血流动力学紊乱病理课件.ppt

Chapter3 HaemodynamicDisorders DepartmentofPathologySchoolofBasicMedicalSciencesSouthernMedicalUniversityDingYanqing Section1Hyperemia Congestion Definition Increasedbloodinanareacomparedtonormal normal ischemia hyperemia congestion Hyperemia Hyperemiaisanactiveprocessresultingfromaugmentedtissueinflowduetoarteriolardilation It salwaysaphysiologicalstateorisgoodforbody e g skeletalmuscleduringexercise instomachrepletewithfood andinflammation Pathologicalchanges Gross Theaffectedtissueareredder warm swelling HyperemiainPneumonia Hyperemia Infection Pneumonia Pathologicalchanges microscope Congestionisapassiveprocessresultingfromimpairedoutflowfromatissue Systemiccongestion inheartfailure Localcongestion isolatedvenousobstruction Congestion Gross Theaffectedtissueareblue redcolor cyanosis edema hemorrhageanddegenerationordeathofparenchyma Congestionandedemaarecommonlyoccurtogether Pathologicalchanges Localincreasedvolumeofbloodinaparticulartissue Longstanding chronic congestionChronichypoxialeadstodegeneration death fibrosis Capillaryruptureleadstoaccumulationofredcelldebrisinthemacrophages Congestionofcapillarybed edema ChronicHypoxia CapillaryRupture Majororgansaffected SubcutaneoustissuesOrgansLiverSpleenLungCavitiesHydrothoraxHydropericardiumAscites Pulmonarycongestion Causes leftheartfailure Etiologyofheartfailure includesmyocardialdamageassociatedwithvalvular coronaryarterial orintrinsicmyocardialinjury Othercauses includebloodlossandperipheralvasodilatation shock pathologicalchanges AcutepulmonarycongestionAlveolarcapillariesfilledwithbloodMaybeassociatedseptaledema intra alveolarhemorrhage Acutepulmonarycongestion Heavywetlungs Deepred Oozebloodyfluidonsectioning deeperred Acutepulmonarycongestion FoamyfluideffusionOozebloodyfluidonsectioning Acutepulmonarycongestion Alveolarcapillariesfilledwithblood intra alveolaredemafluid Acutepulmonarycongestion DilatedbloodvesselscontainingabundantRBC s Protein richedemafluidmayalsobepresent pulmonaryedema intra alverolarhemorrhage chronicpulmonarycongestionSeptathickensandfibrosedAlveolarspacescontainhaemosiderinladenmacrophages HeartFailureCellsGross enlarge heavy firmdarkred fixedbyformalin orrustydiscoloration Chroniccongestionoflung Theseptabecamethickenedandfibrotic ScatteredRBC smaybefoundinthealveoli Hemosiderin ladenmacrophages heartfailurecells inthealveoli congestedcapillariesinalveolarseptum Hemosiderin ladenmacrophages Congestionandfibrousthickeningofalveolarseptum Livercongestion Causes rightheartfailureAnydiseasethatresultsinrightheartfailurecancausechronicpassivecongestionoftheliver ChronicPassiveCongestion Rightheartfailureresultsindelayedemptyingofthegreatveinsandretentionofbloodprimarilyinthecentralveinsoftheliver Thisresultsindilatationofcentralveinsandpoolingofbloodinthesinusoidstowardsthecenteroftheliverlobule Pathologicalchanges AcutelivercongestionCentralvein sinusoids distendedwithbloodCentralhepatocytedegeneration ChroniclivercongestionGross centralregionsredbrownanddepressed surroundinguncongestedliver nutmegliverMicro centrilobularnecrosiswithperiportalfattychangeDeadcellsreplacedbyfibrosis cardiaccirrhosis Hepaticcongestion Nutmegliver Causes rightheartfailure slightlyenlarged capsuleistenseandsmooth coloraredarkredandyellow somewhatsoft Nutmegliver oncutsurface itresemblesabisectednutmeg Howisthenutmeg likeapprearanceformed Nutmeg likeappearanceoncutsectionisproducedbyacombinationofdilated congestedcentralveinsandthesurroundingbrownish yellow oftenfattylivercells Chroniclivercongestion Dilatedofthecentralveinfullofblood Congestionofthesinusoidsinthecentralpartofthehepaticlobular Atrophyofhepetocytesofthecentralzoneoflobule Fattydegenerationinhepatocytesinmidzoneoflobule Sometimes therearenecrosisandhemorrhageinthecentrallabular necrosisofthecentralzoneoftheliverlobular necrosis summary Definition Increasedbloodinanareacomparedtonormal Hyperemiaisanactiveprocessresultingfromaugmentedtissueinflowduetoarteriolardilation Congestionisapassiveprocessresultingfromimpairedoutflowfromatissue Majororgansaffectedofcongestionarelungandliver Pathologicalchanges Theaffectedtissueareblue redcolor cyanosis edema hemorrhageanddegenerationordeathofparenchyma Section3 HaemodynamicDisorders THROMBOSIS Thrombosis Definition Thrombosisisthepathologicformationofasolidmass bloodclot fromtheconstituentsofbloodwithinthenon interruptedheartorvascularsysteminalivingorganism Thrombus Themassitselfistermedthrombus Hemostasis Thrombosis Hemostasisisthenormal rapidformationofalocalized plug atthesiteofvascularinjury Normal bloodflowswithoutclottingInjury bloodclotsThisworksduetoaconstantinteractionbetweenthevascularwall plateletsandthecoagulationcascade Normalendothelium Endothelialcellsmodulateseveralaspectsofnormalhemostasis Thebalancebetweenendothelialanti andprothromboticactivitiesdetermineswhetherthrombusformation propagation ordissolutionoccurs AntithromboticPropertiesAntiplateletAnticoagulantFibrinolyticeffectsProthromboticPropertiesPlateleteffectsProcoagulantAntifibrinolytic PLATELETS Plateletsplayacriticalroleinnormalhemostasis Aftervascularinjury plateletsencounterECMconstituentsandadditionalproteins vWFbeingcritical Uponcontactwiththeseproteins plateletsundergothreereactions 1 adhesionandshapechange 2 secretion releasereaction 3 aggregationSequenceofplateletevents Subendothelium Plateletadhesionandaggregation Cited RobbinsBasicPathology 1 EndothelialInjury Thisisadominantinfluence sinceendotheliallossbyitselfcanleadtothrombosis Itisparticularlyimportantforthrombusformationoccurringintheheartorinthearterialcirculation PlateletAggregation EndothelialinjuryexposestheunderlyingbasementmembraneECM plateletsadheretotheECMandbecomeactivatedbybindingtovWFthroughGpIbplateletreceptors Uponactivation plateletssecretegranuleproductsthatincludecalciumandADP ActivatedplateletsalsosynthesizeTXA2 Activatedplateletsexposephospholipidcomplexesthatprovideanimportantsurfaceforcoagulation proteinactivation ReleasedADPstimulatesformationofaprimaryhemostaticplugbyactivatingplateletGpIIb IIIareceptorsthatinturnfacilitatefibrinogenbindingandcross linking Theformationofthedefinitivesecondaryhemostaticplugrequirestheactivationofthrombintocleavefibrinogenandformpolymerizedfibrinviathecoagulationcascade COAGULATIONCASCADE Proenzymes Enzymes ThrombinformationFibrinogen FibrinFibrinolyticcascade PlasminFibrin FDP CoagulationFactors Coagulationoccursviathesequentialenzymaticconversionofacascadeofcirculatingandlocallysynthesizedproteins Tissuefactorelaboratedatsitesofinjuryisthemostimportantinitiatorofthecoagulationcascade atthefinalstageofcoagulation thrombinconvertsfibrinogenintoinsolublefibrin whichhelpstoformthedefinitivehemostaticplug Coagulationisnormallyconstrainedtositesofvascularinjuryby 1 Limitingenzymaticactivationtophospholipidcomplexesprovidedbyactivatedplatelets 2 Naturalanticoagulantselaboratedatsitesofendothelialinjuryorduringactivationofthecoagulationcascade3 InductionoffibrinolyticpathwaysinvolvingplasminthroughtheactivitiesofvariousPAs Factorsinthrombosis ThreemajorinfluencespredisposetothrombosisEndothelialdamageAlterationsinnormalbloodflowHypercoagulability Virchowtriadinthrombosis injuretoendothelium Injurytoendotheliumleadto ExposessubendothelialECMLeadstoadhesionofplateletsReleaseoftissuefactorLocaldepletionofPGI2andplasminogenactivators Commonplaceofinjuretoendothelium SitesofmyocardialinfarctionUlcerplaquesofatherosclerosisCardiacsurgeryInfectionsofmyocardiumInflammatoryorprostheticvalves Dysfunctionalendothelium Note endotheliumneednotbedenudedorphysicallydisruptedtocontributetothedevelopmentofthrombosis anyperturbationinthedynamicbalanceoftheprothromboticandantithromboticactivitiesofendotheliumcaninfluencelocalclottingeventsSignificantendothelialdysfunction Hypertension Haemodynamicstress TurbulentflowoverscarredvalvesBacterialendotoxinsEvenrelativelysubtleinfluences e g homocystinuria hypercholesterolemia radiation orproductsabsorbedfromcigarettesmoke 2 ALTERATIONINNORMALBLOODFLOW Normalaxialflowofblood LAMINARFLOWTurbulence arterialandcardiacthrombiStasis venousthrombi schematicdiagramoflaminarflow axialflow vesselwall ALTERATIONINNORMALBLOODFLOW disruptedlaminarflowbringsplateletsintocontactwithendotheliumpreventsdilutionbyfreshflowofbloodandhepaticclearanceofactivatedcoagulationfactorsretardsinflowofinhibitorsofclottingfactorsPromotesendothelialcellactivation Turbulenceandstasisleadtothrombosis clinicalsettings ulceratedatheroscleroticplaques aneurysms myocardialinfarction healedrheumaticmitralstenosis atrialfibrillationandarrhythmias sicklecellanaemia 3 Hypercoagulability generallycontributeslessfrequentlytothromboticstatesbutisneverthelessanimportantcomponentintheequation Hypercoagulablestates Primary Genetic CommonMutationinfactorVgene factorVLeiden MutationinprothrombingeneMutationinmethyltetrahydrofolategeneRareAntithrombinIIIdeficiencyProteinCdeficiencyProteinSdeficiencyVeryrareFibrinolysisdefects Secondary Acquired HighriskforthrombosisProlongedbedrestorimmobilizationMyocardialinfarctionAtrialfibrillationTissuedamageCancerProstheticcardiacvalvesDICHeparin inducedthrombocytopeniaAntiphospholipidantibodysyndromeLowerriskforthrombosisCardiomyopathyNephroticsyndromeHyperestrogenicstates pregnancy OralcontraceptiveuseSicklecellanemiaSmoking CanoccuranywhereintheCVSCardiacchambersValvecuspsArteriesVeinsCapillaries Thesizeandshapeofathrombusdependonthesiteoforiginandthecause Anareaofattachmenttounderlyingvesselorheartwall TypesandMorphologyofthrombus ARTERIALTHROMBI Atsitesofturbulence damagedendotheliumUsuallyocclusive Growinretrogradefashionfrompointofattachment Site orderoffrequency Coronary Cerebral FemoralSuperimposedondamagedendotheliumFirmlyadherenttoinjuredarterialwallGraywhitefriable tangledmassofplateletsandfibrin RBCsanddegeneratingWBCs Thrombusincoronaryartery Thrombusincoronaryartery MixedThrombus Mass afriablemeshwork ofplateletsandfibrin RBCsanddegeneratingWBCs linesofZahn Thrombi mixed apparenceslaminationscalledlinesofZahnthatingrossly andmicroscopically theserepresentpaleplateletandfibrinlayersalternatingwithdarkererythrocyte richlayers Suchlinesaresignificantonlyinthattheyrepresentthrombosisinthesettingofflowingblood theirpresencecanthereforepotentiallydistinguishantemortemthrombosisfromtheblandnonlaminatedclotsthatoccurinthepostmortemstate Layering paleplateletandfibrinlayers darkererythrocyte richlayers muralthrombi Occurringinheartchambersorintheaorticlumen theyusuallyadheretothewalloftheunderlyingstructure 1 Abnormalmyocardialcontraction e g arrhythmias dilatedcardiomyopathy ormyocardialinfarction 2 Endomyocardialinjury e g myocarditis cathetertrauma 3 ulceratedatheroscleroticplaquesandaneurysmaldilation MuralThrombus CardiacMuralThrombus Laminatedthrombusinadilatedabdominalaorticaneurysm abdominalaorta VENOUSTHROMBI Phlebothrombosis AtsitesofstasisAlmostinvariablyocclusiveExtendinthedirectionofbloodflowOftencreatesalongcastofveinlumenMoreRBCs hencecalledred stasisthrombiMostcommonsite veinsoflowerextremities 90 Lesscommonsites upperextremities periprostaticplexus ovarianandperiuterineveins Red stasisthrombus Constitution largenumberserythrocytes platelets fibrin Location venoussystem attheendpartofvenousthrombus Gross darkred moist elastic fresh VEGETATIONS ThromboticmassesonvalvesarecalledvegetationsInfectiveendocarditisNon bacterialthromboticendocarditisLibman Sacksendocarditis SLE Vegetations Palethrombus Constitution fibrin platelets fewentrappederythrocytes Location arteria cardiacvalvesandtheinitiativepartofvenousthrombus Morphologicalchanges gray white friable firmlyadherenttothewall Vegetationsonthemitralvalveinrheumaticendocarditis Notethesmallpinkvegetationsalongthelineofclosure Thesethrombiaremadeofplatelets leftatrium leftventricle mitralvalve vegetations vegetations Palethrombus A Thehistologyconsistsofhomogeneoussheetsoffibrinwithoutanyinflammatoryresponse B Organizationofthethrombusbyaningrowthoffibroblastsmaybeseen Fibrinthrombus Microthrombus Constitution fibrinLocation micro circulationinDIC Especiallyincapillariesofkidney lung brainandliver FATEOFTHROMBI PropagationEmbolizationDissolutionOrganisationandRecanalisation ThrombusPropagatedintotheInferiorVenaCava Organisation Recanalisation Organizationandrecanalizationofthrombus Mixtureofredbloodcells plateletsandfibrinOverafewdayscapillaries smoothmusclecellsandfibroblastsgrowintotheembolusfromthevesselwallSurfaceoftheemboluswillbecomeendothelializedRecanalizationmayoccur EFFECTSOFTHROMBUS Arterial Atherosclerosisisamajorinitiator infarctionofdependentparts myocardialinfarction cerebralinfarctionVenous associatedwithstasis infarctionrareduetocollateralbypasschannels localpainanddistaledema embolisationtolungs causingdeath ARTERIALv sVENOUSTHROMBUS Atsitesofturbulence damagedendotheliumUsuallyocclusiveGrowinretrogradefashionfrompointofattachmentSite orderoffrequency Coronary Cerebral FemoralGraywhitefriable tangledmassofplateletsandfibrin RBCsanddegeneratingWBCs AtsitesofstasisAlmostinvariablyocclusiveExtendinthedirectionofbloodflowMostcommon veinsoflowerextremitiesLesscommon upperextremities periprostaticplexus ovarianandperiuterineveinsMoreRBCs hencecalledred stasisthrombi SUMMARY Thrombosis 1 ThrombusdevelopmentdependsontherelativecontributionofthecomponentsofVirchow striad Endothelialinjury Abnormalbloodflow Hypercoagulability primaryorsecondary 2 Thrombimaypropagate resolve organization orembolize 3 Thrombosiscausestissueinjurybylocalvascularocclusionorbydistalembolization HaemodynamicDisorders Section4embolism Definition Detached intravascular solid liquidorgaseousmassthatiscarriedbythebloodtoasitedistantfromitspointoforigin Typesofemboli Thromboembolism 99 Bubblesofair nitrogengas decompressionsickness DropletsoffatBonemarrowAtheromatous cholesterol AmnioticfluidTumorfragmentsForeignbodies suchasbullets Gasembolism Fatembolism Thromboembolism Anembolismisusuallythromboticunlessotherwisespecifiedhencethetermthromboembolism Ischemicnecrosis infarction ofdownstreamtissue Embolimaylodgeanywhereinthevasculartree theclinicaloutcomesarebestunderstoodfromthestandpointofwhetherembolilodgeinthepulmonaryorsystemiccirculations Theconsequencesofthromboembolism Originofemboli Origininsystemicveinandrightheart pulmonaryembolism infarction death ornoanyclinicalsymptom Origininleftheartandsystemicarteries distalsystemicarteriesembolism infarction Pulmonaryembolism TheembolioriginateinsystemicveinsandrightheartOver95 ofpulmonarythrombicomefromthedeeplegveinabovethelevelofthekneeThemostseriousformofthromboembolism Clinicaleffect Majority clinicallysilent 60 80 undergoorganizationIf 60 ofpulmonarycirculationisobstructed SUDDENDEATH rightheartfailure RHF MainpulmonarytrunkSaddleemboliSmallerbranchesSmallmultipleemboli PULMONARYTHROMBOEMBOLISM IfMainpulmonarytrunk massiveemboli suddendeathIfmediumsizedvessels usuallycongestion haemorrhage noinfarctionIfsmallend infarctionMultipleemboli pulmonaryhypertensionwithrightventricularfailure Pulmonarythromboembolism CausesofPulmonarythromboembolismcardiacdiseasescancerprolongedimmobilizationHypercoagulablestates ClinicalsignificancedependsonExtentofemboliNumberofemboliCirculatorystate FATEOFEMBOLImayresolvebyfibrinolysisunresolvedpulmonaryhypertensionpulmonaryvascularsclerosischroniccorpulmonale30 chanceofdevelopingsecondemboli Prophylaxis ElevationElasticbandageEarlyambulationEmbolectomyUMBRELLAfilterininferiorvenacavaThrombolysisfollowedbyanticoagulationwithmonitoring SYSTEMICEMBOLISM Embolisminarterialcirculation SOURCE 80 85 fromintracardiacmuralthrombi2 3areassociatedwithleftventricularwallinfarcts1 4areassociatedwithdilatedleftatria e g mitralvalvedisease 5 cardiomyopathy SYSTEMICEMBOLISM OTHERLESSCOMMONSOURCESAtheroscleroticplaquesAorticaneurysmsInfectiveendocarditisValvularheartdiseasesParadoxicalembolifromvenousthrombiUNKNOWNSOURCES10 15 PARADOXICALEMBOLISM dependontissue svulnerabilitytoischemia caliberoftheoccludedvessel andthecollateralbloodsupply ingeneral causesinfarctionoftheaffectedtissues majorsitesforarteriolarembolization Lowerextremities70 75 gangrene Brain10 Viscera intestines kidneys andspleen 10 Upperlimb7 8 Theconsequencesofembolization Clinicalmanifestations siteandsizeofemboliisimportantfemoralartery gangrenecerebralartery MCA deathinhrs daysTreatment anticoagulantsembolectomy FATEMBOLISM Causes FractureoflongbonesSignificantsofttissuetraumaDiabetesPancreatitis ClinicalManifestations by1to3days PulmonaryInsufficiency Anaemia ThrombocytopeniaConjunctivalpetechiaeMentalconfusionGlobulesoffatinurine FATEMBOLISM MechanismofinjuryMechanical microemboliofneutralfatblockthepulmonaryandcerebralmicrovasculatureBiochemicalinjurytomicrovessels Releaseoffreefattyacidsfromthefatglobules toxicendothelialinjuryandactivationofcoagulationsystem FATEMBOLISM MicroscopicDemonstrationoffatwithfrozensectionsandfatstaining Alcoholinparaffinsectiondissolvesfat Fatstains Oilred O Sudanred Fatembolism sudanredstaining AIRORGASEMBOLISMBubblesofairorgasobstructingcirculationDuringobstetricproceduresChestwallinjury 100cctoproduceclinicaleffectTissuedamage typesAcuteChronic decompressiondiseaseAcute Bends obstructionofsmallvesselsaroundjointsandskeletalmusclescausepatientstodoubleupwithpain Chokes respiratoryandbraininvolvementsuddendeath Caissondiseaseordecompressionsickness atrisk scubadivers workersinoffshoredrillingplatforms underwatertunnelingsystemworkers Whenairembolismissuspectedatautopsyorgansshouldbeopenedunderwatertodetectescapinggas AMNIOTICFLUIDEMBOLISM RarecomplicationoflaborMajorcauseofmaternalmortality86 mortality AMNIOTICFLUIDEMBOLISM Cause Tearinplacentalmembraneorruptureofuterine cervicalveinsleadingtoinfusionofamnioticfluidorfetaltissueintothematernalcirculation CLINICALFEATURES DeepcyanosishypotensiveshockGeneralizedconvulsionsComaExcessivebleedingfrombirthcanalDIC duetoreleaseofthromboplasticsubstances AMNIOTICFLUIDEMBOLISM Thepulmonarymicrocirculationmaycontain squamousepitheliumoffetalskin lanugohair fatfromvernixcaseosa mucinfromfetalrespiratoryorgastrointestinal