Alcohol withdrawal pathophysiology: Difference between revisions
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== Pathophysiology == | == Pathophysiology == | ||
* Prolonged exposure to alcohol results in inhibition of the inhibitory GABA A-type and NMDA-type glutamate receptors located in the CNS. Without the alcohol, greater CNS excitability results, due to lack of inhibition on the CNS inhibitory receptors by alcohol. | * Prolonged exposure to alcohol results in inhibition of the inhibitory GABA A-type and NMDA-type glutamate receptors located in the CNS. Without the alcohol, greater CNS excitability results, due to lack of inhibition on the CNS inhibitory receptors by alcohol. | ||
* Elevated [[norepinephrine]] has been found in the [[CSF]] patients in acute alcohol withdrawal. It is postulated that there is a decreased amount of alpha 2-receptors, resulting in less inhibition of [[presynaptic]] [[norepinephrine]] release. | * Elevated [[norepinephrine]] has been found in the [[CSF]] patients in acute alcohol withdrawal. It is postulated that there is a decreased amount of alpha 2-receptors, resulting in less inhibition of [[presynaptic]] [[norepinephrine]] release. | ||
Revision as of 19:44, 20 February 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]
Pathophysiology
- Prolonged exposure to alcohol results in inhibition of the inhibitory GABA A-type and NMDA-type glutamate receptors located in the CNS. Without the alcohol, greater CNS excitability results, due to lack of inhibition on the CNS inhibitory receptors by alcohol.
- Elevated norepinephrine has been found in the CSF patients in acute alcohol withdrawal. It is postulated that there is a decreased amount of alpha 2-receptors, resulting in less inhibition of presynaptic norepinephrine release.