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Neuro-pharmacology > Alcohol > Flashcards

Alcohol Flashcards

1
Q

Colloquially alcohol refers to

A

ethyl
alcohol or ethanol
(EtOH)

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2
Q

alcohol and quantity

A

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

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3
Q

EtOH administered by

A

oral dose has high bioavailability

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4
Q

Almost exclusively administered as

A

dilute aqueous
solutions

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5
Q

Neutral grain spirits (vodka) are almost pure

A

EtOH in
water

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6
Q

Alcohol has high

A

caloric content but little nutritive value

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7
Q

Alcohol is amphipathic

A

(polar and non-polar
character) and can readily diffuse through cell
membranes

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8
Q

Absorbed readily in the

A

GI

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9
Q

10% is absorbed in the

A

stomach

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10
Q

90% is absorbed in the

A

small intestine

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11
Q

Transport by

A

passive diffusion

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12
Q

Relative concentrations drive rate

A

of uptake

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13
Q

Higher concentration of alcohol is

A

absorbed faster

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14
Q

Rate of passage to the small intestine affects

A

s rate
of uptake

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15
Q

Food in stomach

A

slows passage to intestine –
slower uptake

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16
Q

Carbonation (e.g. champagne)

A

) accelerates passage
– faster uptake

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17
Q

Alcohol dehydrogenase (ADH) is

A

secreted in
gastric fluids

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18
Q

Alcohol dehydrogenase (ADH) is secreted in gastric fluids (3)

A
  • 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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19
Q
  • EtOH readily diffuses into all
A

aqueous fluids/tissues via passive diffusion

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20
Q

Easy access through

A

BBB and placental barrier

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21
Q

Excluded from

A

fat tissues

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22
Q

Sex bias

A

– females tend to have higher %
body fat

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23
Q

Age bias

A

as males age % body fat increases

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24
Q

more fatty tissues means

A

higher blood
concentration

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25
Q

Metabolism - 2 key enzymes

A

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

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26
Q

Metabolism occurs via

A

zero-order
kinetics (fixed rate of metabolism)

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27
Q

ethanol metabolism

A

Ethanol –Alcohol dehydrogenase–> Acetaldehyde — aldehyde dehydrogenase–> acetic acid –acyl-CoA synthase–> Acetyl-CoA -> Krebs cycle

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28
Q

Acetaldehyde

A

Toxic intermediate

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29
Q

Acetaldehyde Toxic intermediate

A
  • Flushing reaction
  • Nausea
  • Headache
  • Tachycardia
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30
Q

Most liver metabolism occurs through

A

ADH & ALDH

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31
Q

Some metabolism through

A

cytochrome P450 family enzymes (leads to drug
interactions)

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32
Q

Drug interactions caused by

A

competition for P450 → elevated drug concentration

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33
Q

Induction of P450 with chronic use →

A

decreased drug concentration

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34
Q

95% of ingested EtOH is metabolized by the

A

liver to CO2 and H2O (excreted
through kidneys)

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35
Q

5% of EtOH is excreted through the

A

e lungs – provides the basis for the
Breathalyzer test

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36
Q

Specific effects –

A

result of interactions with receptors

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37
Q

Specific effects – result of interactions with receptors

A

Cause most of the acute and chronic effects of intoxication
Responsible for most subjective effects of intoxication

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38
Q

Non-specific effects

A

result of interaction with
phospholipid membranes or bodily fluids

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39
Q

Non-specific effects – result of interaction with
phospholipid membranes or bodily fluids

A

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

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40
Q

Ethanol interacts with the _____ receptor at the

A

GABA
receptor at the transmembrane surface of the delta-subunit

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41
Q

EtOH acts as a

A

positive allosteric
modulator of GABAA

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42
Q
  • CNS effects
A

depressant and sedative effects of
EtOH moderated through GABA

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43
Q

EtOH can be _____ & ____ with benzos & barbituates

A

cross-tolerant and crossdependent with benzodiazepines and
barbiturates

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44
Q

At low doses EtOH antagonizes

A

NMDA
receptors

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45
Q

At low doses EtOH antagonizes NMDA
receptors

A

Decreases LTP
* Impairs learning and memory

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46
Q

NMDAR responsible for

A

amnesiac
effects of ethanol

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47
Q

EtOH reduces

A

glutamate release

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48
Q

EtOH reduces glutamate release

A

Measured by microdialysis
Esp. hippocampal glutamate release

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49
Q

Chronic effects on NMDA

A

With prolonged EtOH use NMDA
receptors increase

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50
Q

With prolonged EtOH use NMDA
receptors increase

A
  • Adaptive response
  • Increased in cortex and hippocampus of
    animal models and human alcoholics
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51
Q

Glutamate release increases as a result
of

A

EtOH withdrawal

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52
Q

Glutamate release increases as a result
of EtOH withdrawal

A

Rebound hyperactivity
Can result in seizures as a consequence of
withdrawal

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53
Q
  • Glutamatergic excitotoxicity leads to
A

permanent brain damage in alcoholics

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54
Q

Dopamine

A

EtOH increases the firing rate of VTA
dopamine projections into the nucleus
accumbens

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55
Q

Dramatic decrease in VTA firing on

A

withdrawal – may cause dysphoria of
withdrawal

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56
Q
  • Positive modulator of
A

5HT3
receptors

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57
Q

Positive modulator of 5HT3
receptors

A

Seratonergic input to VTA

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58
Q

Positive modulator of NACh receptors

A

Cholinergic inputs to VTA

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59
Q

Opioid receptors

A

Acute administration of ethanol increases
endogenous opioid activity

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60
Q

Increases release of endorphins from

A

pituitary

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61
Q

impact on opioid receptors Likely contributes to

A

reinforcing effects in VTA →
NAc

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62
Q

Opioid antagonists reduce

A

EtOH selfconsumption in animal models

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63
Q

Chronic administration of ethanol reduces

A

opioid
expression

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64
Q

Contributes to the dysphoric effects of
withdrawal from

A

chronic alcohol use

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65
Q

At low doses alcohol is

A

s anxiolytic, mildly
euphoric, and calming / sedating.

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66
Q

With increasing dose significant cognitive

A

impairment occurs – inhibitions and caution are
decreased, judgement is impaired, and
impulsivity increases.

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67
Q

At high doses emotions are

A

exaggerated and
plastic – prone to outbursts and aggression,
pronounced motor and vision impairment,
unconsciousness, coma, and death

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68
Q

Physiological effects At low doses

A

Diuretic
Sedative and hypnotic
REM sleep both decreased for the first part of the night subsequently increased (second part of the night)
At higher doses – complete REM disruption

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69
Q

Vasodilation

A

Dilation of blood vessels in skin (flushed face, warm skin)
* Feeling of warmth – though increases heat loss (risk of hypothermia)
* Increased cerebral blood flow may lead to decreased risk of dementia

70
Q

Balance and coordination

A

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

71
Q

Non-specific effects on vestibular system

A

Ethanol thins the fluid in the inner ear
* Fluid moves more rapidly leading to
overcompensation

72
Q

Balance easily tested by

A

Romberg sway test

73
Q

The effects of alcohol are greatly diminished with

A

repeated administration

74
Q

Cross-tolerance also develops with other sedative-hypnotic
drugs, particularly

A

benzodiazepines and barbiturates

75
Q

Tolerance develops by several

A

mechanisms
depending on the patterns of use

76
Q

Acute tolerance

A

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

77
Q

Effects associated with intoxication –

A

euphoria, anxiolysis, and mild
stimulation occur when blood alcohol
levels are rising.

78
Q

At plateau or falling doses effects
include

A

sedation, anger, depression

79
Q

Metabolic tolerance

A

– induction of liver
enzymes (ADH and P450) increases the
rate of alcohol metabolism

80
Q
  • Metabolic tolerance can be demonstrated
    in
A

short daily doses (e.g. 7 day dosing in
humans)

81
Q

Pharmacodynamic tolerance

A

Adaptive changes in CNS function in response to chronic alcohol consumption

82
Q

Pharmacodynamic tolerance Contributes to the effects of

A

alcohol withdrawal

83
Q

Pharmacodynamic tolerance (increased)

A

Increased NMDA receptor function,
increased glutamate release

84
Q

Pharmacodynamic tolerance (decreased)

A
  • Decreased GABA receptor function
  • Decreased synthesis and release of opioids
  • Decreased firing of mesolimbic dopamine neurons
85
Q

Behavioural tolerance

A

Environmental cues induce compensatory
physiological changes
Tolerance diminished in novel environment

86
Q

Behavioural tolerance May play a strong role in

A

craving

87
Q

Behavioural changes:

A

Practicing behaviours under the influence of
alcohol leads to improved performance

88
Q

High-functioning alcoholic

A

Practicing behaviours under the influence of
alcohol leads to improved performance

89
Q

Tolerance develops

A

rapidly in animals and humans

90
Q

tolerance Reaches maximum

A

within a few weeks

91
Q

tolerance is

A

Reversible

92
Q

Reversible

A

– tolerance diminishes after 2-3 weeks of
abstinence

93
Q

Repeated exposure leads to more

A

rapid development of
tolerance

94
Q

Physical dependence

A

Prolonged intoxication can result in adaptive changes

95
Q

Prolonged intoxication can result in adaptive changes

A
  • Mechanisms of tolerance esp. pharmacodynamics
  • Restoration of homeostasis in presence of drug
96
Q

Physical dependence Can be readily demonstrated by the

A

development of
symptoms of abstinence syndrome (withdrawal)

97
Q

Withdrawal symptoms begin as early as

A

a few hours after last
dose and severity depends on the duration and dose

98
Q

Acute withdrawal

A

Symptoms of hangover

99
Q

Symptoms of hangover

A

Nausea
* Headache
* Dehydration, dry mouth
* Fatigue
* General malaise

100
Q

Hangover is often described as an

A

early
component of withdrawal

101
Q

Hangover is often described as an early
component of withdrawal may result from

A

m acute tolerance rather than
dependence

102
Q

hangover Alternately considered to be signs of

A

acute
toxicity from alcohol and metabolites

103
Q

Contributors to hangover

A

Toxicity:
Dehydration:
Alcohol-induced gastric irritation
Rebound effects on blood sugar
Congeners

104
Q

Toxicity and hangovers

A

Accumulation of acetaldehyde can have acutely
toxic effects
* Acute effects include nausea, vomiting, and
headache

105
Q

disulfuram

A

toxicity induced demonstrated by use of ALDH inhibitor

106
Q

Dehydration

A

Dry mouth and headache

107
Q

Alcohol-induced gastric irritation

A

Dry-mouth, nausea, and diarrhea

108
Q
  • Rebound effects on blood sugar
A

Hypoglycemia, faintness, fatigue and malaise

109
Q

Congeners

A
  • Ingredients or fermentation byproducts that
    exacerbate condition
    Red wine – tannins, sulfates
  • Distilled spirits – methanol
110
Q

methanol metabolism

A

Methanol – alcohol dehydrogenase -> formaldehyde –Aldehyde dehydrogenase —> formic acid

111
Q

formic acid

A

Toxic end-product of methanol metabolism

112
Q

Formic acid inhibits

A

cytochrome C oxidase

113
Q

formic acid causes

A

cellular hypoxia Blindness, coma, death

114
Q

Withdrawal from chronic alcohol use has an

A

early and late
component

115
Q

Early component alcohol withdrawal

A

Agitation, tremors, muscle cramps, vomiting, nausea, sweating, vivid
dreams (rebound effects on REM), irregular heartbeat
Less severe component of alcohol withdrawal

116
Q

Fewer than 5% of patients hospitalized for alcohol withdrawal go on to

A

develop the late stage of withdrawal

117
Q

Rebound effects
GABAA RECEPTOR

A
  1. Alcohol enhances
  2. GABAA function
    receptor function decreases due to
    pharmacodynamic tolerance
118
Q

GABAA RECEPTOR Rebound effects lead to development of

A

hyperexcitability

119
Q

hyperexcitability GABA

A
  • Tremors
  • Seizures
120
Q

Rebound effects NMDA RECEPTOR

A
  1. Alcohol inhibits NMDAR function
  2. NMDA receptor function and glutamate release `increase with prolonged intoxication
121
Q

NMDA RECEPTOR Rebound effects lead to

A

hyperexcitability

122
Q

hyperexcitability NMDA receptor

A
  • Seizures
  • Glutamatergic excitotoxicity
  • Hallucinations
123
Q

Late withdrawal

A

Delirium tremens (DT)

124
Q

Delirium tremens (DT)

A

Onset ~48 hours after last dose, may last
7-10 days
* Tremors and seizures
Vivid hallucinatory episodes

125
Q

Delirium tremens (DT) - Vivid hallucinatory episodes

A
  • Often terrifying
  • Altered sensorium
  • Paranoid and nihilistic delusions
126
Q

Altered sensorium

A

lack of recognition of
real world

127
Q

Paranoid and nihilistic delusions

A

sense of
doom

128
Q

Management of DT involves
administration of

A

benzodiazepines –
effective due to cross tolerance at
GABAA

129
Q

Severe risk with DTs - Excitotoxicity

A

Irreversible brain damage
Epileptogenesis
Seizures and coma

130
Q

Epileptogenesis

A

kindling effect can
lead to prolonged risk of seizures

131
Q

Severe risk with DTs Altered GABA homeostasis leads to

A

unopposed sympathetic activation

132
Q

Altered GABA homeostasis leads to
unopposed sympathetic activation

A

‘Adrenergic storm’
* Tachycardia, hypertension
* Anxiety, panic attacks, agitation
* Fever, profuse sweating
* Cardiac arrhythmia, risk of stroke,
heart attack

133
Q

Chronic alcohol consumption is a

A

huge financial, health, and social
burden

134
Q

High comorbidities of alcohol abuse in psychiatric illness

A
  • Depression
  • Schizophrenia
  • Bipolar disorder
  • Developmental disorders – including FAS / FASD
135
Q

Chronic heavy drinking can lead to

A

cognitive impairment (some
reversible) and peripheral health effects

136
Q

Cognitive deficits occur with prolonged heavy drinking (6)

A
  • Abstract problem solving
  • Visuospatial abilities
  • Verbal learning
  • Perceptual motor skills
  • Motor skills
  • Memory
137
Q

brain structure changes include

A

Decreased brain volume
Neuronal loss in cortex
Ventricular enlargement

138
Q

Decreased brain volume especially in

A

white matter, hippocampus

139
Q

Neuronal loss in cortex

A

superior frontal association cortex, hypothalamus, pons, thalamus, brainstem,
cerebellum

140
Q

Brain damage mechanisms 3

A

NMDA-mediated excitotoxicity
Homocysteine accumulation
Neurotrophic factors

141
Q

NMDA-mediated excitotoxicity and brain damage

A

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

142
Q

Brain damage mechanisms Homocysteine accumulation

A

Neurotoxic amino acid due to low folates

143
Q

Homocysteine is an

A

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

144
Q

Homocysteine levels are a marker for

A

severity of withdrawal

145
Q

Brain damage mechanisms Neurotrophic factors

A

Reduced levels of brain-derived neurotrophic factor (BDNF) and altered receptor function

146
Q

Acetaldehyde

A

General damage to protein function and DNA

147
Q

Formation of aldehyde adducts correlates with

A

liver damage

148
Q

Acetaldehyde also shown to cause increased

A

reinforcing effects
in the mesolimbic dopamine pathway

149
Q

Acetaldehyde microinjection to VTA can demonstrate

A

self-administration in rats

150
Q

Wernicke
-Korsakoff Syndrome - Alcoholism causes

A

B1-vitamin deficiency

151
Q

Alcoholism causes
B1-vitamin deficiency

A

Poor diet and impaired absorption of B
1
(thiamine)

152
Q

Thiamine required for

A

brain glucose metabolism

153
Q

thiamine deficit causes

A

t causes cell death in mammillary bodies, thalamus,
periaqueductal grey

154
Q

WKS presents as

A

confusion, disorientation, tremors, and
ataxia

155
Q

Wernicke
-Korsakoff Syndrome Leads to significant

A

memory impairment

156
Q

Wernicke
-Korsakoff Syndrome - recall for past events

A

intact

157
Q

Wernicke
-Korsakoff Syndrome - Encoding is

A

inhibited

158
Q

Wernicke
-Korsakoff Syndrome - inhibited encoding

A

repeatedly reading same page,
repeating same stories or asking same questions

159
Q

Wernicke
-Korsakoff Syndrome - can be stopped with

A

thiamine supplement
but damage is irreversible

160
Q

Liver toxicity is a well characterized effect of

A

chronic consumption

161
Q

At lower levels alcohol leads to

A

fatty liver

162
Q

Metabolism of alcohol decreases fat metabolism
leading to

A

reversible accumulation of fats

163
Q

Prolonged use leads to

A

alcoholic hepatitis

164
Q

alcoholic hepatitis

A
  • Inflammation, fever, jaundice
  • Potentially fatal
165
Q

Liver injury leads to

A

scarring

166
Q

Liver injury leads to scarring

A
  • Liver cirrhosis
  • Scar tissue reduces blood flow – secondary
    damage due to ischemia
167
Q

Fetal alcohol syndrome / fetal alcohol spectrum disorder results from

A

developmental
injury to the fetal brain

168
Q

Alcohol effects on the developing fetus - cytotoxin

A

Pre- and post-natal growth disorders

169
Q

Alcohol effects on the developing fetus - Teratogen

A

typical craniofacial changes and variable malformations

170
Q

Alcohol effects on the developing fetus - Neurotoxin

A

structural changes to the CNS and multiple cerebral dysfunctions

171
Q

Alcohol effects on the developing fetus - Behavioural

A

dramatic increase in risk of addictions

Neuro-pharmacology (26 decks)

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