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Ethanol

Ethanol is a potent CNS depressant

Uses

Biphasic effect on the body - low doses causes relaxation and cheerfulness, but higher doses lead to systemic depression - blurred vision, etc

Mechanism

ethanol acts, at least in part on the GABA receptor, enhancing chloride influx and increasing hyperpolarization
inhibits NMDA receptors, decreasing the excitatory effects of glutamate signaling
increases NE activity in the locus coeruleus

Dose and Half Life

Alcohol's effects depend on the blood alcohol concentration (BAC) and depend on many factors. The following are effects on the body at various BAC levels:

0.02 - slight mood changes
0.06 - lowered inhibition, impaired judgment
0.08 - legally drunk, lowered reaction time and control
0.15 - impaired balance, movement, and coordination
0.20 - decreased pain sensation
0.30 - decreased consiousness and reflexes
0.40 - loss of consiousness
0.50 - death

Adverse Drug Reactions

short term

death

long term

Counter-Indications and Drug Interactions

Metabolism and Excretion

ethanol is broken down by alcohol dehydrogenase by the liver into acetaldehyde, and then into acetate by acetaldehyde dehydrogenase
acetate can be used to make energy or converted into fat for storage

Dependency

Alcohol withdrawal can be life-threatening.
Long term use of ethanol produces a decrease in GABA_A receptors. When ethanol is no longer present, the resulting loss of chloride influx and disinhibition causes seizures, anxiety, and anxiety-related symptoms such as tremors, diaphoresis, and tachycardia.
Benzodiazepines can be used to reduce alcohol withdrawal due to increased GABA binding and chloride influx

the HPA axis is also stimulated during withdrawal, leading to elevated corticosteroid levels and symptoms such as fatigue, weakness, hypertension, confusion, and depression