OVERVIEW
 Alcohol
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Benzodiazepines
Opoid
Pharmalocology
Signs & Symptoms
Management
Pharmacology
Acute effect
 Stimulatio of Gamma-Amniobutryic Acid (Gaba) System
 Neurohibitory
Chronis use
 Configuration changes of GABA
 Induces an intensitivity to GABA .. more inhibitor is required to maintain a constant inhibitory
tone.
As alcohol tolerence develops the individual retains arousal at alcohol concentrations which would
normally produce lethargy or even coma in relatively alcohol naïve individuals.
Cessation of alcohol or a rduction from chronically elevated concentrations results in decreased
inhibitory tone.
EXCITATORY AMINO ACIDS-GLUTAMATE
 Binds to the N-METHHYL-D- ASPARTATE (NMDA) receptor, calcium influx leads to Neuronal
excitation.
 Ethanol inhibits Glutamate induced excitation
 Adaption occurs by increasing the number of Glutamate receptors in an attempt to maintain a
normal state of arousal.
 Cessation of alcohol or a reduction from chronically elevated concentrations results in
unregulated excess excitation.
Non -Pharmacological Management
 A calm, non threatening , protective environment with frequent verbal orientation and
reassurance.
 To relieve anxiety and fear and to minimize agitation.
 Intravenous hydration and electrolyte replacement.
 Thiamine
Pharmacological Therapies
 The agent of choice is a Benzodiazepine
 Given orally in milder cases or I.V. in more severe withdrawal states.
Options include
 1. Midazolam administered by infusion and titrated to effect
 2. Diazepam… given initially in titrated doses of 5-10mg at intervals as frequent as every
10 min if necessary until a calm but awake level of consciousness is achieved.
Subsequent dosing at 5-20 mg every 4-6 hours typically required.