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Pmcol 305 > Alcohol > Flashcards

Alcohol Flashcards

1
Q

alcohol

A

ethanol (EtOH)
hydroxyl group (alcohol functional group)

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2
Q

yeast

A

converts sugars to alcohol through fermentation
fast generation time
dried for long-term storage; rehydrated for use
simple fungi = genomes are fully sequenced → can trace metabolic pathways
model organism → aging, DNA repair, brewing

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3
Q

fermentation

A

glucose → 2 pyruvate by glycolysis
pyruvate → 2 acetaldehyde (release of CO2)
acetaldehyde → ethanol by aldehyde dehydrogenase

additional molecules are produced
15% ethanol is toxic to yeast (above requires distillation)

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4
Q

distillation

A

concentrates alcohol to 40%+

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5
Q

proof

A

ABV x 2
max proof is ~190 chemically - alcohol absorbs moisture from the air

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6
Q

ABV

A

alcohol by volume
difference in density of sugar between original and final

= 131.25 x (OG-FG)

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7
Q

wine, beer, and scotch chemistry

A

botanical beverages = plant-based

complex plant chemistry + yeast metabolism [+ conditioning (oxidation of chemicals)] = chemical profile in finished products

anthocyanins, terpenes, tannins, polyphenols, vitamins

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8
Q

alcohol use

A
  1. abstinent
  2. moderate
  3. bingeing: 4 (women) or 5 (men) drinks on one occasion in last 30 days
  4. heavy (alcoholic)

use epidemiological trends and health related effects to set definitions → start to feel negative effects

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9
Q

ethanol in a standardized drink

A

one standardized drink = 0.6 oz
1 oz contains 23.3 g of EtOH

= ~14g of alcohol

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10
Q

absorption

A

absorbed in the small intestine
partially absorbed in stomach - food increases retention time in the stomach = slowed absorption
(low pH does not alter ethanol)

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11
Q

distribution

A

distributes through aqueous tissue
small size = easily distributed to brain → psychoactive effects
volume available for distribution determines BAC
g EtOH / 100 mL of blood

higher proportion of body fat = higher BAC after 1 drink

larger people = lower BAC because of greater body volume
leaner people = lower BAC because of greater water volume

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12
Q

estimate BAC

A

blood alcohol concentration

one drink = 14g EtOH
avg man = 53.4% water; 1L water = 1kg
0.534 x 90.7 kg = 48.4L

14g EtOH / 48.4 L water = 0.29 g/L = 0.029 g / 100 mL

blood = 80.6% water
0.029 g / 100 mL x 0.806 = 0.023 BAC

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13
Q

acute effects of EtOH

A

biphasic
1. as BAC rises (~ 1st hour) = stimulant
triggers VTA → NAc DA release (disinhibition)
- increased sociability, decreased anxiety
2. BAC falls (when stopped drinking) = depressant
potentiation of GABA A receptor IPSP, blocks NMDA receptor EPSPs, blocks select Ca2+ channels
- feel and show inebriation

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14
Q

acute effects in brain

A

inhibited decision making
unstable mood and heightened emotions
decreased anxiety
increased aggression + addiction

impaired memory, balance + coordination, vision
balance: improper cerebellum-mediated modulation of motor signals

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15
Q

acute effects in heart

A

1st phase = increased heart rate
2nd phase = decreased heart rate

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16
Q

acute effects in blood vessels

A

vasodilation
autonomic brainstem nuclei
causes warm skin but decreased core temperature

reduced blood clotting

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17
Q

other acute effects

A

increased salivation + appetite
inhibited ADH hormone = increased urination
reduced perception of pain

increased gastric secretions
overproduction of acid = loss of stomach mucosal lining

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18
Q

mechanism of action

A

depressant: slows neuronal activity
affects neurotransmitters: GABA, glutamate, dopamine + endogenous opioids, other NTs

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19
Q

aggression

A

inhibition of PFC areas that control behaviours
many environmental factors

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20
Q

GABA

A

alcohol increases GABA’s inhibitory actions
potentiates GABA receptors

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21
Q

glutamate

A

alcohol blocks glutamate receptors

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22
Q

dopamine and endogenous opioids

A

alcohol increases the release of dopamine and endorphins in addiction pathways

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23
Q

other neurotransmitters

A

alcohol affects serotonin + endogenous cannabinoids

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24
Q

anxiolytic effects

A

amygdala
decreased activity when threatened = don’t perceive threats

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25
mechanism of reinforcement
acute ethanol inhibits glutamate and stimulates opioid neurons in hypothalamus causes inhibition of GABA interneuron → disinhibition of dopaminergic neuron in nucleus accumbens = phasic firing of dopamine neuron → addiction, reward, motivation
26
metabolism
causes biphasic effects 90% metabolized in liver by alcohol dehydrogenase + acetaldehyde; CYP 2E1 2% excreted by breath, urine, skin 3% metabolized in stomach 5% in brain + epithelium genetic effects on ALDH levels, effects, vulnerability to addiction
27
zero order kinetics
linear elimination curve 0.015 BAC elimination per hour in avg person - same rate
28
driving under the influence
amount of alcohol exhaled is 1/2100 the concentration in blood → breathalyzer tests (concentration in breath x 2100) = BAC 0.05% = provincial limit for suspension 0.08% = federal limit for criminal DUI 0.4-0.5% = lethal
29
the spins
common side effect of excessive drinking BAC ~ 0.04 change in fluid density in semi-circular tubules - alcohol permeates endolymph and cupula; when BAC starts to decline, EtOH diffuses out of cupula first = cupula is more dense than endolymph, cannot stabilize when lying down = sensory fibres are activated → brain interprets activity as motion
30
memory loss
depressed hippocampal activity (black out drunk) septohippocampal pathway is driven by ACh over suppressed activity by high doses = transient anterograde amnesia hippocampal dentate gyrus neurons in medial temporal lobe are susceptible to ethanol damage
31
alcohol-related brain damage
pro-inflammatory signaling that induces cellular damage and death
32
alcohol poisoning
antifreeze (ethylene glycol) → metabolites =glycolic acid and oxalic acid stupor/coma, hyperventilation/arrhythmia/lung edema methanol → metabolites = formaldehyde and formic acid blindness (damage to optic nerve mitochondria); respiratory failure hand sanitizer → isopropanol metabolized to acetone vomiting, coma metabolites are toxic
33
treating methanol poisoning
administration of 1. ethanol out competes methanol for metabolic enzymes = reduces formaldehyde production methanol is excreted unchanged via kidneys 2. fomepizole competitive inhibitor of alcohol dehydrogenase = prevents build up of toxic metabolites
34
lipid theory
early 19th century Meyer-Overton anaesthetics interact with lipid membranes to cause effects → affect Na+ and K+ channels not 100% accurate
35
1980s theory
EtOH inhibits soluble enzyme luciferase
36
EtOH direct effect on DA somas
IV EtOH increases VTA DAergic firing frequency 10-200mM EtOH increases spontaneous VTA firing frequency in vitro EtOH must be applied directly in VTA, not in NAc
37
mechanism of EtOH action
lower [EtOH] = strong potentiation of GABA A receptors (delta subunit → may be extra synaptic) higher [EtOH] = inhibition of ionotropic Glu-NMDA receptors and voltage gated Ca2+ channels = neuronal inhibition, sedative-like effects asphyxiation at lethal doses via depressed activity in autonomic centres
38
input to VTA dopaminergic neurons
GABA interneurons: - NAc - lateral shell, medial shell, and core - ventral pallidum glutamate neurons: - amygdala - medial PFC NE neurons: - locus coeruleus
39
neurotransmitters
glutamate and GABA = most common; balance activation/inhibition → important for EtOH reinforcement Glutamatergic inputs to VTA from PFC, RN GABA-ergic inputs to VTA from NAc, VTA interneurons
40
GABA A receptors
cys-loop ligand gated channel heteropentameric receptors 19 genes = 19 subunits
41
α4δ-containing GABA A receptor
responds to low EtOH; expressed in striatum = part of reward circuit (implicated in addiction) hyperpolarizing currents, threshold mini inhibitory post-synaptic currents EtOH potentiates channels after activation (open longer)
42
NMDA receptors
ionotropic Glu receptor heterotetrameric subunits - 1 NR1 gene, 4 NR2 genes, 2 NR3 genes subunit composition directly affects function 8 NR1 splice variants in humans inhibited by EtOH at high doses → additive effect with GABA potentiation towards overall depressed electrical activity
43
NR1/2C subunit
less sensitive to EtOH than NR1/2A or 2B
44
behavioural tolerance
cerebellum → increased NR1/2C subunits = less sensitive to EtOH masking of inebriation (balance, motor coordination)
45
other input to VTA dopaminergic neurons
receives opioid-ergic input from arcuate nucleus of hypothalamus individuals with low baseline levels of endorphin release more when given alcohol = genetic predisposition to alcohol abuse (addiction is a polygenic disease)
46
control of VTA DAergic firing to NAc
glutamatergic + opioidergic inputs to GABAergic interneurons balance between inputs = baseline GABA activity = tonic firing of VTA → NAc decreased glu inputs + increased opioid inputs = less active GABA interneurons = phasic firing of VTA → NAc GABA inputs are main control
47
acute → chronic effects
tolerance: decreased GABA A receptor expression up-regulation of NMDA receptors and Ca2+ channels = over-active brain, hyperexcitable → emotional volatility
48
cross tolerance
with other drugs that affect GABA receptors (benzos, barbiturates)
49
mechanism of tolerance
- GABA A receptor down-regulation (↓ expression) → subunit compositions and receptor localizations in membrane change - NMDA receptors up-regulated (hyper-excitability) - Ca2+ channel receptors up-regulated = higher excitability
50
metabolic tolerance
up regulation of liver 2E1 enzymes subjects showed elevated CZX metabolism (2E1 substrate) CYP2E1 knockout prevents EtOH induced liver damage; over-active CYP2E1 induces more damage = metabolites are the cause of damage
51
alcohol withdrawal syndrome
hangover physical symptoms: headache, diarrhea, fatigue, restlessness, nausea psychological symptoms: haziness, slower though/cognition, impaired reaction times, poor reasoning symptoms peak as BAC reaches 0 → metabolites reach max concentration = cloud brain functioni
52
congener
minor chemical constituent that gives a distinctive character to wine or liquor (flavour and colour) - responsible for some of its toxic effects e.g. acetone, methanol, acetaldehyde, furfural higher congener content of a drink = increased hangover severity brandy has 37x more than vodka
53
withdrawal
stages 1-4 more severe than most other drugs sympathomimetic effects
54
stage 1 of withdrawal
elevated heart rate/bp diaphoresis tremors no appetite, insomnia
55
stage 2 of withdrawal
hallucinations increased stimulatory response
56
stage 3 of withdrawal
delusions, delirium, amnesia tremors peak 3-4 days after last drink
57
stage 4 of withdrawal
seizure
58
treatment of AWS
prevent stages 3 and 4 reduce over excitation - glutamate antagonists - benzodiazepines or ketamine - clonidine - propranolol - disulfiram - opioid antagonists - SSRI, cannabinoid antagonists
59
glutamate antagonists
e.g. acamprosate reduce hyperexcitability
60
benzos or ketamine
reduce AWS severity
61
clonidine
pre-synaptic α2 adrenergic agonist prevents excessive neurotransmitter release
62
propranolol
β adrenergic antagonist reduces sympathetic effects and tremor
63
disulfiram
enzyme blocker → inhibits acetaldehyde dehydrogenase = buildup of acetaldehyde aversive conditioning prevents alcohol use, does not decrease craving
64
opioid antagonists
naltrexone, nalmefene prevent DA reward by maintaining threshold for DA firing reduce reinforcement by disinhibition
65
neural circuitry - use of imaging + electrophysiology
3D reconstructions to picture synaptic connections, neuronal morphology electrical potentials across particular membranes - track LTP, LTD molecular signaling - how cells are regulating cellular changes that underlie electrical changes
66
long term dependence - neuroadaptations
glutamate, GABA, DA, 5-HT, opioids, CRF changes in reinforcement, enhanced anxiety, increased sensitivity to stress structural neuroadaptations = alterations in the space available for synaptic connections glutamatergic synapses located almost entirely on head of spines (direct opposition of post synaptic membrane)
67
nucleus accumbens
two regions: core and shell core: aversive reinforcement shell: positive reinforcement
68
Spiga et al. 2014
NAc medium spiny neurons spines in healthy control rat: stubby = immature mushroom = mature most pronounced changes observed during withdrawal - less spiny features overall = less activity - long thin spines were most affected
69
adhesion molecules
*********
70
morphological changes in NAc
neurons are continuously altering protein levels and synaptic connections after 1d withdrawal: reductions in dendritic length and branching; increased mature spines in core after 7d withdrawal: shell MSNs length and branching reduced; higher density of immature spines spines are selectively altered (long thin but not mushroom)
71
effects on amygdala
measure of mini inhibitory post synaptic currents = increased GABA release in central and basolateral amygdala
72
gross brain changes
reduced brain volume nutritional deficiency (thiamine [vit B] bc of irritated GI tract) hyperactive Glu systems
73
reduced brain volume
increased stress in brain → ROS/acetaldehyde production = induces neuronal death
74
nutritional deficiency
affects glucose metabolism, protein synthesis, myelin formation = cell death Wernicke's encephalopathy Korsakoff's confabulation → memory loss, disorientation, loss of coordination
75
hyperactive glutamate systems
cause excitotoxicity via excessive Ca2+ influx → cell death
76
increased abuse potential
heart rate biomarker: pharmacological indicator of stimulatory influence due to alcohol reward circuit in the NAc elevates DA levels → brainstem nuclei raise heart rate elevated levels of catecholamines
77
genetic factors affect risk of addiction
low baseline beta-endorphin levels = prone to drinking more alcohol
78
adolescent brains + EtOH
developing brain connections until 25 years = susceptible PFC deficiencies prevent full development of consequential thinking; normally regulates reward-seeking affects long-term hippocampal synaptic plasticity → learning + memory
79
malnutrition
EtOH contains lots of carbs → complex in beer easy to put on weight + metabolic changes in energy usage → brain metabolizes acetate, not glucose
80
CYP2E1 produces ROS
acetaldehyde + ROS ROS react with anti oxidant systems → at elevated levels, overwhelm the systems can react with cellular components → stress cell if it cannot detoxify → membrane + DNA damage, cancer, cell death
81
metabolic switch
metabolism produces high NADH:NAD+ → reduces fatty acid oxidation (decrease use of fat as energy source → stored) cells start to lyse and induce inflammation → hepatitis reversible at early stages
82
fatty liver disease → cirrhosis
TGF-beta cytokine production by infiltrating immune cells triggers transcriptional changes in hepatocytes cells produce collagen → dumped into extracellular space → fibrosis
83
fibrosis
functional liver cells are replaced by fibrous, collagenous matrix (clumps of non-functional tissue) liver irreversibly loses detoxifying capacity
84
cirrhosis
chronic inflammatory state + cell death caused by pro-inflammatory cascade: cell death and reactive species-induced changes to macromolecules facilitate immune infiltration mis-identification of targets: activation of immune cells in the liver → target host antigens
85
progression to cancer
requires massive dysfunction - local inflammatory environment avoids immune recognition and cell death reactive lipids are highly mutagenic
86
retinoic acid receptor
therapeutic target reduces cell proliferation = anti cancer reduced expression in stressed cells
87
increased cancer risk
upper GI tract, colorectal, liver, breat 50% of cancers linked to alcohol consumption upper GI tract susceptible because microflora contribute to EtOH metabolism [acetaldehyde] can reach 10-100x higher than in blood increased production by smoking
88
mechanisms of oncogenesis
4MP: alcohol dehydrogenase inhibitor reduces N2-ethylidene-dG count acetaldehyde + DNA = N2-ethylidene dG → free floating ROS - links to endogenous molecules
89
acetaldehyde
metabolite interferes with DNA synthesis and repair → binds and inactivates DNA repair proteins; causes mutations and chromosomal abnormalities
90
FASD
fetal alcohol spectrum disorder developmental stages in uterus are adversely affected at different times - face + brain development: vulnerable in 3rd week - brain development: vulnerable in 3rd trimester → poor impulse control, planning
91
cannabinoid receptor (29)*************
92
safe level of alcohol consumption
cardioprotective effects vs cardiotoxic effects
93
cardioprotective effects
low doses, 1 drink per 1-2 days beneficial antioxidants in wine → increases HDL = prevention of lipid deposition in arteries, decreased platelet aggreggation = decreased CV disease
94
cardiotoxic effects
cardiomyopathies at high doses EtOH = direct modulator of Ca2+ release → inhibits SR Ca release = negative ionotropic effect acetaldehyde inhibits protein synthesis; damages mitochondria
95

Pmcol 305 (18 decks)

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