病理病生8充血ischemia缺血

DISTURBANCEOFLOCALCIRCULATIONLocalcirculatorychangesofblood changesofbloodcharacterandcontentsofvessel:changesofvascularIncreasedbloodinanareacomparedtoactive(arterial)passive(venous)hyperemia, ACTIVEHyperemiaisanactiveprocessresultingfromaugmentedtissueinflowduetoarteriolardilation (原因sympatheticneurogenicmechanismsreleaseof‘vasoactive’substancesarterialandarteriolarphysiologicalpathological–reactivehyperemia反應(yīng)性(減壓后)PathologicalGross肉眼redinusuallyPathologicalMicroscopically(鏡下–dilatationofthearteriolesandcapillariesSequelsofActive(結(jié)局temporaryreactionofvessels,resumedoncethecausesare(congestion淤血CongestionisapassiveprocessresultingimpairedvenousreturnfromaCAUSESOFvenous pressureontheveincardiacfailure–organsortissues–turnblue-redcolor–dilatationofsmallveinsandcapillariesfilledwithbloodSequelsofCongestionslowingdownofthebloodhypoxia(缺氧reductionofnutritionaccumulationofmetabolicatrophy,degenerationandnecrosisofcellshyperplasiaofconnectiveincreaseofcapillariesincreaseofcapillarieshydrostaticpressureofsmallveinsandcapillariesincreased (hemosiderin-ladenmacrophage含鐵血黃素細(xì)胞pulmonarycongestionbrown congestionofliver→cardiaccirrhosis/congestiveLocalincreasedvolumeofbloodinaparticular1DuetoarteriolarDuetoimpairedvenous2Activee.g.skeletalmuscleduringexercise,InflammationPassiveprocessSystemice.g.cardiacfailureLocale.g.venousobstructionRedChronicPulmonaryHeartfailure Someofthecapillariesruptureanderythrocytestoescape.Theerythrocytesactasforeignbodiesandattractlargephagocyteswhichenterthealveoliandingestthem.ThesemacrophagesfilledwithfragmentsoferythrocytesandhemosiderinChronicCongestionofDilatedofthecentralveinfullofCongestionofthesinusoidsinthecentralpartofthehepaticAtrophyofhepatocytesofthecentralzoneoflobuleFattydegenerationinhepatocytesinmidzoneoflobuleSometimes,therearenecrosisandhemorrhageinthecentralThrombosisisthepathologicformationofasolidmass（bloodclot）fromtheconstituentsofbloodwithinthenon-interruptedheartorvascularsysteminalivingorganism.Thrombus—ThemassitselfistermedCausesand–inhibitionofplateletserveasabarrierbetweenplateletsandsubendothelialstructuressecreteNO,PGI2(prostacyclin),synthesizetissueplasminogenactivator(t-PA) anticoagulant-bindingandinhibitionofthrombinsecreteheparin-likemoleculesandthrombomodulinCausesandEndothelialinjurypromotes–subendothelialECMexposedto–synthesizevonWillebransfactorCausesandEndothelialinjurypromotes–t-PAactivityisblockedbyplasminogenactivatorinhibitor–plateletsbecomesecretionandreleasereaction(vWaggregation(thromboxaneA2,CausesandEndothelialinjurypromotes–tissuefactorfurthertriggerextrinsicbloodcoagulationCausesandCommonplaceofinjureto–myocardial–ulcerplaquesof–cardiac–infectionsof–inflammatoryorprostheticSUMMARY:AntithromboticFibrinolyticeffectsProthromboticPropertiesPlateleteffectsCausesandChangesinbloodslowingofthebloodTurbulenceandstasisleadto-healedrheumaticmitral-atrialfibrillationandCausesandChangesintheconstitutionoftheMutationinfactorVgene/prothrombin/methyltetrahydrofolategeneAntithrombinIII/ProteinC/SdeficiencyVeryrareCausesandChangesintheconstitutionoftheSecondary(Acquired)HighriskforthrombosisProlongedbedrestorimmobilization;MyocardialInfarction;Atrialfibrillation;Tissuedamage;Cancer;Prostheticcardiacvalves;DIC;Heparin-inducedthrombocytopenia;AntiphospholipidantibodyLowerriskforthrombosisCardiomyopathy;Nephroticsyndrome;Hyperestrogenicstates(pregnancy)Oralcontraceptiveuse;Sicklecellanemia;CausesandChangesintheconstitutionofthe andprothrombinchangesinplateletVirchowtriadinWhite gray-white,friable,firmlyadherenttothewall,Platelets,fewfibrin,fewentrappederythrocytes.Whitethrombicardiacvalves:thromboticmassesonvalvesarecalledvegetationsInfectiveNon-bacterialthromboticLibman-SacksendocarditisinitiativepartofvenousMixed(laminated)WhitemixedwithPlatelets,fibrin,erythrocytesandleukocytesatthemiddlepartofvenousleftatrium:ball-shapedaneurysms:muralRedItappearsasfibrinstrandsentanglingtheerythrocytesRedattheendpartofvenousdarkred,moist,elasticMorphologyofFibrin(minute,hyaline)occurinDICandcomposedmostlyoffibrinFateofthrombi Advantagehemostasis–ObstructionofarteriesandObstructionofarteriesandPartialobstructinofanCompleteobsturctionofartery,andnoeffective

Venous

Effectsof–Valvular–HemorrhagicDetached,intravascular,solid,liquidorgaseousmassthatiscarriedbythebloodtoasitedistantfromitspointoforiginTypesof–thrombus、bacterialmass、tumor–bubblesofair/nitrogen–dropletsoffat、amnioticSourceand終點(diǎn)）ofKeepinginthesamedirectionwiththebloodstreamEmboliformedinleftheartchamberandarterialsystemembolismofbranchingofsystemicEmboliofvenoussystemandrightheartchamberembolismofpulmonaryarterialEmboliofportalsystemembolismofportalParadoxicalembolism–EmboliofvenoussystemembolismofarterialsystemRetrogradeembolism–Emboliofinferiorvenacavaembolismofbranchingofinferiorvenacava（下腔靜脈）–PulmonaryembolismArisefromthrombiwithintheofthelowerMuchmorerarelyariseinpelvicveins,therightheart–ArterialArisefrommuralthrombiintheleftheart.Lessoftenarisefromthrombiinanaorticaneurysmorfromotherlargeartery.Fat–FractureoflongbonescontainingfattymarrowFat–Ifasufficientquantityreachesthe respiratory–SomeofthefatpassesthroughthepulmonarycapillariescentralnervoussystemGas–Caissondisease沉箱病ordecompressionsickness減壓病Appearindeep-sea-NitrogenisoflowsolubilityandpersistsasminutebubblesGas–AirItreferstoinvasionoflargequantityofairintocirculationAmnioticfluid–Appearinolder,multiparousAmnioticfluid–Thefindingsinthepulmonaryarteriolesandcapillariesatautopsycompriseepithelialsquamesfromfetalskin,lanugohair,mucinAninfarctisanareaofischemicnecrosiscausedbyocclusionofeitherthearterialsupplyorthevenousdrainageinaparticularCausesofSpasmof–TakeplaceinthediseasedwallofvesselTypesofAnemicinfarct–Insolidorgans,withoutbloodHemorrhagicinfarct–InloosespongyorgansdoublebloodSepticinfarctConditionsforhemorrhageHeavy–conditionsforoutflowofDouble–sourceofbloodLoose–spaceforbloodShapesofthelesion-–Infarcts