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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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Primary Immune Thrombocytopenia
Immune thrombocytopenic purpura
Immune thrombocytopenic purpura or ITP is an autoimmune condition in which the body produces antibodies against its own thrombocytes or platelets, which are destroyed. And this result in purpura, or small bleeding spots beneath the skin.
Normally, when there’s any kind of damage to the blood vessel, hemostasis occurs, which is the process that stops the bleeding and plugs the damaged vessel to limit the blood loss.
And there are two steps: primary and secondary hemostasis. During primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel.
Platelet aggregation is mediated by surface proteins found on platelets, called GP2B3A receptors. While these platelets are aggregating, secondary hemostasis kicks in.
Secondary hemostasis is also called coagulation, because that’s when clotting factors come into play one after another, with a view to cleaving fibrinogen into fibrin.
Then, fibrin forms a protein mesh, kinda like a giant net that covers the platelet plug and stabilizes it.
Now, in ITP, the spleen produces certain IgG autoantibodies which bind to the platelet receptor Gp2B3A, and target the platelet-antibody complexes for destruction in the spleen.
This leads to lowering of platelet counts in the blood, which makes it harder for bleeding to stop. Now, ITP can be acute or chronic.
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