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PSYCH 478 > Topic 25: Alcohol > Flashcards

Topic 25: Alcohol Flashcards

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1
Q

How popular is alcohol?

A

after caffeine, alcohol is the most commonly used psychoactive drug

easily the single most abused drug: $223.5 billion burden in US, $1.90 per drink

88,000 annual deaths in US

long history of use and abuse

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2
Q

What is the historical evidence of alcohol use?

A

archaeological evidence of fermentation from Neolithic period (10,000 BCE)

first fermented beverage was likely mead (fermented from honey)

Egyptians generally credited with first beer

evidence for win production in Babylonia (>1700 BCE)

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3
Q

What are the three classes of alcohols?

A

alcohol is a chemical term for a family of organic compounds containing a hydroxyl group bound to a saturated carbon group

colloquially alcohol refers to ethyl alcohol or ethanol (EtOH)

methyl alcohol (methanol)
ethyl alcohol (ethanol)
isopropyl alcohol (isopropanol)

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4
Q

What is methyl alcohol?

A

methanol

CH3OH

simplest alcohol - toxic

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5
Q

What is ethyl alcohol?

A

ethanol

CH3CH2OH

alcoholic beverages

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6
Q

What is isopropyl alcohol?

A

isopropanol

(CH3)2CH2OH

rubbing alcohol (disinfectant)

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7
Q

What is the pharmacology of alcohol?

A

relative to other drugs, very large quantities of alcohol are required to elicit effects

EtOH administered by oral dose has high bioavailability

almost exclusively administered as dilute aqueous solutions

neutral grain spirits (vodka) are almost pure EtOH in water

alcohol has high caloric content but little nutritive value

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8
Q

What is alcohol absorption?

A

alcohol is amphipathic (polar and nonpolar character) and can readily diffuse through cell membranes

absorbed readily in the GI: 10% of absorption occurs in the stomach, 90& occurs in the small intestine

transport by passive diffusion: relative concentration drive rate of uptake, higher concentration drive rate of uptake, higher concentration of alcohol is absorbed faster

rate of passage to the small intestine affects rate of uptake: food in stomach slows passage to intestine, carbonation accelerates passage

alcohol dehydrogenase (ADH) is secreted in gastric fluids: can break down EtOH in GI preventing uptake, sex difference (60% more ADH activity in males), gastric ADH is inhibited by aspirin

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9
Q

What is alcohol distribution?

A

EtOh readily diffuses into all aqueous fluids/tissues via passive diffusion: easy access through BBB and placental barrier

excluded from fat tissues

sex bias - females tend to have higher % body fat

age bias - as males age % body fat increases: decreased distribution volume leads to higher blood concentration

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10
Q

What is alcohol metabolism?

A

liver metabolism of alcohol depends on the key enzymes alcohol dehydrogenase and aldehyde dehydrogenase

metabolism occurs via zero-order kinetics (fixed rate of metabolism)

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11
Q

What are the steps in the metabolism of ethanol?

A

ADH breaks down ethanol into acetaldehyde

acetaldehyde is a toxic intermediate: flushing reaction, nausea, headache, tachycardia

ALDH breaks down acetaldehyde into acetic acid

ACSS breaks down acetic acid into acetyl-CoA

acetyl-CoA goes to the Kreb’s cycle

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12
Q

What are the steps in the metabolism of methanol?

A

ADH breaks down methanol into formaldehyde

ALDH breaks down formaldehyde into formic acid

formic acid is a toxic end-product: inhibits cytochrome C oxidase, causes cellular hypoxia, blindness, coma, death

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13
Q

What is the metabolism and excretion of alcohol?

A

most liver metabolism occurs through ADH & ALDH

some metabolism through cytochrome P450 family enzymes (leads to drug interactions)

drug interactions caused by competition for P450 –> elevated drug concentration

induction of P450 with chronic use –> decreased drug concentration

95% of ingested EtOH is metabolized by the liver to CO2 and H2O (excreted through kidneys)

5% of EtOh is excreted through the lungs - provides the basis for the Breathalyzer test

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14
Q

What are the specific effects of EtOH?

A

result of interactions with receptors

cause most of the acute and chronic effects of intoxication

responsible for most subjective effects of intoxication

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15
Q

What are the non-specific effects of EtOH?

A

result of interaction with phospholipid membranes or bodily fluids

EtOH interacts with cell membranes causing changes in membrane protein function and cellular dysfunction

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16
Q

How does ethanol interact with GABAA-delta?

A

ethanol interacts with the GABA receptor at the transmembrane surface of the delta-subunit

EtOH acts as a positive allosteric modulator of GABAA

CNS depressant and sedative effects of EtOH moderated through GABA

EtOH can be cross-tolerant and cross-dependent with benzodiazepines and barbiturates

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17
Q

How does ethanol interact with NMDA and glutamate?

A

at low doses EtOH antagonizes NMDA receptors: decreases LTP, impairs learning and memory

NMDAR responsible for amnesiac effects of ethanol: blackouts

EtOH reduces glutamate release: measured by microdialysis, especially hippocampal glutamate release

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18
Q

How are the chronic effects ethanol has on NMDA?

A

with prolonged EtOH use NMDA receptors increase: adaptive response, increased in cortex and hippocampus of animal models and human alcoholics

glutamate release increases as a result of EtOH withdrawal: rebound hyperactivity, can result in seizures as a consequence of withdrawal

glutamatergic excitotoxicity leads to permanent brain damage in alcoholics

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19
Q

How does dopamine interact with EtOH?

A

EtOH increases the firing rate of VTA dopamine projections into the nucleus accumbens: dramatic decrease in VTA firing on withdrawal - may cause dysphoria of withdrawal

positive modulator of 5HT3 receptors: seratonergic input to VTA

positive modulator of NACh receptors: cholinergic inputs to VTA

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20
Q

How does ethanol interact with opioid receptors?

A

acute administration of ethanol increases endogenous opioid activity

increases release of endorphins from pituitary

in animal models increases endorphin and enkepaline synthesis and release in CNS

likely contributes to reinforcing effects in VTA –> NAc

opioid antagonists reduce EtOH self-consumption in animal models

chronic administration of ethanol reduces opioid expression

contributes to the dysphoric effects of withdrawal from chronic alcohol use

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21
Q

What are the behavioral effects of alcohol?

A

at low doses alcohol is anxiolytic, mildly euphoric, and calming/sedating

with increasing dose significant cognitive impairment occurs - inhibitions and caution are decreased, judgement is impaired, and impulsivity increases

at high doses emotion and exaggerated and plastic - prone to outbursts and aggression, pronounced motor and vision impairment, unconsciousness, coma, and death

22
Q

What are the physiological effects of alcohol at low doses?

A

diuretic (increased kidney output - dehydration)

inhibits antidiuretic hormone (vasopressin) release

sedative and hypnotic (sleep-inducing)

REM sleep both decreased (first part of night) and subsequently increased (second part of the night)

at higher doses - complete REM disruption - also subject to rebound on withdrawal (extended REM period on withdrawal)

23
Q

What are the vasodilation effects of ethanol?

A

dilation of blood vessels in skin (flushed face, warm skin)

feeling of warmth - through increases heat loss (risk of hypothermia)

increased cerebral blood flow may lead to decreased risk of dementia

24
Q

What are the balance and coordination effects of ethanol?

A

alcohol intoxication has pronounced motor effects (coordination) and disturbs balance

non-specific effects on vestibular system: ethanol thins the fluid in the inner ear, fluid moves more rapidly leading to overconsumption

balance easily tested by Romberg sway test

25
Q

What is alcohol tolerance?

A

the effects of alcohol are greatly diminished with repeated administration

cross-tolerance also develops with other sedative-hypnotic drugs, particularly benzodiazepines and barbiturates

tolerance develops by several mechanisms depending on the pattern of use

26
Q

What is acute alcohol tolerance?

A

tolerance to the subjective effects of alcohol develop within a single administration session

effects associated with intoxication - euphoria, anxiolysis, and mild stimulation occur when blood alcohol levels are rising

at plateau or falling doses effects include sedation, anger, depression

27
Q

What is metabolic tolerance to alcohol?

A

drug disposition tolerance occurs relatively quickly - induction of liver enzymes (ADH and P450) increases the rate of alcohol metabolism

metabolic tolerance can be demonstrated in short daily doses (e.g. 7 day dosing in humans): daily consumption of 3.2 g/kg body weight (240 mL pure EtOH for 75 kg male), roughly equivalent to 14 beers per day

28
Q

What is pharmacodynamic tolerance to alcohol?

A

adaptive changes in CNS function in response to chronic alcohol consumption: changes in receptor expression

contributes to the effects of alcohol withdrawal

increased NMDA receptor function, increased glutamate release

decreased GABA receptor function

decreased synthesis and release of opioids

decreased firing of mesolimbic dopamine neurons

29
Q

What is classical conditioning in alcohol use?

A

similar to opiates

environmental cues induce compensatory physiological changes

in rodent models alcohol administration decreases body temperature: conditioning leads to a compensatory increase in body temperature based on expectancy

tolerance diminished in novel environment

may play a strong role in craving

30
Q

What are the behavioral changes in alcohol tolerance?

A

practicing behaviors under the influence of alcohol leads to improved performance

rats trained run on a treadmill while intoxicated performed better with time

rats trained on treadmill sober performed poorly when tested after alcohol administration

seen in alcoholism as well: high-functioning alcoholic

31
Q

What is the development of alcohol tolerance?

A

tolerance develops rapidly in animals and humans

reaches maximum within a few weeks: may require 30-50% increased dose

reversible - tolerance diminished after 2-3 weeks of abstinence

repeated exposure leads to more rapid development of tolerance

32
Q

What is physical dependence on alcohol?

A

prolonged intoxication can result in adaptive changes: mechanisms of tolerance especially pharmacodynamic, restoration of homeostasis in presence of drug

can be readily demonstrated by the development of symptoms of abstinence syndrome (withdrawal)

withdrawal symptoms begin as early as a few hours after last dose and severity depends on the duration and dose

33
Q

What is acute withdrawal from alcohol?

A

symptoms of hangover: nausea, headache, dehydration, dry mouth, fatigue, general malaise

hangover is often described as an early component of withdrawal: may result from acute tolerance rather than dependence

alternately considered to be signs of acute toxicity from alcohol and metabolites

34
Q

What are the contributors to a hangover?

A

hangover varies considerably between individuals - not easy to define

generally occurs after a single session of excessive consumption

multiple possible causes

toxicity: accumulation of acetaldehyde can have acutely toxic effects, acute effects include nausea, vomiting, and headache, can be demonstrated by use of ALDH inhibitor - disulfuram

dehydration: dry mouth and headache

alcohol-induced gastric irritation: dry-mouth, nausea, and diarrhea

rebound effects on blood sugar: hypoglycemia, faintness, fatigue and malaise

congeners: ingredients or fermentation byproducts that exacerbate condition, red wine (tannins, sulfates), distilled spirits (methanol)

35
Q

What is early withdrawal to alcohol?

A

withdrawal from chronic alcohol use has an early and late component

early component (8-12 hours after last drink)

agitation, tremors, muscle cramps, vomiting, nausea, sweating, vivid dreams (rebound effects on REM), irregular heartbeat

typically last ~48 hours

less severe component of alcohol withdrawal

fewer than 5% of patients hospitalized for alcohol withdrawal go on to develop the late stage of withdrawal

36
Q

What are the rebound effects of alcohol on the GABAA receptor?

A

alcohol enhances GABAA function

GABAA receptor function decreases due to pharmacodynamic tolerance

rebound effects lead to development of hyperexcitability: tremors, seizures

37
Q

What are the rebound effects of alcohol on the NMDA receptor?

A

alcohol inhibits NMDAR function

NMDA receptor function and glutamate release increase with prolonged intoxication

rebound effects lead to hyperexcitability: seizures, glutamatergic excitotoxicity, hallucinations

38
Q

What is late withdrawal of alcohol?

A

delirium tremens (DT)

onset ~48 hours after last dose, may last 7-10 days

tremors and seizures

vivid hallucinatory episodes: often terrifying, altered sensorium (lack of recognition of real world), paranoid and nihilistic delusions (sense of doom)

39
Q

What are the severe risks of delirium tremens?

A

altered GABA homeostasis leads to unopposed sympathetic activation: “adrenergic storm”, tachycardia, hypertension, anxiety, panic attacks, agitation, fever, profuse sweating, cardiac arrhythmia, risk of stroke, heart attack

excitotoxicity: irreversible brain damage, epileptogenesis: kindling effect can lead to prolonged risk of seizures, seizures and coma

management of DT involves administration of benzodiazepines - effective due to cross tolerance at GABAA

40
Q

What is chronic alcohol exposure?

A

chronic alcohol consumption is a huge financial, heath, and social burden

high comorbidities of alcohol abuse in psychiatric illness: depression, schizophrenia, bipolar disorder, developmental disorder (FAS, FASD)

chronic heavy drinking can lead to cognitive impairment (some reversible) and peripheral health effects

41
Q

What are the cognitive deficits that occur with prolonged heavy drinking?

A

abstract problem solving

visuospatial abilities

verbal learning

perceptual motor skills

motor skills

memory

42
Q

What are the structural changes that occur with prolonged heavy drinking?

A

decreased brain volume (especially white matter, hippocampus)

neuronal loss in cortex (especially superior frontal association cortex), hypothalamus, pons, thalamus, brainstem, cerebellum

ventricular enlargement

43
Q

How is NMDA-mediated excitotoxicity involved with brain damage in alcohol use?

A

sensitization of neuronal cells due to compensatory upregulation of glutamate and NMDAR

44
Q

How is homocysteine accumulation involved with brain damage in alcohol use?

A

neurotoxic amino acid

normally detoxified in a folate-dependent mechanism (low folate in alcoholism)

homocysteine is an agonist at glutamate and glycine sites of NMDAR (exacerbates excitotoxicity)

homocysteine levels are a marker for severity of withdrawal

45
Q

How is neurotrophic factors involved with brain damage in alcohol use?

A

reduced levels of brain-derived neurotropic factor (BDNF) and altered receptor function

46
Q

What is acetaldehyde?

A

aldehydes are highly reactive with protein and DNA

general damage to protein function and DNA

formation of aldehyde adducts correlates with liver damage

acetaldehyde also shown to cause increased reinforcing effects in the mesolimbic dopamine pathway: acetaldehyde microinjection to VTA can demonstrate self-administration in rats

47
Q

What is Wernicke-Korsakoff syndrome?

A

alcoholism causes B1-vitamin deficiency: poor diet and impaired absorption of B1 (thiamine)

thiamine required for brain glucose metabolism: deficit cause cell death in mammillary bodies, thalamus, periaqueductal grey

WKS presents as confusion, disorientation, tremors, and ataxia

leads to significant memory impairment: recall of past events intact, encoding is inhibited - repeatedly reading same page, repeating same stories or asking same questions

degeneration can be stopped by thiamine supplement but damage is irreversible

48
Q

How is the liver impacted by alcohol use?

A

liver toxicity is a well characterized effect of chronic consumption

at lower levels alcohol leads to fatty liver: metabolism of alcohol decreases fat metabolism leading to reversible accumulation of fats

prolonged use leads to alcoholic hepatitis: inflammation, fever, jaundice, potentially fatal

liver injury leads to scarring: liver cirrhosis, scar tissue reduced blood flow - secondary damage due to ischemia

49
Q

What is fetal alcohol syndrome / fetal alcohol spectrum disorder?

A

alcohol has pronounced effects on the developing fetus

fetal alcohol syndrome / fetal alcohol spectrum disorder results from developmental injury to the fetal brain

major cause of intellectual impairment worldwide

50
Q

What are alcohols effects on the developing fetus?

A

cytotoxin: pre and post-natal growth disorders

teratogen: typical craniofacial changes and variable malformations

neurotoxin: structural changes to the CNS and multiple cerebral dysfunctions

behavioral: dramatic increase in risk of addictions

51
Q

How much alcohol is too much during pregnancy?

A

no established guidelines for safe alcohol consumption during pregnancy

ethical restrictions prevent establishing safe guidelines

general advice in North America is no level is safe

studies: ~30% of women self-report consuming some alcohol during pregnancy

PSYCH 478 (28 decks)

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