Post-streptococcal glomerulonephritis pathophysiology: Difference between revisions
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{{Post-streptococcal glomerulonephritis}} | {{Post-streptococcal glomerulonephritis}} | ||
{{CMG}} | {{CMG}} | ||
==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=== | |||
*The exact pathogenesis of [disease name] is not fully 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== | |||
*[Disease name] is transmitted in [mode of genetic transmission] pattern. | |||
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3]. | |||
*The development of [disease name] is the result of multiple genetic mutations. | |||
==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]. | |||
==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
The exact pathology remains unclear, but it is believed to be Type III [[hypersensitivity]] reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the [[glomerular basement membrane]]. [[Complement system|Complement]] activation leads to destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long lasting antibody response. | The exact pathology remains unclear, but it is believed to be Type III [[hypersensitivity]] reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the [[glomerular basement membrane]]. [[Complement system|Complement]] activation leads to the destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long-lasting antibody response. | ||
==References== | ==References== |
Revision as of 17:25, 2 May 2018
Post-streptococcal glomerulonephritis Microchapters |
Differentiating Post-streptococcal glomerulonephritis from other Diseases |
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Directions to Hospitals Treating Post-streptococcal glomerulonephritis |
Risk calculators and risk factors for Post-streptococcal glomerulonephritis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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
- The exact pathogenesis of [disease name] is not fully 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
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
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].
Overview
Pathophysiology
The exact pathology remains unclear, but it is believed to be Type III hypersensitivity reaction. Immune complexes (antigen-antibody complexes formed during an infection) become lodged in the glomerular basement membrane. Complement activation leads to the destruction of the basement membrane. It has also been proposed that specific antigens from certain nephrotoxic streptococcal infections have a high affinity for basement membrane proteins, giving rise to particularly severe, long-lasting antibody response.