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Platelet
FromWikipedia,thefreeencyclopedia

Platelets,alsocalledthrombocytes(thromb+cyte,"bloodclotcell"),areacomponentofbloodwhose
function(alongwiththecoagulationfactors)istostopbleedingbyclumpingandclottingbloodvessel
injuries.[1]Plateletshavenocellnucleus:theyarefragmentsofcytoplasmthatarederivedfromthe
megakaryocytes[2]ofthebonemarrow,andthenenterthecirculation.Theseunactivatedplateletsarebiconvex
discoid(lensshaped)structures,[3][4]23mingreatestdiameter.[5]Plateletsarefoundonlyinmammals,
whereasinotheranimals(e.g.birds,amphibians)thrombocytescirculateasintactmononuclearcells.[6]

Platelets

Onastainedbloodsmear,plateletsappearasdarkpurplespots,about20%thediameterofredbloodcells.The
smearisusedtoexamineplateletsforsize,shape,qualitativenumber,andclumping.Theratioofplateletstored
bloodcellsinahealthyadultis1:10to1:20.
Themainfunctionofplateletsistocontributetohemostasis:theprocessofstoppingbleedingatthesiteof
interruptedendothelium.Theygatheratthesiteandunlesstheinterruptionisphysicallytoolarge,theyplugthe
hole.First,plateletsattachtosubstancesoutsidetheinterruptedendothelium:adhesion.Second,theychange
shape,turnonreceptorsandsecretechemicalmessengers:activation.Third,theyconnecttoeachotherthrough
receptorbridges:aggregation.[7]Formationofthisplateletplug(primaryhemostasis)isassociatedwith
activationofthecoagulationcascadewithresultantfibrindepositionandlinking(secondaryhemostasis).These
processesmayoverlap:thespectrumisfromapredominantlyplateletplug,or"whiteclot"toapredominantly
fibrinclot,or"redclot"orthemoretypicalmixture.Thefinalresultistheclot.Somewouldaddthesubsequent
clotretractionandplateletinhibitionasfourthandfifthstepstothecompletionoftheprocess[8]andstillothers
asixthstepwoundrepair.

Imagefromalightmicroscope(500)froma
Giemsastainedperipheralbloodsmearshowing
platelets(bluedots)surroundedbyredbloodcells
(pinkandcircular)
Anatomicalterminology
[editonWikidata]

Lowplateletconcentrationisthrombocytopeniaandisduetoeitherdecreasedproductionorincreaseddestruction.Elevatedplateletconcentrationis
thrombocytosisandiseithercongenital,reactive(tocytokines),orduetounregulatedproduction:oneofthemyeloproliferativeneoplasmsorcertainother
myeloidneoplasms.Adisorderofplateletfunctionisathrombocytopathy.
Normalplateletscanrespondtoanabnormalityonthevesselwallratherthantohemorrhage,resultingininappropriateplateletadhesion/activationand
thrombosis:theformationofaclotwithinanintactvessel.Thesearisebydifferentmechanismsthananormalclot.Examplesare:extendingthefibrinclotof
venousthrombosisextendinganunstableorrupturedarterialplaque,causingarterialthrombosisandmicrocirculatorythrombosis.Anarterialthrombusmay
partiallyobstructbloodflow,causingdownstreamischemiaorcompletelyobstructit,causingdownstreamtissuedeath.

Contents

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Contents
1
2
3
4
5
6
7
8

Discovery,earlyobservations,andnaming
Measurement
Structure
Symptomsofplateletdisorders
Kinetics
Dynamics
Adhesion
Activation
8.1 Inhibition
8.2 Trigger(Induction)
8.3 Components(Consequences)
8.3.1 GPIIb/IIIaactivation
8.3.2 Granulesecretion
8.3.3 Morphologychange
8.3.4 Coagulationfacilitation
9 Aggregation
10 Woundrepair
11 Plateletcoagulationfactorinteractions
12 Roleinnonhematologicdiseases
12.1 Inflammation
13 Clotformationinnonmammalianvertebrates
14 Testsofplateletfunction
14.1 Bleedingtime
14.2 Multiplatemultipleelectrodeaggregometry
14.3 PFA100
15 Plateletdisorders
15.1 Thrombocytopenia
15.2 Alteredplateletfunction
15.3 Thrombocytosisandthrombocythemia
16 Drugsaffectingplatelets
16.1 Antiinflammatorydrugs
16.2 Drugsthatsuppressplateletfunction
16.2.1 Oralagents
16.3 Drugsthatstimulateplateletproduction
16.3.1 Intravenousagents
17 Therapywithplatelets
17.1 Transfusion
17.1.1 Indications
https://en.wikipedia.org/wiki/Platelet

Theligands,denotedbyletterL,
signalforplatelets(P)tomigrate
towardsthewound(SiteA).Asmore
plateletsgatheraroundtheopening,
theyproducemoreligandstoamplify
theresponse.Theplateletscongregate
aroundthewoundinordertocreatea
captostopbloodflowoutofthe
tissue.

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17.1.1 Indications
17.1.2 Collection
17.1.3 Storage
17.1.4 Deliverytorecipients
17.2 Woundtherapy
18 References
19 Furtherreading
20 Externallinks

Discovery,earlyobservations,andnaming
GeorgeGulliverin1841drewpicturesofplatelets[9]usingthetwinlens(compound)microscopeinventedin1830byJosephJacksonLister.[10]Thismicroscope
improvedresolutionsufficientlytomakeitpossibletoseeplateletsforthefirsttime.WilliamAddisonin1842drewpicturesofaplateletfibrinclot.[11]Lionel
Bealein1864wasthefirsttopublishadrawingshowingplatelets.[12]MaxSchultzein1865describedwhathecalled"spherules",whichhenotedweremuch
smallerthanredbloodcells,occasionallyclumped,andweresometimesfoundincollectionsoffibrinmaterial.[13]Queen'sCollege,Birmingham(apredecessor
collegeofBirminghamUniversity)physicianDrRichardHillNorriswasthefirsttodescribetheactionofplateletsin1880.[14]GiulioBizzozeroin1882studied
thebloodofamphibiansmicroscopicallyinvivo.HenamedSchultz'sspherules(It.)piastrine:littleplates.[15][16]WilliamOslerobservedthemand,inpublished
lecturesin1886,calledthemathirdcorpuscleandabloodplaqueanddescribedthemasacolorlessprotoplasmicdisc.[17]JamesWrightexaminedbloodsmears
usingthestainnamedforhim,andusedthetermplatesinhis1906publication[18]butchangedtoplateletsinhis1910publication[19]whichhasbecomethe
universallyacceptedterm.
Thetermthrombocyte(clotcell)cameintouseintheearly1900sandissometimesusedasasynonymforplateletbutnotgenerallyinthescientificliterature,
exceptasarootwordforothertermsrelatedtoplatelets(e.g.thrombocytopeniameaninglowplatelets).[6]Thrombocytesarecellsfoundinthebloodofnon
mammalianvertebrates.Theyarethefunctionalequivalentsofplatelets,butcirculateasintactmononuclearcells,andarenotsimplycytoplasmicfragmentsof
bonemarrowmegakaryocytes.[6]
Insomecontexts,thewordthrombusisusedinterchangeablywiththewordclot,regardlessofitscomposition(white,red,ormixed).Inothercontextsitisusedto
contrastanormalfromanabnormalclot:thrombusarisesfromphysiologichemostasis,thrombosisarisesfromapathologicandexcessivequantityofclot.[20]Ina
thirdcontextitisusedtocontrasttheresultfromtheprocess:thrombusistheresult,thrombosisistheprocess.

Measurement

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Plateletconcentrationismeasuredeithermanuallyusingahemocytometer,orbyplacingbloodinanautomatedplateletanalyzerusingelectricalimpedance,such
asaCoultercounter.[21]Thenormalrange(99%ofpopulationanalyzed)forplateletsinhealthyCaucasiansis150,000to450,000percubicmillimeter[22](amm3
equalsamicroliter).or150400109perlitre.Thenormalrangehasbeenconfirmedtobethesameintheelderly[23]andSpanishpopulations.[24]

Structure
Structurallytheplateletcanbedividedintofourzones,fromperipheraltoinnermost:
Peripheralzoneisrichinglycoproteinsrequiredforplateletadhesion,activation,andaggregation.Forexample,GPIb/IX/XGPVIGPIIb/IIIa.
Solgelzoneisrichinmicrotubulesandmicrofilaments,allowingtheplateletstomaintaintheirdiscoidshape.
Organellezoneisrichinplateletgranules.AlphagranulescontainclottingmediatorssuchasfactorV,factorVIII,fibrinogen,fibronectin,plateletderived
growthfactor,andchemotacticagents.Deltagranules,ordensebodies,containADP,calcium,serotonin,whichareplateletactivatingmediators.
Membranouszonecontainsmembranesderivedfrommegakaryocyticsmoothendoplasmicreticulumorganizedintoadensetubularsystemwhichis
responsibleforthromboxaneA2synthesis.ThisdensetubularsystemisconnectedtothesurfaceplateletmembranetoaidthromboxaneA2release.

Symptomsofplateletdisorders
Spontaneousandexcessivebleedingcanoccurbecauseofplateletdisorders.Thisbleedingcanbecausedbydeficientnumbersofplatelets,dysfunctionalplatelets,
orveryexcessivenumbersofplatelets:over1.0million/microliter.(TheexcessivenumberscreatearelativevonWillibrandfactordeficiencydueto
sequestration.)[25][26]
Onecangetaclueastowhetherbleedingisduetoaplateletdisorderoracoagulationfactordisorderbythecharacteristicsandlocationofthebleeding.[27]Allof
thefollowingsuggestplateletbleeding,notcoagulationbleeding:thebleedingfromaskincutsuchasarazornickispromptandexcessive,butcanbecontrolled
bypressurespontaneousbleedingintotheskinwhichcausesapurplishstainnamedbyitssize:petechiae,purpura,ecchymosesbleedingintomucousmembranes
causingbleedinggums,nosebleed,andgastrointestinalbleedingmenorrhagiaandintraretinalandintracranialbleeding.
Excessivenumbersofplatelets,and/ornormalplateletsrespondingtoabnormalvesselwalls,canresultinvenousthrombosisandarterialthrombosis.The
symptomsdependonthesiteofthrombosis.

Kinetics
Megakaryocyteandplateletproductionisregulatedbythrombopoietin,ahormoneproducedinthekidneysandliver.
Eachmegakaryocyteproducesbetween1,000and3,000plateletsduringitslifetime.
Anaverageof1011plateletsareproduceddailyinahealthyadult.
Reserveplateletsarestoredinthespleen,andarereleasedwhenneededbyspleniccontractioninducedbythesympatheticnervoussystem.
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Theaveragelifespanofcirculatingplateletsis8to9days.[28]Lifespanofindividualplateletsiscontrolledbythe
internalapoptoticregulatingpathway,whichhasaBclxLtimer.[29]
Oldplateletsaredestroyedbyphagocytosisinthespleenandliver.

Dynamics
Anoverviewsummarizingplateletdynamics,thecomplexprocessofconvertinginactiveplateletsintoaplateletplug,is
essentialEL2.Complicatinganyverbaldescriptionisthefactthatatleast193proteinsand301interactionsareinvolvedin
plateletdynamics.Theseparationofplateletdynamicsintothreestagesisusefulinthisregard,butitisartificial:infact,
eachstageisinitiatedinrapidsuccession,andeachcontinuesuntilthetriggerforthatstageisnolongerpresent,sothereis
overlap.[7]

Plateletsderivefromtotipotent
marrowstemcells

Adhesion
Thrombusformationonanintactendotheliumispreventedbynitricoxide,[30]prostacyclin,[31]andCD39.[32]
EndothelialcellsareattachedtothesubendothelialcollagenbyvonWillebrandfactor(VWF)whichthesecellsproduce.
VWFisalsostoredintheWeibelPaladebodiesoftheendothelialcellsandsecretedconstitutivelyintotheblood.Platelets
storevWFintheiralphagranules.
Whentheendotheliallayerisdisrupted,collagenandVWFanchorplateletstothesubendothelium.PlateletGP1bIXV
receptorbindswithVWFandGPVIreceptorandintegrinalpha2beta1bindwithcollagen.[33]

Activation
Anoverviewofplateletactivationisausefulintroductiontothismultifacetedprocess.[EL3]

Inhibition
Theintactendotheliallininginhibitsplateletactivationbyproducingnitricoxide,endothelialADPase,andPGI2.

Plateletsextrudedfrom
megakaryocytes

EndothelialADPasedegradestheplateletactivatorADP.

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RestingplateletsmaintainactivecalciumeffluxviaacyclicAMPactivatedcalciumpump.Intracellularcalcium
concentrationdeterminesplateletactivationstatus,asitisthesecondmessengerthatdrivesplateletconformationalchange
anddegranulation(seebelow).Endothelialprostacyclinbindstoprostanoidreceptorsonthesurfaceofrestingplatelets.
ThiseventstimulatesthecoupledGsproteintoincreaseadenylatecyclaseactivityandincreasestheproductionofcAMP,
furtherpromotingtheeffluxofcalciumandreducingintracellularcalciumavailabilityforplateletactivation.
ADPontheotherhandbindstopurinergicreceptorsonplateletsurface.SincethethrombocyticpurinergicreceptorP2Y12
iscoupledtoGiproteins,ADPreducesplateletadenylatecyclaseactivityandcAMPproduction,leadingtoaccumulation
ofcalciuminsidetheplateletbyinactivatingthecAMPcalciumeffluxpump.TheotherADPreceptorP2Y1couplestoGq
thatactivatesphospholipaseCbeta2PLCB2,resultingininositol1,4,5trisphosphate(IP3)generationandintracellular
releaseofmorecalcium.Thistogetherinducesplateletactivation.EndothelialADPasedegradesADPandpreventsthis
fromhappening.ClopidogrelandrelatedantiplateletmedicationsalsoworkaspurinergicreceptorP2Y12antagonists.

Trigger(Induction)

3DRenderingofPlatelets

Plateletactivationbeginssecondsafteradhesionoccurs.Itistriggeredwhencollagenfromthesubendotheliumbindswith
itsreceptorsontheplatelet.GPVIisassociatedwiththeFcReceptorgammachainandleadsviatheactivationofatyrosine
kinasecascadefinallytotheactivationofPLCgamma2PLCG2andmorecalciumrelease.
TissuefactoralsobindstofactorVIIintheblood,whichinitiatestheextrinsiccoagulationcascadetoincreasethrombin
production.Thrombinisapotentplateletactivator,actingthroughGqandG12.TheseareGproteincoupledreceptorsand
theyturnoncalciummediatedsignalingpathwayswithintheplatelet,overcomingthebaselinecalciumefflux.Familiesof
threeGproteins(Gq,Gi,G12)operatetogetherforfullactivation.Thrombinalsopromotessecondaryfibrinreinforcement
oftheplateletplug.PlateletactivationinturndegranulatesandreleasesfactorVandfibrinogen,potentiatingthe
coagulationcascade.Soinrealitytheprocessofplateletpluggingandcoagulationareoccurringsimultaneouslyratherthan
sequentially,witheachinducingtheothertoformthefinalclot.

Components(Consequences)

Scanningelectronmicrographof
bloodcells.Fromlefttoright:human
erythrocyte,activatedplatelet,
leukocyte.

GPIIb/IIIaactivation
CollagenmediatedGPVIsignallingincreasestheplateletproductionofthromboxaneA2(TXA2)anddecreasestheproductionofprostacyclin.Thisoccursby
alteringthemetabolicfluxofplatelet'seicosanoidsynthesispathway,whichinvolvesenzymesphospholipaseA2,cyclooxygenase1,andthromboxaneA
synthase.PlateletssecretethromboxaneA2,whichactsontheplatelet'sownthromboxanereceptorsontheplateletsurface(hencethesocalled"outin"
mechanism),andthoseofotherplatelets.Thesereceptorstriggerintraplateletsignaling,whichconvertsGPIIb/IIIareceptorstotheiractiveformtoinitiate
aggregation.[7]
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Granulesecretion
Plateletscontaindensegranules,lambdagranulesandalphagranules.Activatedplateletssecretethecontentsofthese
granulesthroughtheircanalicularsystemstotheexterior.Simplistically,boundandactivatedplateletsdegranulateto
releaseplateletchemotacticagentstoattractmoreplateletstothesiteofendothelialinjury.Granulecharacteristics:
granules(alphagranules)containingPselectin,plateletfactor4,transforminggrowthfactor1,plateletderived
growthfactor,fibronectin,Bthromboglobulin,vWF,fibrinogen,andcoagulationfactorsVandXIII).
granules(deltaordensegranules)containingADPorATP,calcium,andserotonin).
granules(gammagranules)similartolysosomesandcontainseveralhydrolyticenzymes.
granules(lambdagranules)contentsinvolvedinclotresorptionduringlaterstagesofvesselrepair.
Morphologychange

Diagramofthestructureofaplatelet
showingthegranules

Mitochondriahyperpolarizationisakeyeventininitiatingchangesinmorphology.[34]Intraplateletcalciumconcentration
increases,stimulatingtheinterplaybetweenmicrotubule/actinfilamentcomplex.Thecontinuouschangesinshapefromtheunactivatedtothefullyactivated
plateletisbestseenonscanningelectronmicroscopy.[EL4]Threestepsalongthispatharenamedearlydendritic,earlyspreadandspread.Thesurfaceofthe
unactivatedplateletlooksverysimilartothesurfaceofthebrain,withawrinkledappearancefromnumerousshallowfoldstoincreasethesurfaceareaearly
dendritic,anoctopuswithmultiplearmsandlegsearlyspread,anuncookedfryingegginapan,the"yolk"beingthecentralbodyandthespread,acookedfried
eggwithadensercentralbody.Thesechangesareallbroughtaboutbytheinteractionofthemicrotubule/actincomplexwiththeplateletcellmembraneandopen
canalicularsystem(OCS),whichisanextensionandinvaginationofthatmembrane.Thiscomplexrunsjustbeneaththesemembranes,andisthechemicalmotor
whichliterallypullstheinvaginatedOCSoutoftheinterioroftheplateletliketurningpantspocketsinsideout,creatingthedendrites.[EL7]andthenspreadseach
dendriteuntiltheentireOCSbecomesindistinguishablefromtheinitialplateletmembraneasitformsthe"friedegg".Thisdramaticincreaseinsurfaceareacomes
aboutwithneitherstretchingnoraddingphospholipidstotheplateletmembrane.[35]
Coagulationfacilitation
Plateletactivationcausesitsmembranesurfacetobecomenegativelycharged.Oneofthesignalingpathwaysturnsonscramblase,whichmovesnegatively
chargedphospholipidsfromtheinnertotheouterplateletmembranesurface.Thesephospholipidsthenbindthetenaseandprothrombinasecomplexes,twoofthe
sitesofinterplaybetweenplateletsandthecoagulationcascade.Calciumionsareessentialforthebindingofthesecoagulationfactors.

Aggregation

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Aggregationbeginsminutesafteractivation,andoccursasaresultofturningontheGPIIb/IIIareceptor,whichallowsthese
receptorstobindwithvWForfibrinogen.[7]Thereare50100ofthesereceptorsperplatelet.[36]Whenanyoneormoreof
atleastninedifferentplateletsurfacereceptorsareturnedonduringactivation,intraplateletsignalingpathwayscause
existingGpIIb/IIIareceptorstochangeshapecurledtostraightandthusbecomecapableofbinding.[7]
SincefibrinogenisarodlikeproteinwithnodulesoneitherendcapableofbindingGPIIb/IIIa,activatedplateletswith
exposedGPIIb/IIIacanbindfibrinogentoaggregatetogether.GPIIb/IIIacanalsofurtheranchortheplateletsto
subendothelialvWFforadditionalclotstructuralstabilisation.
Classicallyitwasthoughtthatthiswastheonlymechanisminvolvedinaggregation,butthreenewmechanismshavebeen
identifiedwhichcaninitiateaggregation,dependingonthevelocityofbloodflow(i.e.shearrange).[37]

Plateletclumpsinabloodsmear

Woundrepair
Thebloodclotisonlyatemporarysolutiontostopbleedingtissuerepairisneeded.Smallinterruptionsintheendotheliumarehandledbyphysiological
mechanismslargeinterruptionsbythetraumasurgeon.[38]Thefibrinisslowlydissolvedbythefibrinolyticenzyme,plasmin,andtheplateletsareclearedby
phagocytosis.[39]

Plateletcoagulationfactorinteractions
InadditiontointeractingwithvWFandfibrin,plateletsinteractwiththrombin,FactorsX,Va,VIIa,XI,IX,andprothrombintocompleteclotformationviathe
coagulationcascade.[40][41]Sixstudiessuggestedplateletsexpresstissuefactor:thedefinitivestudyshowstheydonot.[40]

Roleinnonhematologicdiseases
Inflammation
Inadditiontobeingthecellulareffectorofhemostasis,plateletsarerapidlydeployedtositesofinjuryorinfection,andpotentiallymodulateinflammatory
processesbyinteractingwithleukocytesandbysecretingcytokines,chemokines,andotherinflammatorymediators.[42][43][44][45]Plateletsalsosecreteplatelet
derivedgrowthfactor(PDGF).

Clotformationinnonmammalianvertebrates
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Insteadofhavingplatelets,nonmammalianvertebrateshavethrombocytes,whichhaveanucleusandresembleBlymphocytesinmorphology.Theyaggregatein
responsetothrombin,butnottoADP,serotonin,noradrenaline,asplateletsdo.[46][47]

Testsofplateletfunction
Bleedingtime
DevelopedbyDukein1910andbearinghisname,itmeasuredthetimeforbleedingtostopfromastandardizedwoundintheearlobewhichisblottedeach30
seconds.Normalwaslessthan3minutes.[48]Moremoderntechniquesarenowused.Anormalbleedingtimereflectssufficientplateletnumbersandfunctionplus
normalmicrovasculature.

Multiplatemultipleelectrodeaggregometry
IntheMultiplateanalyzer,anticoagulatedwholebloodismixedwithsalineandaplateletagonistinasingleusecuvettewithtwopairsofelectrodes.Theincrease
inimpedancebetweentheelectrodesasplateletsaggregateontothem,ismeasuredandvisualizedasacurve.

PFA100
ThePFA100isasystemforanalysingplateletfunctioninwhichcitratedwholebloodisaspiratedthroughadisposablecartridgecontaininganaperturewithina
membranecoatedwitheithercollagenandepinephrineorcollagenandADP.Theseagonistsinduceplateletadhesion,activationandaggregationleadingtorapid
occlusionoftheapertureandcessationofbloodflowtermedtheclosuretime(CT).AnelevatedCTwithEPIandcollagencanindicateintrinsicdefectssuchas
vonWillebranddisease,uremia,orcirculatingplateletinhibitors.ThefollowuptestinvolvingcollagenandADPisusedtoindicateiftheabnormalCTwith
collagenandEPIwascausedbytheeffectsofacetylsulfosalicylicacid(aspirin)ormedicationscontaininginhibitors.

Plateletdisorders
Adaptedfrom[49]
Thethreebroadcategoriesofplateletdisordersare"notenough""dysfunctional"and"toomany".[49]

Thrombocytopenia
Immunethrombocytopenias(ITP)formerlyknownasimmunethrombocytopeniapurpuraandidiopathicthrombocytopenicpurpura
Splenomegaly
Gaucher'sdisease
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Familialthrombocytopenia[50]
Chemotherapy
Babesiosis
Dengue
Onyalai
Thromboticthrombocytopenicpurpura
HELLPsyndrome
Hemolyticuremicsyndrome
Druginducedthrombocytopenicpurpura(fiveknowndrugsmostproblematicisheparininducedthrombocytopenia(HIT)
Pregnancyassociated
Neonatalalloimmuneassociated
Aplasticanemia
Transfusionassociated
Pseudothrombocytopenia
idiopathicthrombocytopenicpurpura
Gilbert'sSyndrome[51]

Alteredplateletfunction
Congenital
Disordersofadhesion
BernardSouliersyndrome
Disordersofactivation
Disordersofgranuleamountorrelease
HermanskyPudlakSyndrome
Grayplateletsyndrome
ADPReceptordefect
Decreasedcyclooxygenaseactivity
Storagepooldefects,acquiredorcongenital
Disordersofaggregation
Glanzmann'sthrombasthenia
WiskottAldrichsyndrome
Acquired
Disordersofadhesion
Paroxysmalnocturnalhemoglobinuria
Asthma[52]
Samter'striad(aspirinexacerbatedrespiratorydisease/AERD)[53]
Cancer[54]
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Malaria[55]
Decreasedcyclooxygenaseactivity

Thrombocytosisandthrombocythemia
Reactive
Chronicinfection
Chronicinflammation
Malignancy
Hyposplenism(postsplenectomy)
Irondeficiency
Acutebloodloss
Myeloproliferativeneoplasmsplateletsarebothelevatedandactivated
Essentialthrombocytosis
Polycythemiavera
Associatedwithothermyeloidneoplasms
Congenital

Drugsaffectingplatelets
Antiinflammatorydrugs
Somedrugsusedtotreatinflammationhavetheunwantedsideeffectofsuppressingnormalplateletfunction.Thesearethenonsteroidalantiinflammatorydrugs
(NSAIDS).Aspirinirreversiblydisruptsplateletfunctionbyinhibitingcyclooxygenase1(COX1),andhencenormalhemostasis.Theresultingplateletsareunable
toproducenewcyclooxygenasebecausetheyhavenoDNA.Normalplateletfunctionwillnotreturnuntiltheuseofaspirinhasceasedandenoughoftheaffected
plateletshavebeenreplacedbynewones,whichcantakeoveraweek.Ibuprofen,anotherNSAID,doesnothavesuchalongdurationeffect,withplateletfunction
usuallyreturningwithin24hours,[56]andtakingibuprofenbeforeaspirinpreventstheirreversibleeffectsofaspirin.[57]

Drugsthatsuppressplateletfunction
Thesedrugsareusedtopreventthrombusformation.
Oralagents
aspirin
clopidogrel
cilostazol
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ticlopidine
ticagrelor
prasugrel

Drugsthatstimulateplateletproduction
thrombopoietinmimetics
desmopressin
factorVIIa
Intravenousagents
abciximab,
eptifibatide
tirofiban
Othersoprelvekin,romiplostim,eltrombopag,argatroban

Therapywithplatelets
Transfusion
Indications
Platelettransfusionismostfrequentlyusedtocorrectunusuallylowplateletcounts,eithertopreventspontaneousbleeding(typicallyatcountsbelow(10109/L)
orinanticipationofmedicalproceduresthatwillnecessarilyinvolvesomebleeding.Forexample,inpatientsundergoingsurgery,alevelbelow50109/Lis
associatedwithabnormalsurgicalbleeding,andregionalanaestheticproceduressuchasepiduralsareavoidedforlevelsbelow80109/L.[58]Plateletsmayalsobe
transfusedwhentheplateletcountisnormalbuttheplateletsaredysfunctional,suchaswhenanindividualistakingaspirinorclopidogrel.[59]Finally,platelets
maybetransfusedaspartofamassivetransfusionprotocol,inwhichthethreemajorbloodcomponents(redbloodcells,plasma,andplatelets)aretransfusedto
addressseverehemorrhage.Platelettransfusioniscontraindicatedinthromboticthrombocytopenicpurpura(TTP),asitfuelsthecoagulopathy.
Collection
Plateletsareeitherisolatedfromcollectedunitsofwholebloodandpooledtomakeatherapeuticdose,orcollectedbyplateletapheresis:bloodistakenfromthe
donor,passedthroughadevicewhichremovestheplatelets,andtheremainderisreturnedtothedonorinaclosedloop.Theindustrystandardisforplateletstobe
testedforbacteriabeforetransfusiontoavoidsepticreactions,whichcanbefatal.RecentlytheAABBIndustryStandardsforBloodBanksandTransfusion
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Services(5.1.5.1)hasallowedforuseofpathogenreductiontechnologyasanalternativetobacterialscreeningsin
platelets.[60]
Pooledwholebloodplatelets,sometimescalledrandomplatelets,areseparatedbyoneoftwomethods.[61]IntheUS,a
unitofwholebloodisplacedintoalargecentrifugeinwhatisreferredtoasasoftspin.Atthesesettings,theplatelets
remainsuspendedintheplasma.Theplateletrichplasma(PRP)isremovedfromtheredcells,thencentrifugedatafaster
settingtoharvesttheplateletsfromtheplasma.Inotherregionsoftheworld,theunitofwholebloodiscentrifugedusing
settingsthatcausetheplateletstobecomesuspendedinthebuffycoatlayer,whichincludestheplateletsandthewhite
bloodcells.Thebuffycoatisisolatedinasterilebag,suspendedinasmallamountofredbloodcellsandplasma,then
centrifugedagaintoseparatetheplateletsandplasmafromtheredandwhitebloodcells.Regardlessoftheinitialmethod
ofpreparation,multipledonationsmaybecombinedintoonecontainerusingasterileconnectiondevicetomanufacturea
singleproductwiththedesiredtherapeuticdose.
Apheresisplateletsarecollectedusingamechanicaldevicethatdrawsbloodfromthedonorandcentrifugesthecollected
bloodtoseparateouttheplateletsandothercomponentstobecollected.Theremainingbloodisreturnedtothedonor.The
Plateletconcentrate.
advantagetothismethodisthatasingledonationprovidesatleastonetherapeuticdose,asopposedtothemultiple
donationsforwholebloodplatelets.Thismeansthatarecipientisnotexposedtoasmanydifferentdonorsandhaslessrisk
oftransfusiontransmitteddiseaseandothercomplications.Sometimesapersonsuchasacancerpatientwhorequiresroutinetransfusionsofplateletswillreceive
repeateddonationsfromaspecificdonortofurtherminimizetherisk.Pathogenreductionofplateletsusingforexample,riboflavinandUVlighttreatmentscan
alsobecarriedouttoreducetheinfectiousloadofpathogenscontainedindonatedbloodproducts,therebyreducingtheriskoftransmissionoftransfusion
transmitteddiseases.[62][63]AnotherphotochemicaltreatmentprocessutilizingamotosalenandUVAlighthasbeendevelopedfortheinactivationofviruses,
bacteria,parasites,andleukocytesthatcancontaminatebloodcomponentsintendedfortransfusion.[64]Inaddition,apheresisplateletstendtocontainfewer
contaminatingredbloodcellsbecausethecollectionmethodismoreefficientthansoftspincentrifugationatisolatingthedesiredbloodcomponent.
Storage
Plateletscollectedbyeithermethodhaveaveryshortshelflife,typicallyfivedays.Thisresultsinfrequentproblemswithshortsupply,astestingthedonations
oftenrequiresuptoafullday.Sincetherearenoeffectivepreservativesolutionsforplatelets,theylosepotencyquicklyandarebestwhenfresh.
Plateletsarestoredunderconstantagitationat2024C(6875.2F).Unitscannotberefrigeratedasthiscausesplateletstochangeshapeandlosefunction.
Storageatroomtemperatureprovidesanenvironmentwhereanybacteriathatareintroducedtothebloodcomponentduringthecollectionprocessmayproliferate
andsubsequentlycausebacteremiainthepatient.RegulationsareinplaceintheUnitedStatesthatrequireproductstobetestedforthepresenceofbacterial
contaminationbeforetransfusion.[65]
Deliverytorecipients

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PlateletsdonotneedtobelongtothesameABObloodgroupastherecipientorbecrossmatchedtoensureimmunecompatibilitybetweendonorandrecipient
unlesstheycontainasignificantamountofredbloodcells(RBCs).ThepresenceofRBCsimpartsareddishorangecolortotheproduct,andisusuallyassociated
withwholebloodplatelets.Aneffortissometimesmadetoissuetypespecificplatelets,butthisisnotcriticalasitiswithRBCs.
Priortoissuingplateletstotherecipient,theymaybeirradiatedtopreventtransfusionassociatedgraftversushostdiseaseortheymaybewashedtoremovethe
plasmaifindicated.
Thechangeintherecipient'splateletcountaftertransfusionistermedthe"increment"andiscalculatedbysubtractingthepretransfusionplateletcountfromthe
posttransfusionplateletcount.Manyfactorsaffecttheincrementincludingtherecipient'sbodysize,thenumberofplateletstransfused,andclinicalfeaturesthat
maycauseprematuredestructionofthetransfusedplatelets.Whenrecipientsfailtodemonstrateanadequateposttransfusionincrement,thisistermedplatelet
transfusionrefractoriness.
Platelets,eitherapheresisderivedorrandomdonor,canbeprocessedthroughavolumereductionprocess.Inthisprocess,theplateletsarespuninacentrifugeand
theexcessplasmaisremoved,leaving10to100mLofplateletconcentrate.Suchvolumereducedplateletsarenormallytransfusedonlytoneonatalandpediatric
patients,whenalargevolumeofplasmacouldoverloadthechild'ssmallcirculatorysystem.Thelowervolumeofplasmaalsoreducesthechancesofanadverse
transfusionreactiontoplasmaproteins.[66]Volumereducedplateletshaveashelflifeofonlyfourhours.[67]

Woundtherapy
Plateletsreleaseplateletderivedgrowthfactor(PDGF),apotentchemotacticagentandTGFbeta,whichstimulatesthedepositionofextracellularmatrix
fibroblastgrowthfactor,insulinlikegrowthfactor1,plateletderivedepidermalgrowthfactor,andvascularendothelialgrowthfactor.Localapplicationofthese
factorsinincreasedconcentrationsthroughPlateletrichplasma(PRP)isusedasanadjunctinwoundhealing.[68]

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Furtherreading
Michelson,AlanD.(2013).Platelets(3rded.).Academic.ISBN0123878373.1351pages60,000references.Excerptsfreeonline.

Externallinks
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