Sideroblastic anemia pathophysiology: Difference between revisions
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==Pathophysiology<ref name="pmid24003969">{{cite journal |vauthors=Fujiwara T, Harigae H |title=Pathophysiology and genetic mutations in congenital sideroblastic anemia |journal=Pediatr Int |volume=55 |issue=6 |pages=675–9 |date=December 2013 |pmid=24003969 |doi=10.1111/ped.12217 |url=}}</ref><ref name="pmid22160084">{{cite journal |vauthors=Fleming MD |title=Congenital sideroblastic anemias: iron and heme lost in mitochondrial translation |journal=Hematology Am Soc Hematol Educ Program |volume=2011 |issue= |pages=525–31 |date=2011 |pmid=22160084 |doi=10.1182/asheducation-2011.1.525 |url=}}</ref>== | ==Pathophysiology<ref name="pmid24003969">{{cite journal |vauthors=Fujiwara T, Harigae H |title=Pathophysiology and genetic mutations in congenital sideroblastic anemia |journal=Pediatr Int |volume=55 |issue=6 |pages=675–9 |date=December 2013 |pmid=24003969 |doi=10.1111/ped.12217 |url=}}</ref><ref name="pmid22160084">{{cite journal |vauthors=Fleming MD |title=Congenital sideroblastic anemias: iron and heme lost in mitochondrial translation |journal=Hematology Am Soc Hematol Educ Program |volume=2011 |issue= |pages=525–31 |date=2011 |pmid=22160084 |doi=10.1182/asheducation-2011.1.525 |url=}}</ref>== | ||
=== Physiology === | |||
The normal physiology of heme synthesis can be understood as follows: | |||
=== Pathogenesis[edit | edit source] === | |||
* The exact pathogenesis of [disease name] is not completely understood. | |||
OR | |||
* It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. | |||
* [Pathogen name] is usually transmitted via the [transmission route] route to the human host. | |||
* Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. | |||
* [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. | |||
* The progression to [disease name] usually involves the [molecular pathway]. | |||
* The pathophysiology of [disease/malignancy] depends on the histological subtype. | |||
== Genetics[edit | edit source] == | |||
[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: | |||
==References== | ==References== |
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Overview
Sideroblastic anemia pathophysiology | |
Sideroblastic (microcytic) anemia |
Pathophysiology[1][2]
Physiology
The normal physiology of heme synthesis can be understood as follows:
Pathogenesis[edit | edit source]
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics[edit | edit source]
[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:
References
- ↑ Fujiwara T, Harigae H (December 2013). "Pathophysiology and genetic mutations in congenital sideroblastic anemia". Pediatr Int. 55 (6): 675–9. doi:10.1111/ped.12217. PMID 24003969.
- ↑ Fleming MD (2011). "Congenital sideroblastic anemias: iron and heme lost in mitochondrial translation". Hematology Am Soc Hematol Educ Program. 2011: 525–31. doi:10.1182/asheducation-2011.1.525. PMID 22160084.