ALCOHOL Other name(s): ethyl alcohol, ethanol, grain alcohol, hootch, liquor, booze, firewater, EtOH Class: alcohols are molecules with a hydroxyl
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1 Other name(s): ethyl alcohol, ethanol, grain alcohol, hootch, liquor, booze, firewater, EtOH Class: alcohols are molecules with a hydroxyl (OH) bound to carbon atoms. In EtOH, the carbon is in an ethyl (CH2- CH3). Also a phytochemical
2 Forms: Comes from fermented plants: Beer (3.2-7%) Wine (12-14%) Fermented then distilled = hard liquor (40-50%) Proof = % x2 (80 proof whiskey is 40% ethanol) 1 drink equivalent contains.6 oz / 18 ml / 3.6 tsp / 14 g / ~1/2 shot glass of pure ethanol
3 History: oldest drug to be used by humans (to reduce anxiety, loosen inhibitions, induce sleep, etc) 2 nd most widely used psychoactive drug in the world ~half of Americans are legally old enough to drink ~70% of those do so Effects: Dosage commonly measured in grams% blood alcohol content (BAC): # of grams (~tsp) of ethanol per 100 ml (~2 cups / 1 pint) blood ED 50 ~.04
4 Effects (cont): Low doses (BAC ~ ): behavioral disinhibition / sociability frontal lobe inhibition anxiolysis (also )reduced anxiety about consequences of violence) reward (nucleus accumbens) respiration increased dilation of blood vessels in skin > decrease in body temp mixture of stimulant and depressant effects partly determined by psychological expectations (set and setting) reduced risk of coronary artery disease & stroke men: 2 drinks / day, women:.5 1 drink / day increases HDL & reduces LDL decreases platelet aggregation relaxation effect?
5 Effects (cont) at higher doses: set & setting less important respiration depressed at higher doses (brainstem inhibition) can eventually stop (LD 50 ~.4) therapeutic safety ratio = 10
6 Chronic use / alcoholism: effects of anxiolysis and reward can lead to selfmedication tolerance & dependence: metabolic: liver upregulates alcohol dehydrogenase accounts for ~25% of tolerance neuronal tolerance behavioral compensation poor executive / frontal lobe function (disinhibition) vitamin B deficiency leads to neurodegeneration Korsakoff s Syndrome liver damage via oxidants produced during metabolism pancreas, GI ulcers, cancer FAS - 1 st trimester (facial abnormalities) / 3 rd trimester (synaptogenesis)
7 PHARMACODYNAMICS non-specific suppression of neuronal function by disturbing the membrane s fluidity (solvent vs. lipid) GABA agonist positive allosteric modulator allows negative chloride ions in to hyperpolarize neuron this has the effect of inhibiting ( shutting down ) neurons indirectly increases DA release from ventral tegmental area (VTA) to the nucleus accumbens (reward system)
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9 PHARMACODYNAMICS NMDA antagonist - inhibits NMDA subtype of glutamate (glu) receptors negative allosteric modulator glu is excitatory inhibiting the function of these receptors also has the effect of shutting down neurons
10 PHARMACODYNAMICS may also: induce release of endogenous opioids triggering DA release into the nucleus accumbens stimulate release of endogenous cannabinoids anandamide augment serotonin activity 5-HT 2 and 5-HT 3 receptors in the nucleus accumbens
11 Chronic use eventually causes: upregulation of excitatory glutamate receptors reduced inhibition by GABA uncontrolled excitation > seizures withdrawal induces seizures in 10% of alcoholics induces hyperexcitability more withdrawals = increased likelihood down-regulation of cannabinoid receptors
12 Other effects: anticonvulsant withdrawal may cause hyperexcitation of neurons > seizures induction of sleep in insomniacs but, REM is depressed
13 Amelioration of withdrawal effects: partially mimic pharmacodynamics glu antagonists / GABAergics (acamprosate, benzodiazepines) Reduction of ethanol intake: blocking opiate release (naltrexone Trexan ) blocking cannabinoid receptors (rimonabant) blocking 5-HT 2 / 5-HT 3 receptors in the nucleus accumbens using a GABAergic NMDA antagonist (just like alcohol - acamprosate) using a dopamine agonist antidepressant (bupropion / Wellbutrin ) to ameliorate chronic hypofunction of the reward system prevent breakdown of acetaldehyde > nausea (disulfiram / Antabuse ) use serotoninergic antidepressants link between 5HT and alcohol consumption (depression)
14 PHARMACOKINETICS: Absorption: oral administration is rapid and efficiently absorbed water & fat soluble easily diffuses across all membranes 1 st pass metabolism: some metabolized in the GI tract by the enzyme alcohol dehydrogenase ~15% in males, ~7% in females females have 50% less alcohol dehydrogenase also less vasculature per body mass
15 PHARMACOKINETICS: maximum blood concentration is reached minutes from the last drink more rapidly absorbed on an empty stomach reduces 1 st pass metabolism exposure to alcohol dehydrogenase Distribution freely permeable to all membranes (BBB / neurons / placenta) evenly distributed throughout entire body
16 Metabolism / Excretion 95% is eventually metabolized by alcohol dehydrogenase mostly in the liver 5% excreted unchanged, mostly through the lungs tight correlation between ethanol levels in excreted breath / blood Steps: alcohol dehydrogenase converts ethanol into acetaldehyde requires co-enzyme - nicotinamide adenine dinucleotide (NAD) rate-limited to 1 drink (~.6 oz)/hr, or 225 ml (~1 cup)/day ~1 pint (2 cups) of 100 proof (50% ethanol) acetaldehyde is toxic and contributes to nausea aldehyde dehydrogenase breaks down acetaldehyde into acetic acid this step is inhibited by disulfiram Antabuse and leads to nausea acetic acid broken down into CO2 and H2O produces energy (calories)
17 on average, 1 drink equivalent is metabolized per hour limited by low supply of NAD relatively constant & independent of dose / BAC zero-order metabolism (due to NAD limitation) no ½-life ( first-order ) as with other drugs with no more ethanol, BAC falls by ~.015 / hr more than 1 per hour = rising BAC
18 BENZODIAZEPINES introduced in mother s little helper diazepam ( Valium ) & chlordiazepoxide ( Librium ) sleeping pills / anti-seizure / anti-anxiety relatively safe (but still may cause dependence ) GABA agonists bind to a specific site on the GABA ion channel receptor facilitates GABA binding with the receptor positive allosteric modulator act mostly in the limbic parts of the brain anxiolytic - blocking GABA sites can cause anxiety well absorbed orally - peak plasma in ~ 1 hr some have metabolites are pharmacologically active zolpidem ( Ambien ) is a partial GABA agonist produces sedation, but not anxiolysis
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20 GAMMA HYDROXYBUTYRATE (GHB) colorless, odorless liquid potent CNS depressant used in other countries as an IV general anesthetic Similar in structure to GABA - synthesized in humans from GABA Effects similar to ethanol often added to alcohol (modern Mickey Finn / date rape) 1 st drug ever on Schedule I and III (for narcolepsy) rapidly absorbed via oral administration peak blood levels in min (longer if taken with food) crosses BBB easily half-life ~ min
21 OTHER DEPRESSANTS, SEDATIVE, HYPONOTICS BARBITURATES inhalants solvents nitrous oxide inhalant anesthetics (isoflurane, etc): ketamine NMDA antagonist related to PCP used as an anesthetic hallucinogenic in adults, but not in children anti-epileptics / neuromodulators used to stabilize neuronal membranes facilitate inhibition / reduce excitation mechanisms largely unknown
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