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Mechanisms of Thrombosis
Maureane Hoffman, MD, PhD
Professor of Pathology
Duke University Medical Center
Durham, NC, USA
Thrombosis
Vascular Injury
endothelial cell
TF
VIIa
TF
Hypercoagulability
The coagulant/anticoagulant
proteins, blood cells and
endothelial cells each play roles
Hypercoagulability is multifactorial
Lifestyle and environmental
factors play critical roles
Hypercoagulability is multifactorial
This is different from
hemorrhagic disorders which
are often single gene defects
Oral contraceptive
5-7
FV Leiden, hetero + OC
30-35
FV Leiden, homozygous
80
FV Leiden, homo + OC
?>100
16
Arterial Thrombosis
Often results from deposition of
atherosclerotic plaque in the wall of an artery
(vascular injury), which narrows the channel
(altered blood flow)
Platelet deposition often linked to arterial
thrombosis
Rupture of the plaque can precipitate acute
thrombosis
Venous Thrombosis
Blocks return of deoxygenated blood
Common in the lower extremities, but can
also occur in the upper extremities
Symptoms include swelling, bluish
discoloration and pain
The most feared complication of venous
thrombosis is pulmonary embolism
Venous Thrombosis
Associated with stasis (immobility)
Associated with hypercoagulability
Inherited disorders (FV Leiden, AT
deficiency, Protein C/S deficiency)
Acquired disorders (obesity, smoking,
inflammation, oral contraceptives, cancer,
antiphospholipid syndrome)
Pulmonary Emboli
Bottom Line
Thromboembolism is multifactorial, and risk
factors accumulate (or even multiply)
Arterial and venous thrombosis have different
mechanisms and, thus, different risk factors
Clinical observation
Histology of thrombotic disorders
Effect of pharmaceutical agents
Animal models
Arterial
Venous
50
40
30
20
10
0
during infusion
4-24 hr
1-7 d
>7d