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. | * It is thought that [[microangiopathic hemolytic anemia]] is mediated by endothelial injury, [[platelet]] activation, micro[[thrombi]] formation, intra-vascular [[hemolysis]] and [[thrombocytopenia]]. | ||
* 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. | |||
* The mechanism of endothelial injury varies depending on the underlying cause. It results in [[platelet]]s aggregation and activation the [[coagulation]] cascade. There is the formation of a [[fibrin]] mesh due to increased activity of [[coagulation]] cascade. | |||
* This results in the formation of micro[[thrombi]] in the [[blood vessel] and reduction of the caliber of the [[blood vessels]]. | |||
* The [[red blood cells]] are fragmented due to mechanical sheering by the micro[[thrombi]]. | |||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
The red blood | The [[red blood cell]]s are physically cut by these protein networks, and the fragments are identical to the [[schistocyte]]s seen on light microscopy. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 21:07, 30 January 2021
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Microangiopathic hemolytic anemia Microchapters |
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Differentiating Microangiopathic hemolytic anemia from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
- It is thought that microangiopathic hemolytic anemia is mediated by endothelial injury, platelet activation, microthrombi formation, intra-vascular hemolysis and thrombocytopenia.
- 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.
- The mechanism of endothelial injury varies depending on the underlying cause. It results in platelets aggregation and activation the coagulation cascade. There is the formation of a fibrin mesh due to increased activity of coagulation cascade.
- This results in the formation of microthrombi in the [[blood vessel] and reduction of the caliber of the blood vessels.
- The red blood cells are fragmented due to mechanical sheering by the microthrombi.
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.