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VeterinaryClinicalPathology兽医临床病理学Prof.ZhaoxinTangCollegeofVeterinaryMedicine,SouthChinaAgriculturalUniversity,Guangzhou,China,51

06422021/02/241PrefaceVeterinaryClinicalPathology:VeterinaryLaboratoryMedicineInclude:1ClinicalHematology2C

linicalbiochemistry3Clinicalcytology4Clinicalmicrobiology5Clinicalparasitology6Clinicaltoxicology2021/02/242PrefaceGeneralLaboratoryconcepts

Veterinarianshavemanychoicesregardinglaboratorytesting.Importantfactorsinclude:--Needandusefulness--Practicality--Co

st-effectiveness--Accuracy--Turnaroundtime2021/02/243CompleteBloodCountandBoneMarrowExamination:generalcommentsandse

lectedtechniques•Completebloodcount•Quantitationtechniques•Bloodsmearanalysis•Otherdeterminations•Bonemarrowexamination•Bonemarrowbiopsyandaspirate

2021/02/244Completebloodcount(CBC)•CBCisaprotestsusedtodescribethequantityandqualityofthecellularelementsinbloodan

dafewsubstancesinplasma.•CBCisacost-effectivescreenthedetectsmanyabnormalitiesanddiseaseconditions.•Bonemarrowexaminationisusedinselectedinstancest

oanswerquestionsthemorereadilyavailableCBCcannot.2021/02/245QuantitationTechniques•Samplesubmission•Microhemot

crit•Hemoglobinconcentration•Cellcounts•AbsolutenucleatedRBCcount•Automatedhematologycellcounters2021/02/246BloodSmearAnalysis•Makingthesmear•Stai

ns•Evaluatingbloodsmears--plateletmorphology--leukocytemorphology--leukocyteestimation--leukocytedifferentialcount--erythrocy

temorphology2021/02/247BoneMarrowExamination•Bonemarrowisusuallyexaminedtoanswercertainquestionthatarosef

romevaluatingtheCBC.•Indicationsforbonemarrowexaminationinclude:--nonregenerativeanemia--Persistentneutropenia--Persistentthromb

ocytopenia--Unexplainedpolycythemiaorthrombocytosis--Atypicalcellsinblood2021/02/248Erythrocytes•Basi

cconceptsoferythrocytefunction,metabolism,productionandbreakdown•Hemesynthesis•Globinsynthesis•Ironmetabolism2021/02/249Erythrocytemetabo

lism•Embden-meyerhofpathway--GlycolysisgeneratesATPandNADH•Pentosephosphatepathway--ThispathwayproducesNA

DPH•Methemoblobinreductasepathway--Methemoglobin(Fe3+)cannottransportoxygen•Rapoport-lueberingpathway--2,3diphosphoglycerat

e(2,3DPG)2021/02/2410RedbloodcellsThefundamentalstimulusforproductionofredbloodcells(erythropoiesis)iserythropoietin(红细胞生成素）,aglyc

oproteinproducedbythekidneysinresponsetorenaltissuehypoxia.Otherhormones,suchascorticosteroids,thyroidhorm

oneandandrogens,stimulatetheproductionorreleaseoferythropoietinbuthavenointrinsicerythropoieticactivity.Theaveragelifespanofacirculatinge

rythrocyteis110-120daysinthedogand68daysinthecat.Agedordamagedredcellsareremovedprimarilybymacrophagesintheliver,spleenandbonemarrow.2021/02/241

1NeutrophilsTheproductionofneutrophils,eosinophilsandbasophilsistermedgranulopoiesis.Theneutrophilsinthebloodstreameithercirculatefreely(the

circulatingpool)oradheretothevascularendothelium(themarginalpool).Inthedogthemarginalpoolandthecirculatingpoolareapproximatelyequal

insize,whilstinthecatthemarginalpoolistwotothreetimeslargerthanthecirculatingpool.Thereisacontinualexchangeof

cellsbetweenthesetwopools.Thehalf-lifeofcirculatingneutrophilsisonly6-14hours,afterwhichtimetheyleav

ethecirculationandpassintothetissuepool.Thecirculatingtimeisshortenedduringacuteinfectionsasneutrophilspasstothes

iteofinfectioninthetissues.Themainfunctionoftheneutrophilisthephagocytosisofpyogenicbacteria.2021/02/2412LymphocytesLymphoidprimitivestemcellsdividea

nddifferentiateintopre-Blymphocytesandpre-Tlymphocytesinthebonemarrow.Pre-TlymphocytesmatureandproliferateintoTcellsinthethymus.Pre-B

cellsproliferateinthebonemarrowandmigratetoperipherallymphoidorgans(spleenandlymphnodes)wherefurtherproliferationta

kesplace.PlateletsPlateletsareproducedfromthecytoplasmofmegakaryocytesOnceinthecirculation,plateletssurvi

vefor8-12days.Upto20-30%ofcirculatingplateletscanbesequesteredinthespleen;thefiguremaybeahighas90%ifthereissplenomegaly.Oldordamagedplateletsarerem

ovedfromthecirculationbythespleen,liverandbonemarrow.2021/02/2413ROUTINEHAEMATOLOGYThecompletebloodcountisanintegralpartofthediagnostici

nvestigationofanysystemicdiseaseprocess.Itconsistsoftwocomponents:Aquantitativeexaminationofthecells,including:packedcellvolume(PCV)totalredcellcount

(RBC)totalwhitecellcount(WBC)differentialwhitecellcountplateletcountmeancorpuscularvolume(MCV),meancorpuscularhaemoglobin(MCH),meancorpus

cularhaemoglobinconcentration(MCHC),totalplasmaproteinconcentration.Aqualitativeexaminationofbloodsmearsforchangesinc

ellularmorphology.2021/02/2414Table1ReferencevaluesforredcellindicesDogsCatsTotalredbloodcells(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)32.0~37.0

30.0~36.0ROUTINEHAEMATOLOGY2021/02/2415REDBLOODCELLINDICESMCV(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)RBCindicesarehelpfulintheclassificatio

nofcertainanemias.ROUTINEHAEMATOLOGY2021/02/2416DifferentialwhitecellcountsThedifferentialwhitecellcountisperformedbycounting200leucoc

ytesinabloodsmear.Thecellsarecountedalongthelongedgeofthesmear,usingthebattlementmeandermethod:fourhigh-powerfieldsarecountedinonedirection,t

henfourmoreinadirectionatrightanglestothefirst,andsoon,followingtheshapeofabattlement.Thepercentageofeachtypeofcellisdetermined.Thispercentageisthe

nmultipliedbythetotalwhitecellcounttoobtainanabsolutecountforeachcelltype.ROUTINEHAEMATOLOGY2021/02/2417Plasmaproteinconcentration(Referencerang

e:60-80g/1forthedogandcat)Totalplasmaprotein(TPP)andPCVshouldbeinterpretedtogether.QualitativeexaminationofabloodsmearAbloodsmears

houldalwaysbeevaluatedwhenautomatedcellcountsaremadeorwhenin-practiceinstrumentationislimitedtoacentrifugeforPCVPrepara

tionofabloodsmearAsmalldropofbloodisplacedononeendofaglassslide,usingacapillarytube.Aspreaderslide(

madebybreakingoffthecomerofanotherslide,afterscoringitwithaglasscutterordiamondwriter)isplacedontotheslide

holdingtheblooddrop,infrontofthedropandatanangleof20-40°.ROUTINEHAEMATOLOGY2021/02/2418ANAEMIAAnaemiaischaracterizedbyanabsolutedecreaseinredc

ellcount,haemoglobinconcentrationandPCV.AcutehaemorrhageAcutehaemorrhagemaybeduetotraumaorsurgery,bleedinggastrointestinalulcersortumours,rupture

ofavasculartumour(e.g.splenichaemangiosarcoma),oracoagulopathy(e.g.warfarintoxicity).Immediatelyfollowingacuteh

aemorrhagetheredcellparameters,includingPCV,arenormalbecausebothredcellsandplasmahavebeenlostinproportion.Compensatorymechanism

ssuchasspleniccontractionmayfurtheroffsetanyfallinPCV.ThePCVfallswhenbloodvolumeisreplacedbyinterstitialfluidandsodoesnotindicatethefullma

gnitudeofbloodlossforatleast24hoursaftertheonsetofhaemorrhage.ROUTINEHAEMATOLOGY2021/02/2419Chronichaemo

rrhageChronicexternalbloodloss(e.g.chronicgastrointestinalhaemorrhage,renalorbladderneoplasia)initiallyr

esultsinaregenerativeanaemiabutgraduallytheanaemiabecomesnon-regenerativeastheironstoresbecomedepleted.Younganimalsbecomeiron-deficientmorebonemarro

wisalreadyveryactiveproducingredcellsquicklythanadultsfollowingbloodloss,partlybecausetheyhavelowironstoresandpartlybecausetheirtomatchtheirgro

wthrateandsohaslesscapacitytoincreaseitsrateofhaemopoiesis.HaemolyticanaemiasMostcasesofhaemolytican

aemiaareimmune-mediated.Inthedogmostcasesofimmune-mediatedishaemolyticanaemia(IHA)areprimary(idiopathic)andaretermedautoimmuneha

emolyticanaemia(AIHA).IHAmayoccurinassociationwith:drugs(e.g.potentiatedsulphonamides);lymphoreticulard

iseases(e.g.lymphoidleukaemia);systemiclupuserythematosus;orinfections(e.g.Babesia,bacterialendocarditis).ROUTINEHAEMATO

LOGY2021/02/2420DISORDERSOFWHITECELLNUMBERNeutrophiliaFigure3.20CausesofneutrophiliaPhysiologicalresponse(fear,excite

ment,exercise)Stress/corticosteroid-inducedAcuteinflammatoryresponse:bacterialinfection(localizedorgeneralized),immune-mediateddiseas

e,necrosis,e.g.pancreatitis,neoplasia,especiallywithtumornecrosis.ChronicgranulocyticleukaemiaNeutrophildysfunctionParaneoplasticsyndromes2021/02

/2421NeutropeniaThethreemaincausesofneutropeniaare:•Anoverwhelmingdemandforneutrophils•Reducedproductionofneutrop

hilsinthebonemarrow•Defectiveneutrophilmaturationinthebonemarrow.Anoverwhelmingdemandforneutrophilsmayoccurwithperacutebacterialinfection

s,especiallyGram-negativesepsisandendotoxaemia.Otherpossiblecausesincludeperitonitis,pyometra（子宫蓄脓）,aspirationpneumoniaandcaninepar

vovirusinfection.DISORDERSOFWHITECELLNUMBER2021/02/2422EosinophiliaEosinophilsaredistributedinthebodyamong

variouspoolsinasimilarwaytoneutrophils,althoughthebonemarrowstoragepoolisminimal.Eosinophilscirculateinthebloodstreamforonlyafewhoursbeforeent

eringthetissues,wheretheymayliveforseveraldays.Theirtwomainfunctionsaretokillparasitesandtoregulateallergicandinflammatoryreactions.EosinopeniaEos

inopeniaincombinationwithlymphopeniaoccursfollowingstress,administrationofcorticosteroidsandinspontaneoushyperadrenocorticism(Cushing

'ssyndrome).BasophiliaBasophilscontaininflammatorymediatorssuchashistamineandheparinandfunctioninasimilarmannertomastcellsinh

ypersensitivityreactions.DISORDERSOFWHITECELLNUMBER2021/02/2423LymphocytosisCausesoflymphocytosis1.Physiologicallymphocytosis,withconcomita

ntneutrophilia,inresponsetoexcitement(especiallycats)2.Strongimmunestimulation(e.g.inchronicinfection,viraemiaorimmune-mediateddisease)3.Ch

roniclymphocyticleukaemia4.Hypoadrenocortiscism(lymphocytosismaybeassociatedwithaneosinophilia)5.Increasednumbersoflarger

eactivelymphocytesmayoccurtransientlyfollowingvaccination6.YounganimalshaveahigherlymphocytecountthanadultanimalsDIS

ORDERSOFWHITECELLNUMBER2021/02/2424LymphopeniaCausesoflymphopeniaarelisted.StressGlucocorticoidtherapyHyperadrenocorticismChylothora

x(lossoflymphocytesintothepleuralspace)Lymphangiectasia(lossoflymphocytesintothegut)Acutephaseofmostviralinfections(e.g.caninedistemper,parv

ovirus,FeLV)Septicaemia/endotoxaemiaDISORDERSOFWHITECELLNUMBER2021/02/2425DogsCatspercentageAbsolutevaluepercentageAbsolutevalue(10/TotalWBCN/a6~17N/

a5.5~19.5Bandneutropils0~30~0.30~30~0.3Neutropils60~773~11.535~372.5~12.5Lymphocytes12~301~4.820~551.5~7Monocytes3~100.2~1.51~40~1.5Eosinopils

2~100.1~1.32~120~1.5basopilsrarerarerareRareReferencerangesfortotalanddifferentialwhitebloodcellcounts2021/02/2426Table2showsthealter

ationsinsomeofparametersinvariousdiseases.LaboratoryassessmentTeststoassessprimaryhaemostasisinclude:PlateletcountB

leedingtimeClotretraction.Teststoassesssecondaryhaemostasisinclude:Wholebloodclottingtime(WBCT)Activatedclottingtime(

ACT)Activatedpartialthromboplastintime(APPT)One-stageprothrombintime(OSPT)Thrombintime(TT)DISORDERSOFWHITECELLNUMBER2021/02/2

427Disseminatedintravascularcoagulation(DIC):Thismaybetriggeredbyawidevarietyofdiseases,includingendotoxaemianeoplas

ia(especiallyhaemangiosarcoma血管肉瘤)acuteinfections(e.g.infectiouscaninehepatitis)haemolyticanaemiapancreatitish

eatstroke.TheclinicopathologicalfeaturesofDICare:•Thrombocytopenia•IncreasedOSPT/APTT•ElevatedFDPs•Lowfibrinogen•Schistocytesinthebloodfilm.D

ISORDERSOFWHITECELLNUMBER2021/02/2428兽医临床病理学CollegeofVeterinaryMedicine,SCAU,Guangzhou,China5106422021/02/2429ClinicalbiochemistryI

ntroductionSerumproteinsTotalproteinandalbuminGlobulinsIndicatorsofrenalfunctionUreanitrogenCreatinineMarkersofhepaticdiseaseAl

anineaminotransferaseAspartateaminotransferaseAlkalinephosphataseGamma-glutamyitransferaseBilirubinBileacidsAmmoniaPancreaticdiseaseAmylaseLipase

ElectrolytesSodium;Potassium;ChlorideMagnesium;Calcium;PhosphorusMuscleenzymesCreatinekinaseAspartate

aminotransferaseCarbohydratemetabolismGlucoseFructosamineLipidmetabolismCholesterolTriglyceridesMiscellaneoustestsIronLeadZincCopperChemicalpr

ofilesandtestselection2021/02/2430SERUMPROTEINSTotalproteinandalbuminPhysiologyThecirculatingproteinsaresynth

esizedpredominantlyintheliver,althoughplasmacellsalsocontributetotheirproduction.Quantitativelythesinglemostimportantp

roteinisalbumin(35-50%ofthetotalserumproteinconcentration).Theotherproteinsarecollectivelyknownasglobulins.Thefunctionsofproteinsaremanyandv

ariedbutincludemaintenanceofplasmaosmoticpressure,transportofsubstancesaroundthebody(e.g.ferritin铁蛋白,ceruloplasmin血浆铜蓝蛋白),humoralim

munity,bufferingandenzymeregulation.IndicationsforassayThemeasurementofproteinsisgenerallyincludedinaninitialhealths

creeninallpatientsbutespeciallywhereintestinal,renalorhepaticdiseaseorhaemorrhageissuspected.AnalysisProteinconcentrationscanbee

stimatedinserum,plasma,urineorbodyfluidswitharefractometerorbyspectrophotometry.Serumalbuminlevelsaremeasuredbybro

mocresolgreendye溴甲酚绿bindingandtheserumglobuliniscalculatedbysubtractionofthealbuminconcentrationfromthetotalprot

einconcentration.2021/02/2431ReferencerangesNeonatesandveryyounganimalshavelowerconcentrationsofalbuminandglobulins(duetominimalquantitiesofimmuno

globulins).Astheanimalgainsimmunocompetencetheproteinconcentrationsrisetoreachadultvalues.Physiologicald

ecreasesinalbuminmaybenotedduringpregnancy.CriticalvaluesMarkedhypoalbuminaemia(<15g/L)isassociatedwiththedevelopmento

fascitesandtissueoedema.Accumulationofperitonealfluidmayoccurathigheralbuminconcentrationsifthereisconcurren

tportalveinhypertension,e.g.inchronicliverdisease.InterferingphenomenaLipaemia,haemolysisandhyperbilirubinaemia

producefalseincreasesintotalproteinconcentrations.DrugeffectsHormoneshaveamarginaleffectonplasmaproteinconcentrations.Corti

costeroidsandanabolicsteroidsmayincreasetheproteinconcentrationduetotheiranaboliceffectswhilethecataboliceffect

softhyroxinecancauseadecrease.SERUMPROTEINS2021/02/2432Figure4.3:Causesofhypoalbuminaemia.IncreasedlossGlomerularproteinlossProtein-losingent

eropathyCutaneouslesions,e.g.bumsExternalhaemorrhageDecreasedproductionHepaticinsufficiencyMalnutritionMaldigestionMalabsorptionSequestra

tionBodycavityeffusionSERUMPROTEINS2021/02/2433GlobulinsAnalysisSerumproteinelectrophoresis(SPE)oncelluloseacetategelsallowsf

ractionationoftheproteins,dependingpredominantlyontheirchargeandsize.Afterstainingforprotein,thecelluloseacetatestripisscannedbyadensitometerwhic

hconvertstherelativeintensitiesoftheproteinbandstopercentagesandgeneratesagraphthatdemonstratestheproteinfractions

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

thologicalcausesarehaemorrhageandprotein-losingenteropathies.SERUMPROTEINS2021/02/2434Figure4.4:Caus

esofhyperglobulinaemia.PolyclonalgammopathyInfections:BacterialdiseaseViraldisease(e.g.FIP)Immune-mediateddiseases:Sys

temiclupuserythematosusRneumatoidartnntisImmune-mediatedhaemolyticanaemiaImmune-mediatedthrombocytopemaNeoplasia,especiallylymph

osarcomaMonoclonalgammopathyNeoplasia:MultiplemyelomaMacroglobulinaemiaLymphosarcomaFelineinfectiousperitonitis(r

are)SERUMPROTEINS2021/02/2435UreanitrogenPhysiology★Dietaryproteinsarehydrolysedintheintestinestotheirconstituentaminoacidswhichmay,inturn,bedegr

adedtoammoniabytheactionofgutbacteria.★Theammoniaandaminoacidsaretransportedtotheliverviatheportalcirculationwheretheyar

eutilizedintheureacycle.★Theureaformedinthehepatocytesisexcretedviathekidneytubules.★Ureaplaysanimportantroleinconcentr

atingtheurine;thepresenceofhighconcentrationsofureaandsodiumchlorideintherenalmedullaryinterstitiumcreatesanosmoticgradientforreabsorp

tionofwater.INDICATORSOFRENALFUNCTION2021/02/2436IndicationsforassayTheureanitrogen(urea)concentrationisoneofth

etestsusedwhenscreeningrenalfunction.Itisoftenmeasuredwhentheclinicalsignsincludevomiting,anorexia,weightloss,polydipsiaandde

hydration.AnalysisUreacanbemeasuredinserum,plasmaandurinebyspectrophotometry.Sticktestsforwholebloodarealsoavailable.ReferencerangesDogs3

.0-9.0mmol/LCats5.0-10.0mmol/LInterferingphenomenalipaemiainterfereswiththeanalysisandproducesvariableeffectsdependingonthemethodology.INDICATOR

SOFRENALFUNCTION2021/02/2437Causesofreducedbloodurea☆Reduceddietaryproteinintakeisassociatedwithalowbloodurea.☆Inaddition,patientswithdif

fuseliverdiseasehaveanimpairedcapacitytosynthesizeureaandreducedhepaticproduction.Wherehepaticdiseaseissuspected,acom

pletebiochemistryproabileacidstimulationtestareindicated.☆Themarkeddiuresis（多尿）associatedwithsomeconditi

ons,especiallyhyperadrenocorticismanddiabetes,resultsinincreasedurinarylossofureawhich,inturn,causesareductionofthebloodurea.INDICATORSOFRENAL

FUNCTION2021/02/2438Causesofincreasedbloodurea☆Increaseddietaryproteinintakeproducesahighlevelofureaintheblood.Amoderateinc

reaseindietaryproteinisnotcommonlyassociatedwithanotableriseinureaabovethereferencerange,buthigh-proteindietscancausesignificantincreases.☆A12-hour

fastisrecommendedbeforesamplingformeasurementofurea.☆Intestinalhaemorrhagealsoresultsinanincreasedconcentrationwhichisr

eportedtocorrelatewiththeseverityofbloodloss.☆Ureaisfreelyfilteredattheglomerulusandreabsorbedintherenaltubules.Therateofreabsorptionishigheratsl

owerurinaryflowrates,e.g.indehydratedpatients.☆Bloodureaisthereforenotareliableestimateoftheglomerularfiltrationrate(GFR

).Increasedureaconcentrationsareassociatedwithconditionsotherthanparenchymalrenaldisease.☆Thepresenceofaconcentratedurinesample(urineSG>1.030indog

s,>1.035incats)supportsthediagnosisofaprerenalazotaemia.INDICATORSOFRENALFUNCTION2021/02/2439CreatininePhysiology◤Cre

atinineisformedfromcreatineinthemusclesinanirreversiblereaction.Thequantityofcreatinineproduceddependsupondiet(smallcontribution)

andthemusclemass.Diseaseaffectingthemusclemassmayaffectthedailycreatinineproduction.◤Bothureaandcreatininearefreelyfilteredatth

erenalglomerulusbutureaissubjecttotubularreabsorptionandthuscreatinineissaidtobeabetterindicatorofGFR.Analysis◤Creatininecanbemeasuredinser

um,plasmaorabdominalfluidbyspectrophotometricmethods.ReferencerangesDogs20-110umol/LCats40-150umol/LINDICATORSOFRENALFUNCTION2021/02/2440Ca

usesoflowserumcreatinine◤Sincethedailyproductionofcreatinineisdependentuponthemusclemassoftheanimal,theb

odyconditionshouldbeconsideredwheninterpretingserumcreatinineconcentrations.Apoorbodyconditionmaybeassociatedwithlowconcentrationswhileminorrises

insuchcasesmaybemoresignificantthaninotherindividuals.Causesofincreasedserumcreatinine◤Decreasedglomerularfilt

rationisthemajorcauseofraisedserumcreatinine.However,approximately75%ofnephronfunctionmustbeimpairedbeforeserumcreatinine(andurea)isincreased.Cre

atinineisconsideredamorereliableindicatorofGFRthanisureanitrogen,sincetherearefewerfactorswhichinfluencetheserumconcentrationofcreatinine.INDICA

TORSOFRENALFUNCTION2021/02/2441►Thebiochemicalparametersusedtoassessliverpathologymaybedividedintotwoclasses:th

ehepaticenzymesthatreflectliverdamageandcholestasis,andtheendogenousindicatorsofliverfunction.►Alanineaminotransferase(ALT)

isthemostusefulenzymeforidentifyinghepatocellulardamageindogsandcatsbutshouldnotbeusedaloneasascreeningtestforliverdisease.►Thep

roductionofotherenzymes,i.e.alkalinephosphatase(ALP)andgamma-glutamyltransferase(GGT),isincreasedsecondarytointra-andextrahepaticcholestasis.

►Theseenzymesaremarkersofcholestaticdisease.►Bilirubin,serumalbuminandserumbileacidsareconsideredtobeindicatorso

fhepaticfunction.►Itiscommonforextrahepaticdisease(e.g.pancreatitis,diabetesmellitus,hyperadrenocorticismandinflammatoryboweldisease)tocauseabnormali

tiesofthesebiochemicalparameters.MARKERSOFHEPATICDISEASE2021/02/2442Alanineaminotransferase(ALT)PhysiologyALTi

sfoundinthecytosolofhepatocytesandinmuscletissueinthedogandcat.Activitiesintheserumareelevatedbyleakageoftheenzymesecondarytoaninc

reaseinhepatocytemembranepermeabilityorcellnecrosis.Theformermaysimplybeaconsequenceofhypoxiaandneednotreflectcellde

ath.IncreasedserumALTmaybenotedwithin12hoursofanacutehepaticinsultbutcantake3-4daystoreachpeaklevelsafterexperimentalcholestasis（胆汁阻塞）.Thedegreeofinc

reaseinenzymeactivitycorrelatesapproximatelywiththenumberofhepatocytesaffectedbutdoesnotindicatethenature,se

verityorreversibilityofthepathologicalprocess.ALTactivityisnotanindicatorofhepaticfunction.IndicationsforassaySerumALTis

ausefulaidinthediagnosisofhepaticdiseaseandismeasuredwheretheclinicalsignsmightsuggestahepatopathy,e.g.weightloss,anorexia,

polydipsia,vomiting,diarrhoea,ascitesandjaundice.AnalysisTheactivityoftheenzyme(ininternationalunits)ismeasuredinserumorpla

smabyspectrophotometricmethodsunderspecifiedconditions.ReferencerangesDogs<100units/LCats<75units/LMARKERSOFHEPAT

ICDISEASE2021/02/2443CausesofraisedALTactivityGuidelinesfortheinterpretationofraisedliverenzymeactivitiesinrelationtoliverdiseasesaregiveni

nChapterliver.ThemajorityofdiseasesthataffectthelivercouldpotentiallycauseanincreaseinserumALTactivitybutthose

pathologicalprocessesthatmightcauseamarkedincreaseincludeparenchymaldisease/damage,cholangitis,cholangiohepatit

is,chronichepatitis,anoxia,cirrhosisanddiffuseneoplasia,e.g.lymphoma(lymphosarcoma).However,insomecasesthesediseasesmaybeaccompaniedbyanegligibleinc

reaseornoincreaseinserumALTactivity.CausesofreducedALTactivityAnartefactualreductioninserumenzymeactivitiesmayresultfromsubstratedepletion.Dil

utionandrepeatassayofthesamplearenecessarytoexcludethisphenomenon.ReducedALTactivities(belowthereferencerange)aregenerallynotconsi

deredtobeofclinicalsignificance,butthepossibilityofchronicliverdiseaseandnutritionaldeficiencies(zincorvitaminB

6)shouldbeconsidered.MARKERSOFHEPATICDISEASE2021/02/2444Aspartateaminotransferase(AST)(seealsoMuscleenzymes)PhysiologyASTislocatedinthemitochondr

iaofthecellandispresentinsignificantquantitiesinhepatocytes,erythrocytesandinmuscle.ASTisthereforenotliver-specifi

cbut,likeALT,itsactivityintheserumiselevatedbyleakageoftheenzymefromthecell.IndicationsforassayASTisincludedind

iagnosticprofilesforinvestigationofsuspectedliverdiseaseormuscledisease.AnalysisTheenzymeactivityismeasuredinserumandheparinizedplasmaby

spectrophotometry.ReferencerangesDogs7-50units/LCats7-60units/LCausesofraisedASTThemostcommoncausesofincreasedASTarehepatic

disease,muscledisease(trauma,inflammation)andhaemolysis.Concurrentmeasurementofotherhepaticenzymes(ALT,ALP,GGT)andhepaticfunctionindicators(a

lbumin,urea,bilirubin,bileacids)areessentialtoestablishtheoriginoftheincreasedserumASTandtoprovidefurtherinformationregardingliverdamageandfunc

tion(seeChapter9).Withrespecttoliverdamage,theserumactivityofASTtendstoparallelthatofALT.MARKERSOFHEP

ATICDISEASE2021/02/2445Alkalinephosphatase(ALP,SAP)PhysiologyIndogsandcatsthereareisoformsofALPlocatedinbrushbordersintheliver,pl

acenta,intestine,kidneyandbone.Inthedogthereisalsoasteroid-inducedisoenzyme(SIALP),theoriginofwhichhasnotbeenf

ullydetermined.TheproductionofSIALPisincreasedbytheadministrationofglucocorticoids(oral,parenteralortopical),byexcessiveproductionofendogenousgluco

corticoids(hyperadrenocorticism)andinassociationwithchronicdisease(e.g.renalorhepatic).Theliverisoenzymeisresponsiblefortheseruma

ctivityinthenormaladultdogandcat.IndicationsforassaySerumALPisoneofthetestscommonlyincludedinscreeningprofilesforhepatic

disease(cholestasis)andhyperadrenocorticism.Itisthereforeusefulwheretheclinicalsignssuggesteitherofthesediagnoses,e.g.

weightloss,anorexia,polydipsia,vomiting,diarrhoea,ascitesandjaundice.AnalysisSerumALPactivityismeasuredinserumorhepar

inizedplasmabyspectrophotometry.ReferencerangesDogs<200units/LCats<100units/LMARKERSOFHEPATICDISEASE2021/02/2446CausesofraisedALPFro

madiagnosticviewpointthemostimportantisoenzymesinsmallanimalsarethebone,hepaticandsteroid-inducedforms.IncreasesinboneALPcausesrais

edserumactivitiesinyounggrowinganimals,butvaluesarerarelymorethantwo-foldgreaterthantheupperlimitoftheadultreferencerange.Thisphysiologicalincrease

inserumALPshouldbeconsidered.Increasesinthehepaticisoenzymearecommonlyassociatedwithcholestaticdisease.Includepanc

reatitis,pancreaticneoplasiaandcholelithiasis.Cholelithsareveryrareinthedog.Theenzymeisgenerallyincludedinprofiles

whereitcontributestothediagnosisofhepaticdisease.ALPshouldnotbeusedalonewhenscreeningpatientsforevidenceofliverdisease.Indogs,theincreaseinALPassoc

iatedwithsteroidadministrationvariesdependingonthepatient,thedrugusedandtherouteofadministration.ALPinthecathasaveryshort

half-lifeandthemagnitudeofincreasenotedinhepaticdiseaseisgenerallylessthanthatrecordedindogs.AnyincreaseinALPisp

robablysignificantinacat.MARKERSOFHEPATICDISEASE2021/02/2447.Gamma-glutamyltransferase(GGT)PhysiologyG

GTisacytosolicandmembrane-boundenzymefoundinhighestconcentrationsinthebrushbordersoftherenalandbileductepithelium.Cholestasisan

denzymeinductionduetoglucocorticoidtherapycauseincreasedserumactivities.IndicationsforassayGGTisusedinconjunctionwithALPandotherliver

testsinthediagnosisandmonitoringofhepaticdisease.ItisthoughttobemoreusefulthanALPinthecatandtheserumactivityindogsdoe

snotappeartobeaffectedbytheadministrationofanticonvulsants.Dogs0-8.0units/LCats0-8.0units/LCausesofincreasedGGTSerumGGTisamarkerforcholes

taticdiseaseinthedogandcat.InthecatitmaybemoreusefulthanALPinthediagnosisofcholestatichepaticdiseaseMARKERSOFHEPATICDISEASE2021/0

2/2448BilirubinPhysiologyBilirubin（胆红素）isderivedfromthecatabolismofhaemoproteinsinthecellsoftheretic

uloendothelialsystem.Thenewlyformedlipid-solublebilirubin(indirect-reactingbilirubin)isthenboundtoalbumin,whichfacilitatesitstransfe

rthroughtheaqueousphaseoftheplasmatotheliver.Inthehepatocytethebilirubinisconjugatedwithglucuronicacid（葡糖醛酸）,creat

ingawater-solublemolecule(direct-reactingbilirubin).IndicationsforassayMeasurementofbilirubinisindicatedwherethereisjaundice（黄疸）oncli

nicalexamination,visibleicterus（黄疸）oftheserumorplasma,orsuspectedhepaticdisease.Clinicaljaundiceinthedogisdetectedwhenthebilirubinisatleast25-

35umol/L.AnalysisThetotalserumbilirubinconcentration(conjugatedandunconjugated)ismeasuredinserumorplasmabyspectrophotometry.Referencera

ngesDogs0-6.8umol/LCats0-6.8umol/LMARKERSOFHEPATICDISEASE2021/02/2449CausesofhyperbilirubinaemiaJaundicemaybecl

assifiedaccordingtotheunderlyingpathologicalprocess:prehepaticjaundice(increasedproductionofbilirubin,e.g.haemolyti

canaemia,andinternalhaemorrhage);hepaticjaundice(failureofuptakeorconjugationofbilirubin);posthepaticjaundice(obstructionofthebiliarysystem).Afu

llhaematologicalproindicatedinalljaundicedpatientstoexcludethepossibilityofprehepaticcauses.Characteristicfindingsthatmaybenotedinha

emolyticanaemiaincludemarkedreticulocytosis(网状细胞过多症，indicativeoferythrocyteregeneration),autoagglutinationoftheredcellsandtheformation

ofspherocytes.Theplateletcountandserumproteinsarecommonlywithinthereferencerangeforthespecies.Theabnormalitiesofbilirubinassociate

dwithhepaticdiseaseandcholestaticdiseasearediscussedmorefully.Previouslyitwasbelievedthatthemeasurementofdirectandindirect-reactin

gbilirubinwouldhelptodeterminethecauseofthejaundice.However,itisnowclearthatthisisnotthecaseinthedogandcatandthathepatic,haemolyticandbiliarytractdis

easesproducevariableincreasesinthesefractions.Differentiationofprehepatic,hepaticandposthepaticjaundicerequ

iresafullhaematologicalandbiochemicalinvestigation(includingmeasurementofredcellmass,examinationofabloodsmearandliverfunctiontes

ts)andmayrequireexaminationofthebiliarytract.Hepaticbiopsymayalsobenecessaryinsomecases.MARKERSOFHEPATICDISEASE2021/02

/2450BileacidsPhysiologyTheprimarybileacidsareproducedintheliverfromcholesterolandarethenconjugatedtotaurine（氨基乙磺酸）orglycine（氨基乙酸）.Theyareexcreted

intothebiliarytreeandstoredinthegallbladder.Gallbladdercontraction(stimulatedbyingestionoffood)releasesthebileacidsintot

heintestineswheretheyfacilitatethedigestionandabsorptionofdietarylipid.Thebileacidsareefficientlyreabsorbedintheileu

m,resultinginverysmallfaecalloss.Thetotalpoolofbileacidsmayundergoenterohepaticcirculationtwotofivetimesduringasinglemeal.Indic

ationsforassayInclusionofbileacidsinaproindicatedwherethereissuspicionofhepaticdisease.Clinicalsignsinsuchpatientsmightincludehepatomegaly（肝大

）,microhepatica（小肝）andabnormalcentralnervoussystemsigns.Thesensitivityofthebileacidassaymaybeincreasedbyusingabileacidstimulationtest.Refere

nceranges(fasted)Dogs0-15umol/LCats0-15umol/LMARKERSOFHEPATICDISEASE2021/02/2451CausesofincreasedbileacidsThef

astingserumbileacidconcentrationmayberaisedinassociationwithprimaryorsecondaryhepaticdisease.Theassayfacilitatesidentificationofhepaticdysfunctionb

utgivesnoindicationastothenatureorreversibilityoftheliverpathology.Valuesexceeding30umol/Larecommonlyassociatedwithhi

stologicallesionsandbiopsymaybehelpfulinthesecases.Itisimportanttorememberthatthehistologicalchangescouldstillbeassociated

withsecondaryhepaticdiseaseeventhoughthefastingbileacidconcentrationis>30umol/L,forexampleinhyperadrenocorticism.Theuse

ofthebileacidstimulationtestmayimprovethesensitivityoftesting.Forthis,serumbileacidconcentrationsaremeas

uredinasamplecollectedaftera12-hourfast(fastingbileacidconcentration)and2hoursafterafattymeal(postprandial（餐后）bileacidconcentration).Inonestudyof108c

ats,thepostprandialbileacidconcentrationwasfoundtohavethehighestsensitivityofanysingletestforthediagnosisoffelineliverdisease.MARKE

RSOFHEPATICDISEASE2021/02/2452AmmoniaPhysiologyDietaryproteinsarehydrolysedintheguttoaminoacidswhich,inturn,m

aybedegradedbyintestinalbacteria,producingammonia.Ammoniaistransportedtotheliverwhereitisusedasaprecursorinth

esynthesisofurea.Increasedbloodammoniaconcentrationsareobservedinsomepatientswithdiffuseliverdisease(withareducedcapacity

forureasynthesis)andinindividualswithportosystemicshunts.IndicationsforassayAmmoniaisusedintheevaluationofhepaticfunction;theindication

sformeasurementarethesameasforbileacids.AnalysisAmmoniaismeasuredinblood,serumorplasmabydryreagentandenzymaticmethods.Samplesshouldbecol

lectedintoachilledsampletubeandstoredoniceuntilanalysis,whichmustbecarriedoutwithin20minutesofcollection.ReferencerangesDogs0-60umol/L

Cats0-60umol/LMARKERSOFHEPATICDISEASE2021/02/2453CausesofincreasedammoniaIncreasedammoniaconcentration

sareassociatedwithfeedinghigh-proteindietsandwithintestinalhaemorrhage(duetotheincreaseddeliveryofaminoacidstotheintestinalbacteria).

Diffusehepaticdisease,resultinginthefailureofconversionofammoniatourea,andportosystemicshunts(congenitalandac

quired)willalsoproduceincreasedserumammoniaconcentrations.MARKERSOFHEPATICDISEASE2021/02/2454PANCREATICDISEASEAmylasePhysiologyAmylase（淀粉酶）is

acalcium-dependentenzyme,producedbythepancreaticacinarcells,whichhydrolysescomplexcarbohydrates.Theenzymepassesdirectlyfromthepan

creasintothecirculationwhereitisfilteredbytherenaltubules;theinactivatedenzymeisreabsorbedbythetubularepithelium.Amylaseactivityinthetissuesofth

edogandcatishighestinthepancreasbutisalsofoundintheintestinesandliver.IndicationsforassayAmylaseshouldbemeasuredwhenthepresentingsignsmightsugge

stpancreatitis（胰腺炎）,e.g.vomiting,abdominalpainoricterus,orwhenthereisfreeperitonealfluid.AnalysisAmylaseacti

vitiesmaybemeasuredinserum,heparinizedplasmaandabdominalfluidusingspectrophotometricmethods.ReferencerangesDogs400-2000units/LCats400-2000un

its/L2021/02/2455CausesofincreasedamylaseThetissuedistributionofamylaseisnotrestrictedtothepancreasandthereforerais

edserumactivitiesarenotspecificforpancreatitis.Reducedglomerularfiltration(prerenal,renal,postrenal)isoftenassociatedwit

hanincreasedserumamylaseactivitybutthisiscommonlylessthantwotothreetimesgreaterthantheupperlimitofthereferencerange

.Serumactivitiesabovethislevelaresuggestiveofpancreatitisbutthedegreeofincreasedoesnotcorrelatewellwiththeseverityofpancreatitis.Ifanazo

taemic（氮血症）patienthasanamylaseactivitytwotothreetimestheupperlimitofthereferencerangethenpancreaticdiseasemustbeconsidered.Thesimultaneousme

asurementofamylaseandlipaseincasesofsuspectedpancreatitisisadvisablewhileadditionaltestsofrenalandhep

aticfunctionshouldalsobeincludedinthebiochemicalprofile.Amylaseisnotareliableindicatorofpancreatitisincats.In

casesthatpresentwithfreeperitonealfluid,fullanalysisofthefluid(proteinconcentration,cellcountsandcytologicalexamination)andmeasur

ementoftheserumandfluidamylaseactivitiesmaybeuseful.Thepresenceofanon-septicexudatewithgreateramylaseactivitythantheserummaybeassociatedwithp

ancreatitisorbowelrupture.PANCREATICDISEASE2021/02/2456LipasePhysiologyLipaseisadigestiveenzyme,producedbythepancreaticacinarcells,thathydrolysestrig

lycerides.Theenzymeisclearedfromthecirculationbyrenalinactivation.Aswithamylase,lipasemayoriginatefrom

pancreaticorextrapancreaticsources.Pancreaticdamageandinflammationresultsinthereleaseoflipaseintothesurroundingglandandperitonealtissuewhichmaycaus

ethedevelopmentofnecrosisintheperipancreaticperitonealfat.IndicationsforassayIndicationsforthemeasurementoflipasearethesameasforamylase.Amylas

eandlipaseassaysshouldbeperformedsimultaneouslyincasesinwhichpancreatitisissuspected,buttheincreasesinenzymeactivitiesareoftennotp

arallel(markedincreasesinoneenzymemaybeassociatedwithminimalincreasesintheother).AnalysisLipaseactivitiesaremeasuredinserum,heparinized

plasmaandbodyfluidsusingturbidimetricmethods.ReferencerangesDogs0-500units/LCats0-700units/LPANCREATICDISEASE2021/02/2457Causesofraisedser

umlipaseSincelipaseoriginatesfrombothpancreaticandextrapancreatictissue,anincreaseinserumactivityisnotdiagnost

icofpancreatitis.Increasedserumactivityisalsonotedinazotaemicpatients,althoughthevaluesgenerallydonotexceedtwotothreetimestheupp

erlimitofthereferencerange.Inaddition,moderateelevationsoflipase(upto5-foldincreases)havebeenreportedinassociationwithadministrationofdexametha

sonewithoutevidenceofhistologicalchangesinthepancreas.Anormallipaseactivitydoesnotprecludepancreaticdisease.Lipasehasbeenrepor

tedtobepersistentlyelevatedincatswithexperimentallyinducedpancreatitisbutthisisnotaconsistentfindinginnatu

rallyoccurringdisease.PANCREATICDISEASE2021/02/2458CARBOHYDRATEMETABOLISMPhysiologyGlucoseistheprincipalsourceofenergyforma

mmaliantissuesandisderivedfromthedietandhepaticgluconeogenesis.Thebloodconcentrationiscontrolledbyhormoneswhichregulateitsentryinto,andremovalfrom,

thecirculation(insulin,glucagon,adrenaline,cortisol).Inthekidneyofthedogandcat,glucoseenteringtheglom

erularultrafiltrateisreabsorbedbytherenaltubules.However,therenalreabsorptionofglucoseisoverwhelmedinthepresenceofblood

glucoseconcentrationsgreaterthan10-12mmol/1,resultinginglucosuria.IndicationsforassayMeasurementofbloodglucoseisessenti

alwherepresentingclinicalsignscouldsuggest：diabetesmellitus(polydipsia,polyuria,weightloss,cataractformation),diabeticketo

acidosis(vomiting,diarrhoea,anorexia)hypoglycaemia(weakness,collapse,seizures,disorientation,depression,blindness).Inaddition,theassayisinc

ludedingeneralhealthscreenswhereitmayprovidesupportiveevidenceforotherdiseaseprocesses(hyperadrenocorticism,hepaticdis

ease).Measurementofthebloodglucoseconcentrationistheidealmethodofmonitoringthestabilizationofdiabeticpatien

tsoninsulintherapyandallowsoptimizationofthetherapeuticregimen.Insuchcases,glucoseismeasuredinsamplescollectedat2-hourlyintervals,allowingca

lculationofthedurationofactionandpeaktimeofactionoftheadministeredinsulin.Glucose2021/02/2459AnalysisReagentstr

ips:Rapid-analysisreagentstripsrequiretheuseofwholebloodwithnoanticoagulant.Laboratoryanalysis:Spectrophotometricmethods(enzymaticorchemical)arcge

nerallyusedforthemeasurementofbloodglucose.Wherein-houseequipmentdemandstheuseofheparinizedplasma,thesamplemustbesepara

tedimmediatelyaftercollection.Thispreventsdepletionoftheplasmaglucosebytheerythrocytes.Collectionofthebloodintofluor

ideoxalateisthepreferredmethodofpreventingerythrocyteglucoseutilizationwhenadelayinanalysisisanticipated,suchasdu

ringtransporttoacommerciallaboratory.ReferencerangesDogs3.5-5.5mmol/LCats3.5-6.5mmol/LGlucose2021/02/2460CausesofhypoglycaemiaMarkedhypo

glycaemia(glucose<2mmol/L)mostcommonlyresultsfromoverproductionofinsulinorexcessiveutilizationofglucosebyneoplasticcells.Insulin

-secretingtumoursofthepancreas(insulinomas)producebiologicallyactivehormonewhichincreasestheuptakeofglucosebythebodytissuesandimpair

shepaticgluconeogenesis,resultinginhypoglycaemia.Inonestudyofdogswithinsulinomasthemean(+SD)plasmaglucoseconcentrationwas2

.14(±0.82)mmol/1.Extrapancrcatictumoursoccasionallycausehypoglycaemiabysecretionofaninsulin-likesubstanceorbyin

creasedutilizationofplasmaglucose.Glucose2021/02/2461Neoplastic:Insulin-secretingtumourofthepancreas(insulinoma)HepatocellularcarcinomaEndocrine:Hy

poadrenocorticismHepaticinsufficiency:CongenitalvascularshuntsAcquiredvascularshuntsChronichepaticfibrosis(cirrhosis)Hepaticnecrosis(e.g.he

patotoxins,bacterialinfection,trauma)GlucoseFigure4.19:Causesofhypoglycaemiainthedog.Catsmayrarelybeaffectedbyinsulinoma.Substratedeficiency:Neonatal

hypoglycaemiaJuvenilehypoglycaemiaHuntingdoghypoglycaemiaGlycogenstoragediseaseSepsis2021/02/2462Causesofhyperglyc

aemiaHyperglycaemiacommonlyresultsfromarelativeorabsolutelackofinsulin.Thisleadstoimpairedtissueutilizationofplasmaglucose

andanincreaseintherateofgluconeogenesis.Mildhyperglycaemia(6.7-10mmol/L)inthedogmaybenotedaspartofanadrenalinestressresponse

orsecondarytoexcessivesecretionoradministrationofotherdiabetogenichormones,inparticularglucocorticoidsan

dprogesterone.Themildhyperglycaemiaisaresultofthehormonalantagonismoftheactionsofinsulin.Inaddition,mildhyperglyca

emiamaybenotedinthepostprandialperiodindogsfedasugar-richdietsuchassemi-moistfoods.Apersistent,moder

atetomarkedhyperglycaemiainthedogisconsistentwithdiabetesmellitus.Suchcasesdonotpresentwithclinicalsigns(polyu

riaandpolydipsia)untiltherenalthresholdforglucoseisexceeded,resultinginosmoticdiuresis.Inthecat,anadrenaline-ind

ucedstressresponsemayproduceamoderateormarkedincreaseinglucoseconcentration.Thediagnosisofdiabetesmellitusisoftendifficu

ltincatsandconfirmationrequiresdocumentationofpersistenthyperglycaemiawithcompatibleclinicalsigns.Glucose2021/02/2463Figure4.20:Causesofhy

perglycaemia.Adrenalinestressresponse(especiallymarkedincats)PostprandialDiabetesmellitusHyperadrenocorticism(dogsandrarelyc

ats)Acromegaly(cats)Acutepancreatitis(dogsandcats)RenalinsufficiencyGlucose2021/02/2464FructosaminePhysiolo

gyFructosamineisaglycatedserumproteinwhichisformedbythenon-enzymaticreactionbetweenasugarandanaminoacid.

Thetotalamountoffructosamineformedisproportionaltotheserumglucoseconcentrationduringthelifespanoftheproteins.Indogsandcat

s,fructosaminehasbeenfoundtobeausefulparameterinthediagnosisandmanagementofdiabetesmellitus.IndicationsforassaySerumfructosamineconcentrations

areusefulinthediagnosisofdiabetesmellitusandinidentifyingpersistenthyperglycaemiaduringtherapy.Measurementoff

ructosaminemayalsobehelpfulinconfirmingthepresenceofpersistenthypoglycaemia.AnalysisFructosamineismeasuredusin

gamethodbasedonthereducingabilityoffructosamineinalkalinesolution.ReferencerangesDogs250-350umol/LCats150-270u

mol/L2021/02/2465CausesoflowserumfructosamineAlowserumfructosamineconcentrationhasbeenrecordedinadogw

ithaninsulin-secretingtumourofthepancreas(insulinoma).Ithasbeensuggestedthatthemeasurementofserumfructosamineinadditiontog

lucoseandinsulinmaybehelpfulinconfirmingthepresenceofinsulinomas.CausesofraisedfructosamineRaisedserumconcentrationso

ffructosaminereflectpersistenthyperglycaemiaoverthepreceding2-3weeks.Indogswithdiabetestheserumfructosamineconcentrationissignifican

tlygreaterthanindogswithotherdiseases.Fructosamineisalsousefulforconfirmingdiabetesmellitusinthecatandcanbehelpfulinidentifyingpersistenthyperg

lycaemiaafterinitialstabilizationoninsulintherapy.Fructosamine2021/02/2466LIPIDMETABOLISMPhysiologyCholesterolisthemostcommonsteroidi

nthebodytissuesandactsasaprecursorcompoundforsteroidhormoneandbilesaltsynthesis.Themajorityofthebody'scholesterolissynthesizedbytheliver,butther

emainderoriginatesfromdietarysources.Excesscholesterolisexcretedinthebile.IndicationsforassayHypercholeste

rolaemiaisoftenassociatedwithendocrinediseaseinthedogandcatandisfrequentlymeasuredaspartofageneralhealth

prothesespecies.Raisedplasmacholesterolaloneisnotcommonlyresponsibleforthedevelopmentofclinicaldiseaseinthed

ogandcat.However,markedhypercholesterolaemiaandhypertriglyceridaemiasecondarytothyroiddysfunctionindogshavebeenassociatedwith

thedevelopmentofperipheralvasculardisease.AnalysisCholesterolconcentrationsareassayedinserum,heparinizedplasmaorEDTA

plasmausingspectrophotometric,automateddirectandenzymaticmethods.Cholesterol2021/02/2467Figure4Causesofalterationsi

nplasmacholesterolconcentrations.HypocholesterolaemiaProtein-losingenteropathyMaldigestion/malabsorptionHepatopathy(portocavalshunt,cirrhosis)Hyper

cholesterolaemiaPostprandialhyperlipidaemiaSecondaryhyperlipidaemia:HypothyroidismDiabetesmellitusHype

radrenocorticismCholestaticdiseaseNephroticsyndrome2021/02/2468CausesofhypercholesterolaemiaAmarginalincreaseinthecholesterolconcentrationmay

benotedinsamplescollectedinthepostprandialperiodversusafastedsample.Thisincreasedlevelgenerallydoesnotexceedthereferencerangeforthespecies

.Hypercholesterolaemiainthedogandcatismostcommonlyassociatedwithendocrinedisease(diabetesmellitus,hypothyroidism,hyperadr

enocorticism).Ineachoftheseendocrinedisorderstheremaybeaconcurrentincreaseinserumtriglycerideconcentration.H

ypercholesterolaemiamayalsobenotedincholestaticdiseaseandglomerulonephritis(肾小球性肾炎）.Furtherspecialistinvestigation(e.g.lipo

proteinelectrophoresis)maybenecessaryifnounderlyingsystemicorendocrinediseasecanbeidentifiedandthehypercholesterolaemiaismarkedandpersistent.2021/

02/2469TriglyceridesPhysiologyThetriglyceridesarethemostabundantlipidsinthebodyandtheirstorageinadiposetissueprovidesanessentialreserveofchemicalen

ergyfortissuerequirements.Theyarederivedfromthedietandalsosynthesizeddenovo（重新）intheliver.IndicationsforassayFastinghypertriglyceridaemiai

nthedogandcatisapathologicalfinding.Thepresenceoflargetriglyceride-richlipoproteinsimpartsaturbiditytotheplasmaor

serum(lipaemia).Triglyceridesshouldthereforebemeasuredinallfastingbloodsamplesthatappeartobelipaemic.Clinicalmanifes

tationsofhypertriglyceridaemiainclude：recurrentabdominalpain,alimentarysigns,seizures.2021/02/2470Causesofhypotriglyceri

daemiaHypotriglyceridaemiahasnotbeenconsistentlyassociatedwithanyspecificdiseaseprocessalthoughithasbeenreportedinseveralcase

sofacuteandchronichepaticdisease.CausesofhypertriglyceridaemiaThemostcommoncauseofapparenthypertriglyceridaemiainthedogandcatisafailur

etoobtainafastingsample(postprandialhyperlipidaemia).Ifhypertriglyceridaemiaisdocumentedinasamplecollectedaftera12-hourfast,endocrinean

dsystemicdiseaseshouldbeexcluded(diabetesmellitus,hypothyroidism,hyperadrencorticism,glomerulonephrit

is).Manydogswithspontaneousacutepancreatitishaveincreasedserumtriglycerideconcentrations.Therelationshipbetweenpanc

reatitisandhyperlipidaemiahasnotbeenfullyelucidatedbutitappearsthattheincreasedtriglycerideconcentrationmay

predisposepatientstopancreaticpathology.2021/02/2471Figure5CausesofhypertriglyceridaemiainthedogandcatPostprandialhyperlipidaemiaSecondaryhy

perlipidaemia:HypothyroidismDiabetesmellitusHyperadrenocorticismAcutepancreatitisPrimaryhyperlipidaemia:Idiopathichyperchylomicron

aemiaoftheMiniatureSchnauzerFamilialhyperchylomicronaemia（乳糜微粒血症）inthecatIdiopathichypertriglyceridaemia2021/02/2472CHEMICALPROFILE

SANDTESTSELECTIONOntheinitialpresentationofanillpatient,aclinicianformulatesalistofdifferentialdiagnosesbasedonthehis

toryandclinicalfindings.Wheretheclinicalfindingsarespecific,e.g.pallorofthemucousmembranessuggestiveofanaemia,thenstepsaretak

entoconfirmthissuspicionandtoelucidatethepossiblecause.Awider,morecomprehensiveinvestigationisnecessarywhenclinicalsignsma

ybecausedbymanymetabolicdisorders;forexample,polydipsiainthedogcouldbetheresultofendocrinedisease,renaldise

aseorhepaticdisease.Theselectionoftestsdependsuponthedifferentialdiagnoses,therangeofconditionsthatmustbeexcluded,theavailabi

lityofthetests,andthecostoftests.Inthecaseofthepolydipsicdog,acost-effectiveprorequiredtocoverthepossibilityoforganfailure(renal,hepa

tic),endocrinedisease(diabetesmellitus,hyperadrenocorticism)andhypercalcaemia.2021/02/2473Someofthesedifferentialsmaybeexcludedorconfirmedonthebasis

ofindividualtests(e.g.ureaandcreatinineforrenaldisease)butinclusioninamorecomprehensiveprothesimultaneousassessmentandcost-effectiveexclusio

nofmanyothercausesofpolydipsia.Whentheclinicalsignsarevagueanda'generalhealthscreen'isrequired,thenitisnecessarytoselectabroadrangeofanalyteswhichw

illreflectanumberofcommondiseasesorpathologicalstates.Theinclusionofteststhatarenotorgan-specificbutwhichprovidege

neralinformationregardingthehydrationandessentialhomeostaticmechanismsisworthwhile,e.g.totalproteins,albumin,electrolytes,glucose.CHEMICALPRO

FILESANDTESTSELECTION2021/02/2474ProfileHealthPre-anaestheticscreen*Extended*healthscreenPolydipsiaprofileSeizureprofileRenalprofileHepaticpr

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

,ALT,ALP,bilirubin,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,dipstickandsedimentexamination).FBC,TP

,albumin,globulin,ALT,ALP,bileacids,urea,creatinine,glucose,calcium,CK,phosphorus,magnesium,electrolytescreenPC

V,TP,albumin,globulin,urea,creatinine,sodium,potassium,calcium,phosphorus,urinalysis(SGdipstickandsedimentexamination)TP,albumin,globulin,

ALT,ALP,AST,GGT,bilirubin,bileacids,cholesterolIndicationsRoutinescreeningScreenforexistingdiseasepriortoroutinesurgeryGastr

ointestinai.endocrinediseaseandnonlocalizingsignsPolydipsiaSeizures,weakness,episodiccollapseMonitoringhepatotoxicity2021/02/24752

021/02/2476GastrointestinalSystemFecalanalysisExaminationofvomitusBloodtestsImagingtechniquesEndoscopy2021/02/2477Dysphagiaandregurgitation•Collect

ahistoryandconductathoroughphysicalexamination•Completeaneurologicalexamination•Observethepatienteating,toassessthelikelystageofthe

swallowingprocessaffected•Plainradiographyofpharynxandoesophagus•Possiblecontraststudies-bariumswallowan

dfluoroscopy•Examinationoforalcavityandpharynxundergeneralanaesthesia•EndoscopicexaminationofpharynxandoesophagusPos

siblediagnosticproceduresforcommonalimentarysymptoms2021/02/2478Vomiting*Collectahistoryandconductathorou

ghphysicalexamination*Characterizethevomitusproduced*Isthevomitingprimaryorsecondary?PRIMARYSECONDARYHaematologyandbiochemistryHaematolog

yandbiochemistryPlainradiographyUrinalysisContraststudiesSpecifictestsofEndoscopy/exploratoryorganfunctionlaparotomyPossiblediagnosticproced

uresforcommonalimentarysymptoms2021/02/2479Diarrhoea•Collectahistoryandconductathoroughphysicalexamination•Physicale

xaminationofthefaecesproduced•Isthediarrhoeaprimaryorsecondary?•Ifprimary,isthediarrhoeaofsmallorlargeintestina

lorigin?PRIMARYSECONDARYSmallintestinalLargeintestinalUrinalysisHaematology/biochemistryFaecalcultureSpecifictestsoforganfunctionFaecalcultureWorme

ggcountWormeggcountRectalexaminationUndigestedfoodanalysisPlainradiographySerumfolate/cobalaminEndoscopy/biopsyTrypsin-likeim

munoreactivityBreathhydrogenassaySugarpermeabilitytestUltrasoundscanEndoscopy/exploratorylaparotomyPossiblediagnosticproceduresforcommonalimentarysym

ptoms2021/02/2480Constipation*Collectahistoryandconductathoroughphysicalexamination*Rectalexamination*Neurologicalexamination*Orthopaedicasses

sment*PlainradiographyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2481Faecaltenesmus(里急后重）•Collectahistoryandconductathoroug

hphysicalexamination•Rectalexamination•Faecalcultureandwormeggcount•Plainradiography•Contraststudies•Ultrasoundscan•Endoscopy

/biopsyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2482Acuteabdomen•Collectahistoryandconductathoroughph

ysicalexamination•Carefulabdominalpalpation•Haematologyandbiochemistry•Plainradiography•Possiblycontraststudies•Paracentesis•Ultrasoundscan•Explorat

orylaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2483Abdominalenlargement•Collectahistoryandcondu

ctathoroughphysicalexamination•Carefulabdominalpalpation•Haematologyandbiochemistry•Plainradiography•Paracentesis（腹腔穿刺）

•Ultrasoundscan•ExploratorylaparotomyPossiblediagnosticproceduresforcommonalimentarysymptoms2021/02/2484FAECALANALYSISPhysicalapp

earanceInitialexaminationofafreshfecalsampleshouldconcentrateonitsphysicalappearance.Inmanycasesofdiarrhoeaitispossibletodecidewhetheritisassociated

withasmallorlargeintestinalproblemusingthecriteriashowninTable8.1.Suchadifferentiationnotonlygivestheclinicianvaluableinformationregardingthelocation

ofthelesionbutconsequentlyassistsintheselectionoffurtherappropriatediagnostictests.Unfortunately,notalldiarrhoeasmaybereadilyclassi

fied,andfeaturesofbothsmallandlargeintestinaldiseasemaybepresent.Thismayreflectasmallintestinalproblemwhichresultsintheabnormalpresenceofn

utrientsorotheragentsinthelargeintestine,therebycausingsignsoflargeintestinaldisease.Alternatively,itmayreflectaconditionthataffectsboththesm

allandthelargeintestineequally.2021/02/2485Table8.1:Characteristicsoffaecespassedinsmallandlargeintestin

aldiarrhoea.Symptom/SignSmallintestineLargeintestineFaecalvolumeIncreasedReducedFaecaltenesmusNonePresentFaecalbloodNone

orchangedOftenpresentFaecalmucusNoneOftenpresentUrgency（尿急）RareOftenpresentDyschezia（排便困难）AbsentOftenpr

esentSteatorrhoea（脂肪痢）OftenpresentAbsentVomitingMayoccurOccursin30%ofcasesWeightlossPresentAbsentFlatus/borborygmi(肠鸣)PresentRar

eCoat/skinconditionPoorNormalAppetiteIncreasedNormalorreduced2021/02/2486Figure8.2Majorcausesofacutediarrhoeaindogsandcats.Endo

parasitism:Hookworms钩虫Whipworms鞭虫Giardiasis贾第鞭毛虫病Dietaryindiscretions:SoiledfoodsScavengingOver-eatingViralinfections:Felinepan

leucopenia猫瘟Canineparvovirus犬细小病毒Coronavirus冠状病毒Bacterialinfection:SalmonellosisCampylobacterinfection弯曲菌Intussus

ception肠套叠Haemorrhagicgastroenteritis2021/02/2487Figure8.3:Majorcauseofchronicdiarrhoeaindogsandcats.Smallintestinaldisease:Lymphocytic

-plasmacyticenteritis淋巴细胞-浆细胞性肠炎EosinophilicenteritisLymphangiectasia淋巴管扩张Lymphosarcoma淋巴肉瘤GiardiasisExocrinepancreati

cinsufficiency(EPI)Colitis:Lymphocytic-plasmacyticEosinophilicHistiocyticGranulomatousLymphosarcomaSystemicdis

ease:Hyperthyroidism(cats)HypoadrenocorticalismHypothyroidism(dogs)ChronicrenalfailureHepaticdiseaseFeLV,FIVandFIP2021/

02/2488Melaena（黑粪症）canbedefinedasthepresenceofchangedbloodinthefaeces.Theappearanceofmelaenawilldependontheextentofbleedinganditsl

ocation,butmalaenicfaecesnormallyappearblackandtarryinconsistency.Thisappearanceisnormallyassociatedwithbleedingintothesmallintestine,althoughmela

enamayoriginatefromthestomachorfromtheoesophagus,pharynx,mouthorrespiratorysystem.Inthelattercasesbloodisswallowedandpa

ssesthroughthealimentarytracttoappearasmelaena,givingtheimpressionofalimentarydisease.Patientswithclottingdisordersmaypresentwithmel

aena,butagaincarefulclinicalexaminationshouldrevealbleedingfromotherlocations,confirmingageneralizeddisorder.Occul

tblood（潜血）referstothepresenceofmicroscopicamountsofbloodthatcanonlybedetectedbylaboratoryanalysis.Greatcareisrequiredininterpretingapositiveres

ultindogsandcatsastheyareoftenfedmeat-baseddiets.Thepresenceofhaemoglobinormyoglobininthedietwillgivefalsepositiveresults.Itisthereforeimportanttopla

cethepatientonameat-freedietforaminimumof3dayspriortotestingforoccultblood.Atruestrongpositiveresultindicatesonlythatbleedingisoc

curringsomewherealongthealimentarytract.2021/02/2489CultureforbacteriaNormalfloraThesmallintestineliesbetweenthealmosts

terilestomach(duetogastricacid)andthelargebacterialpopulationlocatedinthecolon.Bacterialnumbersintheproximalsmallintestinearelowbutn

umbersincreaseintheileum.Theactualnumberspresentinanyindividualwillvarydependingonvariousinternalandexternalfactors.Manyofthe'nor

mal'floraarebeneficialtotheanimalbyproducingvitaminK,biotin,folateandshort-chainfattyacids(SCFAs).If

thenumbersofbacteriapresentinthesmallintestineincrease,smallintestinalbacterialovergrowth(SIBO)develops.Suchaproliferationofbacteriacan

seriouslydamagetheintestinalmucosa.ThepointatwhichbacterialpopulationsinduceclinicalsignsofSIBOwillvarywitheachindividualandthegenusofbacteria

present.2021/02/2490PathogenicbacteriaPathogenicbacteriamayestablishwhenthereisinterferencewiththenormalphysio

logicalregulationoftheresidentflora.Bacterialpropertiesthatpermitpathogenstoestablishinclude:thepresenceofflagellae;productionofenzymessuchasp

roteases;theabilityofbacteriatoadheretothemucosa;andproductionoffactorsthatinterferewithintestinalmotility.Theabilitiestoproduc

eenterotoxinandtoinvadeenterocytessignificantlyincreasepathogenicity.PotentialpathogensincludeSalmonella,Campylobacter,YersiniaandClos

tridiumspeciesandEscherichiacoli.2021/02/2491AnalysisforvirusesCanineparvovirus(CPV-2)infectionusuallyresul

tsinanacuteenteritiswithsecondarybacterialinfection,involvingespeciallySalmonellaandCampylobacterspp.Adefinitivediagnosisofparvovirusinfe

ctionrequirescollectionofafreshfaecalsampleforviralantigendetection.Ideally,samplesshouldbecollectedwithinthefirst2daysofinfectionwhenthel

argestnumberofvirusparticlesarepresent.AcommercialELISAtestkitisavailableforthedetectionofparvovirusantigeninfaeces.Serol

ogycanalsobecarriedoutinordertodetectarisingtitreofantibodyindicatingrecentparvovirusinfection.2021/02/2492EndoparasitesEndoparasi

ticinfectionwithroundworms(ToxocaracanisToxocaracati,Toxascarisleonina)andtapeworms(Dipylidiumcaninum,Taeniaspp.andEchmococcu

s)are,intheauthor'sexperience,veryrarecausesofdiarrhoeaindogsandcats.However,EchinococcusandToxocarabothcarryasignificantpubli

chealthriskandshouldbeidentifiedandtreatedwheneverpossible.2021/02/2493FaecalsmearsFreshfaecalsmearsprovideaquickandcheapmethodofexaminingfaecalsampl

es.However,asthereisnoconcentrationofovaitiseasytomissparasiteeggsorcyststhatarepresentinsmallnumbers.Afreshfecalsampleshouldbemi

xedwithasmallvolumeofphysiologicalsalineonamicroscopeslide.Ifprotozoansaresuspected,onedropofLugol'siodinewillhighlighttheseparasitesbutwillreducet

heirmotility.Anegativeresultmaybeaccurateormayreflectthesmallnumbersofparasiticeggspresent,intermittentexcretion,ortheeffectsofagentssuchasbar

iumsulphate,kaolin,pectinorenemas.2021/02/2494FaecalflotationFaecalflotationisamoresensitivemethodthanth

efaecalsmearforthedetectionofparasiteeggsandcyslbecausethetechniqueconcentratestheirnumbersinasmallvolumeofsoluti

on.Severalmethodshavebeedeveloped,butforthepurposesofthischapterontwomethodswillbedescribed.Faecalsamplesfordetectionofpa

rasiteeggsorcystsmaybepreservedbrefrigerationat+4Cforupto2dayspriortoexamination,butshouldnotbefrozen.Preservationoffaecals

amplesmayalsobecarriedoutusing1partfaecel3partspreservative(1.5gsodiumacetate,2mlglacialaceticacid,4ml40%formalinplus92.5m

lwater).2021/02/2495HepatobiliarySystemIntroductionDiseasesoftheliverfrequentlypresentthesmallanimalclinicianwithad

iagnosticchallenge;signsareoftenvariedandvagueand,despiteawidearrayofdiagnostictestsofbothhepaticdama

geandfunction,thereisrarelyasingletestthatidentifiestheproblemdefinitively.Forexample,jaundiceisoftenconsideredacardinalsignofliverdi

sease,yetcanbecausedbynon-hepaticconditions(e.g.haemolysis,extrahepaticbileductobstruction)aswellasarangeofdifferentliverdiseases.Conversely,signifi

cantliverdiseasecanexistintheabsenceofjaundice.Nevertheless,followingathoroughhistory-takingandcarefulphysi

calexamination,astuteinterpretationofapaneloflaboratorytestsinconjunctionwithradiographicandultrasonographicimagingo

fthehepatobiliarysystemwilloftenpermitapresumptivediagnosistobemade.Inmostcases,however,withtheexceptionof

congenitalportosystemicshunts(PSS),definitivediagnosisofprimaryliverdiseasewillrequirehistopathologicalexaminationoflivertissue.2021/02

/2496Figure9.1:Someofthemorecommonextrahepaticdisordersthatcancauseabnormallivertestresults.AcutepancreatitisDiabetesmellitusExocrinepancre

aticinsufficiencyExtrahepaticbacterialinfectionHyperadrenocortisolismHyperthyroidismHypoadrenocortic

ismHypothyroidismImmune-mediatedhaemolyticanaemiaInflammatoryboweldiseaseProtein-losingenteropathyRight-sidedheartfailureSepticaemiaShock2021/02/24

97Table9.1:Clinicopathologicalabnormalitiesassociatedwithdisturbancesofhepatobiliaryfunction.FunctionAbnormallaborato

rytestresultassociatedwithliverdysfunctionCarbohydratemetabolism:GlucosehomeostasisHyper-orhypoglycaemiaLipidmetabolism:CholesterolFattyacidsLipoprot

einsBileacidsHypo-orhypercholesterolaemiaHypertriglyceridaemiaLipaemiaElevatedbileacidsProteinmetabolism:AlbuminGlobulin

sCoagulationproteinsHypoalbuminaemiaIncreasedacutephaseproteins,immunoglobulinsCoagulopathiesVitaminmetabolism?D

ecreasedfolate,cobalaminVitaminE,vitaminKmaybereduceddependingonthediseaseImmunologicalfunctionsHyperglo

bulinaemiaIncreasedacutephaseproteinsDetoxificationHyperammonaemiaDecreasedureaHyperbilimbinaemia2021/02/2498CLINICOPATHOLOGICALCHANGESINLIVER

DISEASEConsequencesofhepatobiliarydysfunctionThediversefunctionsofthehepatobiliarysystemarereflectedinthediver

seclinicopathologicalchangesthatcanbefoundinliverdisease(Figure9.3).Thedefectivemetabolismandexcretionofbilirubin,causingaccumulationofcirculat

ingbilirubinandthedevelopmentofjaundice,isoftenconsideredthehallmarkofliverdisease,butitisonlyoneofmanyabnorm

allaboratoryteststhatmayfoundinliverdisease.Indeed,evenhyperbilirubinaemiafrombiliaryobstructionisusuallyass

ociatedwithhypercholesterolaemiaandelevationsofcholestaticmarkerenzymes.2021/02/2499Figure9.3:Clinicalsignsofhepatobiliarydisease.Depression,d

ecreasedappetiteandlethargyStuntingandweightlossVomiting,diarrhoea,andgreyacholicfaecesPolydipsiaandpolyuriaAscitesIcter

usAlteredliversizeBleedingtendencyAbdominalpain(rare)Encephalopathy(脑病)2021/02/24100CorrelationwithclinicalsignsThec

linicalsignsofliverdiseasearemanyandvaried(Figure9.3)andmayberelatedtospecificlaboratoryabnormalities.Signsareoftenvagueandnotapparentuntilthereis

significanthepaticdysfunction,whichiswhylaboratorytestingishelpfulindetectingandcharacterizingearlyliverdisease.However,itmustalwaysbereme

mberedthatequallyabnormaltestsmaybesecondarytoaprimarysystemicdisease.Forexample,fattyinfiltrationoftheliverindiabetesmellituscancauseincreasesinseru

mactivitiesofliverspecificenzymesinbothdogsandcats,andcanresultinjaundiceincats.2021/02/24101Depressionan

ddiminishedappetiteThesesignsarereflectionsofdisturbedmetabolisminliverdisease,butarenotassociatedwithspecificlaborat

orytestabnormalities.Anaemiaofchronicdiseasemaybepresent.Abnormallipoproteinandcholesterolmetabolismmayoccur.Hypoglycaemi

aisseeninend-stagediseaseandmaybeoneofmanyfactorsproducingthesignsofliverfailureusuallyattributedtoaccumulationofmetabolictoxins.Stuntingand

weightlossCongenitalPSSandjuvenilehepatopathiesareassociatedwithstunting,butthebiochemicaldisturbancesresponsiblear

emultifarious.Hypoproteinaemiaisoftenassociatedwithmusclewasting.GastrointestinalsignsGrey,acholicfaecesareseeninbiliaryobstruction,andare

thereforeassociatedwithjaundice.Diarrhoeamaybeareflectionofhypoproteinaemiacausingboweloedema,althou

ghlackofluminalbilesaltsandportalhypertensionaremorelikelycauses.2021/02/24102PolydipsiaandpolyuriaThesesignsmaybeassociatedwithlowlevels

ofserumurea,althoughothermechanisms,e.g.hypercortisolism,areinvolvedintheirpathogenesis.AscitesHypoproteinaemiaisarecognizedcauseoftissueflui

daccumulation.However,ascitesismorecommonthangeneralizedoedemainliverdisease,suggestingportalhypertensioninacquiredliverdiseaseisalsoan

importantfactor.IcterusHyperbilirubinaemiacausesjaundice,andmaybeduetoprehepatic(haemolysis)orposthepatic(biliaryobstruction,biliaryleakage)diseas

easwellasprimaryintrahepaticcauses.2021/02/24103LiversizeDiseasescausingalteredliversizearelistedinFigure9.4,buttherearenospecificl

aboratorymarkersofliversizeandmanydiseasesarenotassociatedwithabnormalliversize.Lipaemiamaycorrelatew

ithfattyinfiltrationoftheliver.BleedingtendencyCoagulationtimesareusuallyabnormalifsevereliverdysfunctioncausesbleeding.Generalizedblee

dingandhaemorrhagefromhepaticpeliosis(cats)andvasculartumours,suchasmetastatichaemangi-osarcoma,mayresultinregen

erativeanaemia.HepatoencephalopathyThissyndromeiscausedbyaccumulationoftoxinsbecauseofseverehepaticdysfunctionand/orporto-systemicshuntin

gofblood.Hyperammonaemiaisasensitiveandspecificmarkerforthesyndrome,althoughothermetabolicdisturbancesarei

nvolved.2021/02/24104DIAGNOSTICAPPROACHTOLIVERDISEASEInmostcases,atentativediagnosiscanbededucedfromtheresultsoflaboratorytestsinco

njunctionwithimagingtechniques.However,thedefinitivediagnosisofprimaryliverdiseaseusuallydependsultimatelyonhistologicalexaminationofliverbiopsyspec

imens.Primaryextrahepaticcausesofsecondaryliverdiseasewillhopefullybeidentifiedbeforebiopsyisundertaken.2021/02/24105Thusadiagnosticapp

roachtoliverdiseaseincludes:•Clinicalhistory•Physicalexamination•Laboratorytests•Examinationofasciticfluid•Imaging:R

adiographyUltrasonographyAngiographyScintigraphy•Liverbiopsy.2021/02/24106Theaimsoflaboratorytestingare:•Toidentifyandcharacterizeanyhepaticdysfunc

tion•Toidentifypossibleprimarycausesofsecondaryliverdisease•Todifferentiatecausesoficterus•Toevaluatepotentialanaestheticrisks•Toidentifycause

sofanaemiaofunknownorigin•Toassessprognosis•Toassesstheresponsetoxenobiotics•Tomonitorresponsetotherapy.

2021/02/24107Thereisawiderangeoflaboratorytestsavailableforassessingliverstatus,buttheycanbeconvenientlydiv

idedintofourclasses:•Generalscreeningtests•Markersofliverdamage•Liverfunctiontests•Prognosticindices.Thetestsrou

tinelyavailabletothepractisingveterinarysurgeonandindicationsfortheirusewillbediscussedindetail,andmorespec

ializedtestsmentionedonlybriefly.2021/02/24108UrinarySystemTHEROLEOFCLINICALPATHOLOGYClinicalpathologytestsintheevaluationofapatientforth

epresenceofrenaland/orurinarytractdiseaseshouldbeperformedunderthefollowingcircumstances:•Whenprimaryorsecondaryurinarysystemdiseaseissuspect

edfromthepresentingsigns,clinicalhistoryorphysicalexamination•Whenapatienthasadiseaseinanotherorgansystemthatisknowntobepotentiallyassociatedwithconc

urrentorsecondaryrenalorurinarytractdisease•Whenscreening'atrisk'patientsaspartofageneralhealthcheck(e.g.aspartofageria

tricscreeningprogramme,beforegeneralanaesthesia,orbeforeadministrationofdrugsthatareknowntobepotentiallynephrotoxic,suchasn

on-steroidalanti-inflammatorydrugs,aminoglycosidesoroxytetracycline).2021/02/24109Theaccuratediagnosisofrenalandurinarytractdise

asesrequiresinvestigationbyanyorallofthefollowing:•Fullhistory•Fullphysicalexamination•Imaging:Radiography-plainandcontraststudies;s

ometimesdynamicstudies,Ultrasonography•Urinalysis•Bloodchemistry•Haematology•Microbiologicalcultureandsensiti

vitytesting•Tissuebiopsy•Surgicalexaminationatlaparoscopyorlaparotomy•Post-mortemexamination2021/02/24110Urineshouldbeanalysedwhen:•Thereisachangei

nitsphysicalappearance,e.g.discoloration•Ananimalpassesfrankbloodinitsurine•Ananimalexhibitspolydipsia•Ananimalexhibitspolyuria•Ananimalexhibi

tsurinarytenesmus•Ananimallicksitsexternalgenitaliaexcessively•Ananimalexhibitsincreasedurinaryfrequency•Ananimal

isdehydrated•Ananimalisvomiting•Ananimalhassignsoffluidaccumulationintheabdomen(i.e.ascites)orperipherally(subcutaneousoedema)•Primaryorsec

ondaryrenalorurinarytractdiseaseissuspected•Aurolithhasbeenpassed•Ananimalexhibitspyrexiaofunknownorigin•Itispartofa

routinescreeningtest-juvenile,geriatricorbeforeanaesthesia.2021/02/24111Urinalysisincludesoneormoreofthefollowing:•

Physicalexamination:color,smell,turbidity,content,volume,specificgravity•Chemicalexamination:pH,proteinuria,acetone,glucose,urea•Examinationofs

ediment•Bacterialculture•Viralexamination.2021/02/24112ClinicalpathologypanelforurinarysystemdiseasePlasmaureaBloodurea

nitrogenPlasmacreatinineUrea:creatinineratioTotalplasmaproteinPlasmaalbuminBlasmasodiumPalsmapotassiumPlasmachloridePlasmacalciu

mPlasmaphosphate2021/02/24113GlomerularfunctiontestsindogsandcatsEndogenouscreatinineclearanceExogenouscreatinineclearanceInulin（菊酚）clearan

ceIothalanate(碘酞酸盐）clearanceFiltrationfraction24hoururineproteinexcretionUrinephosphate:urinecreatinine2021/02/24114THANKSFORWATCHING

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