ChapterIIILocalCirculatory

DisturbanceItconsistedof:a.changeinvascularpermeabilityandintegrityhemorrhage出血,edema水腫b.disturbanceofbloodvolumecongestion充血,ischemia缺血c.changeinintrvascularcontentsthrombosis血栓,embolis栓塞

SectionIHyperemiaandCongestionHyperemiaandcongestionarealsoincreasedbloodvolumewithdilatedvesselsinanorganorpartofthebody.

IHyperemia

充血

Arterialhyperemia(activehyperemia)increasedarterialbloodtothepart.(I).Typesofhyperemia1.Physiologicalhyperemia2.Pathologicalhyperemiaa.inflammatoryhyperemiab.collateralhyperemiac.removepressureofhyperemiaIICongestion淤血Congestion(venoushyperemia,passivehyperemia)Increasedvenousbloodtothepartduetoaccumulationofbloodinthevenousvasculartree.Itmaybeeithergeneralorlocal.Generalvenouscongestionisbyfarmostimportant.(I).Cause三個原因1.pressureonthevein靜脈受壓

tumormass,ligature,tightbandage,strangulatedherniaetc.腫瘤團塊、結(jié)扎、繃帶過緊、疝絞窄2.intraluminalocclusionofthe

veinthrombosis靜脈血栓3.cardiacfailure

心力衰竭(II).ChangeandeffectofveneouscongastionChr.Veneouscogestion

Anoxiaincreaseveneouspressureparenchy-interstitialbloodmatouscelltissuevesselsatrophyfibroustissuepermeabilitydegenerationcollagenizationnecrosisofreticulinfiberscogestiveedema(cogestivesclerosis)cogestivehemorrhaga(hemosiderin)

四個后果：淤血性水腫（毛細血管流體靜壓增高）淤血性出血實質(zhì)細胞萎縮、變性壞死間質(zhì)（纖維結(jié)締組織）增生(III).Congestionofmajororgan兩個主要器官1.Chronicveneousncongestionoflungduetoleftheartfailure左心衰

usuallycausedbymitralstenosis二尖瓣狹窄duetorheumaticheartdisease.

Morphylogicalcharacteristic:Earlystage:congestivelung,edemaoflung

Alveoli;largeamountofphagocyticcellsfilledwithyellowbloodpigment(heartfailurecells心衰細胞).Latestage:browninduration肺褐色萎縮Darkbrownincolorandtoughinconsistency.browninduration肺褐色萎縮

含鐵血黃素褐色間質(zhì)增生硬化2.Chronicvenouscongestionofliver:

Occuresearlyingeneralveneouscongestion

duetorightheartfailure右心衰.Motphlogicalchracterisic:

Earlystare:Mutmegliver檳榔肝

Latestage:Cogestiveliversclerosis淤血性肝硬化

Gross:Cutsurfaceshowsamottledappearanceofdarkbrown(congested淤血centerofeachlobule)andlightyellowareas(fatty

changes脂肪變性oflivercells).LM:Centeroftheloule------distendedsinusoids,atrophicdegeneration

livercells.Peripheralpartofthelobule-----fattychangesCogestiveliversclerosis

匯管區(qū)間質(zhì)增生，小葉構(gòu)造完整SectionIIHemorrhage

Hemorrhage出血：escapeofbloodfrombloodvessel

I.ThecauseandmechanismofhemorrhageRuptureofbloodvessel破裂性出血:majorcauseistraumaordisease.RBCleakout漏出性出血:majorcauseisincreaseofpermeabilityofbloodvessel.RBCleakout:

A.damageofvascularwall血管壁內(nèi)皮細胞受損(severeinfectionintoxicationetc.)B.changeinthenumberandqualityofplatelets血小板C.disturbanceofcoagulativemechanism血液凝固性障礙II.ChangeTermsyoushouldunderstand:Internalhemorrhage內(nèi)出血:Hematocele積血:accumulationofbloodinsomaticcavitye.g.Hemothrorax胸腔積血,hemopericardium心包腔積血,hemoperitoneum腹腔積血.

Hematoma血腫:hemorrhageintothetissueformingtumorlikeswelling.Externalhemorrhage外出血:

Externalhemorrhage:Petechiahemorrhage瘀點:minutehemorrhage(pinpoint)inskin,mucusmembrane,serosalsurface.Purpura紫癜:hemorrhageupto1cminsizeinskin,mucusmembraneserosalsurface.Ecchymosis瘀斑:alargeblotchhemorrhage(lessthen1-2cmindiameter)inskin,mucusmembrane,serosalsurface.Rhinorrhagia鼻衄:nasalhemorrhageHemoptysis咯血:hemorrhageofrespectorytract.Hematemesis嘔血:hemorrhageofupperdigestivetractHematochezia便血:hemorrhageoflowerdigestivetractHematuria血尿:hemorrhageofurinarytractIII．EffectsTheeffectsofhemorrhageisdependuponthespeed,theadequacyandpartofhemorrhage.

出血速度、量、部位SectionIIIThrombosisThrombosis血栓形成:formationofasolidorsemisolidmassfromtheconstituentsofthebloodwithinthevescularsystemduringlife.活體心血管腔血液凝固血小板析出粘集形成固體質(zhì)塊Themassitselfistermedathrombus血栓.

BloodcoagulationsystemAnticoagulationsystemI.Theformingconditionand

mechanismofthrombosisTherearetwomajorcourseofthrombosis:兩個基本環(huán)節(jié)Bloodcoagulation

血液凝固Thrombocyticaggregation血小板析出和粘集Therearethreemajorfactorsinthrombusformation.三個條件TheseweredescribedoriginallybyVirchowandareasVirchow’striad.Thethreefactorsare:Endothelialinjury內(nèi)皮細胞受損Changesinthepatternofbloodflow血流狀態(tài)變化Bloodhypercoagubility血液凝固性增高(I).Endothelialinjury:

(1).Plateletadherenceandactivation:adhesionreleasereaction(ADP)aggregation(thromboxaneA2)Endothelialthrombocyticaggregationinjury(2).ExposureofcollagenfibersXII

endogenouscoagulationsystem(3).ReleasethehistofactorsVII

exogenouscoagulationsystem

Bloodcoagulation

Sothat,thethrombosisofclinicaloccursforthemostpartintheendothelialinjury.e.g.a.variousendocarditisb.endophlebitisc.atherosclerosis

d.repeatedperformofvenipuncture

(II).Changesinthepatternofbloodflow1.bloodflowslowly2.turbulance(whirlpool)3.stasisofbloodflow

血流緩慢臨床上多見于：長久臥床旳病人，如手術(shù)后，久病虛弱，心力衰竭及骨折臥床旳病人。Inveins,however,thebloodpressureislowertheninarteries,sothatthrombosisinveinsismoretheninarteries(4times).

據(jù)統(tǒng)計，發(fā)生在V內(nèi)比A內(nèi)多4倍，下肢V比上肢V多3倍，尤其是骨盆內(nèi)V及腿部背面旳深靜脈。

血流漩渦臨床上多見于：①風心二狹，左心房可產(chǎn)生渦流，尤其在擴大旳左心耳內(nèi)。②A瘤或曲張旳V內(nèi)——血液忽然流進寬闊處，產(chǎn)生血栓。③血管分岔處。④淤血時旳V瓣上。(III).Bloodhypercoagubility1.genetichypercoagubility:e.g.V-factormutantgene2.acquiredhypercoagubility:e.g.malignancy,abnormalpregnancy,severetrauma,extensiveburns,

grandoperation

II.CourseofThrombosisandTypes

ofThrombus(I).Courseofthrombosis:(II).TypesofthrombusThethrombuscanbeclassifiedinto4types:四個類型1.Whitethrombus(palethrombus)

血小板粘集為主

Usuallypresentinhighflowarea(heartvalves,ventricles,arteries)Ittendstobemural(adherenttothewallofthevesselorheart)andnon-occlusiveAttachedfriablegraymassofdegranulatedplatelets血小板andfibrin.

2.Mixedthrombus血小板粘集+血液凝固

Itusuallyshowscharacteristiclaminationswhichisproducedbypalepinklayersofplatelets血小板粘集andfibrinalternatewithdarkredlayersofRBC血液凝固層狀血栓

‘Muralthrombus’附壁血栓

Thrombusattachedtovesselwall/heartwall,non-occlusive3.Redthrombus血液凝固Resemblesbloodclots.

Usuallypresentindeepveinsof‘tail’ofextendthrombus延續(xù)性血栓.

‘Extendthrombus’composedofwhite‘head’(initialplateletfibrinnidus)attachtothevascullarwall;mixed‘body’(redandwhitethrombus);redtail(coagulatedredthrombus).4．Hyalinethrombus

(microthrombus,fibrinousthrombus)ItwidespreaddepositionoffibrinandplateletsinmicrovasculaturethroughoutthebodyItismostfrequentlyseenDIC(disseminatedintravascularcoagulation).III.Fateofthrombus(I).Malacia,lysisandabsorpation(II).Organization機化andrecanalization再通a.preventfromamotioingrowthofvascularizedconnectivetissue(granulationtissue)intothethrombuswhichbecomefirmlyattachedtothevascular-wallb.recanalization------contractionandlysisofthethrombusendothelialcellaccompaniedbygrowthofendothelialcellsfromtheadjacentintimalsurfacewithrestorationofafunctionalbloodchannel.(III).Calcificationphlebolith靜脈石,arteriolith動脈石VI.EffectsofThrombus(I).Occlusionofvascularischemia缺血,infarction梗死(II).Embolish栓塞(III).Deformityofheartvalves瓣膜變形Chronicvalvularvitiumoftheheart

(valvularstenosis,valvularinsufficiency)(IV).Widespreadhemorrhage廣泛出血DICconsumptioncoagulopathySectionIVEmbolism

Embolism:Occlusionofsomepartofcardivascularsystembyimpactionofaforeignmasstransportedtothesitethroughthebloodstream.Thisimpactionofforeignmassbeknownasembolus栓子.Theembolusmaybesolid,liquidorgaseous.Typesofemboliare(1).thromemboli,(2).fatemboli,(3).airorgasemboli,(4).amnioticfluidemboli羊水栓塞,and(5).tumoremboli,etc.I.Thewayofpropagationofembolus

1.embolusofvenoussystemandrightheartPulmonaryembolism2.embolusofarterialsystemandleftheartVascularocclusionoccurmostfrequentlyinthespleen,kidney,brainetc.3.embolusofportalsystem4.crossedembolism(paradoxicalembolism)５．retrogradeembolism

II.TypesandEffectsofEmbolism

(I).ThromboembolismThromboembolism血栓栓塞:Anembolusisamassofthrombusinthevascularsystemabletolodgeinavesselandblockitslumen.

Mostemboliarederivedfromthrombi.Over99%ofmajoremboliarederivedfromthrombi.

1.Pulmonaryembolism

Around95%ofpulmonaryembolismoccursindeepveinsofleg;themajorityoftherestoccurinpelvicveinsandaveryfewoccursinthemuralthrombusofrightheart.

Theeffectsofpulmonaryembolidependupontheirsizeandquantity.(1).Mediumandsmallembolimayoccurunnoticedandbelysedwithinthelungortheymaybecomeorganisedandcausesomepermenent.

Pulmonaryembolismissometimeaccompaniedwithvenouscongestionoflung肺淤血;theareamayevenbecomeinfarcted

(2).Largemassivethromboembiareoftenimpactedacrossthebifurcationofoneofmajorpulmonaryarteriesasa‘saddleembolus’adescriptivetermfortheirappearance.Inseverecase,itmayberesultin‘suddendeath’.

Theseareusuallylongthrombiderivedfromlegdeepveinsandhavetheshapeofthevesselsinwhicharose.

Postmortemexamination:LongthrombiretaintheappearanceofathrombuswithlinesofZahnandgranular,friable,consistency

Postmortemclotsappearanceof‘chickenfat雞脂樣andredcurrantjelly果醬樣’,glossy,andelastic彈性.

(3).Alargenumberofsmallthromboliarealsoresultinsuddendeath.

2.Systemicembolism80%ofsystemicemboliariseintheleftheart.

瓣膜贅生物Vegetationsontheheartvalvesareancommonimportantsourceofarterialemboli.(e.g.subacuteinfectiveendocarditis,SBE)Anothercommonsourceofthrombosiswithintheleftheartisthepresenceofmuralthrombus附壁血栓intheatrium(mitralstenosis二尖瓣狹窄)andmuralthrombusduetomyocardialinfarction.Therestoccurinmuralthrombusduetoatherosclerosisoraneurysm動脈粥樣硬化、動脈瘤.

Vascularocclusionsoccurmostfrequentlyinthespleen,kidney,brainetc,mayresultinformationofinfarctionoftheorganinvolved.

Moredramaticconsequencesdevelopasaresultofembolitravellingtotheintestine;thisimpactioncancausedeathofwholesectionsofsmallbowel腸梗死.

Moreseriously,ininfectiveendocarditisthevegetationsconsistofmicro-organisms,usuallybacteria,andareextremelyfriable.(maycausesepticinfarct敗血性梗死)(II).FatembolismFatembolismusuallyarisesfollowingsomeseveretraumawithfracturetolongbones長骨骨折.Fatfromthebonemarrowisreleasedintocirculationandcomestolodgeinvariousorgans.Asimilarsituationarisesinsevereburns嚴重燒傷andinextensivesofttissueinjury脂肪組織嚴重挫傷.

Thediameteroffatglobules>20μm,thecirculatingfatentersthelungandthisindicatesthatitmusttravelbywayofthevenoussystemThediameteroffatglobules<20μm,thatmanyalsoenterthesystemicarterialcirculation.(oftenbringonembolisminvesselsofbrain).Theeffectsoffatembolismdependupontheirpartandquantity.

Fatenterthecirculationinsmallquantities,theeffectsareunnoticed.Fatenterthecirculationinlargequantities(>200g),theeffectsaresevere.(maybringaboutdeathduetorightheartfailure)

病例討論：男性，42歲，因騎車不慎跌倒，右小腿腫痛，急診診療為右小腿脛腓骨骨折，長靴形石膏固定后，回家臥床休息。今后，小腿腫痛逐漸緩解，傷后二周又出現(xiàn)右下肢腫痛，去醫(yī)院復(fù)查，拆除石膏重新包扎，回去后腫脹仍無改善，并漸向大腿發(fā)展，四天后坐起吃飯時，忽然高叫一聲，心跳呼吸停止，急救無效死亡。病人忽然死亡旳原因是什么？

Ａ、肺動脈血栓栓塞Ｂ、脂肪栓塞(III).GasembolismTherearevariouscausesofemboliceventsinvolvinggas.

1.airembolism接近心臟旳大靜脈破裂Thecausesofairembolismaremainlysurgicalwhensomevesselisopentotheair.(iatrogenic)Thisalsooccursinaccidentallywhenpatientsaredisconnectedfromintravenouslinesandairenters.

Thisalsooccursinsuicideattemptswhentheneckveinsarecut.

Thevolumeofairneededtocausedeathinthisfashionisaround100ml.Thepathologicalsignsofthisconditionatautopsyincludevisiblebubblesinthevesselssuchasafrothyballofbloodandairintherightsideoftheheartoccludingoneofthevalves.

2.Decompressionsickness減壓病(caissondisease沉箱病,diver’disease潛水員病)Experiencedbydiverswhentheyaretransferredtoorapidlyfromhightolowpressureenviroments

Athighpressure,increasedvolumesofgas氮氣栓塞dissolveinthebloodandduringrapiddecompressionthesecomeoutasbubbles.

(IV).Amnioticfluidembolism

Withthevastlyincreasedpressuresintheuterusduringdelivery,andthepressureistransferredtotheamnioticfluidwhichmaybeforcedintothematernaluterineveinsTheseamnioticfluidembolitravelinthecirculationandlodgeinthelungs,causingrespiratorydistresslikeotherpulmonaryemboli

Theycanberecognisedhistologicallysincetheycontaintheshedskincellsoftheinfant.

Inthecases,itmaybecausingdeathby(1).anaphylacticshock;(2).reflexangiospasm;(3).DIC(V).Otherembolism

Otherembolicmaterialinclude:tragmentsoftumour(causingmetastases),particlesofforeignmatter.

SectionVInfarction

Infarction:Localizedareaofischemicnecrosiswithinatissueororganproducedbyocclusionofitsarterialsupplyorvenousdrainageduetothromboticorembolicocclusion.Infarctionisischaemicdeathoftissuewithinthelivingbody.Thismeansthatdeathoftissuefromothercauses,suchastoxinsortrauma,isnotinfarctionbutissimplynecrosis,whichisthegeneraltermfordeathoftissuewithinthelivingorganism.

I.TheCausesandConditionofInfarction(I).Thecausesofinfarction1.Thrombolism血栓形成themostcommoncauseofinfarction.(99%ofinfractionarecausedbythromboliceventsandalmostallaretheresultofarterialocclusion.2.Arterialembolism動脈栓塞thromboembolism,maybecauseofinfarctionofspleen,kidney,lungandbrain.3.Arteriospasm動脈痙攣4.Occlusionbypressureonthevessel血管受壓.(II).Theconditionofinfarction1.Thetypesofarterialsupplies

雙重血供Asecondbloodsupplyispresentand,althoughthearterialinflowisblocked,bloodstillenterstheorganfromthissecondsupply.Agoodexampleofthisisthelung,whichhasbothpulmonaryandbronchialarterialsupplies.

Otherexamplesareliverandforearm.2.Thesusceptibilitytoischemiaofeffectedtissues缺血敏感性Differenttissuesshowdifferingsusceptibilitytoischemia.Tissuesalsovaryinthedegreeofischemiathattheycantolerate.Nervecellstolerancetoischemiaarelowest.(3-4minutes)Cardiocytes:(20-30minutes)

Skeletalmusclesandconnectivetissuestolerancetoischemiaaremostpowerful.

II.AppearenceandTypesofInfarctionMorphologicalcharacterandtypesofinfarction1.Anemicinfarct(whiteinfarct)generallytheresultofocclusionofananatomicalorfunctionalend-arteryofasolidorgan實性器官(Thereisnopossibilityofcollateralsuppliestakingover).Suchasheart,kidney,andspleenetc.

Morphologicalcharacter:Wedgeshape

Triangularoncutsurface,withitsbasetowardthesurfaceandapexnearthesiteofocclusion.

Theevolutionofanemicinfarctare:(1).Early,mayappearred(residualbloodorvenousbackflow)(2).Subsequentlybecomepale

(lysisanddecompositionofhemoglobin)(3).laterareddemarcationzoneatthemarginofadjacentnormaltissue(infla