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Psychopharmacology > Alcohol > Flashcards

Alcohol Flashcards

1
Q

What does ethanol look like at low doses?

A

A stimulant

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2
Q

Why does ethanol look like a stimulant at low doses?

A

GABAergic neurons are really sensitive to it

ethanol inhibits GABAergic neurons

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3
Q

What happens when you have a large dose of ethanol?

A

Ethanol inhibits most neurotransmitters in prefrontal cortex

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4
Q

What happens when you have a massive dose of ethanol?

A

Changes membrane fluidity for neurons

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5
Q

What is a sedative-hypnotic?

What is important about them?

A

Drugs that diminish awareness

most dangerous group of drugs

Drugs can kill you
withdrawal can kill you
Only group you can die from if you go cold-turkey

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6
Q

What drugs are in the sedative-hypnotic category?

A

ethanol

barbituates

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7
Q

You take two CNS depressants. What is the pharmacodynamic effect?

A

They can be additive with each other

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8
Q

Can CNS depressants be antagonized by stimulants?

A

Not directly. You just become a wide-awake drunk

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9
Q

Neural and behavioral disinhibition happens as the result of taking a CNS depressant. Why?

A

The drug is working at GABA synapses, antagonizing them. That means that inhibitory neurons are themselves inhibited, creating an excitatory effect

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10
Q

What is the most common drug used in the world?

A

Caffeine

Ethanol is second

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11
Q

Where in the body will alcohol generally be?

A

Aqueous compartments

Very small, so can get through BBB

Water-soluble, so doesn’t clump up in blood

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12
Q

Where is ethanol absorbed?

A

Small intestine. Significant 1st pass metabolism

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13
Q

What does carbonation do to ethanol?

A

Accelerates metabolism

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14
Q

Why do females metabolize alcohol more quickly?

A

More female body is fat

Fat has less water in it than muscle, and therefore tissue with more fat has more water in blood

So, ethanol is more concentrated in blood (water-soluble)

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15
Q

What are pylorospasms?

A

Spasm of the sphincter

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16
Q

Why does the stomach empty more slowly if ethanol is higher than 30%?

A

Because of pylorospasms

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17
Q

What are the two metabolites of alcohol?

A

Alcohol >(alcohol dehydrogenase) > acetaldehyde > (acetaldehyde dehydrogenases) > acetic acid > (oxidation) > CO2, H2O, energy

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18
Q

What two things almost always happen when drug tolerance occurs?

A

Alteration of liver enzymes

Alteration of nervous system (acute/functional tolerance)

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19
Q

What are hepatic enzymes?

A

liver enzymes

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20
Q

What does coffee drinking do to ethanol metabolism?

A

There’s cross-tolerance

Ethanol causes caffeine tolerance

Due to changes in hepatic enzymes

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21
Q

What is the righting reflex?

A

Makes the body go upright

Impaired with ethanol consumption

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22
Q

You lie down in bed and the room is spinning. Why?

A

bedspins

Differences in distribution of ethanol across vestibular apparatus

Makes neurons in inner ear more excitatory where ethanol is not active

This causes weird activation patterns resulting in bedspins

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23
Q

How do you get rid of bedspins?

A

Put your foot on the ground

Gives somatosensory feedback that overrides vestibular feedback

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24
Q

Where does neural activation pathway from vestibular apparatus go?

A

To cerebellum, then to motor/parietal cortex

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25
Q

What does alcohol do to NMDA receptors?

A

Fucks with them to prevent GLU binding

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26
Q

What are the two reasons alcohol effects learning and memory?

A
  1. NMDA receptor not taking in GLU as easy

2. Glutamate RELEASE inhibited in the HC

27
Q

Why do cells die with regards to alcohol / glutamate?

A

Elevated glutamate activity during withdrawal

This causes excessive Ca2+ influx

Influx leads to cell death

28
Q

What are the subunits of GABA receptors?

A

a, B, Y/theta subunits

29
Q

How many classes of GABA receptors are there? What are they called?

A

2: GABA-A and GABA-B

30
Q

‘endogenous’

A

naturally occurring (inside the body)

31
Q

‘exogenous’

A

Comes from outside the body

32
Q

How many GABA molecules do you need to open the GABA-A receptor?

A

Two

33
Q

Where on the GABA-A receptor does ethanol effect?

A

Trick question: facilitates transmission at all three!

a1, B2, or delta

34
Q

Which GABA subunit does GABA bind to?

A

B subunit

35
Q

Which GABA subunit do barbituates bind to?

A

B subunit

36
Q

What subunit does benzodiazepine attach to?

A

Y/Delta

37
Q

What ion comes in when GABA-A receptors open?

A

Cl-, it’s ionotropic

38
Q

What happens to GABA receptors over time when you have a bunch of ethanol?

A

less GABA-A receptors to compensate

39
Q

What happens when you have less GABA-A receptors?

A

increased excitability in the nervous system (less inhibition)

40
Q

What does EtOH do for glutamate?

A

antagonization

41
Q

What receptors does ethanol’s glutamate antagonization affect?

A

both NMDA and AMPA

42
Q

Why (molecularly) will unsupervised ethanol withdrawal cause seizures?

A

There’s a shitload of NMDA and AMPA receptors everywhere, which causes the seizures

43
Q

What takes over as the principal neurotransmitter in the spinal cord?

A

Glycine

44
Q

Chronic

A

Always there. Exposed to drug constantly. Different from ‘repeated’

45
Q

Acute

A

Brief spike in drug concentration, with large periods of lack of drug. Once

46
Q

Kainate

A

Think of it as the same as AMPA

47
Q

Where in the brain do low concentrations of ethanol cause dopaminergic neurons to increase firing rate?

A

The VTA

48
Q

Why do dopaminergic VTA neurons increase firing rate with low EtOH doses?

A

Inhibition of GABAergic neurons there increases activity of DAergic neurons

49
Q

What is the rough rule of thumb for D1 and D2 DA receptors?

A 
D1 = increase in excitability
D2 = decrease in excitability
50
Q

Why is an alcoholic’s stomach hard when you pat it?

A

Liver accumulation of fat

51
Q

Perseveration

A

Continually engaging in the same sequence of behavior, even if it’s maladaptive

52
Q

When would you see the accumulation of fat in the liver due to ethanol? What type of drinking?

A

Chronic drinkers. Constant exposure to ethanol with no letting-up

53
Q

What is the name of the syndrome involving loss of memory/confabulation due to chronic ethanol exposure?

A

Wernicke-Korsakoff’s syndrome

54
Q

What is the word for bullshit / huge intervals of time where memories are made up?

A

Confabulation

55
Q

What area of the brain is damaged with wernicke-korsakoff’s syndrome?

A

Dorso-medial thalamus

56
Q

What is the dorso-medial thalamus part of the circuitry doing?

A

Part of memory circuit
HC talks to mammilary bodies
mammilary bodies talk to dorsomedial thalamus
dorsomedial thalamus to cortex

57
Q

Deficiency in what in the dorsomedial thalamus in wernicke-korsakoff’s?

A

Thiamine deficiency

58
Q

What is the #1 cause of retardation in the US?

A

Fetal alcohol syndrome..

No safe EtOH when pregnant

59
Q

What does fetal alcohol syndrome do cellularly?

A

GABA and GLU systems involved in apoptosis

Apoptosis enhanced by EtOH exposure

60
Q

Why is apoptosis caused with ethanol?

A

more ethanol = more Ca2+ in the cell due to more NMDA

High concentrations of Ca2+ causes apoptosis

61
Q

What does disulfuram do?

A

Blocks breakdown of acetaldehyde

Leads to flushing reaction / hangover

62
Q

Where does EtOH enter the fluid of to cause bedspins?

A

endolymph, changes its density

63
Q

Where does EtOH not enter the fluid of to cause bedspins?

A

perilymph (gel-like)

difference in density causes the bedspins

64
Q

What happens to AMPA and NMDA receptors with repeated use?

A

upregulation of both receptor types

Psychopharmacology (12 decks)

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