HEMOSTAZ

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HEMOSTAZ

• Yard. Doç. Dr. Murat ÖRMEN

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Vascular System
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PRIMER HEMOSTAZ
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Platelet Aggregation
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Function HEMOSTASIS BLEEDING AGREGOMETRI ANIMASYON
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Factor VII Proconvertin, Stable Factor
Biosynthesis Liver, Vitamin K dependent MW
55,000 daltons Plasma Concentration 1 mg/L In
Vivo Half-Life 5 hours Pathology
Hypoproconvertinemia, autosomal recessive
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Factor X Stuart-Prower Factor
Biosynthesis Liver, Vitamin K dependent MW
55,000 daltons Plasma Concentration 5 mg/L In
Vivo Half-Life 65 hours Pathology Stuart
disease, autosomal recessive
Tissue Factor Factor III, Thromboplastin Biosynth
esis Brain, lung, subendothelium MW 45,000
daltons
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Biosynthesis Liver MW 80,000 daltons Plasma
Concentration 29 mg/L In Vivo Half-Life 60
hours Pathology Hageman trait, autosomal
recessive
Factor XII Hageman Factor
High Molecular Weight Kininogen (HMWK) Fitzgerald
Factor MW 120,000 daltons Plasma Concentration
70 mg/L Pathology Fitzgerald trait, autosomal
recessive
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Prekallikrein Fletcher Factor
Biosynthesis Probably Liver MW 107,000
daltons Plasma Concentration 50 mg/L Pathology
Fletcher trait, autosomal recessive
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Factor XI Plasma Thromboplastin Antecedent
Biosynthesis Liver MW 158,000 daltons Plasma
Concentration 4 mg/L In Vivo Half-Life 65
hours Pathology Hemophilia C, autosomal recessive
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Biosynthesis Liver, Vitamin K dependent MW
57,000 daltons Plasma Concentration 4 mg/L In
Vivo Half-Life 20 hours Pathology Hemophilia
B, (Christmas disease) x-linked recessive
Factor IX Christmas Factor
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Factor VIII Antihemophilic Factor vWF von
Willebrand Factor
Biosynthesis Liver, endothelium Factor VIII
Related Antigen, megakaryocyte MW(FVIII vWF)
1.2-2 million daltons (6-10 subunits 200,000
daltons each) Plasma Concentration 7 mg/L
(vWF) In vivo Half-Life 10 hours (Factor
VIII) Pathology Factor VIII-Hemophilia A,
x-linked recessive. vWF-von Willebrands
disease, autosomal dominant
Factor IIa
Factor Xa
or
Procoagulant
Factor VIII
Activation
Factor VIIIa
Inhibition
Anticoagulant
Inactive Fragments
Protein C Complex
Activated Protein C
Protein S
Phospholipid (Platelet Factor 3)
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Biosynthesis Liver, Vitamin K dependent MW
70,000 daltons Plasma Concentration 100 mg/L In
Vivo Half-Life 100 hours Pathology
Hypoprothrombinemia, autosomal recessive
Factor II Prothrombin
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Factor V Proaccelerin, Labile Factor
Biosynthesis Liver, megakaryocytes MW 330,000
daltons Plasma Concentration 5-12 mg/L In Vivo
Half-Life 25 hours Pathology Parahemophilia,
autosomal recessive
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Biosynthesis Liver MW 340,000 daltons Plasma
Concentration 2500 mg/L In Vivo Half-Life 20
hours Pathology Afibrinogenemia, autosomal
recessive. Dysfibrinogenemia, autosomal
dominant
Fibrinogen Factor I
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Prothrombin Time
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Activated PartialThromboplastin Time
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Quantitative Fibrinogen
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Heparin/AT-III Complex
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Minimum Plasma Levels
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Vessels
Coagulation Proteins
Platelets
Fibrinolysis/Inhibitors
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Fibrinolysis
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Biosynthesis Liver MW 90,000 daltons Plasma
Concentration 120 mg/L In Vivo Half-Life 48
hours Pathology Plasminogen deficiency,
autosomal dominant. Dysplasminogenemia,
autosomal recessive
Plasminogen
tPA (tissue Plasminogen Activator)
or
or
Kallikrein
Urokinase
Anticoagulant
Plasminogen
Activation
Plasmin
Procoagulant
Inhibition
Plasmin
a2 - Anti- plasmin
a2 - Anti- plasmin
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Antithrombin-III Inhibitionof Thrombin
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Antithrombin-III Decreased Levels
1. Congenital 2. Acquired decreased
synthesis 3. Acquired increased
utilization 4. Drug-induced
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Protein C
Vitamin K-dependent plasma protein
Inactivates Factors V and VIII Stimulates
fibrinolysis
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Biosynthesis Liver, Vitamin K dependent MW
56,000 daltons Plasma Concentration 3-5 mg/L In
Vivo Half-Life 6-7 hours Pathology Protein C
deficiency, autosomal recessive (?)
Protein C
Thrombo- modulin
Factor IIa
Protein C Activation Peptide
Protein C
Anticoagulant
Activation
Activated Protein C
Inhibition
Activated Protein C
Procoagulant
Protein C Inhibitor
Requires Protein S for functional activity
Protein C Inhibitor
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Deficiencies of Protein C
I. Congenital Hereditary autosomal
dominant II. Acquired A. DIC B. Liver
disease C. During post-operative period D.
Anticoagulant therapy
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Clinical Manifestations
Superficial thrombophlebitis Venous
thromboses in adolescents or young adults
Arterial thromboses rarely observed Skin
necrosis during onset of oral anticoagulant
therapy
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Protein S
Cofactor for Protein C Vitamin K-dependent
protein Enhances binding of Protein C to
phospholipid surfaces
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