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Sindroame hemoragipare
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HEMOSTAZA NORMALA
I. Etapa vasculara
II. Etapa trombocitara
III. Etapa coagulare
IV. Etapa fibrinoliza
HEMOSTAZA NORMALA
I. Endoteliul- functia
1. bariera de permeabilitate2. secretie:- F. Willebrand,
- trombomodulin - ataseaza trombina, proteina C, S
- fibronectina – inhibitorul activatorului tisular al plasminogenului - PGI2 , Endotelina
- adeziunea prin receptori Gp I - colagenul subendotelial
- fibronectin + f. Willebrand prin Gp IIb IIIa
- fibrinogen
II. Etapa trombocitara
- agregarea - ADP subendotelial - Tx A2
- secretia - Ca+2 , Factor 3, 4, serotonina
COAGULAREA - intrinseca - trombocite activate
colagenul subendotelial factorul XII
- XII XII a - XI XI a
- IX IX a
- X Xa
Ca, F3plachetar- fosfolipide,VIII
COAGULAREA - extrinseca
- tromboplastina tisulara
FT
- X Xa
Proteina C- VII
- fibrinogen fibrina +
fibrinopeptid A,B
COAGULAREA - calea comuna
- X Xa
- II IIa
Ca, F3plachetar,V
Proteina C
COAGULAREA
CLASIFICARE
- Etapa vasculara - Purpura vasculara- congenitala
- dobandita
- Etapa trombocitara - Purpura trombocitara
- trombocitopenie - trombopatii
- Etapa coagulare - Purpura deficienta factorilor de coagulare
- congenitala - dobandita
- Etapa reologica - Purpura ortostatica
- Etapa fibrinolizei - Purpura fibrinolitica
- Etapa activare sistem monocit-macrofag - Purpura CID
Purpure vasculare
- congenitaleEhler Danlos osteogeneza imperfectaRendu - Osler
- dobanditescorbutsenilaSindrom Henoch Schonleininfectioasa - meningococcica, viraledisglobulinemii - Waldenstrom, mielom,
disglobulinemie mixta
Boala Rendu Osler- congenitala
autosomal dominantadefect perete venos
(endoteliu, membrana bazala, adventice)
fistule arteriovenoase(mucoasa digestiva, plaman, ficat, splina,
cerebral)
Telangiectazia ereditara
Telangiectazia ereditara
Manifestari clinice
1. telangiectazii cutanate, mucoase 2. epistaxis, hemoptizii, melena 3. anemie feripriva cr4. anevrisme arteriovenoase hepatice cu sindrom hiperkinetic cardiovascular 5. AHC – sugestive boala Rendu
Diagnostic diferential
1. Telangiectaziile sclerodermie (CREST)
2. Pete telangiectatice3. B Fabry (Angiokeratoma corporis
difusum) - boala a metabolismului glicolipidic (ceramide intramacrofagic)
- leziuni nodulare inchise la culoare ( aproape negre) periombilical,
scrotal, cardiac, sistem nervos
CREST
Boala Fabry
Pete telangiectatice
Tratament
1. Suportiv: tamponament nazal, unguente ( dermatol), cauterizari contraindicate
2. Trat anemiei : fier, ac folic, vit B12 la 3 luni
3. Trat chirurgical al fistulelor mari – greu de abordat
2. Purpure vasculare anomalii dobandite
ale tesutului conjunctiv
Purpura de staza
Purpura senila
Scorbutul
Situatii etiologice- alcoolism, copii hraniti exclusiv
cu lapte de vaca - patogenie:
- deficit vit C – deficit de colagen (hidroxiprolina)
- reduce adeziunea, agregarea plachetelor, - clinic : - purura in jurul foliculului pilos, durere - hipercheratoza- rar: HDS, hemoragii musculare - tratament: Vit C iv
3. Purpure vasculare dobandite
- boli infectioase - boli de tesut conjunctiv
- hiper/disglobulinemii - Henoch Schonlein -cauze rare
Purpure vasculare dobandite – boli inflamatorii
- etiopatogenie
- complexe imune circulante - post infectii bacteriene, virale, rickettsi- medicamente – penicilina, sulfamide, allopurinol
Purpura infectioasa
- infectii (virusuri, meningococ, rickettsi)
- patogenie: complexe imune circulante - clinic :
- purura – bule hemoragice – “purpura fulminans “ - tratament – antiinfectios
Sindromul hemolitic uremic
- microtromboze exclusiv in vase renale
- etiologie: infectioasa
- patogenie: - copii, adolescenti- dupa infectii (E Coli, Shigella)
- leziune de celule endoteliale, microtromboze a. aferenta, glomerul
Sindromul hemolitic uremic
- microtromboze exclusiv in vase renale
- etiologie: infectioasa
- clinic: - purpura
- insuf renala acuta - HTA
- AH microangiopatica- evolutie :
- deces prin IRA - 10- 50% cazuri IRC
- tratament - dializa in IRA
Meningococcemie
Purpura fulminans post zona zoster
Endocardita bacteriana
Vasculita poliartrita reumatoida
Manifestari clinice1. purpura2. hemoragii retiniene3. nevrita periferica Tratament
1. Tratatamentul mielom, etc
2. Plasmafereza
Purpura hiperglobulinemica IgA+IgG - boala
Waldenstrom, mielom
Purpura hiperglobulinemica
Hemoragii subunghiale - crioglobulinemie
Purpura Henoch Schonlein- etiopatogenie
infectie streptococica (faringiana – 50%cazuri, respiratorie)
-alergii alimentare, medicamentoase – (chinidina, sulfamide)
membrana bazala capilara – - complexe imune IgA2
Purpura Henoch Schonlein
Manifestari clinice
Manifestari clinice1. purpura2. poliartralgii3. colica abdominala, melena,
rar perforatia intestinala
4. Hematurie, proteinurie – GNA ac mesangiala focala Prognostic
favorabil in generalevolutie cu “valuri purpurice”
Tratament1. Penicilina – infectie streptococica
2. Corticoterapie – 1mg/kg prednison
Prognostic
- favorabil in general- evolutie cu “recidive purpurice”
- IRA - perforatie intestinala
Complicatii
Purpure vasculare rare
- anticoagulante
- autoflagelare
- staza
Necroza cumarinica
Purpura trombocitopenicaI. Productie scazuta de trombocite- trombocitopenia < 100000/mm
3
- Nr redus de megacariocite in maduva1. infiltrat medular : leucemii,
limfoame, mielom, metastaze, granuloame
2. hipoplazie medulara: idiopaticasecundara: radiatii, medicamente,
virusuri
4. anomalii congenitale: pancitopenia Fanconi, trombocitopenia autosomal recisiva, boala May Hegglin, infectii (rubeola)
3. sindr mielodisplazice: idiopaticasecundara: radiatii, medicamente,
virusuri
- scurtarea duratei de viata a trombocitelor
1. Distructie crescuta : - PTI autoimuna acuta, cronica
- purpura posttransfuzionala
- neonatala alloimuna- post medicamentoasa- autoimuna secundara
- trombocitopenia < 100000/mm
3
- nr crescut de megacariocite in maduva
II. Distructie crescuta trombocite:
Trombocitopenia autoimuna idiopatica
- terminologie- trombocitopenie imuna primara
- trombocitopenie imuna primara persistenta 3-12 luni
- trombocitopenie cronica
Trombocitopenia autoimuna idiopatica
- etiopatogenie- autoanticorpi in plasma si pe membrana trombocitelor
- distrugere prematura a trombocitelor in macrofagele splenice
Purpure trombocitopenica autoimuna idiopatica acuta
- etiopatogenie
- autoanticorpi antitrombocitari IgG
- antigene : virus gripal, rubeolic, hepatitic, HIV, Ebstein Barr,
Manifestari clinice
1. purpura2. poliartralgii3. colica abdominala, melena,
rar perforatia intestinala
4. Hematurie, proteinurie – GNA ac mesangiala focala
Manifestari clinice
- clinic- petesii fara splenomegalie
- paraclinic
- trombocitopenie- maduva: megcariocite numeroase
oprite in maturatie,
- TS prelungit
- IgG antiitrombocitari
Maduva:
nu megcariocite trombocitogene
- evolutie- boala autolimitata cu vindecare, - uneori cu purpura “in valuri” - 20% cronicizare
- tratament- cortioterapie in cazuri grave
- plasmafereza in risc de hemoragie cerebrala
Tratament linia I la T‹ 30 0001.Corticoterapia
- Prednison 1-1,5 mg-kgc-zi - Dexametazona 40 mg 4 zile la 28 zile 1-4X - Metilprednisolon pulsterapie 500-1000mg 3 zile lunar 2.Imunoglobuline iv urgente, pre-splen. - Ig in doza mare 1g-kgc 2 zile sau 400mg 5 zile - Ig anti-D pacienti Rd pozitivi
Tratament linia II1.Splenectomia clasica sau laparoscopic-corticorezistenta 6 luni-recidivanti-se poate face la › 50 000 (corticoterapie, Ig.,agonisti ai receptorilor de trombopoietina)-in urgente dupa masa trombocitara - Vaccinare anti S. pneumoniae, N. meningitidis, Haemophilus influenzae
Tratament linia II2.Contraindicatii –refuz splenectomia-Azatriopina, Ciclofosfamida, Vincristin, Ciclosporina A-Danazol- Rituximab-in urgente dupa masa trombocitara -Agonistii receptorilor de trombopoietina Romiplostim s.c. Eltrombopag p.o.
Purpure trombocitopenica autoimuna idiopatica cronica
- etiopatogenie
- anticorpi antitrombocitari anti receptori IIb-IIIa, glicoproteina
Ib
- clinic
- astenie, petesii - “nepalpabile”, fara bule hemoragice, echimoze, - metroragii, sangerari digestive, - fara splenomegalie - paraclinic
- trombocitopenie- maduva: megacariocite tinere
Purpure trombocitopenica autoimuna idiopatica cronica
- femei / barbati = 3/1
- paraclinic
- trombocitopenie
- maduva: megacariocite tinere numeroase oprite in
maturatie,
- TS prelungit
Evolutie- cronica, remisiuni spontane f rare
Tratament- cortioterapie 1mg/kg/zi- 50% remisiune partiala,raspuns la 6 sap
- splenectomie – forme corticorezistente - agonisti de trombopoietina – forme corticorezistente
- imuran – 3 luni +/- vinblastin
- gama globulina iv – 3luni blocarea sistemului monocit-macrofag
- postnatala
- clinic- sindrom hemoragipar imediat dupa nastere
- manifestari grave la urmatorii copii
Purpure trombocitopenica alloimuna
- anticorpi antitrombocitari ce trec placenta
- anti sistemului PI
A1
- clinic
Purpure trombocitopenica posttransfuzionala
- la 7 zile de la transfuzie, masa trombocitara
- anticorpi antitrombocitari - anti sistemului PIA1
- tratament- corticoterapie, plasmafereza,
exanguinotransfuzie
- actiune maduva osoasa
Purpure trombocitopenica postmedicamentoasa
- arabinosid, daunorubicina,- tiazidice, estrogeni
- distructie imuna- antibiotice, sulfamide,
- chinidina, chinina- metildopa
- saruri de aur, - heparina
- mecanism
Purpure trombocitopenica postmedicamentoasa
1. complexe imune anti “ medicament + proteina plasmatica”
- absorbtie nespecifica a complexelor pe trombocit “inocent bystander”
2. medicament fixat pe trombocit, anticorpi anti complex
“ medicament + trombocit”
- clinic- petesii, frecvent sindrom
hemoragic sever, - aparut post medicamentos
- paraclinic
- intreruperea medicatiei, corticoterapie, plasmafereza,
- tratament
- megacariocite normale, intens trombogene ( citoplasma granulata, azurofila, fara vacuole)
TIH- sindrom protrombotic indus de un anticoagulant
Tip I primele 4 zile
- de cauza imuna, severa, progresiva - tromboze arteriale, venoase
Tip II dupa 5-15 zile
- datorata aglutinarii T, usoara, limitata
- paraclinic- trombocitopenie- maduva: megcariocite normale, anomalii morfologice
Purpure trombocitopenica autoimuna secundara
- LES - LLC, limfoame
- HIV
- tratament- zidovudin
Purpure trombotica trombocitopenica
- sarcina, anticonceptionale, infectii - Coxackie, micoplasme, - antibiotice
- morfopatologic
- context
- microtromboza hialina capilara, arteriolara
Purpure trombotica trombocitopenica
- clinic- febra
- purpura - anemie hemolitica microangiopatica
- disfunctie renala severa, - manifestari neurologice
- tratament
- CID
Sindrom hemolitic uremic
- clinic- copii, tineri
- tratament
- IRA, sindr hemoragipar, rar sindrom neurologic
- prognostic- 50-80% mortalitate
- plasmafereza, exanguinotransfuzia
Sindroame hemoragipare prin
anomalii de coagulare si
fibrinoliza
- Etapa coagulare - Purpura deficienta factorilor de coagulare
- congenitala - dobandita
-Etapa fibrinolizei - Purpura fibrinolitica
- anomalii primare ale fibrinolizei- anomalii secundare: CID
COAGULAREA - intrinseca
colagenul subendotelial factorul XII
XII XII akininogenprecalicreina
XI XI a
IX IX a
X Xa
“Complex” la nivelul endoteliuui
COAGULAREA - intrinseca
XII XII akininogenprecalicreina
XI XI a
IX IX a
X Xa
COAGULAREA - extrinsecaVIIIa
Ca, F3plachetar
(1)factor tisular + F VII + Ca
VIII
colagenul subendotelial factorul XII
fibrinogen fibrina
Faza comuna a in coagularea intrinseca si extrinseca X Xa
II IIa
Fibrinoliza
+tPA
Pro UK
PAI
trombina
Plasminogen
Plasmina-
+
+
Fibrina
PD Fibrina
fibrinogen fibrina
Anticoagularea naturala
X Xa
II IIaInactiveaza Va
Proteina CProteina S
Proteina C a
Trombomodulina + trombina
Inactiveaza VIIIa
Antitrombina
Sindrom hemoragic prin anomalii de coagulare
1. Hemofilia A deficienta factor VIII
- anomalia genei F VIII – bratul lung cromozom X - mutatii punctiforme, deletii importante
- boala afecteaza aproape exclusiv barbatii, deoarece la femei heterozigote cromozomul X asigura sinteza necesara de f VIII
- incidenta 1/ 10 000
Hemofilia A - deficienta factor VIIIX
y xx
Xy
Xyx
xXy
Xy
Xy x
xx
xX Xy
xx
xxX
XX X
y
Generatia I
Generatia II
Generatia III
Generatia IV
X
Xy
Factorul VIII – proteina 80 000 daltoni, pe suprafata f. von Willebrand
F VIII – sintetizat in ficat- concentratie plasmatica = 10 g/l
- durata de viata 8-12 ore
Hemostaza normala necesita activitate – 25% f VIII
- Clinic
- copii - baieti, tineri - hematoame, hemartroza,
- hemoragii: muschi,
orofaringe, cerebrale
Hemofilia A
Hemartroze – hemofilia A
- Diagnostic paraclinic
- T sangerare = normal - T coagulare = prelungit - T protrombina = normal - T tromboplastina partial
activata = prelungit
- AND fetal
- Concentratie F VIII = scazuta
- Forme- severe …….. 1% activitate f VIII
- medii …….. 1-5% activitate f VIII
- usoare …….. 5% activitate f VIII
- f usoare .… 5 - 25% activitate f VIII
Tratament
• Profilactic de 2X pe saptamana• CurativKogenate 1000 UI 15 flOctanate 500 UI 13 fl• 1UI/kgc factor VIII creste concentratia
plasmatica cu 1%
Tratament
- crioprecipitat plasma Forme medii
Forme usoare
- desmopresin – creste nivelul F VIII
- EACA – inainte de extractii dentare inhibitor de fibrinoliza ( inhiba activatorul tisular plasminogen)
Tratament
- concentrat de factor VIII - prin absorbtie pe anticorpi monoclonali sau f VIII recombinat
- chirurgia majora, ortopedica - cu pretestarea inhibitorului FVIII – pentru nivel 50% a FVIII,2 sapt - adm la interval de 8 ore sau 12 ore
- profilactic - la simptome, fara hematoame, a redus hemartroza
Forme severe
1. Hemofilia B – boala Christmas deficienta factor IX
- Anomalia genei IX – bratul lung cromozom X
- mutatii punctiforme, 1/3 spontane- microdeletii
- 800 pattern- uri de anomalii moleculareex: factor IX Leiden – 11 mutatii punctiforme
- Factor IX - sinteza hepatica dependenta de vit. K
- 20% din hemofilii
1. Hemofilia B – boala Christmas deficienta factor IX
- Paraclinic – concentratia fact IX < 1%
- Tratament – plasma proaspata, - complex protrombinic liofilizat ( risc de tromboze)
- Clinic – sindrom hemoragipar expresie fenotipica variabila
- ameliorare la pubertate, sub androgeni
1. Boala fon Willebrand- precursor F Willebrand sintetizat de endoteliu si megacariocite- functii F Willebrand
- adeziunea trombocit la endoteliu- transportor f VIII
- TS - prelungit- agregare plachetara la ristocetina= absenta - APTT– normal, T Quik-normal- concentratia de F Willebrand - scade
- concentratia plasmatica: 10 mg/dl
- tratament: crioprecipitat, desmopresin
- Boala Von Willebrand - 1 la 100 – 500 persoane este cea
mai comuna anomalie mostenita de sangrare
- FvW - glicoproteina multimerica heterogena secretata de endoteliu si
plachete
1. favorizeaza adeziunea plachetelor la receptori subendoteliali
2. transportor plasmatic al F VIII- nivel palsmatica 10mg/L
– reduceri modeste FvW sau modificare moleculara determina S hemoragipar
Boala von Willebrand:- boala autosomal dominanta, forma
heterozigota vWf este produs de gena normala
- BvW tip I - nivel descrescut cu 50% al FvW
- Clinic: sangerare la traumatisme, chirurgie, epistaxis, hemoragii mici mucoase, subcutanate
- Diagnostic: - TS > - nivel plasmatic vWF < - aglutinare la ristocetina< (activitate
biologica)- spectru normal al multimerilor la
electroforeza in agaroza
- activitatea F VIII scazuta
- Boala von Willebrand: - BvW tip II - nivel noraml FvW
disfunctional pentru multimerii cu greutate moleculara mare si medie, fenomen detectat la electroforeza in agaroza
- BvW tip II a - deficienta a FvW cu greutate moleculara mare sau medie, mutatie in
domeniul A2 – deficienta de secretie sau proteoliza a multimerilor vWF, - FvW si F VIII – concentratii normale
- BvW tip II b – descrestere FvW cu greutate moleculara mare, legare inadecvata de
plachete si eliminare a Pl+FvW anormal, cu trombocitopenie secundara
- mutatie in domeniul I ce se laga de glicoproteina Ib IX
- - FvW si F VIII – concentratii
normale
- BvW tip III - autosomal recesiva- incidenta 1 la 1 milion
- parinti heterozigoti pentru defecte diferite sau homozigoti pentru acelasi defect – FvW absent + F VIII redus
Clinic: sangerari de mucoase + hemartroze
- BvW tip IIn- defect legare FvW de F VIII
- Clinic:
- TS - prelungit- Agregare plachetara la ristocetina= absenta - APTT– normal, T Quik-normal- Concentratia plasmatica F Willebrand - scade
- femei si barbati- hemoragii cutanate si mucoase
- Tratament: crioprecipitat, desmopresin
- forme:- usoare, medii, severe
- DG. paralinic:
- Tratament- concentrate de F VIII
- menoragia – contraceptive orale
- DDAVP sau desmopresina (vaspresina) – creste retentia de fluide – stimuleaza
eliberarea FvW- nu in tipul IIa !!!
Deficienta factor XI
- Tratament – plasma proaspata inghetata o infuzie/zi
- transmitere autosomal recesiva - mai frecventa la evrei din Ashkenazi
- Clinic – sangerare posttraumatica - menometroragii
Deficienta de factor V, VII. X si II
- Tratament – plasma proaspata inghetata o infuzie/zi
- transmitere autosomal recesiva - rare
- Clinic – sangerare posttraumatica - menometroragii
Afibrinogenemia si disfibrinogenemia
- Tratament – plasma proaspata inghetata
- Clinic – sangerare - tromboze in disfibrinogenemie (rar)
- Paraclinic- afibrinogenemie: scaderea concentratie de fibrinogen
- disfibrinogenemie: - Timp protrombina prelungit - Timp tromboplastina prelungit
- Timp trombina prelungit
1. Deficienta dobandita a factorilor de coagulare
- vitamina K -- plante- sintetizata de flora intestinala
vit K
epoxidaza
reductaza
vit K epoxid
Anticoagulanti cumarinici
- Deficienta vitamina K influenteaza -- f II- f VII- f IX- f X
- proteina C si S
- Cauze deficienta vitamina K -- aport insuficient- antibioterapie per os- sindr biliar obstructive- f X- boli hepatocelulare grave- antagonisti de vit K
- Clinic -- sindrom hemoragipar functie de deficienta de vit K- forme usoare - severe
- Tratament - - plasma proaspata, sange proaspat - vit K parenteral – 10mg - restabileste depozitele hepatice in 8 -10 ore
- paraclinic -- TC – prelungit, T Quik - prelungit
- Cauze de sangerare in boli de ficat
- scade sinteza : fibrinogen, protrombina, fact V, VII, IX, X, - scade sinteza: proteina C,S,
antitrombina III - CID - vit K - scade absorbtia si metabol - monocit - macrofag
insuficient functional
- fibrinoliza sistemica primara - trombocitopenie
Coagulare intravasculara diseminata
Sindrom clinicopatologic caracterizat prin formarea unor retele de fibrina intravascular.
Coagulare intravasculara diseminata
Mecanism: -generarea necontrolata de trombina -expunerea la nivele patologice de FT -supresia mecanismelor anticoagulante fiz. -fibrinoliza anormala
Coagulare intravasculara diseminata
Insuficienta organica multipla: -depozite de fibrina in vasele mici si medii -afectarea circulatiei:F,R, creier,plaman -ischemie -hemoliza intravasculara
Coagulare intravasculara diseminata
Consumul trombocitelor si factorilor de coag. - sangerare difuza -fibrinoliza -PDF, d-Dimeri
Coagulare intravasculara diseminata
- infectii sistemice: stafilo, meningococ, B Gram neg
- sindr obstetricale: avort, eclampsie, dezlipire placenta - neoplazii: LAM, adenocarcinoame - hemoliza intravasculara- distructii tisulare: traumatisme, arsuri, etc- leziuni endoteliu: SHU, GNA, hemangiom cavernos- ciroza
Factori etiologici
XII a
PDF exces in microcirculatie
XII a
Tromboze
Fibrinoliza in excesActivare coagulare in microcirculatie
Sangerare difuza
XII a
PDF exces in microcirculatie
PDFcoagulare fibrinoliza
Tromboze Sangerare difuza
- neurologic : semne focar, convulsii, coma
- piele : ischemie focala, gangrena
- plaman : SDRA
- gastrointestinal : sangerare acuta
- laborator : trombocite <, F VII, V<, Fibrinogen<, PDF> 4g/dl, AH microangiopatica
- petesii,- sangerare - pe mucoase -(gastrointestinala, hemoptizieepistaxis) - neurologica
Coagulare intravasculara diseminata
Coagulare intravasculara diseminata
CID – dg. paraclinic 1. trombocitopenie
2. AH microangiopatica
schizocite
3. TC >, aPTT >, TQ >
5. PDF+++4. Fibrinogen <
- Tratament
- tratamentul bolii de baza - reechilibrare hidroelectrolitica - heparina –1000 UI/ora, 5000 UI la 4ore - EACA = 4-6g/24 ore
( blocheaza PDF)
Coagulare intravasculara diseminatacronica
-hemangioame gigante-carcinoame metastatice-fetus mort
CID cronic– dg. paraclinic 1. Trombocite-N sau usor
2. AH microangiopatica
schizocite3. aPTT -N, TQ -N
5. PDF+++4. Fibrinogen -N
- Fibrinoliza
activator tisular plasminogen
plasminogen tromb
plasminafibrina
anti plasmina2
PAI
- Fibrinoliza primara
- deficitul anti plasmina2
- scade mult fibrinogenul
- sindrom hemoragipar
- aPTT, T Quick – aproape normale - trombocite normale
- paraclinic
- tratament - plasma proaspata, EACA
ELEMENTE CLINICE DIAGNOSTIC DIFERENTIAL
- varsta, sex - Sindromul hemoragipar
- conditii de declansare - purpura - localizare - leziuni palpabile, buloase,
micronecrotice - acuta, cronica
- hemoragii: mucoase, articulare, SNC
ELEMENTE PARACLINICE DIAGNOSTIC DIFERENTIAL
- Timp sangerare - Trombocite - Timp coagulare
- concentratie f VIII, IX, von willebrand
- aPTT - t Quick
- PDF - liza cheagului
- fibrinogen