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Autoimmune hemolytic anemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hemolytic disease of the newborn
Paroxysmal nocturnal hemoglobinuria
Pyruvate kinase deficiency
Sickle cell disease (NORD)
Folate (Vitamin B9) deficiency
Vitamin B12 deficiency
Anemia of chronic disease
Iron deficiency anemia
Vitamin K deficiency
Langerhans cell histiocytosis
Essential thrombocythemia (NORD)
Polycythemia vera (NORD)
Acute intermittent porphyria
Porphyria cutanea tarda
Disseminated intravascular coagulation
Von Willebrand disease
Monoclonal gammopathy of undetermined significance
Thrombotic thrombocytopenic purpura
Antithrombin III deficiency
Factor V Leiden
Protein C deficiency
Protein S deficiency
Coagulation disorders: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Leukemias: Pathology review
Lymphomas: Pathology review
Macrocytic anemia: Pathology review
Microcytic anemia: Pathology review
Mixed platelet and coagulation disorders: Pathology review
Myeloproliferative disorders: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Plasma cell disorders: Pathology review
Platelet disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
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Factor V Leiden and Pregnancy Success Story
Factor V Leiden Thrombophilia
Acquired & Inherited Thrombosis Syndromes
venous sinus thrombosis and p. 515
Factor V Leiden is a disorder where blood clots form more easily due to a mutation in a clotting protein called factor V. Factor V Leiden is the most common hypercoagulable disorder in people of caucasian descent, and was named after the town Leiden in Holland, where the disease was first described.
Now, Factor V Leiden is a hemostasis disorder.
Hemostasis is the process where blood flow is stopped after there’s damage to a blood vessel, and it has two steps.
Primary hemostasis involves the formation of a platelet plug at the site of injury, and secondary hemostasis involves the coagulation cascade, where several clotting factors come into play to form a fibrin mesh over the platelet plug to reinforce it - forming a blood clot.
Hemostasis can be both stimulated, and inhibited by several factors.
One way to stimulate hemostasis is with thrombin, or factor II, which increases platelet activation, and cleaves several factors involved in secondary hemostasis to their active form.
So one way to inhibit hemostasis is actually to inhibit thrombin.
This happens with the help of anticoagulant proteins like protein C. Protein C is a vitamin K dependent circulating plasma protein produced in the liver along with a cofactor called protein S.
Both protein C and S interact with a protein called thrombomodulin, which is on the surface of intact endothelial cells that line our blood vessels.
So, let’s say you cut your finger and now a blood clot has formed.
When there’s a lot of thrombin around a damaged blood vessel, excess thrombin binds to thrombomodulin and it can no longer participate in the coagulation cascade.
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