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,
where do you get DVT from
popliteal femoral iliac veins
what leads to DIC
disseminated intravascular coagulation can be caused by shock infection pregnancy with malignancy.
what is the second most common medical complication
VTE venous thrombi embolism
what is the most common cause of preventable hospital death
pulmonary embolism
what is a parodoxical embolus
when it will pass from right side to left of the heart by a septal defect
what is the vulnerability to hypoxia of neurons heart and fibrous tissue
3-4 min neuron, 20-30- heart, and hours for fibrous tissue
what the inherirted hypercoagulabilities with highes relative risk
antithrombin deficiency 10x but only 5% of pop, prothrombin mutation 7%, defeciecy in protein c and protein s 5% and 10 rr
what should you look for before oral contraceptives prescription
possible factor 5 leiden because it will increaase rr by 34.7
what are some threpuetic options for thrombosis
heparin LMW heparis, throbolysis, warfarin, ASA PGP 2B/3a inhibititors.
what is purple skin syndrom
3% of people who go on warfarin will get this common on toes and skin reversible with heparin.
what percent of thrombosis is accounted by factor 5 leiden
About 50%
how do you test for factor 5 and prothrombin
DNA genetic tests.
what is the overall risk of thrombosis
1:1000 adults children less need several factors to really be at risk.
