causes of thrombosis
virchow’s triad:
1 - injury to vessel wall
2 - increased coagulability
3 - decreased flow
hemostasis
thrombosis
thrombus
coagula that forms inside blood vessels or heart chambers
clot
coagula outside of blood vessels or in vessels after death
pathogenesis of thrombosis - endothelial injury
1 - injury/loss to endothelial cells 2 - inflammation 3 - anatomic alterations - plaques 4 - trauma/surgery 5 - endothelial dysfunction
pathogenesis of thrombosis - abnormal blood flow
pathogenesis of thrombosis - hypercoagulability
1 - primary (genetic)
common: factor V (G1691A), prothrombin (G20210A), (C677T) mutations, or increased factors VIII, IX, XI, or fibrinogen
rare: protein C or S, or antithrombin III deficiency
2 - secondary (acquired) - cardiac failure, tissue damage, oral contraceptives, hyperestrogenic state, disseminated cancer, increased platelets, lifestyle
heparin-induced thrombocytopenia (HIT)
unfractionated heparin induces formation of antibodies against heparin-platelet factor 4
anti phospholipid antibody syndrome
ventricular mural thrombosis
vegetations
- endothelial injury from bacteria, antibodies, trauma
venous thrombosis - phlebothrombosis
venous thrombosis - thrombophlebitis
- can be sterile due to trauma or septic due to bacteria
thrombosis of microcirculation - DIC
- fibrin thrombi consume platelets and coagulation proteins which leads to bleeding disorder
outcomes of thrombosis (4)
1 - lysis (dissolution)
2 - organization in connective tissue
3 - propagation towards heart
4 - embolization
five most frequent types of embolisms
1 - pulmonary thromboembolism 2 - systemic embolism 3 - fat embolism 4 - air embolism 5 - amniotic fluid embolism
embolus
- can be part of thrombus, fat, cholesterol, gas, part of a tumor, bone marrow, foreign body, amniotic fluid
pulmonary thromboembolism
systemic thromboembolism
fat embolism
air embolism
caisson disease
- focal necrosis (femur, humerus, tibia)
amniotic fluid embolism