Microangiopathic hemolytic anemia pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
In diseases such as hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, as well as malignant hypertension, the endothelial layer of small vessels are damaged with resulting fibrin deposition and platelet aggregation. | |||
In all causes, the mechanism of MAHA is the formation of a [[fibrin]] mesh due to increased activity of the system of [[coagulation]]. | In all causes, the mechanism of MAHA is the formation of a [[fibrin]] mesh due to increased activity of the system of [[coagulation]]. | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
The red blood cells are physically cut by these protein networks, and the fragments are identical to the schistocytes seen on light microscopy. | The red blood cells are physically cut by these protein networks, and the fragments are identical to the schistocytes seen on light microscopy. | ||
==References== | ==References== |
Revision as of 14:07, 21 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
In diseases such as hemolytic uremic syndrome, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, as well as malignant hypertension, the endothelial layer of small vessels are damaged with resulting fibrin deposition and platelet aggregation. In all causes, the mechanism of MAHA is the formation of a fibrin mesh due to increased activity of the system of coagulation.
Microscopic Pathology
The red blood cells are physically cut by these protein networks, and the fragments are identical to the schistocytes seen on light microscopy.