00:00 / 00:00
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
0 / 13 complete
0 / 2 complete
Disseminated Intravascular Coagulation (DIC)
Acquired Coagulation Defects
acute myelogenous leukemia p. 437
amniotic fluid emboli p. 693
Ebola p. NaN
endotoxins p. 129, 131
meningococci p. 140
microangiopathic anemia p. 415
placental abruption p. 659
schistocytes in p. 422
Waterhouse-Friderichsen syndrome p. 353, 724
Disseminated intravascular coagulation, or DIC, describes a situation in which the process of hemostasis, which is when after blood vessel wall injury, liquid blood rapidly becomes a gel, called coagulation or clotting, starts to run out of control.
When this happens, lots and lots of blood clots start to form in blood vessels serving various organs, leading to organ ischemia.
DIC, though, is also called a consumption coagulopathy, because all this clotting consumes platelets and clotting factors.
Without enough platelets circulating in the blood, other parts of the body begin to bleed with even the slightest damage to the blood vessel walls. So paradoxically, patients have too much and too little clotting.
Normally, after a cut and damage to the endothelium, or inner lining of blood vessel walls, there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow.
After that, some platelets adhere to the damaged vessel wall, and become activated and then recruit additional platelets to form a plug.
The formation of the platelet plug is called primary hemostasis.
After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around in the blood.
The coagulation cascade starts when one of these proteins gets proteolytically cleaved.
This active protein then proteolytically cleaves and activates the next clotting factor, and so on.
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