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Endothelial injury
This is the dominant influence
Thrombosis results from exposed ECM and tissue factor and platelet adhesion
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Alteration of Flow
Normal blood flow is laminar with cellular elements located
centrally in the vessel lumen separated from the endothelial wall by
a plasma clear zone. Stasis and turbulent flow disrupt laminar flow
with a number of consequences:
platelets contact endothelium
Stasis elicits thrombosis in the venous system, cardiac chambers
and aneurysmal dilatations.
Plaques disrupt laminar flow in addition to producing endothelial
injury.
Anything that promotes blood viscosity (hyperviscosity syndromes)
promotes stasis (polycythemia, sickle cell, dehydration, etc.).
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Hypercoagulability
An alteration of coagulation that predisposes to thrombosis, this is the least frequent
cause for thrombosis but allows the simplest opportunity for intervention.
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Hypercoagulability
Acquired Hypercoagulability:
1. Oral contraceptives or hyper-estrogenic states (pregnancy) create
hypercoagulability by increasing the synthesis of coagulation factors and
deceased production of antithrombin III.
2. Certain malignancies and disseminated cancers release procoagulant tumor
products.
3. Advanced age is associated with increased platelet aggregation.
4. Smoking
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Morphology of Thrombi
Thrombi may form any where in the vascular
system, they vary in size and shape depending
on their site of origin and how firmly they are
attached at their origin.
Arterial thrombi Click to edit Master text styles
Found in areas of active flow
Second level
● Third level
Commonly show layering of platelets & fibrin (Lines of ● Fourth level
Zahn)
● Fifth level
Cardiac & aortic thrombi tend to be non-occlusive
(↑↑↑flow).
Tend to propagate distally often with embolization (can
propagate retrograde)
Atherosclerotic plaques, endothelial injury, areas of
turbulent flow serve as nidus
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Venous thrombosis:
1. Characteristically in areas of low/no flow or turbulent flow.
2. Superficial thrombi usually occur in enlarged saphenous veins.
3. Deep vein thrombi (DVT) generally occur in veins proximal to the knee and due to
the abundant collateral venous system are asymptomatic in 50 % of instances prior
to an embolic event. The situations associated with increased risk of DVT are legion,
anything that involves prolonged immobilization (? > 8 hours, particularly associated
with dehydration) CHF, trauma (including surgical), pregnancy and post-partum
states* and malignancy.
4. Often associated with inflammatory changes ( thrombophlebitis).
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The Fate of the Thrombus
Once formed the thrombus has a limited number of fates:
1. Propagation with subsequent vessel occlusion, depending
on the location and type of vessels the sequelae may be
minor (superficial vein thrombosis) or catastrophic (stroke,
MI, etc.).
2. Embolization to downstream sites (PE)
3. Dissolution by fibrinolytic activity (a therapeutic intervention)
4. Organization & recanalization, endothelial cells, smooth
muscle cells and fibroblasts create vascular channels in the
thombus.
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Embolism
● Fourth level
● Fifth level