Test Bank For Rodak's Hematology 6th Edition By Jeanine Walenga, Elaine Keohane, Larry Smith 9780323530453 Chapter 1-43 Complete Guide .

HEMATOLOGY II n




REVIEWER NOTES n




KYLE BERNIE S. RAMOS 2022
n n n n




Reference: Rodak's Hematology Clinical Principles and Applications 6th Edition & Hematology_112 L
n n n n n n n n n n n


ecture - J.A. Ganding, RMT
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, Introduction: Hemostasis n


HEM_112:nHEMATOLOGYn2nLECTUR
En(PRELIMINARY)
SirnJomarnAdamsnGanding,nRMT
OUTLINE ABNORMALnSTATE
I. DefinitionnofntermsnrelatedntonHemostasis ● Thrombosis
A. PrimarynHemostasis ○ Excessivenclottingninsidenthenbloodnvesseln→norgan
1. Platelets
ndeprivationnofnoxygennandnnutrientsn→ntissue/celln
2. VascularnSystem
3. Mechanism death.
B. SecondarynHemostasis ● Hemorrhagicndisease
1. Coagulationnfactors ○ Noncoagulationn→ndeficientnprocoagulants.
2. CoagulationnInhibitor
3. Mechanism KEYnCOMPONENTSnOFnHEMOSTASIS
C. Fibrinolysis
● Cellularncomponents:
NOTE:nThencontentsnofnthisnreviewernisnmostlynfromntheninstructor’ ○ CellsnofnthenVascularnIntiman(EndothelialnCells)
snlecture.nPleasenreadnRodak'snHematologyn6thnEditionnfornanm ○ ExtravascularnTissuenFactornBearingnCells
orendetailednstudy.nThanknyou! ○ Platelets
● Plasmancomponents:
HEMOSTASIS ○ Coagulationnproteinsn-nfavorsncoagulation
○ Fibrinolyticnproteinsn-
ntriggersnfibrinolysisntonendnclotting.

○ Inhibitors:
(1) Fornfibrinolysisn-
ninhibitsnunderntimenclotting;nincomplet

entissuenrepair.
(2) Forncoagulationn-
neliminatesnbystandernclotnformationninsid

enthenbloodnvessel.

PRIMARYnHEMOSTASIS
● ActivatednbynSMALLninjuriesninnbloodnvessels.
● Rapid,nshort-livednreponse.
● “Firstnaid”;nfirstntonbenactivated.

● Hemostasisnisnancomplexnphysiologicnprocessnthatnkeeps
ncirculatingnbloodninnanfluidnstaten(Rodak’sn6thnEd).
COMPONENTS
● involvesntheninteractionnofnvasoconstriction,nplateletn ● VascularnSystem
adhesionnandnaggregation,nandncoagulationnenzyme ○ Arteries
nactivationntonstopnbleedingn(Rodak’sn6thnEd). ○ Veins
● Anprocessninnwhichnbloodnisnretainednwithinnthenvascular ○ Capillariesn-nsmallest.
nsystemnduringninjury.

● Responsiblenfornbothncoagulationnandnmaintainingnbloodnin “ThenmainncomponentnresponsiblenfornPrimarynHemostasisnisny
nliquidnstate. ournVascularnIntima/nEndothelium/nEndothelialnCellsn-
● “Bloodnshouldncoagulatenatnthenperfectntime,nperfectnplace ninnernmostnlayernofnthenBloodnVessel.”n-nJAnGanding

,nandnfornthenrightnpurpose.”n-nJAnGanding.
● Platelets
BLOODnENVIRONMENT
● InsidenthenBloodnVessel MECHANISM
○ Normal 1. VascularnSystem
○ Noncoagulationn→nremainnfluidnfornbloodnflow/nblood ○ Contractsntonsealnthenwoundn(vasoconstriction)n→n
ncirculation.
Initialnhemostaticnresponsenofnthenbodyn→nprevents
nexcessivenbloodnloss.
● OutsidenthenBloodnVessel
○ Duringninjury/ntissuendamage 2. Platelets
○ Needsncoagulationn→nhemostaticnreaction ○ Thrombocytesnfillnthenopennspacentonformnanplateletn
plugn(primarynhemostaticnplug),nmadenupnofnplatelets
nalone.




1 RAMOS

, INTRODUCTION:nHEMOSTASIS

FIBRINOLYSIS




● AlsonknownnasnThrombolysis.
AdditionalnInfo: ● Finalnstagenofncoagulation.
● VascularnIntimancontainsnanninternalnelasticnlaminan(elastin ● Onlynhappensnwhennthenwoundnisnalreadynsealed,nread
nandncollagen)nwherenwhennplateletsnarenexposednto,nthenl
ynfornvascularnrepair.
atternisnactivatednenablingnadhesionntonthensitenofninjury. ● Digestionnofnfibrinnclotnkeepsnthenvascularnsystemnfreeno
● Essencenofnfibroblastsn- fndepositednfibrin/nfibrinnclotn →nImportance?nFibrin/nfibri
nfornvascularnrepairnandncellngenerationnfornclosingn
nnclotncannclognthenbloodnvesselsn(magigingnbarado).
theninjury.
MECHANISM
SECONDARYnHEMOSTASIS ● Releasenofntissuenplasminogennactivator.
○ Plasminogennisnanzymogenn(inactive)nthatnneeds
nthrombinn(activator)ntonbenconvertedntonplasmin.

● Conversionnofnplasminogenntonplasmin.
● Conversionnofnfibrinntonfibrin-degradationnproduct.
○ Plasminninducesnfibrinnclotntonlyseninnordernt
onre-establishnbloodnflow.

REVIEWnQUESTIONS
● Whatnarenthenkeyncomponentsnofnhemostasis?
● Whatnarenthencellularncomponents?
● Whatnarenthenplasmancomponents?
● Whatnisnthendifferencenbetweennprimarynandnsecondary
nhemostasis?

● Betweennthentwontypesnofnhemostasis,nwhatnisnrapid?nAn
dnwhatnisndelayed?nWhatnisnthenresponsenfornsmallninjurie
s?nLargeninjuries?
● Activatednwhennprimarynhemostasisnisnnotnenough. ● Whatnarenthencomponentsnofnprimarynhemostasis?
● ActivatednbynLARGEninjuriesntonbloodnvessels. ● Whatnarenthencomponentsnofnsecondarynhemostasis?
● Delayed,nlong-termnresponse. ● Thisnisnalsontermednasnthenprimarynhemostaticnplug.
● Thisnisnalsontermednasnthensecondarynhemostaticnplug.
COMPONENTS ● Whatnisnthenimportancenofnfibroblastsninnthenvascula
rnintima?
● Coagulationnfactors
● Whatnisnthenfactornthatnpreventsnfibrinnclotnfromnbreaking?
○ Promotesncoagulation;nprocoagulants.
● Itnisnthenlastnstagenofncoagulation.
● Coagulationninhibitors
○ Preventsnanynunwantednclotnformation.

MECHANISM
1. Interactionnofncoagulationnfactorsntonproducenanfibrin
nclotn(secondarynplateletnplug).

○ InducednbynCoagulationnFactornI
○ Thrombinn→nultimate/needednproteinntonconvert
nfibrinogenntonfibrin.

2. FibrinnStabilization
○ FactornXIIIn→npreventsnfibrinnclotnfromnbreaking.




2 RAMOS

, MEGAKARYOCYTOPOIESIS PART I n n


HEM_112:nHEMATOLOGYn2nLECTUR
En(PRELIMINARY)
SirnJomarnAdamsnGanding,nRMT
OUTLINE ● MegakaryocytopoiesisnPathway
I. Megakaryocytopoiesis ○ HematopoieticnStemnCelln(Pluripotent)n→nCommon
A. Definitionnofnterms nMyeloidnProgenitorn(Multipotent)n→

B. Sitenofnorigin Megakaryocyte-ErythrocytenProgenitorn–nCFU-
II. Stagesn n of Development GEMMnxnThrombopoietinn→nMegakaryoblastn(Precur
A. ProgenitornCells sor)
B. Megakaryoblast
● “Nakadependensanhormonen(TPO/EPO)nkungnanong
C. Promegakaryocyte
nprecursorncellnangnmapo-produce”n-nJAnGanding
D. Megakaryocyte
III. Thrombocytopoiesis
IV. Platelets NOTE:nPluripotentnvsnMultipotent
V. HormonesnandnCytokinesnofnMegakaryopoiesis ○ Pluripotentn-
ngeneratesncellsnofnallnlineagesn(ex.nHSCn-
NOTE:nThencontentsnofnthisnreviewernisnmostlynfromntheninstructor’ ncommitsntonanspecificnlineageneithernCMPnornCLP)
snlecture.nPleasenreadnRodak'snHematologyn6thnEditionnfornanm ○ Multipotentn-
orendetailednstudy.nThanknyou!
ndividesnintondifferentncellsn(ex.nCMPndifferentiat

esnintonWBCs,nRBCs,n&nPlatelets)
MEGAKARYOCYTOPOIESIS
● IsnitndifferentnfromnMegakaryopoiesis?nNO,nbothntermsnare
STAGESnOFnDEVELOPMENT
nthensame.
● Innthisnportion,nthendifferentnstagesnofnMegakaryopoiesisna
● ThenproductionnandndevelopmentnofnanMegakaryocyte.
rentranscribed,nfromnthenprogenitorsntonthenprecursorsnandn
○ Takennote:nMegakaryocytesnarendifferentnfrom
thenundifferentiatedntonthendifferentiated.
nThrombocytes.


MEGAKARYOCYTEnPROGENITORS
BONEnMARROW




● Sitenofnoriginnfor:
NOTE:nThenCFU-GEMMnwillngivenrisentonthenMegakaryocyte-
○ Megakaryocytopoiesisn- Erythrocyten ProgenitornwhichnwillnreactnwithnTPO,nMeg-CSF,nandnIL-
nproductionnofnMegakaryocytes. 3ntondevelopninton BFU-
○ Thrombocytopoiesisn-nproductionnofnplatelets. Meg.nThenordernofnsucceedingncellsnarenfromnleastntonmostnmature.
● WherenmaturenMegakaryocytesnarenlocalizedninnthenalb ● BurstnFormingnUnitn-nMegakaryocyten(BFU-Meg)
uminalnsurfacen ornnon- ○ Dividesnintonhundredsnofndaughterncells.
bloodnsurfacenofnthensinusoidnliningnendothelialncellsn→ni ○ Undergoesnmitoticndivision.
nnpreparationnfornplateletnshedding. ● ColonynFormingnUnitn-nMegakaryocyten(CFU-Meg)
○ Dividesnintondozensnofndaughterncells.
○ Undergoesnmitoticndivision.
● LightnDensitynCFUn-nMegakaryocyten(LD-CFU-Meg)
○ Unablentondividenbynmitosis
○ Undergoesnendomitosisn-
nanformnofnmitosisnthatnlacksntelophasenandncytokinesi

sn(separationnintondaughterncells).
○ Megakaryocytesndiscontinuentongrow.
○ WillnemployntheirnmultiplenDNAncopiesntonsynthesize
nabundant/largerncytoplasm,nwhichnultimatelyndiffer

entiatesnintonplatelets.

1 RAMOS