THEME 3: HEMOSTATIC DISORDERS AND ATHEROSCLEROSE
LECTURE 33 & 34 – PRIMARY HEMOSTASIS
Thrombophlebitis = vascular inflammation. Swelling of the leg due to coagulation
due to cancer.
Patients with cancer are more likely to develop thrombosis. In the first 3 months:
x54.
Khorana risk score:
But: when you have thrombosis, chance of developing cancer is increased (10% gets cancer within 3
years). In case of provoked thrombosis (clear causing factor), 1,6% develops cancer.
When having cancer AND thrombosis: chance of dying is big (within 6 months).
In cancer patients, anticoagulation with low molecular weight are preferred over vitamin K
antagonists. Treatment with LMWH improves 1-year survival of cancer patients, but no additional
benefit.
Mechanism of hemostasis:
- Vessel injury = major trigger
Vasoconstriction; reduction of blood
flow
Subendothelial collagen exposure
platelet adhesion and aggregation;
formation of platelet plug
These two form primary hemostasis:
closing the “hole”
Tissue Factor in the blood blood
coagulation; formation of fibrin
Bleeding can take many forms:
, Small spots: problem with primary hemostasis.
Thrombosis has different ways to present itself:
Primary hemostasis; platelet plug:
1. Adhesion of platelets
2. Aggregation of platelets
3. Platelet plug formation
Platelets with receptors:
Platelet adhesion:
- Binding to collagen via glycoprotein receptors on
platelet membrane
GPVI and GPIa bind to collagen
Von Willebrand factor binds to collagen. At high
shear VWF binds to GPIb
Platelet aggregation:
- Integrin receptor which can bind to fibrinogen,
fibronectin, VWF
- Receptor needs to be activated, rested state in the circulation
- The morphology of the platelets change when activated
Thromboxane is secreted by platelets, secreting other platelets.
Platelets have receptors – P2Y, PAR1 and TXA2R – which bind
LECTURE 33 & 34 – PRIMARY HEMOSTASIS
Thrombophlebitis = vascular inflammation. Swelling of the leg due to coagulation
due to cancer.
Patients with cancer are more likely to develop thrombosis. In the first 3 months:
x54.
Khorana risk score:
But: when you have thrombosis, chance of developing cancer is increased (10% gets cancer within 3
years). In case of provoked thrombosis (clear causing factor), 1,6% develops cancer.
When having cancer AND thrombosis: chance of dying is big (within 6 months).
In cancer patients, anticoagulation with low molecular weight are preferred over vitamin K
antagonists. Treatment with LMWH improves 1-year survival of cancer patients, but no additional
benefit.
Mechanism of hemostasis:
- Vessel injury = major trigger
Vasoconstriction; reduction of blood
flow
Subendothelial collagen exposure
platelet adhesion and aggregation;
formation of platelet plug
These two form primary hemostasis:
closing the “hole”
Tissue Factor in the blood blood
coagulation; formation of fibrin
Bleeding can take many forms:
, Small spots: problem with primary hemostasis.
Thrombosis has different ways to present itself:
Primary hemostasis; platelet plug:
1. Adhesion of platelets
2. Aggregation of platelets
3. Platelet plug formation
Platelets with receptors:
Platelet adhesion:
- Binding to collagen via glycoprotein receptors on
platelet membrane
GPVI and GPIa bind to collagen
Von Willebrand factor binds to collagen. At high
shear VWF binds to GPIb
Platelet aggregation:
- Integrin receptor which can bind to fibrinogen,
fibronectin, VWF
- Receptor needs to be activated, rested state in the circulation
- The morphology of the platelets change when activated
Thromboxane is secreted by platelets, secreting other platelets.
Platelets have receptors – P2Y, PAR1 and TXA2R – which bind
