Thrombosis Flashcards
Describe the process of protein C and protein S in stopping hemostasis
They inhibit factor V and VIII to stop clotting
Describe the antithrombin in stopping hemostasis
- made in liver & circulates in blood
- binds to thrombin to stop clotting
What happens if we have too much hemostasis
arterial thrombosis: stroke, heart attack
venous thrombosis: DVT, PE
What are the thrombotic mechanisms and risk factors associated with arterial clotting
- underlying vascular disease
- excess platelet activation
What are the thrombotic mechanisms and risk factors associated with venous clotting
- stasis
- failure to regulate thrombin generation
Describe the difference between arterial and venous clots
Arterial: primarily platelets with a little bit of fibrin
Venous: primarily fibrin with a little bit of platelets
Describe the difference in treatment between arterial and venous clotting
Arterial: RF mods & antiplatelet drugs (ASA)
Venous: prophylaxis, blood thinners
What things can cause both arterial and venous thrombosis
- antiphospholipid antibodies
- myeloproliferative disorders
- heparin induced thrombocytopenia
Describe superficial thrombophlebitis
inflammation of superficial veins (tributaries of great saph)
What are the 5 major thrombophilias
Traditional (multiple mutations, rare, strong)
- antithrombin deficiency
- protein C deficiency
- protein S deficiency
Modern (point mutations, common, weak)
- factor V Leiden
- prothrombin gene mutation
Which thrombophilias have a failure to control thrombin generation
- factor V leiden
- prothrombin gene mutation
- protein C & S deficiency
Describe the pathophysiology of factor V leiden
Point mutation in factor V gene at critical site involved in binding of fV to APC (protein C)
List some acquired triggers for thrombosis
- immobilization
- surgery
- trauma
- pregnancy/post partum
- estrogens
- age
Which genetic thrombophilias are generally weaker/asymptomatic
Which genetic thrombophilias are generally stronger/more symptomatic
