Alcohol withdrawal pathophysiology: Difference between revisions

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Revision as of 19:27, 20 February 2014

For patient information click here.

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

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.

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 '''For patient information click [[Alcohol withdrawal (patient information)|here]].'''
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+{{CMG}}; {{AE}} {{ADI}}
+== 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.