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83 Cards in this Set

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Alcohol belongs to which group of compounds?
Sedative-hypnotics & anxiolytics
Diverse group of compounds that depress CNS and behavior- also includes barbiturates, hypnotics, and anxiolytics
Elimination and excretion pathway of alcohol
Alcohol -> Acetaldehyde -> Acetic Acid -> Carbon Dioxide + Water + Energy
What enzyme converts alcohol into acetaldehyde?
Alcohol dehydrogenase
Rate limiting step
What enzyme converts acetaldehyde into acedic acid?
Acetaldehyde dehydrogenase
What causes flushing, nausea, headache, increased heart rate and why?
Build-up of acetaldehyde when aldehyde dehydrogenase is less active
Asian Flush??
10% of Asians have the gene that codes for the homozygous inactive form of acetaldehyde dehydrogenase- even small amounts of alcohol lead to high concentration of acetaldehyde
Homozygous for active form of acetaldehyde dehydrogenase
Effect: mild or no flushing
Heterozygous form of acetaldehyde dehydrogenase
Effect: get sick, flushing
Homozygous for inactive form of acetaldehyde dehydrogenase
Effect: severe flushing, alcohol is toxic
Sex differences in metabolism
Men have first pass metabolism of alcohol b/c alcohol dehydrogenase is 60% more active in male stomachs- effect is less alcohol gets into the small intestine/ bloodstream.
Women have less active alcohol dehydrogenase in female stomach, so more alcohol goes straight into the intestine/bloodstream- greater health problems for female alcoholics.
In women, small difference b/n IV and Oral BAC.
In men, large difference b/n IV and Oral BAC- men lose a lot of ETOH orally.
Disinhibition- relaxed, more social
100-150 mg/100ml
Sedative effects- slurred speech, falling out of chair, really drunk
150-300 mg/100ml
Stupor- under the table, barfing, can barely talk or stand
300 mg/100ml
(LD50)Lethal- death via respiratory depression
400 mg/100ml
Cognitive effects of alcohol
decreased memory (especially storage), greyouts (retrieval limited to when person drinks again), blackouts; mood changes- Low BAC= euphoria, friendly & High BAC= greater hostility; expectancy matters
Acute tolerance of alcohol
BAC on rising phase = BAC on falling phase, but different effects- rising phase-> increased body sway/impairment/"intoxicated", falling phase-> normal body sway, no impairment, "sober", TOLERANT
Chronic tolerance of alcohol
After 7 days of drinking, more rapid decrease in blood alcohol levels, illustrates tolerance. Pharmacokinetic tolerance: inducing enzymes that break down ETOH (you see and increase in both alcohol dehydrogenase and P450 liver enzymes -> more rapid tolerance, blood levels reduced). Shift to the right in curve representing degree of intoxication vs. BAC (expression depends on set and setting, as well as learning).
Withdrawal: hangover
low blood sugar levels, dehydration, irritated stomach, decreased REM- stopped by drinking a little more-> hangover is partly a mini-withdrawal- residual acetaldehyde, loss of body fluids, etc.
Withdrawal: severe, lethal effects
delirium tremens (DT's) characterized by seizures, hallucinations; cramps, nausea, tremors; treated by administering another sedative hypnotic like diazepam (BZD)
Actions @ NMDA & GABA receptors
NMDA antagonist, GABAa agonist
Alcohol's interation w/other drugs
Cross tolerance & additive effects w/antibiotics, anxiolytics, anticonvulsants (all act @ GABAa receptor)
What increases absorption of alcohol?
Harder drinks (greater alcohol concentration), carbonated drinks (champagne), empty stomach (nothing blocking the movement of material from the stomach into the small intestine)
Fetal Alcohol Syndrome
Blocking of NMDA receptors during development triggers widespread apoptotic neurodegeneration
The controlled destruction of cells.
see apoptotic neurodegeneration w/alcohol, barbiturates, BZDs- BUT NOT w/antagonists or agonists @ dopamine receptors, muscarinic antagonists, glutamate receptor antagonists
Pharmacological treatment of alcoholism
Antabuse (disulfiram)- blocks acetaldehyde dehydrogenase -> increased levels of acetaldehyde -> sickness (mixed results).
SSRIs- relieve anxiety, depression (withdrawal effects)
First barbiturate
Barbital (Veronal)
Phenobarbital (Luminal)
long-acting (8-12 hrs), surgery/anxiety treatment, less lipid soluble
Pentobarbital (Nembutal)
intermediate-acting (2-8 hrs), helps induce sleep
Secobarbital (Seconal)
short-acting (1-4 hrs)
Thiopental (Pentothal)
ultra-short-acting (5-30 min.), most lipid soluble, high abuse potential, commonly used on street
Medical Uses for barbiturates
sleep induction (short action), anticonvulsants, anaesthetics, sedatives, alcohol withdrawal, anxiolytics (all long action)
Duration of action determines use
Illicit Use of barbiturates
used for effects similar to alcohol; often used with other drugs (stimulants or opiates- smoothes the high); rapid tolerance (faster than alcohol); severe withdrawal; low safety margin (50% of drug related suicides)
Meprobamate (Miltown)
Anxiolytic, treatment of anxiety and depression, thought to have less aversive effects, actually very dangerous
What's different about second generation anxiolytics?
They don't act @ GABA receptor- act on serotonin autoreceptor; effective but take weeks to have effects
Medical Uses of anxiolytics
Pathological anxiety, severe emotional distress, relief from agitation and alcohol withdrawal, sedation(sleep-inducing), pre-surgery sedation & amnesia, anticonvulsants
Therapeutic Effects of anxiolytics
Calming & relaxation (desired effects); side effects- motor incoordination, intoxication (like alcohol), memory loss, sedation & sleep, deep sleep and coma, respiratory depression
BZDs vs. Barbiturates
BZDs/anxiolytics have less tolerance effects (less dose required, not as dangerous), lower likelihood of abuse (SA), safer drugs
Date rape cases
Rohypnol (flunitrazepam, BZD), "Micky Finn" (chloryl hydrate, tasteless pill-barb), GHB (hydroxybutyric acid, neither barb/BZD but same effect)
BZD Binding
Neocortex, hippocampus, cerebellum, olfactory bulb- binds to GABAa receptor
GABA neurotransmission
Major inhibitory NT, hyperpolarizes neurons
GABA Synthesis
Glutamate -glutamate acid decarboxylase(GAD)-> GABA
What enzyme converts GABA back into glutamate and succinate?
GABA aminotransferase
GABA transporters
GAT-1,2,3 (astrocytes)
GAT-1 (on pre-synaptic terminal)
Ionotropic Receptor
fast-acting, ligand-gated ion channel regulated by NTs that bind to specific sites; composed of several subtypes that come together in cell membrane; ion channel @ center
GABAa receptor
Metabotropic Receptor
slow-acting; composed of single large protein in cell membrane that activates G proteins (G-protein coupled)
GABAb receptor
GABAa receptor
Ionotropic, Cl- selective(forms chloride channel), composed of 5 subunits (each w/number of isoforms), GABA increases Cl- conductance, hyperpolarization
GABAa agonist
Muscimol, binds @ site where GABA binds
GABAa antagonist
Bicuculline, binds @ site where GABA binds
Evidence for unique BZD and BARB sites
no direct action by themselves, do not inhibit GABA binding, do not effect GABA release (don't act presynaptically) -> allosteric modulators, act @ different sites from each other and different site than GABA
Allosteric Modulation
Change conformation of GABAa receptor complex so that GABA works better -> greater Cl- conductance, hyperpolarization
How do Barbiturates affect Cl- channel openings?
Increase long DURATION open states, no change in # of openings- easy to kill yourself b/c channels are stuck open, neurons can't fire and perform normal functions
How do BZDs affect Cl- channel openings?
Increase FREQUENCY (# of times the channel opens), do not change duration
Inverse agonists
First example were drugs that act at BZD site on GABAa receptor: B-carbolines, negatively modulate: decrease Cl- conductance, reduced inhibition (produce extreme anxiety and panic)
Which subtypes of the GABAa receptor are sensitive to diazepam?
alpa-1,2,3,5 (point mutations)
sedative and amnesic effects
anxiolytic effects
Endogenous ligands ar BDZ site
steroid metabolites of progesterone and deoxycorticosterone
Why can't you inject marijuana/cannabinoids?
b/c they're like an oil- very lipid soluble
What are cannabinoids?
Psychoactive compounds of marijuana plant, over 60-vary tremendously in potency (eg. delta-9-tetrahydrocannabinol)
What is Marijuana?
mixture of leaves, stems, tops (all contain cannabinoids)- contain up to 8-10% THC (more potent today)
form of marijuana smoked in a pipe, dried resin from top of female plant, THC usually 2-5% but up to 15% (highest concentration, so can smoke less)
Hash Oil
compressed hashish, organic extraction- dissolved in alcohol, filtered, evaporated, left w/dark brown oily substance- THC usually ~10-20%, up to 70% (pure cannabinoid- drop put on cigarette and smoked)
Synthetic Cannabinoids
Developed for research, more potent than naturally occurring cannabinoids, but water soluble (can work w/them)- synthetic antagonists, Rimonabant; agonist- WIN 55212
Cannabinoid Absorption
very lipid soluble, good absorption if smoked (20-37%), rapid peak (15 min).
Slow absorption w/oral administration, 1st pass metabolism & degradation in stomach- blunted "high" effect reported
Cannabinoid Routes
smoked via joint, water pipe (bong-less drug lost)
Cannabinoid Metabolism and Clearance
Rapid initial drop due to redistribution to fats, slow metabolism in liver, metabolites may persist for weeks.
*Major biologically active compound may be metabolite
1) Primary metabolite of delta-9-THC (11-hydroxy-THC) is more potent
2) Delay between peak plasma levels and reported "high" (peak psychoactive effect after metabolism of delta-9-THC)
Cannabinoid Behavioral Effects: Low-Moderate doses
disinhibition, relaxation, drowsiness, feeling of well being, exhilaration, euphoria, sensory-perceptual changes, STM impairment (very clear lab evidence), balance/stability impaired, decreased muscle strength, small tremor, poor on complex motor tasks, increase hunger (munchies)
Cannabinoid Behavioral Effects: High doses
pseudohallucinations, synesthesias, impaired judgment/reaction time, pronounced motor impairment, increasingly disorganized thoughts, confusion, paranoia, agitation, anxiety (set and setting), NOT LETHAL EVEN @ VERY HIGH DOSES (very large safety margin)
melding of senses (eg. sounds have colors)
Repeated Administration of Cannabinoids
Chronic THC -> fairly rapid tolerance, huge down-regulation of cannabinoid receptors in caudate (fewer receptors for drug to bind to).
Tolerance *rats*: BP, HR, Operant responding (mixed)
Tolerance *humans*: "High" (mixed)
Potential Medical Uses of Cannabinoids
decreases glaucoma, antiemetic (reduces nausea and vomiting- chemotherapy), anticonvulsant, enhances appetite (AIDS patients), analgesic
pure THC vs. marijuana controversy
few clinical trials report THC isn't effective medically, users claim marijuana is effective
Cannabinoid receptor
localization: high density in hippocampus, conserved across mammalian species, both CB-1 and CB-2 (peripheral) receptors are G protein coupled, receptor density very high, located pre-synaptically @ axon terminal, Gi- inhibits formation of cAMP
Endogenous cannabinoids (endocannabinoids)
act as retrograde messengers w/in the brain- released from post-synaptic cell and bind to CB-1 receptors on pre-synaptic terminal: decrease calcium conductance, decrease NT release
endocannabinoid, arachidonic acid derivative, synthesized as needed (too lipid soluble to be stored in vesicles); inhibit cAMP via cannabinoid receptor, inhibit binding of cannabinoids, only weak agonist @ CB-1 receptor, decrease motor activity, antinociceptive effects
2-arachidonyl glycerol
endocannabinoid, full agonist @ CB-1, higher concentration (more active) in brain than anandamide
Locus of cannabinoid actions
*Hippocampus- memory effects
*Mesostriatal DA system- reward
*Basal ganglia, cerebellum- motor activity
*Spinal cord & peripheral tissue- analgesic effects
Reinforcement of cannabinoids
Self-administration blocked by CB-1 antagonist and naltrexone, preexposure enhances SA and conditioned place preference (mixed), CB-1 knockouts also altered SA of alcohol, opioids, cocaine, and nicotine