Immune Thrombocytopenia pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
*Immune thrombocytopenia arises from [[platelets]], which are [[blood]] cells that are normally involved in [[hemostasis]]. | *Immune thrombocytopenia arises from [[platelets]], which are [[blood]] cells that are normally involved in [[hemostasis]]. | ||
*It is understood that Immune thrombocytopenia is caused by destruction of one's own platelets and megakaryocytes. | *It is understood that Immune thrombocytopenia is caused by destruction of one's own platelets and megakaryocytes. | ||
*The progression to immune thrombocytopenia usually involves the [[genetic]] predisposition, immune dysregulation and environmental factors which lead to [[autoimmunity]]. | *The progression to immune thrombocytopenia usually involves the [[genetic]] predisposition, immune dysregulation and environmental factors which lead to [[autoimmunity]]. | ||
*[[Molecular mimicry]] between foreign [[antigens]] and [[autologous]] platelet antigens leads to activation of [[cross-reactive]] [[B cell|B]] and [[T cell]], starting [[autoimmune response]]. | *[[Molecular mimicry]] between foreign [[antigens]] and [[autologous]] platelet antigens leads to activation of [[cross-reactive]] [[B cell|B]] and [[T cell]], starting [[autoimmune response]].<ref name="LiSullivan2018">{{cite journal|last1=Li|first1=June|last2=Sullivan|first2=Jade A.|last3=Ni|first3=Heyu|title=Pathophysiology of immune thrombocytopenia|journal=Current Opinion in Hematology|volume=25|issue=5|year=2018|pages=373–381|issn=1065-6251|doi=10.1097/MOH.0000000000000447}}</ref> | ||
==Genetics== | ==Genetics== | ||
Revision as of 00:59, 27 January 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Maryam Barkhordarian, M.D.[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- Immune thrombocytopenia arises from platelets, which are blood cells that are normally involved in hemostasis.
- It is understood that Immune thrombocytopenia is caused by destruction of one's own platelets and megakaryocytes.
- The progression to immune thrombocytopenia usually involves the genetic predisposition, immune dysregulation and environmental factors which lead to autoimmunity.
- Molecular mimicry between foreign antigens and autologous platelet antigens leads to activation of cross-reactive B and T cell, starting autoimmune response.[1]
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Li, June; Sullivan, Jade A.; Ni, Heyu (2018). "Pathophysiology of immune thrombocytopenia". Current Opinion in Hematology. 25 (5): 373–381. doi:10.1097/MOH.0000000000000447. ISSN 1065-6251.