thrombosis-200612182626.pdf in all patients

Education

1. IkramUllah
M.PhilMLSc

2. Thrombosis
Thrombosis
Formationofasolidorasemisolidmassfromthe
constituentsofbloodwithinvascularsystem
Thrombus
Anaggregationofbloodfactorsprimarilyplateletsand
fibrinwithentrapmentofcellularelements,frequently
causingvascularobstructionatthepointofits
formation.

3. Three primary abnormalities that lead to thrombus
formation (called Virchow’s triad):

4. Endothelial Injury
Endothelialinjuryisanimportantcauseofthrombosis,
particularlyintheheartandthearteries
Formationofthrombiinthecardiacchambersaftermyocardial
infarction
Overulceratedplaquesinatheroscleroticarteries,oratsitesof
traumaticorinflammatoryvascularinjury
Dysfunctionalendotheliumelaboratesgreateramountsof
procoagulantfactorsandsynthesizeslesseramountsof
anticoagulantmolecules.
Hypertension,turbulentbloodflow,bacterialproducts,
radiationinjury.

5. Abnormal Blood Flow
Turbulencecontributestoarterialandcardiacthrombosis
bycausingendothelialinjuryordysfunction,aswellasby
forminglocalpocketsofstasis.
Stasisisamajorfactorinthedevelopmentofvenous
thrombi
Stasisandturbulentbloodflowbothpromoteendothelial
cellactivationandenhancedprocoagulantactivity
Stasisallowsplateletsandleukocytestocomeintocontact
withtheendotheliumwhentheflowissluggish
Stasisalsoslowsthewashoutofactivatedclottingfactors
andimpedestheinflowofclottingfactorinhibitors

7. Turbulentandstaticbloodflowcontributetothrombosis
inanumberofclinicalsettings
Abnormalaorticandarterialdilationscalledaneurysms
createlocalstasisandconsequentlyafertilesitefor
thrombosis
Ulceratedatheroscleroticplaques
Mitralvalvestenosisresultsinleftatrialdilation
Hyperviscositysyndromesincreaseresistancetoflow
Deformedredcellsinsicklecellanemiacausevascular
occlusions

8. Hypercoagulability
Itislooselydefinedasanyalterationofthecoagulation
pathwaysthatpredisposesaffectedpersonstothrombosis
Hypercoagulabilitycontributesinfrequentlytoarterialor
intracardiacthrombosisbutisanimportantunderlying
riskfactorforvenousthrombosis
Primary(inherited)hypercoagulabilitymostofteniscaused
bymutationsinthefactorVandprothrombingenes
Secondary(acquired)hypercoagulabilityisseeninmany
settings
Cardiacfailure,stasisorvascularinjury,oralcontraceptive
useandthehyperestrogenicstateofpregnancy

10. Arterialorcardiacthrombitypicallyariseatsitesof
endothelialinjuryorturbulence
Venousthrombicharacteristicallyoccuratsitesof
stasis
Thrombioccurringinheartchambersorintheaortic
lumenaredesignatedmuralthrombi
Arterialthrombiaretypicallyrelativelyrichin
platelets,astheprocessesunderlyingtheir
developmentleadtoplateletactivation

12. Venousthrombi(phlebothrombosis)frequently
propagatesomedistancetowardtheheart,forminga
longcastwithinthevessellumenthatispronetogive
risetoemboli
Thrombionheartvalvesarecalledvegetations
Bacterialorfungalblood-borneinfectionscancause
valvedamage,leadingtothedevelopmentoflarge
thromboticmasses
Sterilevegetationsalsocandeveloponnoninfected
valvesinhypercoagulablestates

13. Fate of the Thrombus
Propagation
Embolization
Dissolution
Organization
Recanalization

14. Thrombiaresignificantbecausetheycauseobstructionof
arteriesandveinsandmaygiverisetoemboli.
VenousThrombosis(Phlebothrombosis)
Mostvenousthrombioccurineitherthesuperficialorthe
deepveinsoftheleg.
Lower-extremityDVTsareassociatedwithstasisand
hypercoagulablestates
Commonpredisposingfactorsincludecongestiveheart
failure,bedrestandimmobilization
Trauma,surgery,andburnsnotonlyimmobilizeapatient
butarealsoassociatedwithvascularinjury,procoagulant
release,increasedhepaticsynthesisofcoagulationfactors,
andreducedt-PAproduction

17. Disseminated Intravascular Coagulation
Disseminatedintravascularcoagulation(DIC)isthe
suddenorinsidiousonsetofwidespreadthrombosiswithin
themicrocirculation
Itmaybeseenindisordersrangingfromobstetric
complicationstoadvancedmalignancy
Thethrombiaregenerallymicroscopicinsize,yetso
numerousastooftencausecirculatoryinsufficiency,
particularlyinthebrain,lungs,heart,andkidneys
Thewidespreadmicrovascularthrombosisconsumes
plateletsandcoagulationproteins(consumption
coagulopathy),andatthesametime,fibrinolytic
mechanismsareactivated