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10 Cards in this Set

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EtOH dose-dependent acute central effects
-100-300 mg/dL (.1-.3%) : cerebellar effects, ie incoordination
-300-400: midbrain - temp regulation, spinal reflexes
-450-600: respiratory center depression (cause of death, coupled with aspiration of vomit)
EtOH MOA
-"fluidizes" membranes and affects the membrane components
-potentiates GABA-A inhibition, like other non-selective CNS depressents
-may even affect other NT - Receptor systems
how do EtOH pharmacokinetics relate to [EtOH]blood?
zero order elimination, due to the quickly saturable levels of NAD+.
disulfiram MOA?
inhibits aldehyde dehydrogenase, potentiating hangover. also inhibits Dopamine Beta Hydroxylase, thus emptying NE stores, leading to hypotension
why are effects on men/women different?
same size woman has a smaller volume of distribution than a man. thus her EtOH will be more concentrated
EtOH effects on organs besides CNS?
-liver: increases FG - fatty liver
-Kidney - inhibits vasopressin (ADH) release - diuresis
-CV - cutaneous dilation - heat loss
-Heart - dilated cardiomyopathy
possible drug interactions with EtOH?
-competes w/ drugs oxidized by microsomial system (warfarin, phenytoin, barbiturates - these are oxidized 100% by microsomal system)
-pt on MAOi's - tyramine, from wine, can potentiate effects due to NE and lead to rapid HTN
what does an ethanol blood % mean?
% * 1000 = mg/dL, so 80mg/dL blood = 0.08%
how does EtOH's actions compare to other non-selective CNS depressents?
less potent, but same idea - as dose increases, you move from disinhibition - sedation - hypnosis - ataxia - coma - death
3 ways of EtOH metabolism
1. ADH then Aldehyde Dehydrogenase, w/ NAD+ for both
2. Microsomal EtOH Oxidizing System
3. Catalases