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Lecture 5

PSYT 301 Lecture Notes - Lecture 5: Alcohol Tolerance, Palpebral Fissure, Alcohol Dehydrogenase

Course Code
PSYT 301
Kathryn Gill

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Introduction to alcohol: historical and social issues + epidemiology, patterns of
alcohol use and abuse
after alcohol is drunk, it is rapidly and completely absorbed from the entire GI tract as
it can diffuse easily across all biological membranes
most from upper intestine due to large SA
often takes 15-60mins for alcohol to be absorbed and have max concentration in the
blood, faster for people with empty stomachs as most bypasses gastric metabolism
metabolism: approx. 95% of the alcohol a person ingests is enzymatically
metabolized by the enzyme alcohol dehydrogenase (ADH), other 5% excreted
through the lungs usually
women have higher BAC than men due to the following 3 factors:
women have about 50% less gastric metabolism of alcohol because of a
lower level of gastric ADH enzyme
men may have a greater ratio of muscle to fat than do women, men thus have
a larger vascular compartment and therefore alcohol is somewhat more
diluted in men
women with higher body fat than men concentrate alcohol in plasma raising
pharmacodynamics: general theories that it follows regular depressant action, others
that as it is water and lipid soluble, it can dissolve through nerve membranes and
distort the membrane, resulting in a nonspecific and indirect depression of neuronal
function, however this does not account for the evidence that alcohol may disrupt
neurotransmitter action (GABA and glutamate)
ethanol disrupts glutaminergic neurotransmission by depressing the
responsiveness of NMDA receptors to released glutamate
ethanol may induce opioid release, which in turn triggers dopamine release in
the brain reward system
chronic alcohol consumption results in augmentation of serotonergic activity
and serotonin dysfunction has been postulated to play a role in the
pathogenesis of some types of alcoholism
chronic alcohol consumption stimulates the formations of the endogenous
neurotransmitter for cannabinoid receptors (anandamide) -- plays a big part in
the craving aspect of alcohol withdrawal
Overview of the pharmacological effects of alcohol; focus on FAS
graded, reversible depression of behaviour, mental functioning and cognition is the
primary pharmacological effect of alcohol, at low doses, respiration increases but at
moderate doses, respiration becomes depressed
dilates blood vessels, decrease in body temperature
chronic abuse of alcohol leads to heart disease but low doses can increase HDL and
lower LDL -- leading to better heart health
can cause low sexual performance and a loss of sexual restraint
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increased sociability, decreased inhibitions, diminution of attention, judgement and
control, slowed information processing and loss of efficiency in critical performance
can lead to violence crimes -- almost half of homicides and assaults involved alcohol,
alcohol may reduce anxiety about the consequences of aggressive behavior
chronic alcohol consumption is associated with severe executive function deficits, the
existence of persistent executive function deficits could affect the capacity to
maintain abstinence
ethanol inhibits cognitive functioning and produces blackouts by suppressing
production of memory proteins in the hippocampus, blocks glutaminergic NMDA
receptors and may produce neurosteroids that interfere with memory consolidation
side effects: reversible drug-induced dementia, may become labile, delusions
hallucinations, uncoordinated motor behaviour, in the long term liver damage and the
destruction of nerve cells may occur, possible cancers, pancreatitis, chronic gastritis,
peptic ulcers
FAS: occurs in the offspring of mothers who have high blood levels of alcohol during
critical stages of fetal development
CNS dysfunction, including low intelligence and microcephaly, mental
retardation, behavioural abnormalities
retarded body growth rate
facial abnormalities (short palpebral fissures, short nose, wide-set eyes, small
congenital heart defects and malformed eyes and ears
not full blown FAS might be categorized as ARND (alcohol-related
neurodevelopmental disorder)
binge drinking increased risk of child mental health issues (ADD, ADHD)
Neurobiology of alcohol; focus on the neurotransmitters GABA and NMDA
Etiology of alcohol/drug dependence; focus on genetic factors, twin, adoption and
linkage studies
three types of alcohol tolerance:
metabolic tolerance: the liver increases its amount of drug-metabolizing
enzyme -- accounts for at most 25% of the tolerance to alcohol
tissue, or functional tolerance: neurons in the brain adapt to the amount of
drug present, tolerant people at same BAC appear less intoxicated
associative, contingent or homeostatic tolerance: a variety of environmental
manipulations can counter the effects of ethanol, and counter responses are
a possible mechanism of tolerance
after physical dependence develops, withdrawal of alcohol results in a period of
rebound hyperexcitability that can lead to convulsions
alcohol-use disorders are associated with depressive episodes, severe anxiety,
insomnia, suicide and the abuse of other drugs, continued heavy alcohol use also
shortens the onset of heart disease, stroke, cancers and liver cirrhosis, can also
cause mild anterograde amnesias, temporary cognitive deficits, sleep problems, and
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