Thrombosis Flashcards
Properties of anticoagulant factors
Natural anticoagulant proteins are reduced at birth
Liver produces coagulation proteins
–> liver disease leads to deficiency and/or decreased clearance of activation factors, increasing the risk of coagulopathy/thrombosis
Inflammation increases FVIII activity
Fibrinogen properties
Made in liver
Normal levels in infancy
Not vitamin K- dependent
Acute phase reactant
Factor VIII properties
Made in liver and endothelial cells
Normal or high levels in infancy
Not Vitamin K-dependent
Acute phase reactant
Factor IX properties
Made in liver
Low levels in infancy
Vitamin-K dependent
vWF properties
Made in endothelial cells and megakaryocytes
Normal/high levels in infancy
Not vitamin K-dependent
Acute phase reactant
Protein C
Made in liver
Low levels in infancy, normalizes in adolescence
Vitamin K-dependent
Must be activated by thrombin/thrombomodulin complex
AD inheritance
Protein S
Made in liver, endothelial cells, megakaryocytes, brain tissue
Low levels in infancy
Vitamin-K dependent
Inflammation increases C4b binding protein, reduced free protein S
Normalized by 6-12 months of age
Antithrombin (AT)
Made in liver
Low levels in infancy, normalized by 6-12 months of age
Not vitamin K dependent
Thrombophilia
a predisposition to develop thrombosis
Can be due to venous thrombotic events or arterial events
Can be inherited or acquired
Antithrombin
Made in liver
neutralized thrombin (IIa), Xa, IXa
Heparin potentiates activity
Has 2 binding sites: one is heparin binding site, other is reactive center
AT-III Deficiency
Thrombotic events (venous events more common)
40% of events spontaneous
High rate of PE
Very high rate of recurrence
Homozygous - fetal demise
AD inheritance
Type 2 Heparin Binding defects less likely to have thrombosis
Protein C deficiency
Varies with age, does not normalize until adolescence
Mainly venous events
Possible association with arterial stroke
70% spontaneous thrombosis
High risk of recurrence
