Hemolytic-uremic syndrome pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*It is understood that Hemolytic Uremic Syndrome is the result of microvascular endothelial cell damage characterized by Thrombotic Microangiopathy (TMA) in renal glomeruli, gastrointestinal tract, brain and | *It is understood that Hemolytic Uremic Syndrome is the result of microvascular endothelial cell damage characterized by Thrombotic Microangiopathy (TMA) in renal glomeruli, gastrointestinal tract, brain and pancrease in all of which the main lesion is the thickening of vessel wall (mainly in capillaries and arterioles), microthrombi in platelets and obstruction of vessel lumen( partial or complete). Loss of physiological resistance to thrombus formation, complement consumption, leukocyte adhesion to damaged endothelium, abnormal release of Von Willibrand Factor (vWF) and fragmentation, and increased vascular shear stress lead to further amplification of microangiopathy. Congenital predisposing conditions like complement factor abnormalities may play a role in recurrent and familial forms. | ||
*Typical/ | *Typical/ shiga-toxin associated hemolytic uremic syndrome (HUS) is usually caused by E.Coli. Serotype O157:H7 is most commonly seen in USA and Europe, although other serotypes less commonly associated include O26:H11, O103:H2, O121:H19, O145:NM and O111:NM. Other strains, specially O111:H serotype is frequently found in other countries as well. | ||
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host. | *[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. | *Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. | ||
Revision as of 23:17, 2 August 2018
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Hemolytic-uremic syndrome Microchapters |
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Differentiating Hemolytic-uremic syndrome from other Diseases |
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Hemolytic-uremic syndrome pathophysiology On the Web |
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Risk calculators and risk factors for Hemolytic-uremic syndrome pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- It is understood that Hemolytic Uremic Syndrome is the result of microvascular endothelial cell damage characterized by Thrombotic Microangiopathy (TMA) in renal glomeruli, gastrointestinal tract, brain and pancrease in all of which the main lesion is the thickening of vessel wall (mainly in capillaries and arterioles), microthrombi in platelets and obstruction of vessel lumen( partial or complete). Loss of physiological resistance to thrombus formation, complement consumption, leukocyte adhesion to damaged endothelium, abnormal release of Von Willibrand Factor (vWF) and fragmentation, and increased vascular shear stress lead to further amplification of microangiopathy. Congenital predisposing conditions like complement factor abnormalities may play a role in recurrent and familial forms.
- Typical/ shiga-toxin associated hemolytic uremic syndrome (HUS) is usually caused by E.Coli. Serotype O157:H7 is most commonly seen in USA and Europe, although other serotypes less commonly associated include O26:H11, O103:H2, O121:H19, O145:NM and O111:NM. Other strains, specially O111:H serotype is frequently found in other countries as well.
- [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
[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
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].