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Lecture 4

PSYT 301 Lecture Notes - Lecture 4: Aldehyde Dehydrogenase, Alcoholic Hepatitis, Alcohol Tolerance


Department
Psychiatry
Course Code
PSYT 301
Professor
Kathryn Gill
Lecture
4

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Lecture 4: Introduction to Alcohol cont’d
Last time:
Opioid substitution method: can’t just hand out methadone and expect addicts to be “cured”,
must be combined with psychotherapy and other treatment methods
Alcohol-health burden + epidemiology (patterns of use and abuse):
high alcohol tolerance observed amount alcoholics, thus less relationship between
BAL and impairment
some have extremely high tolerance (.6-.8) -- usually a sign of chronic
alcoholism
Metabolic pathways: Ethanol -(ADH)> acetaldehyde -(ALDH)> acetate, oxidation
(95% of metabolism)
MEOS (cytochrome P4502E1): also metabolizes toxins and potential drugs, if
more metabolites are produced due to alcoholism -- harsher on liver, more
free radicals present
CYP2E1 is very active in oxidizing chemicals to reactive intermediates
(eg. benzene, acetaminophen, halothane), thus increased toxicity in
heavy drinkers and alcoholics. catalytic turnover cycle results in the
production of relatively large amounts of reactive oxygen
intermediates such as the superoxide radical and hydrogen peroxide
ADH exists in multiple polymorphic forms
oriental mutation (affects ALDH metabolism): single base pair
mutation in the enzyme -- negative risk factor in the development of
alcoholism, extreme adverse reactions (flushing, nausea, heart
arrhythmias), caused by buildup of acetaldehyde
Antabuse: usually lasts 4 days to synthesize new ALDH enzymes
must be able to commit to taking the pill, or else the treatment is not effective
usually inflammation of the liver is caused by endotoxins from the gut, as well as
acetaldehyde
Liver disease caused by alcohol metabolism:
fatty liver
alcoholic hepatitis
cirrhosis (scar tissues, nodules)
20% of alcoholics
morbidity common (jaundice, ascites, bleeding, infections,
encephalopathy)
liver cancer
american survey of 36,000 people found that 12 month prevalence of AUD was
13.9% and lifetime prevalence of AUD was 29.1%
people with AUDs have much higher rates of accidents -- more often seen in trauma
(orthopaedics - broken bones) and emergency
screening is more important to catch alcoholics in these scenarios (in primary
and secondary care)
GI effects: esophageal disease, stomach/bowel
Liver effects: fatty liver, alcoholic hepatitis, cirrhosis
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