Central pontine myelinolysis pathophysiology: Difference between revisions

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Revision as of 00:37, 1 August 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Overview

Pathophysiology

. Given the importance of the maintenance of cell volume within the CNS, mechanisms underlying the release of osmolytes assume major significance. In this context, we review recent evidence obtained from our laboratory and others that indicates that the activation of specific G-protein-coupled receptors can markedly enhance the volume-dependent release of osmolytes from neural cells. Of particular significance is the observation that receptor activation significantly lowers the osmotic threshold at which osmolyte release occurs, thereby facilitating the ability of the cells to respond to small, more physiologically relevant, reductions in osmolarity. The mechanisms underlying G-protein-coupled receptor-mediated osmolyte release and the possibility that this efflux can result in both physiologically beneficial and potentially harmful pathophysiological consequences are discussed.

Pathogenesis

It is understood that central pontine myelinolysis is caused by rapid correction of hyponatremia.
The CNS is particularly susceptible to reductions in plasma osmolarity, specially during hyponatremia which is the most commonly encountered electrolyte disturbance.
When decrease in the plasma osmolarity happens , neural cells first swell but then they are able to regain their original volume through the:
1. Release of inorganic and organic osmolytes
2. Exit of osmotically obligated water

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

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@@ Line 5: / Line 5: @@
 ==Overview==
 ==Pathophysiology==
-===Physiology===
+. Given the importance of the maintenance of cell volume within the CNS, mechanisms underlying the release of osmolytes assume major significance. In this context, we review recent evidence obtained from our laboratory and others that indicates that the activation of specific G-protein-coupled receptors can markedly enhance the volume-dependent release of osmolytes from neural cells. Of particular significance is the observation that receptor activation significantly lowers the osmotic threshold at which osmolyte release occurs, thereby facilitating the ability of the cells to respond to small, more physiologically relevant, reductions in osmolarity. The mechanisms underlying G-protein-coupled receptor-mediated osmolyte release and the possibility that this efflux can result in both physiologically beneficial and potentially harmful pathophysiological consequences are discussed.
-The normal physiology of [name of process] can be understood as follows:
 ===Pathogenesis===
-*The exact pathogenesis of [disease name] is not completely understood.
-OR
+*It is understood that central pontine myelinolysis is caused by rapid correction of [[hyponatremia]].
-*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].
+*The [[CNS]] is particularly susceptible to reductions in [[plasma osmolarity]], specially during [[hyponatremia]] which is the most commonly encountered [[electrolyte disturbance]].
-*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
+*When decrease in the plasma [[osmolarity]] happens , neural cells first swell but then they are able to regain their original volume through the:
-*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
+*#Release of  inorganic and organic osmolytes
-*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
+*#Exit of osmotically obligated water
-*The progression to [disease name] usually involves the [molecular pathway].
+*
-*The pathophysiology of [disease/malignancy] depends on the histological subtype.
 ==Genetics==