thrombosis Flashcards
what is virchow’s triad
endothelial injury, blood stasis or turbulence of blood flow, blood hypercoagulaboilty
what dirction do thrombi grow
toward the heart
what are some antiplatelete effects
no binding to endothelium and PGI2 and NO prevent platelet adhesion
what are some anticoagulant properties
herparin like molecule activate anti thrombin 3, thrombomodulin activates protein c
what are some fibronlytis properties
endothelium made tPA
what inhibits platelests
ASA?
what is the diffence between a hemostatic plug and a clot
plug is still reversible whereas a clot is not
how does turbulence and stasis of effect thrombosis
turbulance will enhance endothelial injury and stasis leads to venous thrombosis,
what happens to von willebrand factor with increased blood flow
it will unfold and become more sticky.
what makes the fibrin clot
when the plug made of fibrin gets cross likes it will make the fibrin clot.
how does the degradation process start
plasminogen is converted to plasmin and then it degrades the clot.
tell me about pulmonary thrombolism
small will be silent, medium will have an acute respiratory and cardiac symptoms and fear, large right heart failure and collapse, massive sudden death with saddle embolus.
what are some causes of hypercoagulability primary
Factor 5 leiden mutation, antithrombin 3 deficeincy, protein c or s defeciency, prothrombin G20210A gene mutation
what are some causes of hypercoagulability secondary
anti phospholipid syndrome, lups anticoagulant, cancer, nephrotic syndrom, contraceptive pills, smoking, prolonged immobilazation.
what are some other hypercoagulability states
heparin induced thrombocytopenia, and antiphospholipid syndrom [lupus] antibodies to phospholipids, invitro inhibits coagulation in vivo indueds it,