泌尿系统疾病英文课件

泌尿系统疾病英文泌尿系统疾病英文1Section 1 Introduction A.Anatomy of A.Anatomy of kidney kidney Cut surface of Cut surface of kidneykidney Cortex Cortex Medullary Medullary Renal papilla Renal papilla Calyx Calyx Renal pelvis Renal pelvis Section 1 Introduction A.Ana2B.Histology of kidney Nephrons:Nephrons:capillary tuft capillary tuftGlomerulus Glomerulus bowmans capsulebowmans capsule (capsular Space)(capsular Space)proximal convoluted proximal convoluted tubule tubulerenal tubulesrenal tubules distal convoluteddistal convoluted tubule tubule B.Histology of kidney Nephron3C.Ultrastructure of glomerulus 1.Glomerular filtration 1.Glomerular filtration barrier:barrier:basement membrane(B.basement membrane(B.M)M)endothelial cell endothelial cell Visceral epithelial cell Visceral epithelial cell(podocyte),foot-process(podocyte),foot-process have plenty negative ion have plenty negative ion substances(heparan etc)substances(heparan etc)C.Ultrastructure of glomerulu4 2.Glomerular mesangium structure 2.Glomerular mesangium structure mesangial cell mesangial cell mesangial matrix mesangial matrix,2.Glomerular mesangium struc5D.Classification of urinary system disease 1.Glomerulonephritis 1.Glomerulonephritis 2.Pyelonephritis 2.Pyelonephritis 3.Tumor of kidney 3.Tumor of kidney 4.Tumor of bladder 4.Tumor of bladder D.Classification of urinary 6大家有疑问的，可以询问和交流大家有疑问的，可以询问和交流可以互相讨论下，但要小声点可以互相讨论下，但要小声点可以互相讨论下，但要小声点可以互相讨论下，但要小声点大家有疑问的，可以询问和交流可以互相讨论下，但要小声点7D.ClassificationofGlomerulonephritisD.ClassificationofGlomerulonephritisprimary Glomerulonephritisprimary Glomerulonephritis(1)glomerularminor1esion(2)focalandsegmentalglomerularchangeA.focalnephritisB.focalandsegmentalglomerulosclerosis(3)diffuseglomerulonephritisA.membranousglomerulonephritis(membranousnephropathy)B.proliferativeglomerulonephritisa.mesangialproliferativeglomerulonephritisb.endocapillaryproliferativeglomerulonephritisD.Classification of Glomerulo8c.mesangiocapillaryglomerulonephritis(membranoproliferativeglomerulonephritistypeIandIII)d.crescenticglomerulonephritise.IgAnephropathyC.sclerosingglomerulonephritis(4)unclassifiedglomerulonephritissecondary Glomerulonephritissecondary Glomerulonephritis (1)1upusnephritis(2)nephritisofHenoch-Schonleinpurpura(3)anti-GBMnephritis,Goodpasturesyndrome c.mesangiocapillary g9Section 2 Glomerulonephritis(GN)A.Definition A.Definition Glomerulonephritis Glomerulonephritis is is a a hypersensitivity hypersensitivity inflammatory inflammatory disease.disease.It It cause cause by by various various immune immune complex complex and and appear appear diffuse diffuse glomeruli glomeruli proliferative proliferative inflammation inflammation in in bilateral kidneys bilateral kidneys shortenedformshortenedformSection 2 Glomerulonephritis(10B.Mechanisms of glomerular damageIt is clear that GN can be readily induced by It is clear that GN can be readily induced by antigen-antibody reactions.antigen-antibody reactions.1.Antigens 1.Antigens Endogenous antigen(intrinsic Endogenous antigen(intrinsic)GBM,endothelial cell,mesangial cell GBM,endothelial cell,mesangial cell Exogenous antigen(Exogenous antigen(incoming)bacteria,virus,fungus,parasit,drug ect bacteria,virus,fungus,parasit,drug ect B.Mechanisms of glomerular da112.Immune injury mechanisms2.Immune injury mechanisms(1)immune complexs formed In situ(10%)immune complexs formed In situ(10%)(immune complex nephritis in situ)(immune complex nephritis in situ)Antibodies react directly with,intrinsic Antibodies react directly with,intrinsic tissue antigen(GBM,EC,MC)or antigen tissue antigen(GBM,EC,MC)or antigen planted(non-glomerular antigen)planted(non-glomerular antigen)2.Immune injury mechanismsimm12YY YYYYYYYYGBM-autoantigenimmunecomplexsformedInsituimmunecomplexsformedInsituYY YYYYYYYYGBM-autoantigenimm13 Immunofluorescent(IF)appear linear pattern:Immunofluorescent(IF)appear linear pattern:Green color linear fluorescenceGreen color linear fluorescencefibrin Immunofluorescent(IF)appea14(2)Circulating immune complexs deposition(2)Circulating immune complexs deposition(90%)(90%)The antigen and antibody have not The antigen and antibody have not immunologic specificity for glomerular immunologic specificity for glomerular constituents,antigen-antibody complexs constituents,antigen-antibody complexs are formed in the circulation and then are formed in the circulation and then deposit in the glomeruli.IF appear deposit in the glomeruli.IF appear granular pattern.granular pattern.(2)Circulating immune complex15泌尿系统疾病英文课件16SimulativepictureofcapillarytuftSimulativepictureofcapillarytuftSimulative picture of capillar17IFappeargranularpattern.IFappeargranularpattern.IF appear granular pattern.18ImmunecomplexComplementactivatedComplementactivatedmononuclearcellmononuclearcell activatedactivated plateletMCMCcytokinescytokinesC5-9C5-9C3,C5aC3,C5aneutrophilneutrophilInjuryofglomeruliInjuryofglomeruliReleasingproleaseReleasingproleasefreeradicalsfreeradicalsarachidonicacidarachidonicacidExudation,proliferativeinflammationExudation,proliferativeinflammationImmune complexComplement activ19C.Commonglomerulonephritis.AcutediffuseproliferativeGNcalledalso:endocapillaryproliferativeGN,endothelial-mesangialproliferativeglomerulonephritispost-streptococcusGNC.Common glomerulonephritis 20DefinitionDefinition MC and EC mainly/diffusely proliferationMC and EC mainly/diffusely proliferationinmostofinmostofglomeruliinbothkidneys.glomeruliinbothkidneys.ItsabnormalreactiveinflammationorItsabnormalreactiveinflammationorproliferative proliferative inflammation.inflammation.FrequentlyinchildrenFrequentlyinchildrenEtiologyEtiology AssociatedwithA-haemolyticstreptococcal(type12,4,1)AssociatedwithA-haemolyticstreptococcal(type12,4,1)infection.Within1-4weeksafterinfection,notatthattime.infection.Within1-4weeksafterinfection,notatthattime.Otherorganisms:pneumococci,viruses,Malariaetc.Otherorganisms:pneumococci,viruses,Malariaetc.,Definition,21Morphology Grossly:Grossly:“big and red kidneybig and red kidney”“”“flea-bitten kidneyflea-bitten kidney”Enlargement,Enlargement,tightcapsula,tightcapsula,Dark-redcolourDark-redcolourbleedingpointbleedingpointparasite parasite Morphology Enlargement,parasit22LM:LM:1.glomeruli:1.glomeruli:a.proliferativalteration:a.proliferativalteration:Alltheglomeruliareenlarge,andfilledwithcellsAlltheglomeruliareenlarge,andfilledwithcells(mesangial and endothelia cellmesangial and endothelia cell),capillarylumen),capillarylumennarrowed.Butparietalepitheliumwithouthyperplasianarrowed.Butparietalepitheliumwithouthyperplasiab.Exudativealteration:b.Exudativealteration:variableinfiltrationofpolymorphonuclearleukocytes,variableinfiltrationofpolymorphonuclearleukocytes,RBCincapillarytuftandBowmanscapsule.RBCincapillarytuftandBowmanscapsule.c.thrombosisandfibrinoidnecrosisofcapillarytuft,c.thrombosisandfibrinoidnecrosisofcapillarytuft,bleeding.bleeding.2.Renaltubulesalteration:2.Renaltubulesalteration:degenerationofepithelialcells,redcellandleukocytedegenerationofepithelialcells,redcellandleukocytecastsetc.castsetc.3.Interstitialalteration:3.Interstitialalteration:congestion,edema,inflammatorycellinfiltratingcongestion,edema,inflammatorycellinfiltratingneutrophilsneutrophilsLM:neutrophils23BiopsyofaspirationinkidneyBiopsyofaspirationinkidneyglomerule enlarge,andfilledwithcells(mesangial and endothelia cell),capillarylumennarrowed.parietalepitheliumwithouthyperplasianeutrophilsneutrophilsBiopsy of aspiration in kidney24泌尿系统疾病英文课件25silverstainingsilverstainingGBM,MesangialdarkcolourGBM,MesangialdarkcolourMassonstainingMassonstainingoutGBM,Eosin-proteindepositeoutGBM,Eosin-proteindepositesilver stainingMasson staining26EMandIF:EMandIF:endothelialcellandmesangialcellendothelialcellandmesangialcellproliferating,inthebasementmembraneandproliferating,inthebasementmembraneandunderthepodocytehaveunderthepodocytehavehump-shapedhump-shaped deposite.deposite.IFappeargranularpattern-IFappeargranularpattern-IgG.C3(+)IgG.C3(+)EM and IF:27IFappeargranularpatternIFappeargranularpatternhump-shapedhump-shaped deposite.deposite.Camelpeak-likeIF appear granular patternhump28Clinical-pathologicalcorrelationAcutenephritissyndromeAcutenephritissyndromeUrinealteraion:Oliguria(lowerthan400ml/24h)oranuria(lowerthanOliguria(lowerthan400ml/24h)oranuria(lowerthan100ml/24h)100ml/24h)Proteinuria,cast(+)Proteinuria,cast(+)HematuriaHematuriaEdema(sodium,waterretention)Edema(sodium,waterretention)Hypertension(bloodvolume)Hypertension(bloodvolume)heartfailureheartfailurehypertensiveencephalopathyhypertensiveencephalopathyGlomerulefiltrationGlomerulefiltrationazotemiarenalfailureazotemiarenalfailurediureticagentdiureticagentmilliliterRemove,saveupRemove,saveup,Clinical-pathological correlat29Result:95%wouldbecured,5%mightturntochronic95%wouldbecured,5%mightturntochronicGN,andfewcasesdeveloprapidlyprogressiveGN,andfewcasesdeveloprapidlyprogressiveGN.GN.1%developetoheartfailure,renalfailureandfemaleYoungadultfrequently,malefemalecauseofdeath:causeofdeath:pulmonaryhemorrhage,renalfailurepulmonaryhemorrhage,renalfailure,Clinic:seldom,40DiffusemembranousGN（membranousnephritis)Earlychronicnephritis,thedurationisslowEarlychronicnephritis,thedurationisslowandprognosisisrelativelygoodandprognosisisrelativelygood Diffuse membranous GN（mem411.Pathology1.Pathology(1)LM:basement(1)LM:basementmembranediffuselymembranediffuselythickenedverymuchthickenedverymuch(platinicring-like),but(platinicring-like),butthecapillarylumenisthecapillarylumenisnotobstructedusually.notobstructedusually.Nocellproliferation.Nocellproliferation.1.Pathology(1)LM:basement 42(2)grossly:“bigandwhitekidney”.(2)grossly:“bigandwhitekidney”.(3)EM:Thereare“dome”and“spike”.Domeis(3)EM:Thereare“dome”and“spike”.Domeisthedeposit,spikeistheproliferationofthedeposit,spikeistheproliferationof“basementmembranesubstance”.SotheBM“basementmembranesubstance”.SotheBMbecomesthickenedandlatestageBMbecomesbecomesthickenedandlatestageBMbecomes“moth-eaten”like.“moth-eaten”like.(4)IF:(4)IF:granularpattern-IgG.C3(+)(2)grossly:“big and white ki43Slide 21.29“spike”“spike”“dome”“dome”“moth-eaten”like“moth-eaten”liketheproliferationof“basementmembranesubstanceimmunecomplexdepositSlide 21.29“spike”“dome”“moth-44MassonstainingMassonstainingoutGBM,Eosin-proteindepositeoutGBM,Eosin-proteindepositeMasson staining452.Clinical-pathologicalcorrelation2.Clinical-pathologicalcorrelationTypicalnephroticsyndromeTypicalnephroticsyndromeHighproteinuria(osmoticpressureofHighproteinuria(osmoticpressureoffiltrationbarrierincreasefiltrationbarrierincrease)Highedema(proteinslosecolloid-osmosisHighedema(proteinslosecolloid-osmosis pressurepressuredecrease)decrease)HighcholesterolemiaandlipidemiaHighcholesterolemiaandlipidemiaLowbloodalbumin(proteinslose)Lowbloodalbumin(proteinslose),highhighhighlow2.Clinical-pathological corre463.Result3.ResultThedurationisslow.MostofcasesdevelopThedurationisslow.Mostofcasesdeveloprecurrent,inlatestageanumberofglomerulirecurrent,inlatestageanumberofglomerulidevelopfibrosis,somecasesmaybecure.developfibrosis,somecasesmaybecure.3.Result 47DiffusemembranousproliferativeGNDiffusemembranousproliferativeGN（mesangiocapillaryGN)mesangiocapillaryGN)ItisachronicprogressivenephritisanditaffectsItisachronicprogressivenephritisanditaffectsthemesangiumandcapillaryofglomerulus.Itisthemesangiumandcapillaryofglomerulus.Itismoreseriousthanmembranousnephritis.Itsmoreseriousthanmembranousnephritis.Itsprognosisisworse,easiertotransittoatrophicprognosisisworse,easiertotransittoatrophickidney.kidney.Diffuse membranous prolifer481.Pathology1.Pathology(1)LM:LM:TheglomerulusTheglomerulusbecomeslobulatedbecomeslobulatedcapillarywallcapillarywallthickenedandthickenedandlumennarrowedlumennarrowedSomehyalineSomehyalineglomeruliwouldglomeruliwouldbeseen.beseen.1.Pathology LM:49(2)EM:Mesangialcellandmesangialmatrix(2)EM:Mesangialcellandmesangialmatrixproliferateverymuchfurthermore,theywouldproliferateverymuchfurthermore,theywouldinsertintothecapillarywall,theBMshowinsertintothecapillarywall,theBMshowsplitting(twolayer).Makingthelumenserioulysplitting(twolayer).Makingthelumenserioulynarrow,theimmunedepositcanbeseennarrow,theimmunedepositcanbeseenelsewhere(mesangiumandcapillarywall).elsewhere(mesangiumandcapillarywall).(3)IF:granularpattern-(3)IF:granularpattern-IgG.C3(+)-IgG.C3(+)-Mesangium,Mesangium,capillarywalldeposit.capillarywalldeposit.(2)EM:Mesangial cell and 50Slide 21.37Mesangialcellandmesangialmatrixproliferateverymuchandinsertintothecapillarywall,theBMshowsplitting(twolayer).Railway-likeSlide 21.37Mesangial cell and 512.Clinical-pathologicalcorrelation2.Clinical-pathologicalcorrelationTheearlystage:proteinuriaandhematuriaismildTheearlystage:proteinuriaandhematuriaismilddegree.degree.ThedisorderaffectBM:nephroticsyndromeThedisorderaffectBM:nephroticsyndromeThelatestage:hypertensionandrenalfailure.Thelatestage:hypertensionandrenalfailure.2.Clinical-pathological corre523.Result3.ResultTheprognosisisworseeasiertotransittoTheprognosisisworseeasiertotransittoatrophickidney,the50%ofcasesdevelopatrophickidney,the50%ofcasesdevelopchronicrenalfailurewithin10years.chronicrenalfailurewithin10years.3.Result The prognosis is w53.Minimalchangeglomerulonephritis（Lipoidnephrosis)1.Pathology:1.Pathology:(1)Glossly:bigandwhitekidney(1)Glossly:bigandwhitekidney(2)LM:glomerulinochangeatall(2)LM:glomerulinochangeatalltubules:fattydegeneration.tubules:fattydegeneration.(3)EM:TheuniquechangeunderEMisfoot(3)EM:TheuniquechangeunderEMisfootprocessesfusion.Nodepositatall.processesfusion.Nodepositatall.Minimal change glomerulone54bigandwhitekidneybigandwhitekidneybig and white kidney55Slide 21.30Slide 21.3056Slide 21.32Slide 21.32572.Clinical-pathologicalcorrelationNephroticsyndrome(three-highandone-low)Nephroticsyndrome(three-highandone-low)(1)Highproteinuria(mainlyisalbumin)(1)Highproteinuria(mainlyisalbumin)(2)Hypoalbuminemia(2)Hypoalbuminemia(3)Highedema(3)Highedema(4)Hyperlipidemiaandhypercholesterolemia(4)Hyperlipidemiaandhypercholesterolemiahighhighhighlow2.Clinical-pathological corre58Injory of glomerular capillary wallFiltrationofalbuminGenerousproteinuriaGenerousproteinuriaplasmaproteinHypoalbuminemiaplasmacolloidosmoticpressureWaterintotissueedemablood volume glomerular filtration rate Aldosterone and antidiuretic hormone SodiumandwaterretentionaggravatingHighproteinuriaHypoalbuminemiaHighHighedemaedemaInjory of glomerular capillary59HyperlipidemiaHyperlipidemiaandhypercholesterolemiaandhypercholesterolemiaindefiniteindefiniteHypoalbuminemiaLipoproteinssynthesisinliverdisorders of lipid granule transportation in blood and breakdown of peripheral lipid proteins 3.Result3.ResultTheprognosisisgood90%ofcasesinchildrenTheprognosisisgood90%ofcasesinchildrenwouldbecurewithcortisonewouldbecurewithcortisoneHyperlipidemia indefiniteHypoa60.DiffusesclerosingGN（Chronicnephritis)ThistypeisthefinalresultofalotofGN(end-stageThistypeisthefinalresultofalotofGN(end-stagekidney),itscharacterismajorityofnephrons(glomeruli)kidney),itscharacterismajorityofnephrons(glomeruli)becomehyalinized,fibrosis,souremia,even.renalfailurebecomehyalinized,fibrosis,souremia,even.renalfailurePathologiccharacter:Pathologiccharacter:(1)(1)majorityofnephrons(glomeruli)becomehyalinized,majorityofnephrons(glomeruli)becomehyalinized,fibrosisfibrosis(2)(2)ResidualnephronsbecomecompensativehypertrophyResidualnephronsbecomecompensativehypertrophy(3)(3)Grossly“granularatrophyofkidney”Grossly“granularatrophyofkidney”.Diffuse sclerosing GN（Ch61causes:causes:621.Morphology:(1)grossly:granularatrophyofkidney(1)grossly:granularatrophyofkidneyGranulecollectingareasofGranulecollectingareasofcompensativehypertrophynephronscompensativehypertrophynephronsDepressed-collectingareasDepressed-collectingareasoffibrosisofnephronsoffibrosisofnephrons1.Morphology:Granule collecti63泌尿系统疾病英文课件64(2)LM:(2)LM:MostofglomeruliarepartiallyorcompletelyMostofglomeruliarepartiallyorcompletelyscarredandsomeconvertedtohyalinemassesscarredandsomeconvertedtohyalinemassesthenearbytubulesareatrophyandfibrosis;thenearbytubulesareatrophyandfibrosis;Fibrosisofinterstitialtissueisprominent,andFibrosisofinterstitialtissueisprominent,andthereisaninflammatoryinfiltrationinstromathereisaninflammatoryinfiltrationinstromaRelativelynormalglomerulioccurcompensation,Relativelynormalglomerulioccurcompensation,glomerulioccurhypertrophyandtubulesdilateglomerulioccurhypertrophyandtubulesdilate(2)LM:65FobrosisandhyelinzedofglomeruliatrophyandfibrosisoftubulesatrophyandfibrosisoftubulescompensativehypertrophycompensativehypertrophyofnephronandtubulesdilateofnephronandtubulesdilateaninflammatoryinfiltrationinstromaaninflammatoryinfiltrationinstromaFobrosis and hyelinzed of glom66泌尿系统疾病英文课件672.Clinical-pathologicalcorrelationChronicnephritissyndromeChronicnephritissyndrome(1)Renalfailure:azotemia(1)Renalfailure:azotemiauremiauremia(2)Hypertension(2)Hypertension(3)Proteinureaandedemaarenotsevere(3)Proteinureaandedemaarenotsevere(4)Polyuriaandnocturia(4)Polyuriaandnocturiarenin2.Clinical-pathological corre683.ResultPrognosisisverybad,thedeathcausesare:Prognosisisverybad,thedeathcausesare:(1)uremia(1)uremia(2)Hypertensionalheartdiseaseandcerebral(2)Hypertensionalheartdiseaseandcerebralhemorrhagehemorrhage(3)Infection(3)Infection3.Result Prognosis is very ba69VIIIgANephropathyIgANephropathy(BergerDisease):isthemostIgANephropathy(BergerDisease):monglomerulardisease.PresenceofprominentIgAdepositsinthemesangialPresenceofprominentIgAdepositsinthemesangialregions.Dxbyimmunocytochemicaltechniques.regions.Dxbyimmunocytochemicaltechniques.FrequentcauseofrecurrentgrossormicroscopicFrequentcauseofrecurrentgrossormicroscopichematuria,nephroticsyndromemaybepresent.hematuria,nephroticsyndromemaybepresent.Affectchildrenandyoungadults,.Affectchildrenandyoungadults,.Associatedwithglutenenteropathy,liverdisease.Associatedwithglutenenteropathy,liverdisease.VII IgA NephropathyIgA Nephrop70Slide 21.39IgA depositionSlide 21.39IgA deposition71VIIIFocalSegmentalGlomerulosclerosis(FSG):Sclerosisofsomeglomeruli;portionsofcapillarySclerosisofsomeglomeruli;portionsofcapillaryinvolved.Clinicallyshownephroticsyndromeorinvolved.Clinicallyshownephroticsyndromeorheavyproteinuria.Idiopathicrespondspoorlytoheavyproteinuria.Idiopathicrespondspoorlytosteroidsandprogresstochronicrenalfailure.steroidsandprogresstochronicrenalfailure.Causes:associatedwithHIV,drugabuse,sicklecellCauses:associatedwithHIV,drugabuse,sicklecelldisease,IgAnephropathy,certaininheriteddiseasedisease,IgAnephropathy,certaininheriteddiseaseandasprimarydisease,idiopathic.andasprimarydisease,idiopathic.VIII Focal Segmental Glomerulo72Sclerosisofsomeglomeruli;portionsofcapillaryinvolved.Sclerosis of some glomeruli;p73Section3PyelonephritisA.Definition:A.Definition:PyelonephritisisasuppurativeinflammationofPyelonephritisisasuppurativeinflammationofrenalpelvis,renalstromaandrenaltubes,itisrenalpelvis,renalstromaandrenaltubes,itiscausedbypyogenicbactericinfectiondirectlycausedbypyogenicbactericinfectiondirectlyNotirritabilityNotirritabilitySection 3 Pyelonephritis A.De74B.EtiologyandpathogenesisB.Etiologyandpathogenesis.Etiology:colonbacilli(60-80%).Etiology:colonbacilli(60-80%)proteusproteusstaphylococcietcstaphylococcietcAges:child-bearingagefemalesandinfantsAges:child-bearingagefemalesandinfantsfrequently,female:male=910:1frequently,female:male=910:1Inclinic:highfever,achingpaininthewaist,Inclinic:highfever,achingpaininthewaist,hematuria,pyuria.hematuria,pyuria.irritation sign of bladder:irritation sign of bladder:urinaryfrequency,urinaryfrequency,urgency,ururgency,urodyniaodynia.uremiarenalfailureuremiarenalfailureratio,B.Etiology and pathogenesis 75.Infectivepath.Infectivepath1.Ascendinginfection:(urethrainfection,mainpath)1.Ascendinginfection:(urethrainfection,mainpath)urethraurethrabladderbladderureterureterrenalpelvisrenalpelvis renalrenalstromaandrenaltubules(glimerulusnotaffected).stromaandrenaltubules(glimerulusnotaffected).Organism:colonbacilli,womenaffectmoreeasilyOrganism:colonbacilli,womenaffectmoreeasilyonesideki