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12023/3/31ReviewUrinarysystem-kidneys,ureters,urinarybladderandurethra.Kidneystructureandfunctioniscomplexandimportant:nephron(腎單位)Primarykidneyfunction-excretethewasteproductsofmetabolisminurine.Morethan1700Lofblood/dayconvertedto1Lofurine.Preciseregulationofthebody’swaterandsaltconcentration;maintainsappropriateacidbalanceofplasma;servesasanendocrineorgan.22023/3/31RenalDiseases
1.Glomerular(腎小球)
diseases
Primaryglomerulonephritis(腎小球腎炎)SecondaryglomerulonephritisSystemicrenaldiseaseHereditaryrenaldisease2.DiseasesaffectingtubulesandinterstitiumAcutetubularnecrosisTubulointerstitialNephritis:
Pyelonephritis(腎盂腎炎)3.Diseasesofrenalbloodvessels4.TumorsRenalcellcarcinoma,
Wilmstumor(Nephroblastoma),
Urothelialtumors32023/3/31KeypointsPrimaryGlomerularDiseases:Definition,pathogenesis,clinicalsyndromes,morphologyofeachtypePyelonephritis:Infectiouspathway,pathologicfeatureofacuteandchronicdisease,clinicalmanifestationsComparisonofglomerulardiseasesandpyelonephritisComparisonofRenalcellcarcinomaandWilm’stumorUrothelialcarcinomaofurinarybladder42023/3/31Glomerulonephritis(GN)-腎小球腎炎DefinitionGN:nonsuppurativeinflammation,
hypersensitiveimmunemechanism.Mainclinicalmanifestations:proteinuria,hematuria,edema,hypertension,renalinsufficiency52023/3/3162023/3/3172023/3/3182023/3/31ThereisevidenceGNisinducedbyantigen-antibodyreactions(immunemechanisms).Glomerular
depositsofimmunoglobulinswithvariouscomplementproteinsarefound.Cell-mediatedimmunemechanismsalsoplayaroleincertainglomerulardiseases.
PathogenesisofGN
92023/3/31Antigen:
1)Exogenous:Drugs,Foods,Pathogenicorganisms2)Endogenous:
a.Non-glomerularantigens
(nuclear,cytoplasm,tumorcell,immunoglobulins)b.Glomerularantigens(GBM,cells)Antibody:
IgG、IgA、IgM102023/3/31Ag+Ab=ImmuneComplex(IC)
SolublecirculatingIC:DepositionintheglomerulusInsituIC:Antibodiesreactinginsituwithintheglomerulus,eitherwithinsolublefixed(intrinsic)glomerularAgorwithmoleculesimplantedwithintheglomerulus.112023/3/31OnceIClocalizeintheglomerulus,howdoesglomerulardamageensue?MediatorsofimmuneinjuryComplement-leukocytemediatedmechanismisonewell-establishedpathwayOthermediatorsinclude:Monocytes/Macrophages,Platetes,Residentglomerularcells,Fibrin-relatedproducts.Antibodiesdirectlydamageglomeruliafterbindingwithantigenswithinglomeruli.122023/3/31GlomerularsyndromesanddisordersAcuteNephriticSyndrome
hematuria,redcellcastinurine,azotemia,oliguria,hypertension2.NephroticSyndromeClinicalcomplexwhichincludes:(1)Massiveproteinuria,dailylossof≥3.5gofprotein/day.(2)Hypoalbuminemiawithplasmaalbuminlevels≤30g/L.(3)Generalizededema,themostobviousclinicalmanifestation.(4)Hyperlipidemia,andlipiduria(lipidintheurine)littleornoazotemia,hematuria,orhypertension.
132023/3/313.RapidlyProgressiveNephriticSyndromerapidandprogressivelossofrenalfunction,severeoliguria,nephriticsyndrome,renalfailure4.AsymptomaticHematuriaorProteinuria
frequentlyrecurrentgrossormicroscopichematuria,proteinuria
5.Acuterenalfailure6.Chronicrenalfailure
142023/3/31MasangialcellMasangialmatrix(足C)ParietalepitheliumFenestraeinendotheliumVisceralepithelium(Podocyte)FootprocessEndotheliumBowmanspaceGBMCapillarylumen152023/3/31a.入球小動脈b.出球小動脈
c.腎小囊基底膜d.壁層上皮細胞e.腎小囊腔f.GBMg.臟層上皮細胞h.內(nèi)皮細胞i.系膜細胞腎小球162023/3/31172023/3/31a.腎小囊基底膜b.腎小囊腔c.臟層上皮細胞d.GBMe.內(nèi)皮f.系膜細胞182023/3/31PathologicchangesofGNHypercellularity:1.Cellularproliferation:
MsorEn2.Leukocyticinfiltration:neutrophils,monocytes,lymphocytes3.FormationofcrescentsBasementmembranethickening:1.Depositionofamorphouselectron-densematerial2.IncreasedsynthesisofGBMproteincomponentsHyalinosisandsclerosis:
192023/3/31MethodsLM:
HEPASMMassonPASIF:
IgGIgAIgMetcEM:
electrondensedeposit202023/3/31MinimalChangeDisease
(腎小球微小病變)
(LipoidNephrosis)
212023/3/31Morphology:
LM:GlomuruliareofnormalappearanceProximaltubularcellsareoftenheavilyladenwithlipidsEM:Diffuselossof
podocytesfootprocesses
(onlyobviousglomerularabnormality)IF:Negative222023/3/31Minimalchangedisease232023/3/31Clinicalfeatures:Relativelybenigndisorder,
nephroticsyndrome,children,renalfunctionpreserved,nohypertension,
>90%
ofcasesrespondtoashortcourseofcorticosteroidtherapy,
goodprognosis.Pathogenesis:immunedysfunction→cytokineelaboration→damagevisceralepithelialcell→proteinuria
MCD242023/3/31
MembranousNephropathy
(膜性腎?。?/p>
(MembranousGN)
252023/3/31LM:
Basicchange-diffusethickeningoftheGBMSmallspikelikeprotrusions-severecases262023/3/31IF:
Typicalgranulardeposition
ofIgGandcomplementalongGBM.272023/3/31EM:
(Spikeanddomepattern)Electron-densesubepithelialdepositionsnestleagainstGBMSpikelikeprotrusionsofGBMareseparatedbydepositions.
Podocyteslosefootprocesses.282023/3/31MembranousGN
MembranousNephropathy正常292023/3/31Clinicalfeatures:Adults30-50,insidiousdevelopment,nephroticsyndrome,Doesnotresponsewelltocorticosteroidtherapy.Etiology:Idiopathic;secondary(hepatitisB,malignanttumor,SLE,exposuretoinorganicsalts,drugs)Progress:Slowlyprogressivedisease.Pathogenesis:Chronicimmunecomplexnephritis
MN302023/3/31
DiffuseMembranoproliferativeGN
(彌漫性膜增生性腎小球腎炎)
(MPGN)312023/3/31MorphologyMesangialcellproliferationandinfiltratingleukocytesmakeglomerulilargewithlobularappearance.GBMthickened,oftenshowsadoublecontouror“tramtrack”appearanceEMandIFfindingsyields2subtypes
322023/3/31TypeI:(2/3cases)EM:Subendothelialelectron-densedeposits.IF:C3andIgG,earlycomplementcomponents(C1qandC4),suggestICpathogenesis.332023/3/31TypeII:(DenseDepositDisease,DDD)
EM:Depositionofunknownmaterialgivesthe
GBMaribbon-likeelectron-densestructure.IF:C3ispresent.IgGandearly-actingcomplementcomponentsusuallyabsent342023/3/31DiffuseMembranoproliferativeGN正常352023/3/31Clinicalfeatures:Idiopathicnephroticsyndrome(10%-20%)Prognosisuniformlypoor.40%→end-stagerenalfailure,30%→variabledegreeofrenalinsufficiency,30%→nephroticsyndromewithoutrenalfailure.TypeIIhasworseprognosis,withrecurranceafterrenaltransplantation.
MPGN362023/3/31DiffuseProliferativeGN
(彌漫性增生性腎小球腎炎)
DiffuseEndocapillaryGN
(彌漫性毛細血管內(nèi)增生性腎小球腎炎)
Poststreptococcal,PostinfectiousGN
(感染后腎小球腎炎)372023/3/31LM:
UniformlyincreasedglomerularcellularityCharacteristicchange:proliferationofendothelialandmesangialcells,withneutrophilandmonocyteinfiltrates.382023/3/31IF:
GranularIgGandcomplementdepositsalongGBM392023/3/31EM:Immunecomplexesdepositionarrayedassubepithelial
“humps”nestledagainstGBM.402023/3/31Endothelial+MscellsproliferationNeutrophilinfiltrate“Hump”likesubepithelialdeposition
PathogenesisofDffuseProliferativeGN
正常412023/3/31Clinicalfeatures:Abruptonset,nephriticsyndrome,grosshematuria,lowserumcomplement.Poststreptococcalcases:serumantistreptolysinOtiters↑Prognosis:Mostchildrenrecover.Pathogenesis:immunologicallymediateddiseaseDiffuseProliferativeGN422023/3/31CrescenticGN
(新月體性腎小球腎炎)
RapidlyProgressiveGN
(快速進行性腎小球腎炎)432023/3/31Morphology:
1.Glomerulishowcrescent
formation
2.Crescentsformedbyparietalcellproliferation
andmonocyte
migrationintoBowman’space.
3.Fibrinstrandsprominentbetweencellularlayersincrescents.
4.CrGNdividedinto3groupsbasedonimmunefindings442023/3/31
TypeICrGN:Anti-GBMdisease
1.
Clinically-Goodpasturesyndrome
2.Serum-Anti-GBMantibodiespresent(helpfulindiagnosis)
3.IF:lineardepositsofIgGandC3onGBM
4.Treatment:plasmapheresis452023/3/31TypeIICrGN:Immunecomplex-mediateddisorder
Potentialcomplicationofanyimmunecomplexnephritis,includingPoststreptococcalGN,LupusNephritis,IgAnephropathy.
TypeIIICrGN:Pauci-immunetypeCrGN
1.
Definedbylackofanti-GBMantibodiesorICbyIFandEM.
2.
MostpatientshaveserumANCA(Anti-NeutrophilCytoplasmicAntibody).
3.Componentofsystemicvasculitis:Wegner’sgranulomatosis,Microscopicpolyarteritis
462023/3/31正常ParietalcellsproliferationMigrationofmonocytesFibrinins
RapidlyProgressive/CrescenticGNCrescentsformation472023/3/31Clinicalfeatures:Nephriticsyndrome,oliguria,azotemia,ProteinuriaPrognosis:roughlyrelatedtonumberofcrescents.
RPGN482023/3/31
IgANephropathy
(IgA腎病)492023/3/31LM:lesionsvaryconsiderablyFocalGNCrescenticGNDiffuseMsPGN502023/3/31IF:
CharacteristicfeatureismesangialdepositionofIgA,oftenwithC3.512023/3/31EM:confirmsthepresenceofIFdepositioninmesangium.522023/3/31
IgANephropathyClinicalfeatures:Recurrentmicroscopicorgrosshamaturia;
mostcommonGNworldwide,Usuallyaffectschildrenandyoungadults
Typicalacutenephriticsyndromein5-10%Subsequentcoursehighlyvariable.Manypatientsmaintainnormalrenalfunctionfordecades,25%-50%progresstochronicrenalfailureover20years.532023/3/31IgANephropathyPathogenesis
IncreasedIgAsynthesis(marrow).ReducedIgAclearanceIgAandIgAcomplexestrappedinmesangium,andactivatealternativecomplementpathway,andinitiateglomerularinjury.542023/3/31ChronicGlomerulonephritis
(慢性腎小球腎炎)
SclerosingGlomerulonephritis
(硬化性腎小球腎炎)552023/3/31
ChronicGNClinicalCoursePooroutcomeinallformsofGN
Clinically-chronicrenalfailure,firstnotedinyoungandmiddle-agedadults20%-nohistoryofsymptomaticrenaldisease30%to50%requirehemodialysisorrenaltransplantation562023/3/31Macroscopic:
KidneyssymmetricallycontractedKidneysurfacesred-brownanddiffuselygranular.End-stagekidney,reducedsize572023/3/31End-stagekidneys-microscopic
Scarring(hyaline)ofglomeruli(difficulttodiscernnatureoforiginallesions)
Atrophyandreplacementofmanytubulesincortex.Markedinterstitialfibrosisandlymphocytesinfiltration
Smallandmedium-sizedarteries
thickwalled,withnarrowedlumina.582023/3/31RenalDiseases
1.Glomerular(腎小球)
diseases
Primaryglomerulonephritis(腎小球腎炎)SecondaryglomerulonephritisSystemicrenaldiseaseHereditaryrenaldisease2.DiseasesaffectingtubulesandinterstitiumAcutetubularnecrosisTubulointerstitialNephritis:
Pyelonephritis(腎盂腎炎)3.Diseasesofrenalbloodvessels4.TumorsRenalcellcarcinoma,
Wilmstumor(Nephroblastoma),
Urothelialtumors592023/3/31Glomerulonephritis(GN)-腎小球腎炎DefinitionGN:nonsuppurativeinflammation,
hypersensitiveimmunemechanism.Mainclinicalmanifestations:proteinuria,hematuria,edema,hypertension,renalinsufficiency602023/3/31MinimalChangeDisease
(腎小球微小病變)
(LipoidNephrosis)
612023/3/31Minimalchangedisease622023/3/31
MembranousNephropathy
(膜性腎病)
(MembranousGN)
632023/3/31MembranousGN
MembranousNephropathy正常642023/3/31
DiffuseMembranoproliferativeGN
(彌漫性膜增生性腎小球腎炎)
(MPGN)652023/3/31DiffuseMembranoproliferativeGN正常662023/3/31DiffuseProliferativeGN
(彌漫性增生性腎小球腎炎)
DiffuseEndocapillaryGN
(彌漫性毛細血管內(nèi)增生性腎小球腎炎)
Poststreptococcal,PostinfectiousGN
(感染后腎小球腎炎)672023/3/31Endothelial+MscellsproliferationNeutrophilinfiltrate“Hump”likesubepithelialdeposition
PathogenesisofDffuseProliferativeGN
正常682023/3/31CrescenticGN
(新月體性腎小球腎炎)
RapidlyProgressiveGN
(快速進行性腎小球腎炎)692023/3/31正常ParietalcellsproliferationMigrationofmonocytesFibrinins
RapidlyProgressive/CrescenticGNCrescentsformation702023/3/31TubulointestitialNephritis(TIN)TIN-groupofrenalinflammatorydiseasesprimarilyinvolvinginterstitiumandtubules.Glomerulimaybesparedoraffectedlateindiseasecourse.MostTINcausedbybacterialinfection.
Renalpelvisprominentlyinvolved-pyelonephritis.712023/3/31AcutePyelonephritisCommonsuppurativeinflammationofkidneyandrenalpelvis,causedbybacterialinfection.Almostalwaysassociatedwithinfectionofthelowerurinarytract.722023/3/31Principalorganisms-entericgram-negativerods.Mostcommon-E.coliBacteriareachkidneyby2routes:
1)Mostimportantandcommonroute-lowerurinarytract(ascendinginfection).2)Lesscommonroute-bloodstream(hematogeousinfection).Wheredobacteriacomefrom?732023/3/31PredisposingfactorsinrecurrentinfectionUrinaryobstruction:CongenitaloracquiredInstrumentation:Cystoscopy,catheterizationVesicoureteralreflux(VUR):CongenitalPregnancySexandage:Sexualinjury,benignprostatehyperplasiaPre-existingrenallesions:CauseintrarenalscarringDiabetesmellitusImmunosuppressionandImmunodeficiency742023/3/31Macroscopicfindings:DiscreteyellowishraisedabscessesGrosslyapparentontherenalsurfaceWidelyscatteredorlimitedtooneregion752023/3/31Microscopicfindings:Characteristicsuppurativenecrosisorabscessformationwithinrenalparenchyma.Neutrophilinfiltrateandcastswithintubularlumen.Pyelonephrosis,necrotizingpapillitisorpapillarynecrosis.762023/3/31AcutePyelonephritisClinicalCourse
EvidenceofsystemicinfectionUrinaryfindings-pyuriaandbacteriuriaClinicalcourse-benignandself-limited.Necrotizingpapillitisassociatedwithmuchpoorerprognosis.772023/3/31ChronicPyelonephritisChronicpyelonephritis–morphologicallydefinedentityInflammationpredominantlyinterstitialwithscarringofrenalperanchymaGrosslyvisiblescarringanddeformityofpelviccalycealsystemImportantcauseofchronicrenalfailureTwoforms-obstructiveandreflux-associatedpyelonephritis782023/3/31Macroscopicfindings:Characteristic-Unevenscarring,asymmetricallycontractedkidneyHallmark-scarringinvolvingpelvisorcalycesleadingtopapillarybluntingandmarkedcalycealdeformity792023/3/31MicroscopicfindingslargelynonspecificUneveninterstitialfibrosis,
chronicinflammatoryinfiltrate,occasionallywithneutrophils.LesionsinvolvecalycealmucosaandwallDilationorcontractionoftubuleswithcolloidcastsGlomerulosclerosisandarteriolosclerosis802023/3/31ChronicPyelonephritisClinicalCourseRenalinsufficiencyorhypertension,orfoundonroutinemedicalexamination.Ultrasonographyfindingsarecharacteristic.Absenceofsignificantbacteriuriashouldnotruleoutthisdisease.Tubulardysfunctionoccursinbilateral&progressivecasesGlomerulosclerosismaydevelopandleadtochronicrenalfailure.812023/3/31GNPyelonephritisEtiology
AgInflammationImmunereactiontypeIIINon-suppurativeLocationGlomeruliRangeDiffuseorFocalClinically
Proteinuria,hematuria,BUNScrNoirritationofurethraTreatmentCorticosteroidtherapyKidneytransplantationG-Bacteria,E.coliSuppurativeinflammationTubulointerstitiumCalyceal&pelvismucosaFocalBacteriuria,PyuriaTubulardysfunctionBladderandurethrairritationAntibioticsRemovepredisposingfactors822023/3/31Renalneoplasms832023/3/31Renaltumors
epidemiologyBenigntumorshavenoclinicalsignificance-corticalpapillaryadenomaormedullaryfibroma.Renalcellcarcinoma-mostcommonprimarymalignanttumorofkidney,followedinfrequencybynephroblastomaandprimarytumorsofcalycesandpelvis.Otherrenalcancersrare.Tumorsoflowerurinarytractaretwiceascommonasrenalcellcarcinoma(e.g.urinarybladdercarcinoma)842023/3/31DerivedfromrenaltubularepithelialcellsRepresents80%-85%ofprimarymalignantkidneytumorsMostcommon-60-70years.M:F=2:1RiskhigherinsmokersandwithexposuretocadmiumRisk30foldhigherinacquiredpolycysticdiseaseasacomplicationofchronicdialysis.RenalCellCarcinoma852023/3/31Newclassificationbasedonmoleculartumororiginssecondarytorecentadvancesintumorgenetics.Threemostcommonforms:1.Clearcellcarcinoma2.Papillaryrenalcellcarcinoma3.ChromophoberenalcarcinomaNewClassificationofRCC862023/3/3170%to80%ofrenalcellcancersMostaresporadic,somearefamilialassociatedwithvonHipple-Linda(VHL)disease.VHL-autosomaldominantdiseasecharacterizedbypredispositiontoavarietyofneoplasms.Germ-linemutationofVHLgeneandlossofsecondallelebysomaticmutationresultsinhemozygouslossofVHLVHLgeneisatumorsuppressorgeneonchromosome3p25ClearCellCarcinoma872023/3/31Macroscopic:Ariseanywhereinrenalcortex
WelldemarcatednoduleCutsurfaceyellowtoorange
togray-whitewithprominentareasofcysticchangeand
necrosisorhemorrhage.Occasionaldirectinvasionintotheperinephricfatandadrenalgland.882023/3/31Microscopicfindings:
Classic-
clearcellswithvacuolated(lipid-laden)cytoplasm,smallandroundnuclei,welldelineatedcellmembrane,cellswithpinkgranularcytoplasmresemblingtubularcells.
StromausuallyscantbuthighlyvascularizedAbortivetubules,clusterincords
ordisorganizedmasses892023/3/31Papillaryrenalcellcarcinoma10%-15%ofallrenalcancersEtiology-overdoseofMETprotooncogeneonchromosome7q31.Familialcases:chromosome7trisomy,andmutationofMETgenecommonlyseen.Sporadiccases:chromosome7trisomywithoutMETgenemutation,andtrisomyof16,17andlossofchromosomeY.902023/3/31MacroscopicfindingsMultilocalandbilateralgrowthLessvibrantlyorange-yellow,duetolowerlipidcontent.912023/3/31HistologicfindingsPapillarygrowthpattern,papillawithfibrovascularcoresCytoplasmclearoroftenpink922023/3/31Chromophoberenalcarcinoma5%ofrenalcellcancersNamederivesfromfactcellsstainmoredarkly(lessclear)Arisefromcorticalcollectingductsortheirintercalatedcells.Uniqueinhavingmultiplelossesofentirechromosomes1,2,6,10,13,17and21-extremehypodiploidy.Ingeneralhasgoodprognosis932023/3/31Macroscopicfindings:Tan-brownnoduleHistologicfindingsClearflocculentcytoplasmwithprominent,distinctcellmembranes.Nucleisurroundedbyhalosofclearedcytoplasm.EM-macrovesicles942023/3/31RCCClinicalcourseVariableclinicalmanifestationscreatedifficultandchallengingdiagnosticproblemsCharacterisedbytriadofpainlesshematuria,long-standingfever,anddullflankpainSometimesdetectedaftermetastasisPrevalentlocationsformetastases-lungandbone952023/3/31WilmsTumor
Nephroblastoma
(腎母細胞瘤)962023/3/31Grossfindings:Large,solitary,well-circumscribedmassCutsurface-soft,homogenous,tantogray972023/3/31Microscopicfindings:RepresentsdifferentstagesofnephrogenesisClassictriphasiccombinationofblastemal,stromalandepithelialcellstypesobservedinmostlesionsBlastemalcomponent:SheetsofsmallbluecellswithfewdistinctivefeaturesEpithelialdifferentiation:abortivetubulesandglomeruliStromaldifferentiation:Smoothmuscle,adipisetissue,cartilage,osteoidandneurogenictissue982023/3/31WilmsTumorClinicalcourseReadilypalpableabdominalmass.Mayhavefever,abdominalpainPrognosisgenerallyverygood.Excellentresultsobtainedwithcombinationofnephrectomyandchemotherapy.2yearsurvivalrateupto90Tumorswithdiffuseanaplasia,especiallywithextrarenalspreadhaveleastfavorableoutcome.992023/3/31Urothelialneoplasms
(尿路上皮腫瘤)
(Transitionalneoplasms)1002023/3/31OccurintransitionalepitheliumfromrenalpelvistourethraFocusonhistologicpatternsandclinicalimplicationsinurinarybladdertumors.1012023/3/31Macroscopicfindings-Tumorsarisinginurinarybladderrangefromsmallbenignpapillomastolargeinvasivecancers1022023/3/31Classification
ofurothelialneoplasmsarisinginurinarybladderBenigntumor:PapillomaMalignanttumor:urothelialcarcinoma1)lowGrade2)highGrade
1032023/3/31Veryrarebenigntumor,usua
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