v. hyper coagulation state
DESCRIPTION
Hyper Coagulation StateTRANSCRIPT
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Hyper coagulation state
Najmeh VaghefMsc student in Tarbiat modares university
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Introduction Definition of thrombus Review of coagulation triangular and it’s
relation with hyper coagulation Categories of thrombosis (arterial and
venous) and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation state
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Introduction Definition of thrombus Review of coagulation triangular and it’s
relation with hyper coagulation Categories of thrombosis(arterial and venous)
and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation to state
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Thrombus:A mass consist of blood elements that exist in circulation.
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Introduction Definition of thrombosis Review of coagulation triangular and it’s
relation with hyper coagulation Categories of thrombosis (arterial and
venous) and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation to state
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Procoagulant role of Elndothelial cells
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Anticoagulant role of Endothelial cells
No Ecto ADPase PGI2 Heparan sulfate Thrombomadulin tpA
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Platelet
Number Function
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Platelet Activation Pathways
ADP
Adrenaline
PlateletGpIb
Exposed Collagen
Endothelium
vWFAdhesionAdhesion
THROMBIN
GpIIb/IIIaGpIIb/IIIa Aggregation
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Coagulation Factors and inhibitors
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Introduction Definition of thrombosis Review of coagulation triangular and it’s
relation with hyper coagulation Categories of thrombosis (arterial and
venous) and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation to state
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Thrombosis:
ArterialIschemia and Infarctus
VenousEdema and emboli
(white thrombus)
(red thrombus)
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Inheritedhypercoagulable
states
Inheritedhypercoagulable
statesAcquired
hypercoagulablestates
Acquiredhypercoagulable
states
ThrombosisThrombosis
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Etiology of arterial thrombosis
Atherosclerosis Hypertension Hyper vescositemia Diabetic mellitus Hyper lypemia Vacuities Anti phospholipids syndrome
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Some hematological syndromes: TTP ,HUS, HITTS, Myeloprotive disorders,
Increase some proteins and amino acids: Lpa )LDL+Apoa(, Homocystein ) aquired and hereditary( ,Factor VII
Etiology of arterial thrombosis
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Homocysteinemia and hyper coagulation state Increase connection of Lpa to fibrin
Bad functional of Endothelial Cells )Anticoagulant surface change to procoagulant surface (
Reduced thrombomadulin Reduced tpA Reduced APC Increase factor )V(
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Treatment of arterial thrombosis
Anti platelet Anticoagulant If homocysteinemia exists with
thrombosis +foliate
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Etiology of venous thrombosis
Stasis Hyper coagulability Endothelial injury
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Virchow’s Triad
Hypercoagulability Endothelial injury Venous flow
disturbance )stasis or turbulence(
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Hyper coagulability
Protein defects:
Factor )V( Leiden ) 20-40%( G to A mutation at base pair 1691
results in amino acid 506,Glu instead of Arg
Prothrombin 20210 )6%()G to A(Defect or deficiency of protein C )4%( )outozomal dominant(
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Defect or deficiency of Protein S )3-4%( ) outozomal dominant( pregnancy and estrogens reduced protein S
Dysfibrinogenemia ) 3% (Antithrombin deficiency ) 1% (
)outozomal dominant ( acquired deficiency of it happened in sever obesity , liver disease , chronic renal failer , using ocp ,immature neonates
Hyper coagulability
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Dysplasminogenemia ) <1% (Reduced Heparin cofactor IIElevation of PAI-1Elevation of Coagulation factors
VII,VIII,IX,X,XI and IIReduction of protein Z Xa
Z XvitK
Hyper coagulability
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Hematologic diseases :DICHITTSAnti phospholipid syndromeTTPHUSPlatelet disordersHomocysteinemia
Hyper coagulability
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Risk factors for venous thrombosis
Age Prolonged immobility Obesity Neurological disease Cardiac disease Pregnancy Oral contraceptive (ocp) if the patient has
the factor ( V ) leiden mutation the risk is increased 28-fold
Surgery Malignancy
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Treatment of venous thrombosis
Anti fibrin-generating agents )Heparin, Hirudin, argatroban, LMW Heparin, Warfarin (
Lyses of cloths with thrombolytic therapy ) tpA, Streptokinase, Urokinase(
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Introduction Definition of thrombosis Review of coagulation triangular and it’s
relation with hyper coagulation categories of thrombosis (arterial and
venous) and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation to state
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3 questions in thrombosis
Thrombosis is venous or arterial ?Cause of thrombosis : acquired or hereditary?Acquired:
Vascular disorders ) atherosclerosis , diabetic mellitus , vacuities , homocysteinemia (
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Acquired
Blood flow disorders:
Stasis )immobility , CHF( Hypervescoshtemia ) P.V ,Leukemia ,
plasma cell disorders , sickle cell anemia
Platelet disordersMyeloprolifrativedisorders ,
thrombocytosis , hyper lypemia , PNH
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Acquired
Coagulation and Fibrinolytic disorders
Malignancies , nephritic syndrome , trauma , hyperthyroidism , liver disease , operation
Hematological disorders TTP , HUS , HITTS , DIC
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What cases need to follow up? Answer :
Familial thrombosisRecurrent autonomous thrombosis
Thrombosis in youth Surface migrant thrombofelebitsThrombosis in unusual sitesRecurrent abortions
Cases that need to follow up for hyper coagulation state
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Introduction Definition of thrombosis Review of coagulation triangular and it’s
relation with hyper coagulation Divided thrombosis tow categories (arterial
and venous) and review of their etiology and their treatments
The importance of getting case report properly and familial history of thrombosis
Review of lab tests for diagnostic of hyper coagulation to state
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Lab tests for diagnostic of hyper coagulation state
Factor ( V ) leiden Antithrombin III Prothrombin 20210 Protein C Protein S Protein Z Homocystein Specific platelet protein and increase of it’s
metabolism Decrease of fibrinolytic action ACLA, LACT, dRWVT D-dimmer , PTT
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Thank you for your
attention
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Thank you