Neutropenia pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Neutropenia may develop as a result of one of the three mechanisms: Impaired [[granulocyte]] production, margination, and peripheral destruction. Genes involved in the pathogenesis of neutropenia include ''ELA2'', ''HAX1'', and ''CXCR4''. | |||
==Pathophysiology== | ==Pathophysiology== | ||
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'''3) Peripheral destruction''' | '''3) Peripheral destruction''' | ||
*Autoimmune [[hemolysis]] | |||
*Drug-induced [[hemolysis]] | |||
===Genetics=== | ===Genetics=== | ||
Revision as of 15:42, 10 October 2016
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Neutropenia Microchapters |
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Diagnosis |
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Neutropenia pathophysiology On the Web |
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American Roentgen Ray Society Images of Neutropenia pathophysiology |
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Risk calculators and risk factors for Neutropenia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Neutropenia may develop as a result of one of the three mechanisms: Impaired granulocyte production, margination, and peripheral destruction. Genes involved in the pathogenesis of neutropenia include ELA2, HAX1, and CXCR4.
Pathophysiology
Pathogenesis
Neutropenia may develop as a result of one of the three mechanisms:
1) Impaired granulocyte production
- Hematologic malignancy with bone marrow infiltration
- Myelosuppressive chemotherapy or other medications that are toxic to the bone marrow
- Nutritional deficiencies
2) Margination (process where free flowing blood cells exit circulation)
- Splenic sequestration
- Adherence to the vascular endothelium
3) Peripheral destruction
Genetics
Genes involved in the pathogenesis of neutropenia include ELA2, HAX1, and CXCR4.