v. hyper coagulation state
DESCRIPTION
Hyper Coagulation StateTRANSCRIPT
Hyper coagulation state
Najmeh VaghefMsc student in Tarbiat modares university
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
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
Thrombus:A mass consist of blood elements that exist in circulation.
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
Procoagulant role of Elndothelial cells
Anticoagulant role of Endothelial cells
No Ecto ADPase PGI2 Heparan sulfate Thrombomadulin tpA
Platelet
Number Function
Platelet Activation Pathways
ADP
Adrenaline
PlateletGpIb
Exposed Collagen
Endothelium
vWFAdhesionAdhesion
THROMBIN
GpIIb/IIIaGpIIb/IIIa Aggregation
Coagulation Factors and inhibitors
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
Thrombosis:
ArterialIschemia and Infarctus
VenousEdema and emboli
(white thrombus)
(red thrombus)
Inheritedhypercoagulable
states
Inheritedhypercoagulable
statesAcquired
hypercoagulablestates
Acquiredhypercoagulable
states
ThrombosisThrombosis
Etiology of arterial thrombosis
Atherosclerosis Hypertension Hyper vescositemia Diabetic mellitus Hyper lypemia Vacuities Anti phospholipids syndrome
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
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(
Treatment of arterial thrombosis
Anti platelet Anticoagulant If homocysteinemia exists with
thrombosis +foliate
Etiology of venous thrombosis
Stasis Hyper coagulability Endothelial injury
Virchow’s Triad
Hypercoagulability Endothelial injury Venous flow
disturbance )stasis or turbulence(
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(
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
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
Hematologic diseases :DICHITTSAnti phospholipid syndromeTTPHUSPlatelet disordersHomocysteinemia
Hyper coagulability
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
Treatment of venous thrombosis
Anti fibrin-generating agents )Heparin, Hirudin, argatroban, LMW Heparin, Warfarin (
Lyses of cloths with thrombolytic therapy ) tpA, Streptokinase, Urokinase(
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
3 questions in thrombosis
Thrombosis is venous or arterial ?Cause of thrombosis : acquired or hereditary?Acquired:
Vascular disorders ) atherosclerosis , diabetic mellitus , vacuities , homocysteinemia (
Acquired
Blood flow disorders:
Stasis )immobility , CHF( Hypervescoshtemia ) P.V ,Leukemia ,
plasma cell disorders , sickle cell anemia
Platelet disordersMyeloprolifrativedisorders ,
thrombocytosis , hyper lypemia , PNH
Acquired
Coagulation and Fibrinolytic disorders
Malignancies , nephritic syndrome , trauma , hyperthyroidism , liver disease , operation
Hematological disorders TTP , HUS , HITTS , DIC
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
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
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
Thank you for your
attention
Thank you