| what is the difference in composition between venous and arterial thrombi? | venous thrombi: mostly fibrin and erythrocytes, some platelets
arterial thrombi: mostly platelets in the core |
| what is Virchow's triad and what does it compose of? | Virchow's triad are the three factors that can lead to venous thrombosis, they are: hemodynamic changes (stasis), endothelial wall injury and hypercoagulation |
| what do hemodynamic changes in Virchow's triad mean? and when does it happen? | turbulence (disorganized blood flow) and stasis (static pockets of blood)
it happens after long periods of inactivity of the skeletal muscle pump (long flights, bed rest) and during pregnancy |
| what does hypercoagulation in Virchow's triad mean? and when does it happen? | hypercoagulation is the increased amount of clotting factors
it can happend during surgery (endothelial damage), birth control medication and genetics |
| what could cause damage to the endothelial lining (Virchow's triad)? | infection, chronic inflammation, toxins like tobacco smoke, hypertension or shear stress |
| what is the difference between venous and arterial thrombi regarding embolization | venous thrombi: only a part/tail of the thrombus becomes an embolus, can become a pulmonary embolism or cause an embolic stroke in the brain
arterial thrombi: often the entire thrombus becomes an embolus, can effext any organ |
| what is the cause of arterial thrombosis? | often atherosclerosis, a plaque that ruptures and to which platelets adhere |
| what drugs/structures can be used to treat venous thrombosis? | heparin: increases the activity of antithrombin, increasing the inhibition of factor Xa and thrombin
vitamin K antagonists (warfarin): inhibition of vitamin K unables it to modify a lot of coagulation factors, less clotting as a result
fibrinolysis (recombinant tPA): tPA will turn plasminogen into plasmin and plasmin will digest the clots.
dabigatran, lepirudin, desirudin: direct inhibitors of either thrombin or factor Xa, no fibrin mesh formed. |
| what drugs/structures can be used to treat arterial thrombosis? | Aspirin: inhibits cyclooxygenase, prevents autofeedback mechanism that amplifies platelet activation
ADP-receptor antagonist (clopidogrel): inhibits ADP receptor, ADP cannot bind, less platelets will be attracted.
PAR1 inhibition: thrombin cannot bind to its receptor, cannot amplify the cascade.
receptor integrin alpha 2b beta 3 inhibition: reduces platelet aggregation by inhibiting binding of platelets to fibrinogen |
| what step in hemostasis should treatments target in both venous and arterial thrombosis? | venous thrombosis: step 3; coagulation cascade
arterial thrombosis: step 2; platelet plug formation |
