiveresultindogsandcatsastheyareoftenfedmeat-baseddiets.Thepresenceofhaemoglobinormyoglobinint

hedietwillgivefalsepositiveresults.Itisthereforeimportanttoplacethepatientonameat-freedietforaminimumof3dayspriortotestingforoccultblood.Atru

estrongpositiveresultindicatesonlythatbleedingisoccurringsomewherealongthealimentarytract.2021/02/2489Cu

ltureforbacteriaNormalfloraThesmallintestineliesbetweenthealmoststerilestomach(duetogastricacid)andthelargebacterialpopulationlocat

edinthecolon.Bacterialnumbersintheproximalsmallintestinearelowbutnumbersincreaseintheileum.Theactual

numberspresentinanyindividualwillvarydependingonvariousinternalandexternalfactors.Manyofthe'normal'floraarebeneficialtotheanimalbypro

ducingvitaminK,biotin,folateandshort-chainfattyacids(SCFAs).Ifthenumbersofbacteriapresentinthesmallintestineincrease,smallintestinalbacteria

lovergrowth(SIBO)develops.Suchaproliferationofbacteriacanseriouslydamagetheintestinalmucosa.Thepointatwhichbacterialpopulationsinducecl

inicalsignsofSIBOwillvarywitheachindividualandthegenusofbacteriapresent.2021/02/2490PathogenicbacteriaPathogenicbacteriamayestablishwhe

nthereisinterferencewiththenormalphysiologicalregulationoftheresidentflora.Bacterialpropertiesthatpermit

pathogenstoestablishinclude:thepresenceofflagellae;productionofenzymessuchasproteases;theabilityofbacteriatoadheretothemucosa;andproductio

noffactorsthatinterferewithintestinalmotility.Theabilitiestoproduceenterotoxinandtoinvadeenterocytessignific

antlyincreasepathogenicity.PotentialpathogensincludeSalmonella,Campylobacter,YersiniaandClostridiumspeciesandEscherichiacoli.2021/02/2491Analys

isforvirusesCanineparvovirus(CPV-2)infectionusuallyresultsinanacuteenteritiswithsecondarybacterialinfection,inv

olvingespeciallySalmonellaandCampylobacterspp.Adefinitivediagnosisofparvovirusinfectionrequirescollectionofafreshfaecalsampleforviralantig

endetection.Ideally,samplesshouldbecollectedwithinthefirst2daysofinfectionwhenthelargestnumberofvirusparticlesarepresent.AcommercialELI

SAtestkitisavailableforthedetectionofparvovirusantigeninfaeces.Serologycanalsobecarriedoutinordertodetectarising

titreofantibodyindicatingrecentparvovirusinfection.2021/02/2492EndoparasitesEndoparasiticinfectionwithroundworms(ToxocaracanisToxocar

acati,Toxascarisleonina)andtapeworms(Dipylidiumcaninum,Taeniaspp.andEchmococcus)are,intheauthor'sexperience,veryrarecausesofdiarrhoeaindogsandcat

s.However,EchinococcusandToxocarabothcarryasignificantpublichealthriskandshouldbeidentifiedandtreatedwheneverpossi

ble.2021/02/2493FaecalsmearsFreshfaecalsmearsprovideaquickandcheapmethodofexaminingfaecalsamples.However,asthereisnoconcentrationofo

vaitiseasytomissparasiteeggsorcyststhatarepresentinsmallnumbers.Afreshfecalsampleshouldbemixedwithasmallvolumeofphysiolo

gicalsalineonamicroscopeslide.Ifprotozoansaresuspected,onedropofLugol'siodinewillhighlighttheseparasitesbutwillre

ducetheirmotility.Anegativeresultmaybeaccurateormayreflectthesmallnumbersofparasiticeggspresent,intermittentexcretion,ortheeffectsof

agentssuchasbariumsulphate,kaolin,pectinorenemas.2021/02/2494FaecalflotationFaecalflotationisamoresensitivemethodthanthefaecalsm

earforthedetectionofparasiteeggsandcyslbecausethetechniqueconcentratestheirnumbersinasmallvolumeofsolution.Severalmet

hodshavebeedeveloped,butforthepurposesofthischapterontwomethodswillbedescribed.Faecalsamplesfordetectionofparasiteeggso

rcystsmaybepreservedbrefrigerationat+4Cforupto2dayspriortoexamination,butshouldnotbefrozen.Preservationoffaecalsamplesmayalsobecarriedout

using1partfaecel3partspreservative(1.5gsodiumacetate,2mlglacialaceticacid,4ml40%formalinplus92.5mlwater).2021/02

/2495HepatobiliarySystemIntroductionDiseasesoftheliverfrequentlypresentthesmallanimalclinicianwithadiagnosticchal

lenge;signsareoftenvariedandvagueand,despiteawidearrayofdiagnostictestsofbothhepaticdamageandfunction,thereisrarel

yasingletestthatidentifiestheproblemdefinitively.Forexample,jaundiceisoftenconsideredacardinalsignofliverdisease,yetc

anbecausedbynon-hepaticconditions(e.g.haemolysis,extrahepaticbileductobstruction)aswellasarangeofdifferentliverdiseases.Conversely,significantlive

rdiseasecanexistintheabsenceofjaundice.Nevertheless,followingathoroughhistory-takingandcarefulphysicalexamination,as

tuteinterpretationofapaneloflaboratorytestsinconjunctionwithradiographicandultrasonographicimagingofthehepatobiliarysystemwilloftenpermi

tapresumptivediagnosistobemade.Inmostcases,however,withtheexceptionofcongenitalportosystemicshunts(PSS),definitivedia

gnosisofprimaryliverdiseasewillrequirehistopathologicalexaminationoflivertissue.2021/02/2496Figure9.1:Someo

fthemorecommonextrahepaticdisordersthatcancauseabnormallivertestresults.AcutepancreatitisDiabetesmellitusExocrinepanc

reaticinsufficiencyExtrahepaticbacterialinfectionHyperadrenocortisolismHyperthyroidismHypoadrenocorticismHypothyroidismImmune-mediated

haemolyticanaemiaInflammatoryboweldiseaseProtein-losingenteropathyRight-sidedheartfailureSepticaemiaShock2

021/02/2497Table9.1:Clinicopathologicalabnormalitiesassociatedwithdisturbancesofhepatobiliaryfunction.FunctionAbnormalla

boratorytestresultassociatedwithliverdysfunctionCarbohydratemetabolism:GlucosehomeostasisHyper-orhypogly

caemiaLipidmetabolism:CholesterolFattyacidsLipoproteinsBileacidsHypo-orhypercholesterolaemiaHypertri

glyceridaemiaLipaemiaElevatedbileacidsProteinmetabolism:AlbuminGlobulinsCoagulationproteinsHypoalbuminae

miaIncreasedacutephaseproteins,immunoglobulinsCoagulopathiesVitaminmetabolism?Decreasedfolate,cobalaminVitaminE,vitaminKmaybereduce

ddependingonthediseaseImmunologicalfunctionsHyperglobulinaemiaIncreasedacutephaseproteinsDetoxificationHyperammonaemiaDecreasedureaHyperbili

mbinaemia2021/02/2498CLINICOPATHOLOGICALCHANGESINLIVERDISEASEConsequencesofhepatobiliarydysfunctionThediversefunctionsofthe

hepatobiliarysystemarereflectedinthediverseclinicopathologicalchangesthatcanbefoundinliverdisease(Figure9.3).Thedefectivemetabolisma

ndexcretionofbilirubin,causingaccumulationofcirculatingbilirubinandthedevelopmentofjaundice,isoftenconsideredthehallmar

kofliverdisease,butitisonlyoneofmanyabnormallaboratoryteststhatmayfoundinliverdisease.Indeed,evenhyperbilirubinaemiafrombiliaryobstruc

tionisusuallyassociatedwithhypercholesterolaemiaandelevationsofcholestaticmarkerenzymes.2021/02/2499Figure9.3:Clinicalsignsofhepatobi

liarydisease.Depression,decreasedappetiteandlethargyStuntingandweightlossVomiting,diarrhoea,andgreyacholicfaecesPolydipsiaandpol

yuriaAscitesIcterusAlteredliversizeBleedingtendencyAbdominalpain(rare)Encephalopathy(脑病)2021/02/24100CorrelationwithclinicalsignsTh

eclinicalsignsofliverdiseasearemanyandvaried(Figure9.3)andmayberelatedtospecificlaboratoryabnormalities.Signsareoftenvagueandnotapp

arentuntilthereissignificanthepaticdysfunction,whichiswhylaboratorytestingishelpfulindetectingandcharacterizingearlyliverdisease.However,itmus

talwaysberememberedthatequallyabnormaltestsmaybesecondarytoaprimarysystemicdisease.Forexample,fattyinfiltrationofth

eliverindiabetesmellituscancauseincreasesinserumactivitiesofliverspecificenzymesinbothdogsandcats,andcanresultinjaundiceincats.2021/02/24101Depre

ssionanddiminishedappetiteThesesignsarereflectionsofdisturbedmetabolisminliverdisease,butarenotassociatedwi

thspecificlaboratorytestabnormalities.Anaemiaofchronicdiseasemaybepresent.Abnormallipoproteinandcholesterolmetabolismmayocc

ur.Hypoglycaemiaisseeninend-stagediseaseandmaybeoneofmanyfactorsproducingthesignsofliverfailureusuallyattributedtoaccumulationofmetabolictox

ins.StuntingandweightlossCongenitalPSSandjuvenilehepatopathiesareassociatedwithstunting,butthebiochemicaldisturbancesresponsi

blearemultifarious.Hypoproteinaemiaisoftenassociatedwithmusclewasting.GastrointestinalsignsGrey,acholicfa

ecesareseeninbiliaryobstruction,andarethereforeassociatedwithjaundice.Diarrhoeamaybeareflectionofhypo

proteinaemiacausingboweloedema,althoughlackofluminalbilesaltsandportalhypertensionaremorelikelycauses.2021/02/24102PolydipsiaandpolyuriaThes

esignsmaybeassociatedwithlowlevelsofserumurea,althoughothermechanisms,e.g.hypercortisolism,areinvolvedintheirpat

hogenesis.AscitesHypoproteinaemiaisarecognizedcauseoftissuefluidaccumulation.However,ascitesismorecommont

hangeneralizedoedemainliverdisease,suggestingportalhypertensioninacquiredliverdiseaseisalsoanimportantfactor.IcterusHyperbilirubinaemi

acausesjaundice,andmaybeduetoprehepatic(haemolysis)orposthepatic(biliaryobstruction,biliaryleakage)di

seaseaswellasprimaryintrahepaticcauses.2021/02/24103LiversizeDiseasescausingalteredliversizearelistedinFig

ure9.4,buttherearenospecificlaboratorymarkersofliversizeandmanydiseasesarenotassociatedwithabnormalliversize.Li

paemiamaycorrelatewithfattyinfiltrationoftheliver.BleedingtendencyCoagulationtimesareusuallyabnormalifsevereliverdysfu

nctioncausesbleeding.Generalizedbleedingandhaemorrhagefromhepaticpeliosis(cats)andvasculartumours,suchasmetastatichaemangi-osarcoma,mayresultinregen

erativeanaemia.HepatoencephalopathyThissyndromeiscausedbyaccumulationoftoxinsbecauseofseverehepaticdysfunctionand/orporto-systemicsh

untingofblood.Hyperammonaemiaisasensitiveandspecificmarkerforthesyndrome,althoughothermetabolicdisturbancesareinvolved.2021/02/241

04DIAGNOSTICAPPROACHTOLIVERDISEASEInmostcases,atentativediagnosiscanbededucedfromtheresultsoflaboratorytestsinconjuncti

onwithimagingtechniques.However,thedefinitivediagnosisofprimaryliverdiseaseusuallydependsultimatelyonhistologicalexaminationofliverbiopsy

specimens.Primaryextrahepaticcausesofsecondaryliverdiseasewillhopefullybeidentifiedbeforebiopsyisundertaken.2021/02/24

105Thusadiagnosticapproachtoliverdiseaseincludes:•Clinicalhistory•Physicalexamination•Laboratorytests•Examinationofasciticfluid•Imaging:Radiography

UltrasonographyAngiographyScintigraphy•Liverbiopsy.2021/02/24106Theaimsoflaboratorytestingare:•Toidentifyandc

haracterizeanyhepaticdysfunction•Toidentifypossibleprimarycausesofsecondaryliverdisease•Todifferentiatecausesoficterus•Toevaluatepotentialanaesthet

icrisks•Toidentifycausesofanaemiaofunknownorigin•Toassessprognosis•Toassesstheresponsetoxenobiotics•Tomonitorresponsetotherapy.2021/02/24107Ther

eisawiderangeoflaboratorytestsavailableforassessingliverstatus,buttheycanbeconvenientlydividedintofourclasses:•Generalscreeningte

sts•Markersofliverdamage•Liverfunctiontests•Prognosticindices.Thetestsroutinelyavailabletothepractis

ingveterinarysurgeonandindicationsfortheirusewillbediscussedindetail,andmorespecializedtestsmentionedonlybriefly.2021

/02/24108UrinarySystemTHEROLEOFCLINICALPATHOLOGYClinicalpathologytestsintheevaluationofapatientforthepresenceo

frenaland/orurinarytractdiseaseshouldbeperformedunderthefollowingcircumstances:•Whenprimaryorsecondaryurinarysystemdiseaseissuspectedfromth

epresentingsigns,clinicalhistoryorphysicalexamination•Whenapatienthasadiseaseinanotherorgansystemthatisknowntobepotentiallyassociatedwithconcurrent

orsecondaryrenalorurinarytractdisease•Whenscreening'atrisk'patientsaspartofageneralhealthcheck(e.g.aspartofageriatricscreeningprogramme,beforegeneral

anaesthesia,orbeforeadministrationofdrugsthatareknowntobepotentiallynephrotoxic,suchasnon-steroidalanti-inflammatorydrug

s,aminoglycosidesoroxytetracycline).2021/02/24109Theaccuratediagnosisofrenalandurinarytractdiseasesrequ

iresinvestigationbyanyorallofthefollowing:•Fullhistory•Fullphysicalexamination•Imaging:Radiography-plainandcontraststudies;som

etimesdynamicstudies,Ultrasonography•Urinalysis•Bloodchemistry•Haematology•Microbiologicalcultureand

sensitivitytesting•Tissuebiopsy•Surgicalexaminationatlaparoscopyorlaparotomy•Post-mortemexamination2021/02/24110Urineshouldbeanalysedwhen:•Th

ereisachangeinitsphysicalappearance,e.g.discoloration•Ananimalpassesfrankbloodinitsurine•Ananimalexhibitspolydipsia•Ananimal

exhibitspolyuria•Ananimalexhibitsurinarytenesmus•Ananimallicksitsexternalgenitaliaexcessively•Ananimalexhibitsincreasedurinaryfrequen

cy•Ananimalisdehydrated•Ananimalisvomiting•Ananimalhassignsoffluidaccumulationintheabdomen(i.e.ascite

s)orperipherally(subcutaneousoedema)•Primaryorsecondaryrenalorurinarytractdiseaseissuspected•Aurolithhasbeenpassed•Ananimalexhi

bitspyrexiaofunknownorigin•Itispartofaroutinescreeningtest-juvenile,geriatricorbeforeanaesthesia.2021/02/24111Urinalysisincludesoneormoreofthefollow

ing:•Physicalexamination:color,smell,turbidity,content,volume,specificgravity•Chemicalexamination:pH

,proteinuria,acetone,glucose,urea•Examinationofsediment•Bacterialculture•Viralexamination.2021/02/24112Clinicalpathologypanelfor

urinarysystemdiseasePlasmaureaBloodureanitrogenPlasmacreatinineUrea:creatinineratioTotalplasmaproteinPlas

maalbuminBlasmasodiumPalsmapotassiumPlasmachloridePlasmacalciumPlasmaphosphate2021/02/24113Glomerularfunctiontestsindogsan

dcatsEndogenouscreatinineclearanceExogenouscreatinineclearanceInulin（菊酚）clearanceIothalanate(碘酞酸盐）clearanc

eFiltrationfraction24hoururineproteinexcretionUrinephosphate:urinecreatinine2021/02/24114THANKSFORWATCHING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，

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