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addiction day Flashcards

1
Q

Neurobiology of Addiction

A
  1. Addiction is a chronic, progressive behavioral disorder whose central feature is compulsive drug use despite adverse consequences
  2. Addiction pathophysiology involves the brain reward system and the alterations that reward enhancing drugs effect on this system
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2
Q

Ventral Tegmental Area (VTA)

A

Location of dopamine cell bodies that projects to nucleus accumbens (reward center) and prefrontal cortex (executive control)

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3
Q

Nucleus Accumbens (NA)

A
  1. The “reward center” of the brain.
  2. Integrates VTA (dopamine) and PFC (glutamate) inputs to determine motivational output.
    - Incentive (appetitive)
    - Reward (consummatory)
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4
Q

Prefrontal Cortex (PFC)

A
  1. Exerts executive control over midbrain structures
  2. Judgment
  3. Cost-benefit analysis
  4. Consider Further PFC delineation next
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5
Q

With increasing addiction, frontal lobe structures can become

A

less active (less glutamate) and even atrophy allowing increasing, maladaptive addictive (more DA) behaviors to occur. (risk calculations are in error, emotional valence is put onto the addictive substance and response prevention falters

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6
Q

DLPFC-=

A

statistical analysis, prioritizing, top down control center:(failure to assess the risks of a behavior ie drunk driving)

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7
Q

VMPFC=

A

assigns emotional valience (drinking feels good, less stress, more social)

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8
Q

OFC-

A

impulse prevention ( I can beat up that football player, grope that model, drive my car)

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9
Q

ACC=

A

vigilance(Scanning environment for next beer, vodka, bar…)

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10
Q

Decision Making is

A

Glutamate Driven via PFC structures

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11
Q

Limbic Drive is

A

Dopamine Driven

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12
Q

D3 receptors govern

A

static levels of DA neuronal activity to allow homeostatic wakefulness, alertness, etc

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13
Q

D2 receptors are

A

pulsatile depending on motivation, drive, reward expectations

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14
Q

Effects of Drugs and ‘Addictive Behavior’ on the Brain Reward Pathways

A 
1. All act in brain limbic reward pathways to either:
enhance dopamine (DA) release 
enhance DA effects in the Nucleus Accumbens (Nac) or related structures or produce effects similar to DA
2. Drug-induced states are important motivators/reinforces of initial drug use
3. Chronic use leads to reward circuitry changes that promote more future drug use
- Increased limbic function
- Decreased PFC function
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15
Q

The VTA barn supplies DA to

A

the nucleus accumbens (NAc)

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16
Q

The Amygdala assigns a

A

pleasure, threat, or an emotional value to the linkage between 1 and 2 (perhaps this is the terrain of the ranch or how much the horses are to be fed?)
1-3 are the Limbic Addiction Pathways that are excessive in addictive behaviors

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17
Q

With increasing addiction, frontal lobe structures can become

A

less active (less glutamate) and even atrophy allowing increasing, maladaptive addictive (more DA) behaviors to occur. (risk calculations are in error, emotional valence is put onto the addictive substance and response prevention falters

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18
Q

Summary

A
  1. Must know the neurotransmitters involved in normal reward and addiction (DA/GLU)
  2. Must know functional brain areas
  3. Must know if areas become more or less active with addiction
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19
Q

alcohol binds to

A

GABA-A receptor

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20
Q

Intoxication/Withdrawal Alcohol

A
  1. Anxiolysis
  2. Disinhibition
  3. Slurred Speech
  4. Ataxia
  5. Sedation/Stupor
  6. Respiratory Supression
  7. Coma
  8. Death

Rx with support, restraint, protect airway, ventilate

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21
Q

alcohol withdrawal

A
  1. Agitation, Insomnia
  2. Tremor
  3. GI upset
  4. Inc Pulse, HR, BP
  5. Seizures
  6. Hallucinations
  7. Delirium
  8. Death

Rx with benzodiazepines (cross reactive) until vital signs and withdrawal symptoms normalize

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22
Q

Intoxication/Withdrawal Sedatives (Benzodiazepines, Barbiturates)

A
  1. Anxiolysis
  2. Slurred Speech
  3. Ataxia
  4. Sedation/Stupor
  5. Respiratory Supression
  6. Coma
  7. Death

Rx with support, restraint, protect airway, ventilate
Reverse with flumazenil
For benzodiazepines
Will not work for alcohol or barbiturates

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23
Q

withdrawal symptoms with benzo and barbs

A
  1. Agitation, Insomnia
  2. Tremor
  3. GI cramps
  4. Hypereflexia
  5. Inc HR
  6. Seizures
  7. Hallucinations
  8. Delirium
  9. Death

Rx with benzodiazepine replacement until vital signs and withdrawal symptoms normalize

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24
Q

Stimulants and the D2 ReceptorCocaine, Amphetamine

A
  1. Stimulants block dopamine reuptake, may reverse it

2. The net effect is more DA availability in the mesolimbic system which allows increased CNS arousal and excitability

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25
Q

Intoxication of Stimulants

A
  1. Elevated mood and esteem
  2. irritability
  3. Insomnia
  4. Appetite loss
  5. Dilated pupils
  6. Racing heart
  7. Inc BP, elevated temp
  8. Hyperreflexia
  9. Psychosis
  10. Cardiac arrest
  11. seizure

Rx with support, and use meds to reverse specific intoxication symptoms

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26
Q

withdrawal of stimulants

A
  1. Fatigue
  2. Anhedonia
  3. Depression
  4. Increased sleep
  5. Increased appetite
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27
Q

Opiates and the Opioid System

A
  1. affect mu, delta, kappa receptors

2. many prescription narcotic pain meds are naturally occurring alkaloids (poppy), some are synthetic

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28
Q

Mu (OP3,MOP) reduces

A

pain, increases positive emotion,

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29
Q

Rx opiates are often

A

full agonists and very effective at activating endogenious opioid receptors

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30
Q

Kappa(OP2, KOP)/delta(OP1, DOP) allows

A

mild analgesia

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31
Q

They are g protein linked and cause neuronal hyperpolarization via

A

cAMP reduction and increased K+ influx and decrease Ca++ efflux –> Increases descending midbrain pain inhibitory paths
Next increasing serotonin and enkephalin firing

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32
Q

Many prescription narcotic pain meds are naturally occurring alkaloids (poppy), some are synthetic

A
  1. Morphine, codeine,oxycodone, hydrocodone, tramadol
  2. They tend to activate the Mu, OP3, MOP receptors to control pain and improve the emotional state associated with said pain
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33
Q

Intoxication of Opiates

A
  1. Elevated mood
  2. Pupil constriction
  3. Respiratory suppression
  4. Gag reflex loss
  5. Low HR, BP
  6. Constipation

Rx with support, protect airway and use naloxone to reverse

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34
Q

dopamine lives in

A

ventral tegmental area (VTA) –> location of dopamine cell bodies that project to nucleus accumbens (reward center)

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35
Q

prefrontal cortex does

A
  1. judgement
  2. cost-benefit analysis
  3. exert executive decision
36
Q

dorsal lateral prefrontal cortex

A

does statistical analysis, prioritizing, top down control center (failure to assess the risks of a behavior –> drunk driving)

37
Q

ventral medial prefrontal cortex (VMPFC)

A

assigns emotional valience (drinking feels good, less stress, more social)

38
Q

orbital frontal cortex (OFC)

A

impulse prevention (drinking and driving is bad) –> but for addictive pts have cold OFC

39
Q

ant. cingulate (ACC)

A

vigilance (in ADHD you get light up all over not just ACC)

40
Q

Hallucinogens

A

Phencyclidine (PCP), lysergic acid (LSD), mescaline, peyote, psilocybin

Treatment is supportive

41
Q

intoxication of hallucinogens

A

Intoxication=

  1. Perceptual distortion
  2. Hallucinations
  3. Depersonalization
  4. Nystagmus
  5. Tremors
  6. Hyperreflexia
  7. Racing heart
  8. Flashbacks
  9. Paranoia
42
Q

Cannabis

A

Intoxication=

  1. Elevated mood
  2. Expansive thought
  3. Sedation
  4. Pupil constriction
  5. Red conjunctiva
  6. Increased appetite
  7. Panic
  8. Paranoia
43
Q

Stages

A
  1. Precontemplation
  2. Contemplation
  3. Preparation
  4. Action
  5. Maintenance
44
Q

Precontemplation to Contemplation

A
  1. Consciousness raising
  2. Emotional arousal/Dramatic release
  3. Social liberation/Environmental reevaluation
45
Q

Contemplation to Preparation

A

Self-reevaluation

46
Q

Preparation to Action

A

Self-liberation/Commitment

47
Q

Action to Maintenance

A
  1. Countering/Counterconditioning
  2. Environmental control
  3. Rewards
  4. Helping relationships
48
Q

chloride ion goes into

A

GABA-A receptor

49
Q

intoxication is always the opposite of

A

withdrawal

50
Q

gaba must be bound to GABA receptor

A

in order for benzo to work

51
Q

alcohol withdrwal

A
  1. delirium tremor (can’t remember about any exp)
  2. hallucinations (doc, I saw the strangest thing!)
    - -> usually visual hallucination
52
Q

lorazepam is the DOC for alcohol withdrwal ??? (check with the lecture audio)

A

b/c no worries about liver failure

53
Q

what are the two addictive stimulants and the D2 receptor?

A

cocaine, amphetamine

54
Q

stimulants block dopamine

A

reuptake, may reserve it

55
Q

the result of stimulants such as cocaine and amphetamine are

A

the net effect of more DA availability in the mesolimbic system (positive symptoms for shcizo) which allows increased CNS arousal and excitability

56
Q

intoxication of cocaine lead to

A

by blocking the reuptake of neurotransmitter leading to

  1. elevated mood and esteem
  2. irritability
  3. insomnia
  4. appetite loss
  5. dilated pupils
  6. cardiac arrest –> can lead to death
  7. seizure
  8. causes vasospasm
57
Q

withdrawal of stimulants (cocaine and amphetamine)?

A
  1. anhedonia
  2. depression
  3. increased sleep
  4. increased appetite
  5. fatigue
58
Q

trazodone and clonidine

A

prevent the sleeping withdrawal effect

59
Q

what opiate receptor is responsible for reducing pain, and feeling good (positive emotion)?

A

Mu

60
Q

what are some intoxication symptoms of opiates?

A
  1. elevated mood
  2. pupil constriction
  3. resp. suppression
  4. loss of gag reflex
  5. constipation
61
Q

what are the withdrawal symptoms of opiates?

A
  1. restless
  2. watery eyes
  3. yawning
  4. dilated pupils
  5. muscle cramps
  6. agitation –> probably the most important withdrawal symptom
  7. goose flesh, lacrimating
62
Q

what are some of the drugs that are hallucinogens?

A
  1. phencyclidine (PCP)

2. lysergic acid (LSD)

63
Q

what are some of the intoxication symptoms of hallucinogens such as PCP and LSD?

A
  1. perceptual distortion
  2. hallucinations
  3. depersonalization
  4. nystagmus
  5. tremors
64
Q

the only drug that causes vertical nystagmus

A

PCP

65
Q

intoxication of cannabis

A
  1. elevated mood
  2. red conjunctiva
  3. pupil constriction
66
Q

what is harm reduction?

A

to make the drug intake safer and healthier

67
Q

stages?

A

precontemplation –> contemplation –> preparation –> action –> maintenance

68
Q

what is the characteristic of contemplation to preparation?

A

self-reevalution

69
Q

prep to action?

A

self-liberation/commitment

70
Q

what are action to maintenance

A
  1. countering/counterconditioning
  2. environmental control
  3. rewards
  4. helping relationships
71
Q

what is precontemplation?

A

unaware of the problem

72
Q

what is contemplation?

A

aware of the problem but ambivalent about action

73
Q

what is preparation?

A

first decision to change –> small steps taken

74
Q

what is action?

A

change begins –> trial and error

75
Q

what is maintenance?

A

new behaviors practiced –> focus on relpase prevention

76
Q

Harm reduction

A

Replace harmful inhaled tobacco smoke with nicotine (full agonist is replaced with full agonist)
Prevents withdrawal
Easier withdrawal
Avg cigarette has 1.1 mg nicotine, cigar 20 mg…
Side effects similar to smoking too many cigarettes at once (activating)
? E-cigarette use
Used like a patch to detox
Used like methadone maintenance to avoid withdrawal
Data hinting that this may not be helpful…

77
Q

Antidepressant Bupropion SR Mechanism for Smoking Cessation

A

Blocks neuronal reuptake/recycling of NE and DA

Generally this improves alertness, attention, concentration, motivation…

78
Q

The twice daily Slow Release (SR) product is also approved for

A

smoking cessation

79
Q

By blocking Dopamine (DA) and Norepinephrine (NE) transporters, these transmitters build up in synapses and activate neurons in the area.

A

This may desensitize DA reward circuitry so cigarette based activation is not missed by the patient
This may provide alertness, energy, better cognition and mood so that cigarette effects are not missed

80
Q

A partial nicotine receptor agonist

A

Replace a full agonist (nicotine) with a partial agonist

81
Q

Varenicline

A
  • Instead of full nicotine agonism and reward pathway firing,
  • Varenicline does this partially allowing this system to be active, avoid most withdrawal
  • And provide some of the benefits of nicotine use without the harm
82
Q

Chronic use leads to reward circuitry changes that promote more future drug use

A
  1. Increased limbic function

2. Decreased PFC function

83
Q

The Amygdala assigns

A

a pleasure, threat, or an emotional value to the linkage between 1 and 2 (perhaps this is the terrain of the ranch or how much the horses are to be fed?)

84
Q

The VTA barn supplies DA to

A

the nucleus accumbens (NAc)

85
Q

With increasing addiction, frontal lobe structures can become

A

less active (less glutamate) and even atrophy allowing increasing, maladaptive addictive (more DA) behaviors to occur. (risk calculations are in error, emotional valence is put onto the addictive substance and response prevention falters

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