Thrombosis
Thrombus
Thrombi
ANTITHROMBOTIC PROPERTIES
? Inhibition of platelet aggregation,
PGI2,NO,ADPase
? Anticoagulant -binding and inhibition of
thrombin,Antithrombin III acceleration
by heparin-like molecules,thrombomodulin
activation of protein C/S,?2-macroglobulin.
? Fibrinlysis,Tissue plasminogen activator (tPA)
PROTHROMBOTIC PROPERTIES
? Simulation of platelet aggregation
(adhesion),von Willebrand factor,
platelet-activating factor.
? Procoagulation factors,Tissue factor,
binding factors IXa and Xa,Factor V.
? Inhibition of fibrinolysis,t-PA inhibitor.
? Fig 5-5
? Fig 5-6
THREE INFLUENCES OF THROMBOSIS
? Endothelial injury (most important),
Alone can induce thrombosis.
? Alterations in normal flow.
? Hypercoagulability.
When the last two are both present,
endothelial injury is not requisite.
? Fig 5-8
Endothelial injury
? Ulcerative atherosclerosis
? Transmural myocardial infarction
? Vasculitis
? Trauma
? Radiation
? Bacterial toxins
Alterations in normal blood flow
? Platelets activated by contact with
endothelium.
? Slowed flow retards dilution of activated
clotting factors and hepatic clearance.
? Stasis or turbulence retards the inflow of
inhibitors.
? Turbulence may induce endothelial injury
Hypercoagulable states
Primary (genetic):
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Other combined deficiency
Hypercoagulable states
Secondary (acquired):
High risk:
Prolonged bed rest or immobilization.
Myocardial infarction,Tissue damage
(surgery,fractures,burns),Cardiac failure,
Cancer,Acute leukemia,DIC,
Myoproliferative disorders,Prosthetic
cardiac valves,Homocystinuria,
Thrombotic thrombocytopenia.
Hypercoagulable states
Secondary (acquired):
Low risk:
Atrial fibrillation,Cardiomyopathy,
Nephrotic syndrome,Hyperlipidemia,
Late pregnancy/postdelivery,
Oral contraceptives,Lupus anticoagulant,
Sickle cell anemia,Smoking,
Thrombocytosis.
White thrombus
Mixed thrombus
Red thrombus
Fibrin thrombus
Types of thrombus
Absorption
Organization
Calcification
Detachment
Fate of thrombus
Ischemia
Congestion
Heart valve disease
DIC
Embolism
Effects of thrombosis
Thrombus
Thrombi
ANTITHROMBOTIC PROPERTIES
? Inhibition of platelet aggregation,
PGI2,NO,ADPase
? Anticoagulant -binding and inhibition of
thrombin,Antithrombin III acceleration
by heparin-like molecules,thrombomodulin
activation of protein C/S,?2-macroglobulin.
? Fibrinlysis,Tissue plasminogen activator (tPA)
PROTHROMBOTIC PROPERTIES
? Simulation of platelet aggregation
(adhesion),von Willebrand factor,
platelet-activating factor.
? Procoagulation factors,Tissue factor,
binding factors IXa and Xa,Factor V.
? Inhibition of fibrinolysis,t-PA inhibitor.
? Fig 5-5
? Fig 5-6
THREE INFLUENCES OF THROMBOSIS
? Endothelial injury (most important),
Alone can induce thrombosis.
? Alterations in normal flow.
? Hypercoagulability.
When the last two are both present,
endothelial injury is not requisite.
? Fig 5-8
Endothelial injury
? Ulcerative atherosclerosis
? Transmural myocardial infarction
? Vasculitis
? Trauma
? Radiation
? Bacterial toxins
Alterations in normal blood flow
? Platelets activated by contact with
endothelium.
? Slowed flow retards dilution of activated
clotting factors and hepatic clearance.
? Stasis or turbulence retards the inflow of
inhibitors.
? Turbulence may induce endothelial injury
Hypercoagulable states
Primary (genetic):
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Other combined deficiency
Hypercoagulable states
Secondary (acquired):
High risk:
Prolonged bed rest or immobilization.
Myocardial infarction,Tissue damage
(surgery,fractures,burns),Cardiac failure,
Cancer,Acute leukemia,DIC,
Myoproliferative disorders,Prosthetic
cardiac valves,Homocystinuria,
Thrombotic thrombocytopenia.
Hypercoagulable states
Secondary (acquired):
Low risk:
Atrial fibrillation,Cardiomyopathy,
Nephrotic syndrome,Hyperlipidemia,
Late pregnancy/postdelivery,
Oral contraceptives,Lupus anticoagulant,
Sickle cell anemia,Smoking,
Thrombocytosis.
White thrombus
Mixed thrombus
Red thrombus
Fibrin thrombus
Types of thrombus
Absorption
Organization
Calcification
Detachment
Fate of thrombus
Ischemia
Congestion
Heart valve disease
DIC
Embolism
Effects of thrombosis
