Addiction Flashcards

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1
Q

Children of alcoholics are _ times more likely to become alcoholics

A

4
ex. alcoholic biological parent > risk

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2
Q

Provide the twin probandwise concordance rate equation and the variables involved

A

2C/(2C+X)

C = Concordant pairs (match, twin is also alcoholic
X = Discordant pairs (mismatch, twin is not an alcoholic

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3
Q

Which type of twins have a higher probandwise concordance of alcoholism according to Heath et al., 1997?

A

Monozygotic twins, = evidence of genetic influence

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4
Q

What are the differences in addiction rates between men and women?

A

Historically, men had increased addiction rates but now this is changing because females have faster transition from experimentation to addiction

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5
Q

Does level of response to alcohol predict subsequent abuse? (Schuckit, 1994)

A
  • low reponders to alcohol are more likely to become alcoholics than high responders
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6
Q

In the study conducted by Heath et al, what were the 2 primary results?

A
  • In males, MZ twins had higher concordance rate (more likely that both twins get alcoholism)
  • In females, the rates of alcoholism are lower but same pattern is noticed in concordance rate
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7
Q

What does your response level to alcohol reflect metabolically?

A

Your ability and speed of metabolizing alcohol

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8
Q

How is alcohol metabolized?

A

1.) Converted into acetaldehyde via alcohol dehydrogenate (ADH)
2.) Acetylaldehyde is converted into acetic acid via ALDH (Acetyladehyde Dehydrogenase) where it can be excreted from the body

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9
Q

What happens if ALDH is not working?

A

Acetaldehyde cannot be broken down/slower breakdown (bad! 10-13x more toxic than alcohol)
*this is responsible for alcohol intolerance and drunkness
- genetic link! People who lack this enzyme are less likely to become alcoholics cause it feels terrible to drink it

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10
Q

What gene associated with the ALDH enzyme can determine one’s response level to alcohol?

A

ALDH2 gene, locatred on chromosome 12
- there are 2 different types of the gene: the functional one (ALDH1) and dysfunctional (ALDH2) caused by a 1 point mutation in a base pair
- inherit 1 from each parent (homozygous for ALDH2 = least tolerant to alcohol)

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11
Q

What happens if ADH is not working correctly?

A

alcohol cannot be broken down and the concentration of blood alcohol changes

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12
Q

What are the 4 “C”s of alcoholism?

A

CRAVINGS
loss of CONTROL
COMPULSION to use
use despite CONSEQUENCES

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13
Q

How do drugs affect the dopaminergic system?

A

stimulate the reward system of the brain to release dopamine
- brain’s most powerful reward incentive, usually suppost to reward behaviours that are beneficial to survive

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14
Q

Describe the dopamine reward pathway

A
  • dopaminergic cells originate in the VTA (ventral tegmental area), axons cluster into medial forebrain bundle and synapse onto the nucleus accumbens = dopamine release
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15
Q

rank these in order of most dopamine above baseline to least:
food,nicotine, cocaine, exercise, meth, sex

A

meth (1100%)>cocaine (350%)>nicotine (225%)>sex (160)>food (130%)>exercise (115%)

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16
Q

What happens to dopamine responses with addiction?

A
  • eventually, a ton of dopamine doesn’t elicit a pleasurable feeling
  • all increase dopamine in the synapse, drugs like cocaine block transporters
  • dopamine receptors decrease with chronic drug abuse as a homeostatic response (receptors will grow back when you stop but it will take much longer, exercise might speed this up)
17
Q

What happens to PFC and FC activity in addicts?

A
  • less activity in cocaine addicts
    =poor decision making, lack of self regulation and use despite consequences, dramatisized the need for drugs
18
Q

How does PFC development affect addiction risk?

A

PFC is not fully developed until mid-twenties
- more vulnerable to develop addiction if prefrontal cortex not formed yet

19
Q

def drug cue

A

cues that are associated with drug that create anticipation

20
Q

How do context-associated cues cause cravings? (mind)

A
  • glutamate (excitatory neurotransmitter) increases every time drug is used in the presence of a cue, anytime a cue is encountered, drug is expected “glues-together neurons
    *makes withdrawal very hard
  • addicts have increased activity in the ACC (anterior cingulate cortex), primes the brain to get ready to expect the drug
  • if drug doesn’t come, you get withdrawal
  • alcohol cues can speed up brain activity in order to compensate for it’s effects, can get anxiety hallucinations and even death (can’t quit drinking cold-turkey)
21
Q

Re-exposure to drug-associated cues elicits_

A

physiological withdrawal syndrome

22
Q

What is one of the most common reasons for overdose?

A

Change in environment with the same dose, body can’t anticipate drug because there are no familiar cues = does is more lethal

23
Q

What is the active ingredient in marijuana?

A

THC

24
Q

What happens when THC is injected into the nucleus accumbens?

A

extracellular dopamine is increased (almost as high as cocaine, ~300% over baseline

25
Q

How does THC activate the rewards system?

A
  • GABA (inhibitory neurotransmitter) usually blocks dopamine release from dopamine cell, housed in inhibitory neuron
  • we have natural endocanabinoids, one of which is anandemide
  • anandemide binds to cannabinoid receptor and allows dopamine release (blocks release for GABA)
  • THC mimics anandamide, binding to canabinoid receptors, blocking gaba and releasing dopamine in the same way but at supernatural levels b/c much more thc than anandemide usually available
26
Q

What is the similarity between rewards processing for exercise vs canabis?

A

when we exercise, we get more endocanabinoids, increases dopamine

27
Q

What are the consequences of chronic canabis use on the brain?

A
  • can lead to marijuana use disorder (30% of all users)
  • blunts the release of dopamine to naturally rewarding stimuli, causing drug dependency
  • also associated with schizophrenia and psychosis
28
Q

How does psilocybin work?

A
  • naturally-occurring hallucinogenic
  • had very similar structure to serotonin, can bind to it’s receptors
  • when consumed, psilocybin is metabolized into psilocin which looks even more like serotonin
  • can help you feel calm and enhance mood, more direct than SSRIs but tend to have the same effect
29
Q

How does receptor occupancy translate to dosage of psilocin?

A
  • the higher amount of serotonin receptors bound to psilocyn increases with dose until 75% when it maxes out
30
Q

Is psilocybin addictive or toxic?

A
  • not very addictive, similar to food
  • not very toxic
31
Q

How does psilocybin affect drug resistant non-responders?

A

reduced depressive symptoms, ppl had side effects 77% but more minor

32
Q

How does psilocybin affect alcohol addiction (overall amount of drinking days)

A

reduced the # of heavy drinking days