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Lecture 3

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Carleton University
PSYC 3403
Tarry Ahuja

Lecture 3 Overview - Pharmacokinetics of ethanol - Pharmacokinetics of ethanol - Pharmacological effects - Psychological effects - Tolerance and dependence - Side effects and toxicity Ethyl alcohol - Depressant used primarily for recreational purposes • Really fast crash (dancing then passed out) - Second most widely used psychoactive substance in the world - If you double the percentage of the alcohol, that is the proof (ex: 40% alcohol = 80 proof) - One drink equivalent 10cc (1/3 oz) of 100% ethanol - Body reduces BAC by 0.015g % in 1 hour - Soluble in both water and fat • Moves easily throughout our body (gets through everywhere) - Rapidly and completely absorbed by G.I. - Higher absorption in women - BBB (blood brain barrier) is permeable to alcohol - Crosses placental barrier and enters fetal brain Ethyl alcohol (absorption) Ethyl alcohol (metabolism) - 95% of alcohol is metabolized by alcohol dehydrogenase - 85% of metabolism occurs in the liver - 15% by first-pass metabolism • As soon as you consume, enters your system - Empty stomach vs. food-filled stomach • Afull stomach will drain slowly, and allow the alcohol dehydrogenase (in G.I. tract) to break the alcohol molecules down.An empty stomach will drain much faster, and this stops the alcohol dehydrogenase (in G.I. tract) from breaking down the alcohol - Breakdown of alcohol: KNOW THIS FOR MIDTERM!!! • Alcohol dehydrogenase determines how fast we break down alcohol • Rate limiting step: something that slows down the breakdown of alcohol • Get acetaldehyde after alcohol breakdown • Then aldehyde dehydrogenase breaks down the acetaldehyde • Essentially left with energy, carbon dioxide, and water Ethyl alcohol (metabolism) cont’d - Max EtOH metabolized in 24 hours is 170g - Average person metabolizes 7-8g (or 10mL) of 100% alcohol per hour (one drink per hour) - This is equal to one (1) drink equivalent (10mL of 100% alcohol) - Consumption > 1 drink equivalent/hour • Beginning to get intoxicated. Can’t digest fast enough - If consumption and body weight are known, BAC can be calculated - BAC of 0.08g % = intoxicated - **KNOW HOW TO GET BAC BASED ON THIS CHART!!!** (@38 minutes) Consequences for driving with a 0.05 to 0.08 BAC **DON’T NEED TO KNOW THIS!!** - First time • 3-day licence suspension • 150$ administrative monetary penalty - Second time (within 5 years) • 7-day licence suspension • Mandatory alcohol education program • 150$ administrative monetary penalty - Third time (within 5 years) • 30-day licence suspension • Mandatory alcohol treatment program • Six-month ignition interlock licence condition • 150$ administrative monetary penalty - Subsequent infractions (within 5 years) • 30-day licence suspension • Mandatory alcohol treatment program • Six-month ignition interlock licence condition • Mandatory medical evaluation • 150$ administrative Ethyl alcohol (gender differences) - Women have a lower level of gastric alcohol dehydrogenase • Men have more of the enzyme that breaks down alcohol (alcohol dehydrogenase), so more of the alcohol gets in women’s blood than men’s - Men have a greater ratio of muscle/fat • Larger vascular compartment - Women have higher body fat, this concentrates alcohol in plasma - IV = direct into blood, so concentration is high quickly - Drinking orally takes time, gets lower max (has to go through GI tract, first pass metabolism) - Decays at roughly the same rate regardless of how it is taken Pharmacodynamics - Unitary hypothesis of action • When asked back in the day about how they thought alcohol was working, this hypothesis implies that it affects many parts of the body - Alcohol has been shown to affect: • Glutamate systems • GABAsystems • Intracellular transduction processes Pharmacodynamics (GluR) - Inhibits NMDAreceptors • Decreasing level of excitation (blocking excitatory receptor) - Chronic exposure causes up-regulation of NMDAR • When receptors are being blocked by alcohol, the body produces more receptors to up-regulate - Withdrawal can lead to hyperexcitability (ex: seizures) • Chronic drinking, and body has up-regulated the # of NMDAreceptors, and you suddenly stop, so now there are too many receptors and the system is over excited - Acamprosate - Acamprosate structurally similar to glutamate • It will bind to glutamate more easily Pharmacodynamics (GABA) - Activates GABAR, results in neuronal inhibition - Binds to specific site on GABA R A - May reduce both panic and anxiety • When in anxious situations, people drink to calm themselves down • Increase in inhibition from the GABAsystem - GABAagonistic action linked to positive reinforcing effects of the drug Pharmacodynamics (opioid receptors) - Alcohol dependents and offspring show deficit in opioid activity - EtOH (alcohol) induces opioid release, dopamine release • Might be drinking unconsciously due to the opioid release (get back to a level they should naturally be at) - Naltrexone blocks opioid release, reduces craving • Helps with alcohol addiction (to reduce it) Pharmacodynamics (5-HT receptors) - Agonistic action on 5-HT 2-3located on DAneurons in nucleus accumbens • Activating serotonin 5-HT neurons • Receptors on DAneurons that alcohol activates and makes you feel good - Antagonistic drugs block these receptors reduce EtOH intake (ex: sertraline) - 5-HT transporter dysfunction may be involved Pharmacodynamics (cannabioid R) - Chronic exposure leads to formation of endogenous NT anandamide • Endogenous = produce within yourself - Anandamide activates cannabinoid receptor, possible down-regulation • Down-regulation = decrease in receptor - Abstinence lead to hyperactive receptor activation, promotes cravings Pharmacological effects - Graded reversible depression of behavior and cognition • For each dose you take, something is increasing at a consistent rate • Not graded = take one pill and feel good, a second pill feel great, but a third pill could kill you  Don’t want this. Things are not working consistently • As # of drinks consumed increases, motor skills and cognition decrease - reversible - Depression of respiration • If drink too much (extreme alcoholic), they don’t die because of drinking too much, but die from respiratory failure - Additive effects with other sedative-hypnotic compounds • Mixing meds with alcohol can kill you - Reduction in circulatory function, dilates blood vessels • When you drink, circulatory function is compromised (ex: don’t feel cold) - Low doses reduce risk of coronary artery disease and stroke • On semi-regular bases, in low doses, in some individuals - Increase in HD-lipoprotein and HD-cholesterol • HDL (ex: avocados) vs. LDL (ex: French fries)  If you drink, there is actually an increase in the good (HDL) fats - Up to 2 to 2½ drinks per day is good. Ex: red wine and vodka (straight up). Cannot be mixed or sugary drinks - Benefits erased if smoking Overview - Psychological effects - Tolerance and dependence - Side effects and toxicity - Teratogenic effects - Pharmacological treatment Psychological effects - Intoxication is associated with violent crimes: • Physical altercation (fighting) • Rape • Sexual assault  Direct correlation between drinking and these events - Alcohol is implicated in more than half of all homicides (50%) - Activation of GABAsystem • Reduces anxiety by activating GABAsystem • GABAis inhibitory- raising level of inhibition, and lowers level of anxiety - Activation of DA(dopamine) system • Impulse control is reduced  Ex: don’t keep your mouth shut, and can get you into trouble • Increases aggression - Depression of glutamate system • Impaired cognitive function  Ex: can’t do simple math when buying a hotdog on the street after bar • “Alcohol myopia”  Ex: poor decision making/priorities skewed (low priority becomes high priority) • Cognitive and attentional deficits  Ex: repeat themselves, not making sense when talking to people  Depression of glutamate systems due to alcohol Toleran
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