PSY 134 - alcohol

what is alcohol

functional group (-OH), found in all glucose substances

ethanol (ethyl alcohol)

derived from fermentation, distillation for higher concentrations

alcohol on reproductive toxicity

low doses (risky sexual behavior; yields unwanted pregnancy, venereal diseases), high doses (sexual dysfunction; males - ED/low testosterone, females - anovulation/early menopause)

type I alcoholism

guilt/fear, generally begin later in life; most female alcoholics are type I

type II alcoholism

thrill-seeking, antisocial, criminality; genetic vulnerability, begin early; mostly male

DSM-V Criteria for AUD (Alcohol Use Disorder)

REMOVED legal problems, ADDED craving

Alcohol absorption

water soluble but small (so passive diffusion), 20% stomach 80% small intestine, rate hindered by food in stomach

Females have higher BALs

less body fluid (so higher concentration), lower ADH (alcohol dehydrogenase) levels (so less alc metabolism); *NOTE: no diff in BAL when IV admin

Alcohol metabolism

95% liver; microsomal ethanol oxidizing system (MEOS) via CYP2E1 converts alcohol to acetaldehyde at 0.5 standard drinks per hour; aldehyde dehydrogenase (ALDH) converts acetaldehyde (carcinogenic poison) to acetate

disulfiram

ALDH inhibitor; used to treat alcoholism (creates aversion)

ADH vs MEOS

two pathways for alcohol metabolism; ADH in GI tract (prevents absorption) vs MEOS in liver (promotes metabolism)

specific symptoms of alcohol withdrawal

dose-dependent; early stage (up to 36-48 hours; anxiety up to convulsions and sympathetic response) vs late stage (after 2-4 days, lasting 2-3 days; DTs, which can be deadly)

Delirium tremens (DTs)

tremors, anxiety, insomnia, paranoia, hallucinations; high fever, death secondary to complicating illness, shock/hypothermia

physiological symptoms of alcohol withdrawal (in rodents)

CNS hyperactivity (vs CNS depression during intoxication); tremors, spasticity, teeth chattering, convulsions, death

Sxs of alc WD from animal studies

increase in seizures (scales w # of experiences); increased ICSS threshold

anxiety during alc WD from animal studies

fewer/shorter contacts, longer latency + fewer entries, further distance traveled, more marbles buried

acute tolerance

within a single exposure, derivative of BAL; subjective (don’t feel drunk), objective (don’t look drunk)

chronic functional tolerance (behavioral tolerance)

finger-finger test; abstainers (steep drop off in performance), light drinkers (same steepness, but at a higher BAC), heavy drinkers (less steep, even higher BAC); influenced by associative/instrumental learning

“dirty drug”

a drug that interacts with multiple receptors and pathways; as opposed to a clean drug which has a single, specific target

Alcohol = GABA A agonist and non-competitive NMDA antagonist

chronic effects: reduced Cl- influx (GABA A downregulation), increased Glu levels (dampened GABA effects, strengthened NMDA effects), increased Ca influx (NMDA upregulation)

treating alcoholism: acamprosate

NMDA/mGlu5 antagonist (so less Glu reward); poor PO availability

treating alcoholism: naltrexone

mu opioid antagonist; gold standard