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psychology of addiction > Psychology of Addiction Midterm 2 > Flashcards

Psychology of Addiction Midterm 2 Flashcards

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1
Q

2 types of stimulant sympathomimetics

A

direct and indirect sympathomimetics

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2
Q

what are direct sympathomimetics

A

Drugs that increase activity of the sympathetic nervous system (SNS) through direct action on adrenergic receptors
- many direct sympathomimetics have medical uses but few have abuse potential

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3
Q

example of direct sympathomimetics

A

Salbutamol: an adrenergic beta 2 receptor agonist used to treat asthma

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4
Q

What are direct sympathomimetics

A

drugs that mimic direct sympathomimetics by increasing availability of monoamines (DA, NE, and 5-HT) in the synapse, which can occur through
1. increased NT release
2. Blocking NT reuptake
3. blocking NT metabolism

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5
Q

Example of indirect sympathomimetics

A

occur through 5 different DA receptors, 2 families of NE receptors, and 7 families of 5-HT receptors
examples include cocaine and amphetamine

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6
Q

How does cocaine lead to an increase of DA release

A

Cocaine will block reuptake by occupying DA transporters

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7
Q

How does amphetamine lead to increase in DA release?

A

Amphetamine increases DA release, creates more vesicles containing DA for release

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8
Q

What are non-sympathomimetic stimulants

A

drugs with stimulant properties that operate through other mechanisms

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9
Q

Examples of non-sympathomimetic stimulants

A

Caffeine - blocks adenosine receptors (by binding to them); adenosine normally inhibits DA and glutamate activity
Nicotine - binds to acetylcholine receptors, and mimics actions of acetylcholine; it raises DA, glutamate, and gamma-aminobutyric acid (GABA) levels

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10
Q

What system do CNS stimulants induce arousal in

A

Sympathetic nervous system

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11
Q

what mediates release of DA in the mesolimbic system

A

Psychostimulant (reward) mediates DA release regardless of specific mechanisms

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12
Q

what mediates locomotor effects

A

mediated by nigrostriatal pathway

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13
Q

what plant is cocaine derived from

A

Erythroxylon coca, plant from South America (argentina, bolivia, colombia, ecuador, peru)

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14
Q

earliest mention of using cocaine leaves for anti-fatigue properties

A

early as 3000 BC and maybe even 8000 BC

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15
Q

how did spanish colonists use cocaine leaves

A

given to slaves to enhance/sustain performance in silver mines

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16
Q

What famous drink used cocaine and during what time period was this used

A

Coca-cola; from 1891-1903

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17
Q

What act restricted cocaine for medical use only in 1914

A

Harrison Anti-Narcotic Act
- outlawed possession, use, and distribution for anything outside medical use in the US

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18
Q

Order of likelihood of addiction given any use within a year (greatest likelihood of addiction first)

A

Heroin, Cocaine, analgesics, marijuana, stimulants, and alcohol

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19
Q

How does intranasal cocaine use affect the human body over time?

A

destroys mucus membranes and perforate the palate

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20
Q

What is freebasing and when was it popular

A

Freebasing was popular from late 70s to mid 80s and is a purified form of cocaine w/ higher melting point than powdered cocaine and can be smoked creating a quicker, more intense high

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21
Q

How is freebase created

A

mix powdered cocaine w/ ammonia and product extracted using ether creates the freebase pure cocaine crystals

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22
Q

Problem with freebase

A

highly flammable

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23
Q

What was the smokable form of cocaine in the mid 1980s

A

Crack cocaine is powdered cocaine mixed with baking soda and water to create rocks that can be smoked and are safer than freebase

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24
Q

what are the acute health effects of cocaine

A
  • changes in heart rate (increase)
  • increase systolic blood pressure
  • increases in total peripheral resistance (TTR)
  • risk of heart attack
  • risk of stroke
  • permanent cardiac conduction abnormalities (ex: right bundle branch block)
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25
Q

What are the long term health effects of cocaine

A
  • kidney damage
  • enlargement of the heart
  • artery blockage
  • cardiac conduction abnormalities
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26
Q

T or F: are there naturally occurring amphetamines?

A

False

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27
Q

What drug was first synthesized in Germany in 1887 by Romanian chemist Lazar Edeleanu?

A

Dextroamphetamine (d-amphetamine)

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28
Q

why was d-amphetamines stopped being sold as over counter drugs during the 1960s

A

their abuse potential and psychosis inducing properties were recognized

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29
Q

What is d-amphetamine used to treat today

A

popular drug to treat ADHD but it has clear abuse potential

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30
Q

What properties do all stimulants have and can lead to symptoms similar to schizophrenia

A

all stimulants have psychosis inducing properties and if abused can lead to same symptoms presented by someone with schizophrenia

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31
Q

what group has the most prescriptions for brand/general adderall

A

22-44 have the highest number and continue to increase

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32
Q

What new drug was approved in 2008 and is a DA, NE, and 5-HT agonist

A

vyvanse

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33
Q

does Vyvanse or Adderall xr generate more revenue

A

Vyvanse with 2014 million while adderall has 364 million

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34
Q

4 reasons stimulants can become addictive

A
  1. tolerance and withdrawal
  2. preoccupation with obtaining, using, and running out
  3. abuse by college students w/ and w/o ADHD is common
  4. large underground market (opiates, subaxone)
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35
Q

What is the methylated derivative of amphetamine

A

methamphetamine

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36
Q

what is methamphetamine synthesized from

A

ephedrine discovered in 1919 by akira ogata

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37
Q

why is methamphetamine more potent than amphetamine

A

Because methamphetamine can cross the BBB more readily

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38
Q

what country dealt with a widespread use of methamphetamine after World War 2

A

Japan with 550000 abusers in 1954

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39
Q

what was methamphetamine renamed

A

crystal meth in the 80s after a more pure form was created in San Diego

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40
Q

what are the health effects of methamphetamine

A

similar to cocaine but 2 main exceptions
1. chronic use leads to meth mouth
2. chronic use also leads to formication

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41
Q

what is meth mouth

A

lack of saliva that leads to tooth decay and gum disease

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42
Q

what is formication

A

crawling sensation under the skin that leads to obsessive skin picking of the face and body

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43
Q

how is cocaine used in medicine currently

A

used as a local anesthetic in very restricted applications (mucous membranes)
- procaine is used in most situations

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44
Q

how are amphetamines currently used

A

weight control and ADHD

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45
Q

what are the behavioral effects of cocaine and methamphetamines

A
  • repetitive thoughts/behaviors
  • obsessions and compulsions
  • checking behaviors
  • dismantling intricate items (cars, electronics)
  • paranoia
  • skin picking
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46
Q

how do behavioral effects differ between cocaine and methamphetamines

A

behaviors last longer for methamphetamines because it has longer half life

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47
Q

what is the half life for cocaine

A

6 hours

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48
Q

what is the half life for methamphetamines

A

12-16 hours

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49
Q

what is the binge cycle for cocaine and methamphetamines

A

tolerance and craving build rapidly creating an addictive cycle
- euphoria and dysphoria interchange
- leads to paranoia
- ends with psychosis (delusions, hallucinations)

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50
Q

phases of withdrawal for cocaine and methamphetamines

A

protracted phases during which episodic craving and cue-induced craving increase over course of 3 to 4 months making relapse likely

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51
Q

specific phases of cocaine withdrawal and how long each phase lasts

A

Crash ( 9hrs to 4 days)
- insomnia
- irritability
- anxiety
Withdrawal (1 to 10 wks)
- anhedonia
- decreased energy
- limited interest in environment
Extinction (indefinite)
- brief episodic craving
- cue induced craving
Relapse
- occurs during withdrawal or extinction phases
End result is abstinence if they dont relapse

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52
Q

how many time stronger is the release of DA in stimulants than any natural reinforcer

A

10 times

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53
Q

how do stimulants alter neural structure directly

A

they increase dendritic spine branching in both mesolimbic and mesocortical DA systems

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54
Q

What are opiates

A

drugs derived directly from the opium poppy

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55
Q

what are opioids

A

semi and fully-synthetic form of opiates that are manufactured chemically

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56
Q

how are opiates formed

A

resin gum from cuts in unripe poppy pods are scraped and dried to make opium

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57
Q

how long have opium poppies been cultivated

A

since at least 3400 BC in Southwest asia

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58
Q

what law outlawed production, use, possession, and distribution of opium except for medical use

A

Harrison Narcotics Tax Act in 1914

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59
Q

where does 90% of the world’s opium supply come from

A

Afghanistan

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60
Q

how was morphine first discovered?

A

in earyl 1800s, morphine was isolated from dried opium poppy resin by Friedrich Serturner

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61
Q

what is morphine named after

A

named after the greek god of dreams, Morpheus

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62
Q

steps to produce heroin #1

A
  1. opium boiled in water to create brown liquid
  2. impurities are scraped from top, lime is added, produce morphine alkaloid
  3. solution is filtered to remove impurities
  4. ammonia is added and solution is reheated
  5. morphine collects as a solid at the bottom
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63
Q

what percent of heroin #1 is raw opium

A

10%

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64
Q

name for converting morphine to heroin base

A

heroin #2

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65
Q

steps to produce heroin #2

A
  1. morphine base is mixed with acetic acid and heated to 85 C for 2 hours
  2. morphine dissolves
  3. upon cooling, morphine and acetic acid bond chemically to form heroin
  4. heroin is dissolved in water and sodium bicarbonate is added, producing heroin base
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66
Q

What percent of heroin #2 raw opium and how is it injested

A
  1. 15-20% raw opium
  2. snorted (not smoked)
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67
Q

Steps to make heroin #3

A
  1. heroin #2 is mixed with hydrochloric acid and stirred until it dries
  2. dried paste is crushed to form “brown sugar”
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68
Q

percent of heroin #3 that is raw opium

A

20-30% pure and is smoked

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69
Q

Steps to produce heroin #4

A
  1. hydrochloric acid and ether are added to heroin base (heroin #2)
  2. product is filtered and dried to form white powder
  3. powder is compressed into bricks with a heroin press
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70
Q

percent of heroin #4 that is raw opium

A

80-90% pure and is injectable

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71
Q

what are opiates used for in medicine but what are the dangers of it

A

are effective pain relievers, but have addictive properties

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72
Q

Strength of different analgesics

A

weakest: paracetamol, aspirin, ibuprofen
Strongest: c-8813, BDPC, sufentanil

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73
Q

relative strength of morphine

A

oral morphine has strength of 1 for a 10mg tab
IV morphine has a strength of 3 for a 3.33mg injection

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74
Q

What are endogenous opioids

A

neuropeptides produced by the body that have morphine like actions

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75
Q

What are 3 examples of endogenous opioids

A

Enkephalins, dynorphins, and endorphins

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76
Q

when are enkephalins produced

A

released during or after exercise

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77
Q

What endogenous opioids are produced when injured or stressed

A

Dynorphins and endorphins

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78
Q

What are the 4 sources of opioids

A

opiates, opioids (semi synthetic derivatives), synthetic opioids, and endogenous opioid peptides

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79
Q

what are the 4 examples of opiates?

A

opium, morphine, codeine, and thebaine

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80
Q

what are the 5 examples of semi synthetic opioids

A

heroin, hydromorphone, hydrocodone, oxycodone and etorphine

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81
Q

what are the 4 examples of synthetic opioids

A

methadone, meperidine, propoxyphene, fentanyl

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82
Q

what is the dilemma with exogenous opioids

A

nothing relieves pain as well as exogenous opioids, but nothing is more addictive as well

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83
Q

what group of individuals become addicted to pain prescriptions

A

genetically vulnerable

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84
Q

by how much has prescription opioid death increased by and why?

A

increased by 6x from 1999-2014 and synthetic narcotics are increasingly involved

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85
Q

What was the national drug prescription overdose deaths in 1999? 2017?

A

3,442 in 1999 and continued to increase until reaching 17,029 in 2017

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86
Q

What types of prescription of overdose deaths have increased/decreased from 1999 to 2017?

A

Prescription opioids w/ other synthetic narcotics has increased especially after 2013, but just prescription opioids (w/o other syn narcotics) has decreased since 2013

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87
Q

what drugs do people with prescription addiction do people turn to and why?

A

People turn to heroin because it is cheaper and more available

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88
Q

by how much have heroin related deaths increased since 1999 and why

A

eight fold because syn narcotics like fentanyl are increasingly involved

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89
Q

What is the national heroin overdose death in 1999 and in 2017?

A

1999: 1960
2017: 15482

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90
Q

what age group had the most deaths in 2014 due to heroin

A

25-34 yo with 8 deaths per 100000 people

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91
Q

what age group had the most deaths in 2014 due to opioids?

A

45-54 yo with 11.7 per 100000 people

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92
Q

what are the physiologic effects of heroin?

A
  • decrease in body temp
  • decrease in stress hormones (lowers pituitary function, part of the L-HPA axis)
  • decrease respiration
  • decrease cough reflex
  • induces nausea
  • causes orthostatic hypotension
  • decreases gastrointestinal efficiency
  • causes itching
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93
Q

what are behavioral effects of heroin

A
  • pain relief
  • intoxication (including profound euphoria)
  • impaired cognitive function
  • blocked memory function
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94
Q

what are the medical uses for heroin?

A

anti-diarrhea properties
- used to save lives during dysentery epidemics during 19th century pain relief
balanced anesthesia
- used different opioids before and during surgery to induce analgesia (pain relief), amnesia, muscle relaxation, and abolition of reflexes (fentanyl, alfentanil, remifentanil)

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95
Q

what is the peak time of smoked heroin

A

peak in 1-5 min and declines rapidly to minimum limits within 30 minutes

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96
Q

why is heroin a prodrug

A

it has no pharmacological activity, but its metabolites do heroin metabolizes into 6-monoacetylmorphine and morphine

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97
Q

what does koob say is the classic drug of addiction

A

opioids

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98
Q

what does opioid drug taking induce?

A

intense intoxication/euphoria

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99
Q

what does intense intoxication/euphoria promote?

A

repeated use via positive reinforcement mechanisms

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100
Q

what increases with repeated drug use

A

tolerance quickly develops so intake escalates

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101
Q

what symptoms of withdrawal develop with increased tolerance to drugs

A

profound dysphoria, discomfort, and somatic symptoms of withdrawal

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102
Q

what symptoms follow after withdrawal symptoms emerge?

A

preoccupation and craving

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103
Q

how is drug taking maintained

A

through strong negative reinforcement mechanisms

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104
Q

what are people who are not likely to be addicted called

A

chippers, don’t get addicted because they are able to maintain quasi-controlled use patterns

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105
Q

what does early outcome data suggest about addiction as a condition and likelihood of death?

A

heroin is a lifelong addiction and half of addicts die

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106
Q

what were the results for the 581 male heroin addicts admitted to the California Civil Addict Program at a 33 yr follow up?

A
  • half dead
    of those alive:
  • 21% tested positive for heroin (10% refused urinalysis)
  • 40.5% used heroin in the past year
  • 19.4% used cocaine (10.3% used cocaine) in the past year
  • 11.6% used amphetamine (meth)
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107
Q

what was the predominant treatment for heroin addicts in the California Civil Addict Program experiment?

A

methadone maintenance was the predominant treatment

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108
Q

what replaced methadone maintenance as the main heroin addict treatment

A

suboxone

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109
Q

why was methadone maintenance replaced as a treatment

A

methadone itself is addictive as an opioid

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110
Q

what organization does not use maintenance therapy to treat heroin addiction

A

Narcotics Anonymous which helped addicts with self health groups

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111
Q

Employment status for people who are/were heroin addicts

A

59% full time
9% retired
12% unemployed
6% students
11% part time
4% homemaker

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112
Q

Average length of heroin clean time

A

11.7 years

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113
Q

years heroin drug free percentages

A

9% less than a year
33% 1-5 years
17% 6-10 years
11% 11-15 years
11% 16-20 years
19% more than 20 years

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114
Q

what is opioid intoxication

A

intoxication following injection of smoking 1-3 mg of heroin or 3-15 mg of morphine which is described in 4 stages

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115
Q

what are the 4 stages of opioid intoxication

A
  1. rush
  2. nod
  3. high
  4. being straight
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116
Q

duration and effects of rush stage

A

duration: 45 s
effects: intense pleasure, with waves of intense euphoria likened to sexual orgasm. Visceral sensation occur, with facial flushing and deepening of voice. Rush is resistant to tolerance

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117
Q

duration and effects of nod stage

A

duration: 15-20 min
effects: a state of escape from reality that can range from sleepiness to virtual unconsciousness. Addicts are described as calm, detached, and very uninterested in external events

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118
Q

what is the duration and effects of high stage

A

duration: several hours
effects: stage follows rush, it is a general feeling of well-being that can extend hours beyond the rush, shows tolerance

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119
Q

duration and effects of being straight stage

A

Duration: up to 8 hours
effects: the point at which a user is no longer experiencing the rush, nod, or high but also is not yet experiencing withdrawal. This state can last up to 8 hrs following an injection or smoking of heroin

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120
Q

what is opioid tolerance

A

tolerance to the sedative, euphoric and analgesic properties of opioids builds rapidly

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121
Q

those who are addicted can inject up to ____________________________________________

A

70 times the lethal dose for a drug naïve individual

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122
Q

what does tolerance do

A

shortens duration of drug action

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123
Q

what is it called when tolerance is built from switching from codeine to morphine

A

cross tolerance

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124
Q

2 reasons that tolerance occurs

A
  1. neuro-adaptive down-regulation of the opioid system
  2. conditioning to place of use and associated compensatory body reactions in the opposite direction of opioid effects
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125
Q

early opioid drug use is driven by

A

positive reinforcement aka feeling of elation/euphoria

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126
Q

what drives opioid drug use after tolerance develops

A

negative reinforcement (avoiding withdrawal)

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127
Q

what are the opioid withdrawal symptoms

A

profound dysphoria
depression
anxiety
yawning
lacrimation (tear production)
rhinorrhea (runny nose)
perspiration
goosebumps
tremor
pupil dilation
loss of appetite and weight
vomiting
restlessness
diarrhea
insomnia
dehydration
hyperglycemia
increased body temp
increased blood pressure
elevated pulse

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128
Q

how long does it take for heroin withdrawal symptoms to peak

A

48-72 hours

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129
Q

many treatment providers believe that what should be prevented?

A

acute withdrawal that is why they use maintenance therapy

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130
Q

what is more protracted than heroin withdrawal

A

methadone and suboxone withdrawal (aka treatment meds used)

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131
Q

is opioid withdrawal life threatening

A

no

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132
Q

how long do some opioid withdrawal such as increased pain, stress sensitivity, dysphoria, and metabolic changes can last for and what is the phenomenon called

A

symptoms can last up to 5 months and are known as post-acute withdrawal

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133
Q

what happens to a baby if a mother takes opioids

A

because opioids can cross the placental barrier, infants born to opioid addicted mothers suffer withdrawal

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134
Q

what type of receptors are opioid receptors

A

g protein coupled receptors w/ seven transmembrane spanning regions

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135
Q

what are the 3 types of opioid receptor subtypes

A

mu, delta, and kappa

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136
Q

what is the endogenous opioid for the mu receptor subtype

A

beta-endorphin enkephalin

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137
Q

what is the endogenous opioid for the delta receptor subtype

A

enkephalin beta endorphin

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138
Q

what is the endogenous opioid for the kappa receptor subtype

A

dynorphin

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139
Q

what kind of properties do opioids have that cause animals to self-administer the drug when delivered directly into the brain

A

analgesic properties

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140
Q

analgesia occurs through direct injection through various sites:

A
  • raphe nuclei
  • periaqueductal gray
  • certain medullary nuclei
  • spinal cord
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141
Q

are opioids dopamine agonists

A

no

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142
Q

what opioid receptor is the most important for the addictive properties of opioids

A

mu opioid receptor

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143
Q

what role do delta and kappa receptors play in opioid addiction

A

implicated in tolerance and dysphoria

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144
Q

what causes analgesia properties

A

caused by direct inhibition of nociceptive activity in both the brain and spinal cord

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145
Q

what is nociception

A

sensory nervous system response to harmful or potentially harmful stimuli

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146
Q

what causes intoxication in opioid usage

A

blocking the affective component of pain in the brain

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147
Q

what organic substance is considered an alcohol

A

any organic substance with a hydroxyl functional group, bound to a saturated carbon atom

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148
Q

what are 4 types of alcohol

A

ethanol
2-propanol
methanol
butanol

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149
Q

alcohol can be found in all ___________ containing substances

A

glucose

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150
Q

what type of alcohol is safe for consumption

A

ethanol

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151
Q

how does alcohol occur naturally

A

through fermentation

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152
Q

what occurs during fermentation

A

when glucose and water are converted to ethanol and carbon dioxide in the presence of yeast

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153
Q

at are the 5 requirements for fermentation

A
  1. sugar or starch (to make glucose)
  2. water
  3. heat
  4. ferment (yeast)
  5. air
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154
Q

what is an example of naturally occurring fermentation

A

fruit over ripening which can lead to 12% alcohol

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155
Q

what is distillation required for

A

to yield more concentrated levels of alcohol

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156
Q

what occurs when alcohol is distilled

A

a fermented mixture is heated and ethanol vapors which boil off at a lower temp (78 degrees) than water (100 degrees), and are trapped and condensed

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157
Q

different beverages use different__________________

A

use different plant sources of glucose for fermentation and distillation

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158
Q

Alcohol use in US compared to European nations

A

Alcohol use and dependence rates in the US are similar to those observed in many European nations, difference is that US does more binge drinking

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159
Q

Total Alcohol consumption in L per Capita in US

A

Total: 9.08
Beer: 5.11
Wine: 1.67
Spirits: 2.29

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160
Q

Alcohol dependence in US (percentage)

A

4.1%

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161
Q

Alcohol Use by gender

A

Women increased by 15.8% (almost equal to men consumption)
went from 59.6 to 69

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162
Q

Alcohol use by Race/ethnicity Percent change from 2001-2002 to 2012-2013

A

Asian or Pacific Islander: 29.1%
Native American: 27%
Black: 24.2%
Hispanic: 17.2%
White 8.3%

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163
Q

Alcohol Use Percent Change by Age group

A

18-29: 9.6%
30-44: 10.6%
45-64: 11.8%
greater than 65: 22.4%

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164
Q

High Risk Drinking Percent Change by Gender

A

Women: 57.9%
Men: 15.5%

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165
Q

High Risk Drinking Percent Change by Race

A

Black: 62.4%
Asian or Pacific Islander: 56.5%
Hispanic: 40.6%
Native American: 40.3%
White: 23%

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166
Q

High Risk Drinking Percent Change by Age Group

A

18-29: 14.2%
30-44: 37%
45-64: 49.3%
Greater than 65: 65.2%

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167
Q

Alcohol Use Disorder Percent Change by Gender

A

Women: 83.7%
Men: 34.7%

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168
Q

Alcohol Use Disorder Percent Change by Age Group

A

18-29: 44.4%
30-44: 47.4%
45-64: 81.5%
greater than 65: 106.7%

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169
Q

Alcohol Use Disorder Percent Change by Race/Ethnicity

A

Black: 92.8%
Asian or Pacific Islander: 77.8%
Hispanic: 51.9%
Native American 37.2%
White: 47.2%

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170
Q

What is the most abused substance in Western culture and causes more harm to individuals and families than any other substance

A

Alcohol

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171
Q

one possible reason discussed in class for why alcohol consumption has increased?

A

Advertisments of alcohol is more common nowadays

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172
Q

What is the cost of excessive drinking on US economy?

A

250 billion

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173
Q

Top 5 Drugs that Cause the Most harm

A

from greatest harm to least:
Alcohol
Heroin
Crack Cocaine
Methamphetamine
Cocaine

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174
Q

Cost of excessive drinking on workplace productivity and health care

A

180 billion in workplace productivity and 28 billion in healthcare costs

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175
Q

Cost of excessive drinking on law enforcement and in motor vehicle accidents

A

25 billion in law enforcement costs
13 billion in motor vehicle accidents
(44 billion when associated w/ healthcare and law enforcement costs included)

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176
Q

what percent of males and females have experienced one or more alcohol-related adverse events?

A

60% of males and 30% of females

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177
Q

what percent of intimate partner violence is alcohol involved in?

A

55%

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178
Q

what percent of women sexually assaulted or raped by adulthood, how many involve alcohol use

A

25% are SA
half of these involve alcohol use

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179
Q

what percent of traffic fatalities involve alcohol

A

1/3 or 33.333%

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180
Q

what is the leading cause among 8-34 year olds in the US

A

traffic fatalities, specifically those involving alcohol

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181
Q

Age group with the highest percent of heavy use, binge use, and normal use?

A

21-25 yo had the highest percent at 69.3%
Heavy use: 13.1%
Binge use: 30.2%
Normal Use: 26%

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182
Q

Why is alcohol an unusual substance in terms of behavioral effects

A

it has both stimulant (reward) and sedative (anxiolytic) properties

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183
Q

why are males more likely to drink

A

reward properties

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184
Q

why are females more likely to drink

A

for the anxiolytic effects

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185
Q

T or F: behavioral effects are dose dependent?

A

True

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186
Q

What typical behavior occurs from 0.3 to 0.4 (general anesthesia to death) level of alcohol

A
  • increased sedation/hypnosis
  • approaching general anesthesia
  • approaching coma
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187
Q

What typical behavior occurs from 0.05 to 0.08 (relief from anxiety to disinhibition) level of alcohol

A
  • Personality changes
  • Relief from anxiety
  • social lubricant (more talkative, assertive)
  • Disinhibition
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188
Q

What typical behavior occurs from 0.08 to 0.15 (disinhibition to sedation) level of alcohol

A
  • significant disinhibition (life of party)
  • impaired judgment
  • impaired cognition
  • impaired motor function
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189
Q

What typical behavior occurs from 0 to 0.05 (normal to relief from anxiety) level of alcohol

A

Normal behavior

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190
Q

What typical behavior occurs from 0.15 to 0.30 (sedation to general anesthesia) level of alcohol

A
  • marked ataxia (staggering/slurred speech)
  • major motor impairment
  • impaired reaction time
  • blackouts
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191
Q

What is the lethal dose of alcohol for 50% of people

A

0.4 gm%

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192
Q

Alcohol pharmacokinetics

A

when the alcohol readily crosses cell membranes in most parts of the body

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193
Q

what organs absorb alcohol

A

20% absorption by the stomach
80% absorption by the small intestine
80-90% absorption in 30-60 min

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194
Q

T or F: BAL levels are higher when food is in the stomach

A

False

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195
Q

How long does it take for peak alcohol levels to occur on an empty stomach?

A

.8 Hours and peak is at 0.08 g/210 L

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196
Q

How long does it take for peak alcohol levels to occur on a full stomach?

A

1 hour and peak is at 0.045 g/210 L

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197
Q

How many drinks does it take for a 140 lb man to go above the legal drinking limit?

A

3 drinks, causes a .08 blood alcohol level

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198
Q

How many drinks does it take for a 140 lb woman to go above the legal drinking limit?

A

3 drinks, causes a .10 blood alcohol level

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199
Q

under normal conditions at what rate is alcohol metabolized

A

1/2 drink per hour

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200
Q

For an alcoholic, at what rate is alcohol metabolized

A

1 drink per hour

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201
Q

What enzyme metabolizes drugs and other foreign compounds in the body

A

CYP2E1

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202
Q

what is the reaction for breaking down alcohol

A

Alcohol is catalyzed by CYP2E1 and with NAD+ will make acetaldehyde which is then converted into acetate

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203
Q

What causes the hangover symptoms

A

Excess acetaldehyde that cannot be broken down will cause hangover symptoms

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204
Q

What are two byproducts of breaking down alcohol

A

2 NADH

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205
Q

What genetic variation causes the greatest vulnerability to alcohol

A

ALDH^1/ALDH^1 is the fastest alcohol metabolism and is the most vulnerable

206
Q

What genetic variation results in intermediate metabolism

A

ALDH2^1/ALDH2^2

207
Q

What alcohol variation has complete protection from alcoholism

A

ALDH2^2/ALDH2^2

208
Q

How does Disulfiram effect alcohol metabolism

A

Disulfiram will mimic ALDH2^2/ALDH2^2 genotype and inhibit acetaldehyde from converting into acetate

209
Q

Definition of alcohol use disorder

A

a problematic pattern of X use leading to clinically significant impairment or distress, as manifested by at least 2 at the following within a 12 month period (look at alcohol notes for the 11 possible X patterns)

210
Q

Is alcohol heritable?

A

Yes, it is highly heritable

211
Q

having 1 alcoholic parent increases risk of alcoholism by?

A

400%, this does not change even if child is raised in non-alcoholic homes

212
Q

Having 2 alcoholic parents increases risk of alcoholism by?

A

over 600%

213
Q

Explain exp of Men Who later developed alcohol abuse

A

Alcohol-naïve sons were brough in to a lab and were then given a drinks and asked to describe their high from drinking. Those that did not develop alcoholism later on reported a more intense high. Both groups peaked around the same time. Results demonstrate how those who develop alcoholism must drink more in order to achieve the same high

214
Q

How many alleles were identified in 2017 in a GWAS of drinking among 112117 pp in UK

A

14

215
Q

Alcohol consumption is a (1) and (2) trait

A
  1. complex
  2. multifactorial
216
Q

What were the results from 2023 meta-analysis of GWAS

A
  1. 19 SNPs (single nucleotide polymorphisms) were associated with general risk of addiction
  2. substance specific risk at
    - 9 loci for alcohol
    - 32 for tobacco
    - 5 loci for cannabis
    - 1 locus for opioids
217
Q

What is alcohol withdrawal

A

it is a rebound effect of a chronically sedated CNS), produces hyper-excitability

218
Q

risk of alcohol withdrawal

A

withdrawal after chronic abuse can be life threatening if benzodiazepines are not used for acute symptoms

219
Q

What are the stages of acute alcohol withdrawal

A

Early and late stage

220
Q

Signs and time period for early stage of alcohol withdrawal

A

Early stage lasts from a few hours to 48 hours
signs include:
- anxiety
- anorexia
- insomnia
- tremor
- mild disorientation
- convulsions
- sympathetic response

221
Q

Signs and time period for late stage of alcohol withdrawal

A

Begins after2-4 days and lasts 2-3 days
Signs include:
- delirium tremens

222
Q

what is the most severe alcohol withdrawal state

A

Late stage
symptoms include:
tremors, anxiety, insomnia, paranoia, disorientation, sweating, nausea vomiting, diarrhea, fever, agitation, hallucination, fever

223
Q

what is alcohol tolerance

A

Occurs when more alcohol is needed to attain effects that are used to be felt at a lower dose

224
Q

what is dispositional tolerance

A

increased ability to metabolize alcohol through alcohol dehydrogenase and other liver enzymes

225
Q

How long does it take for dispositional tolerance to double due to heavy drinking

A

Only 3-14 days

226
Q

what is functional tolerance

A

the need for higher blood levels to achieve intoxication via neuroadaptive changes to the CNS

227
Q

What is acute functional tolerance

A

greater intoxication is observed on the ascending limb of the BAL curve than at the same dose on the descending limb

228
Q

What is chronic functional tolerance

A

increase in intake needed to produce intoxication; heavy drinkers are less likely impaired on motor coordination tasks than light drinkers at same BAL

229
Q

what is behavioral functional tolerance

A

better performance on behavioral tasks by performing them repeatedly while intoxicated

230
Q

Is alcohol toxic

A

yes at extremely high doses

231
Q

How many alcohol related ER visits were ther in 2009

A

650000

232
Q

How many Alcohol related ER visits for those under the age of 21

A

200000

233
Q

what percent of college students drive with BAL above legal limit

A

25%

234
Q

how many students injured each year due to alcohol related accident

A

500000

235
Q

how many assaults by person who was drinking

A

100000

236
Q

What conditions does alcohol contribute to

A
  1. liver damage (fatty liver disease, hepatitis, cirrhosis)
  2. heart disease
  3. neurological disorders
  4. type 2 diabetes
  5. certain cancers
    - ex esophageal cancer when drinking hard liquor
  6. Korsakoff syndrome
  7. fetal alcohol syndrom
237
Q

what is a teratogen

A

an agent that causes birth defects
- ex: alcohol

238
Q

Fetal Alcohol Syndrome Symptoms

A
  • small eye openings
    -smooth philtrum
  • thin upper lip
  • less developed brain
239
Q

what percent of pregnant women in the US have reported drinking in last month (during 2015)

A

10%, with 1/3 reporting binge drinking

240
Q

what are some lifelong characteristics of fetal alcohol syndrome

A

they can occur without outward indication of exposure and can lead to:
- social skill problems
- adult substance abuse
- altered brain function

241
Q

What are the neurobiological effects of alcohol

A

alcohol has widespread and diverse effects throughout the body, including CNS, that are still not fully understood

242
Q

What are alcohol’s sites of cellular action

A

alcohol does not bind to a given receptor class but instead interacts w/ specific neuronal elements called ethanol receptive elements

243
Q

what are the ethanol receptive elements

A
  • GABA receptors
  • 5-HT receptors
  • K channels
  • Ca channels
  • G proteins
  • protein kinases
  • mhu opioid receptors
  • synaptic sites in CNS neurons
244
Q

Alcohol neurobiologic effects are difficult to quantify and see what is specifically effected

A

true

245
Q

Alcohol Reward Neurocircuit

A

Interneurons stimulate the:
1. VTA
- dopamine is then sent to frontal cortex, Nucleus accumbens, amygdala
- Opioid peptides are sent to opioid receptors
2. AMG
- also has opioid peptides and receptors along with GABA and cannabinoid receptors present
3. Nucleus accumbens
- has opioid, cannabinoid, and GABA receptors present

246
Q

where is the extended amygdala circuit in alcohol neurocircuit

A

Circuit includes the Nucleus accumbens, the BNST, and the Amygdala

247
Q

How does alcohol affect GABA

A

inhibits GABA release in the VTA which will indirectly lead to increase in DA levels

248
Q

How does acetaldehyde affect the VTA

A

it increases its DA levels

249
Q

What partially reduce self administration in animals

A
  • DA receptor agonists
  • opioid receptor antagonists
  • GABA receptor antagonists
250
Q

Problem with promising receptors that show reduction in self administration in animals

A

these drugs were not effective in humans

251
Q

What kind of mouse did not self administer alcohol

A

Mhu opioid receptor knockout mice

252
Q

what kind of mice self administered more alcohol

A

Cannabinoid, delta opioid receptor, and neuropeptide Y1 knockout mice

253
Q

What are blunted striatal responses to reward associated with

A

Various addictions including alcohol

254
Q

Which substances favor hypoactivation

A

Alcohol, Cannabis, Cocaine, and Nicotine

255
Q

what 3 thing is heavy drinking in teen years associated with?

A
  1. faster gray matter loss
  2. slower white matter growth
  3. poor subcortical cortical connectivity
256
Q

what predates addiction

A

the hypoactivation response pattern that affects active and abstinent addicts

257
Q

what does acute alcohol withdrawal activate

A

it activates the limbic-hypothalamic adrenal axis, primary stress response system

258
Q

what were the results of the corticotropin releasing factor immunoreactivity (CRF-IR) exp in rat amygdalas

A

For the first 4 hours, levels of CRF-IR in both the withdrawal and control group were the same
BUT halfway through the 6-8 hour slot, the withdrawal group had a spike in the CRF-IR levels that last up to the 12 hr mark

259
Q

During the CRF-IR exp, what NT were affected

A

NE levels rose and neuropeptide Y decreased
(increase in NE is associated w/ social anxiety
(decrease in neuropeptide Y is also associated w/ anxiety and emotional reactivity

260
Q

what is protracted abstinence

A

it is stage where a negative emotional state is induced and can last for months

261
Q

what long term behavioral effect may occur during alcohol protracted abstinence

A
  1. disruptions in sleep for years
  2. bad mood
  3. homeostatic pt is shifted to allostatic state
262
Q

what is the psychoactive ingredient in tobacco

A

nicotine

263
Q

what is tobacco

A

the dried leaves of nicotiana tobacum which grow in south and north america

264
Q

3 ways of tobacco ingestion

A
  1. smoked (cigars, cigarettes)
  2. chewed (chew)
  3. snorted (snuff)
265
Q

what kind of cancer is chew associated with?

A

mouth cancer

266
Q

how far can tobacco be traced

A

8000 years

267
Q

Where does the US fall in tobacco consumption

A

in the middle with about 1250-1499 cigarettes/person

268
Q

what regions in US have the highest rates of smoking

A

Midwest and South

269
Q

what is a common pattern in the regions where smoking is highest

A

they have the shortest life expectancies aka worst health

270
Q

what tobacco product is most popular

A

cigarettes

271
Q

what is the lowest US life expectancy

A

it is 72.9 to 77.4 yrs and is in the south

272
Q

what year did tobacco products start to decrease and why?

A

Around 1945-1955, people started to figure out that smoking can cause cancer so public campaigns began to discourage smoking

273
Q

what products does tabacco smoke contain

A

nicotine, carbon monoxide, and tar

274
Q

what is tar

A

residual substance left after nicotine is removed and contains several toxins such as carcinogens and tumor initiating agents

275
Q

what major toxic agents are most present in cigarettes

A

Acetaldehyde 800 microg (cilia toxic agent)
NO2 350 microg (toxic agent)
catechol 270 microg (cocarcinogen)

276
Q

what alternative tobacco administration route has recently become more popular

A

vapes

277
Q

what is different bw vapes and cigarettes

A

have less carcinogens, but have a higher nicotine blood plasma level that creates a more intense stimulant effect

278
Q

Since 2011, how much has cig use changed

A

Decreased from 16% in 2011 to 8% in 2018

279
Q

How has e-cig usage changed since 2011

A

Increased from less than 2% to 21%

280
Q

What type of cigarette has the highest nicotine level

A

new generation e cigs have the highest nicotine levels that occur at an hour in

281
Q

what is the peak level and time for a cigarette

A

Cigarette peaks at 15 ng/ml and occurs at 10 min in

282
Q

What are the different parts of the hookah

A

Tobacco bowl, ashtray, neck, hose, water bowl, and mouth piece

283
Q

what is the percent of people 12+ that have used tobacco

A

67.5%

284
Q

what percent of people have smoked a cigarette

A

62.8%

285
Q

what number of people are dependent on cigarettes in a given moment

A

22.9 million

286
Q

what is the medical cost due to tobacco use

A

170 billion

287
Q

what are some of the issues or conditions that tobacco can cause

A
  • heart disease
  • stroke
  • lung disease
  • eye disease
  • immune system problems
  • arthritis
  • erectile dysfunction
288
Q

is the leading cause of preventable death

A

smoking

289
Q

how many people die each year due to smoke related illness

A

480000

290
Q

how many people have a disease due to smoking

A

16 million

291
Q

by how much does the life expectancy of a smoker decrease when compared to a non-smoker

A

die 10 years earlier

292
Q

For men, what is the survival probabilities for current smokers vs non current smokers

A
  1. discrepency starts at 40 yo
  2. by the time you reach 80, there is a 12 yr gap bw smokers and non smokers
293
Q

for women, what are the survival probabilities for current vs non current smokers

A
  1. discrepancy starts at 50 yo
  2. At age 80, the gap increases to 11 years bw smokers vs non smokers
294
Q

what 2 kinds of exposure can lead to adverse outcomes during pregnancy

A

smoking and second-hand smoke

295
Q

what are some of the pregnancy adverse outcomes due to smoking

A
  1. low birth weight
  2. childhood ADHD and conduct problems
    - smoking leads to down regulation of DA levels in general
  3. asthma
  4. SIDS
  5. Vulnerability to drug use in teen years
296
Q

What were the results of the 2019 study of e cigs association to lung injury (EVALI)

A
  • 34 deaths
  • THC present in most samples
  • causes still not fully understood
297
Q

What are the psychological effects of nicotine use?

A
  • mild euphoria
  • increased energy
  • heightened arousal
  • reduced stress
  • anxiolytic effects
  • reduced appetite
  • mild pain reducing qualities
298
Q

what are the behavioral effects of nicotine use?

A
  • improved attention
  • shortened reaction time
  • better problem solving
  • improved cognition
  • increased heart rate and blood pressure
299
Q

what are the pharmacokinetics associated with nicotine use

A
  • inhaled cig and vapes reach brain in 8 s
  • almost all nicotine is delivered through the lungs
  • large individual diff in blood plasma nicotine observed from the same dose
300
Q

how long does it take nicotine to reach the brain

A

8 seconds

301
Q

what are the levels like for people who are addicted to nicotine

A

Those who are addicted will maintain high blood levels of nicotine throughout the day
- smoke a new cig every .5 to 1 hour or when the blood plasma nicotine drops

302
Q

what level of nicotine does an addicted person try to maintain

A

around a 20 ng/ml blood nicotine concentration

303
Q

T or F: different tobacco preparations will lead to the same blood concentration curves

A

False

304
Q

When does the peak concentration for cigarettes occur

A

within 10 min then will gradually decrease

305
Q

When does the peak concentration for oral snuff occur?

A

At 30 min, it increase quickly, peaks, then decreases a little

306
Q

when does the peak concentration occur for chewing tobacco

A

It occurs in 30 min, it will increase quickly then peak and level off (does not really decrease)

307
Q

when does the peak nicotine concentration occur for nicotine gum

A

Peaks at 30, will gradually increase, peak and then gradually decrease

308
Q

During what age group does prevalence of smoking increase sharply

A

from 12 to 17

309
Q

what is the rate for prevalence of smoking during adulthood

A

rates fall slowly across adulthood

310
Q

how long does it take 50% of teens who try smoking to become daily smokers

A

4-5 years

311
Q

can a person be biologically predisposed and quickly develop nicotine withdrawal symptoms

A

yeah

312
Q

what is the term used for people who maintain low nicotine use patterns and are less likely to become addicted

A

chippers

313
Q

at what age do converted chippers usually stop or decrease their smoking habits

A

in their 20s

314
Q

What is required for people to never return to light smoking

A

those that smoke 15+ cigs a day for at least 2 years never return to light smoking

315
Q

what is nicotine abstinence syndrom

A

the withdrawal effects due to prolonged nicotine use

316
Q

what are the somatic symptoms for nicotine withdrawal?

A
  • bradycardia (slowed heart rate)
  • gastrointestinal discomfort
  • increased appetite
  • weight gain
317
Q

what are the affective symptoms for nicotine withdrawal

A
  • depression
  • irritability
  • dysphoria
  • anxiety
  • difficulty concentrating
318
Q

What is the neural cause for many of the symptoms during nicotine withdrawal

A

Dopamine depletion in mesolimbic DA system cause a lot of the nicotine withdrawal symptoms

319
Q

Normal neural response pattern

A

Substance naive response pattern:
Neural firing (tonic activity) is consistent and when a reward cue is present, there is a reward delivery causing phasic response
Satiation will occur after phasic response is over and will return to normal tonic activity (same levels as before the cue)

320
Q

Sensitized neural response pattern

A

Experience dependent response pattern:
there is reduced tonic activity (both in # of neural firings and their intensity)
when a reward cue is present, a sensitized phasic activity is immediately triggered (greater activity than normal)
reward deliver occurs in the midst of the phasic activity
satiation occurs after phasic activity is over and goes back to reduced tonic activity

321
Q

How long does nicotine acute withdrawal last

A

Koob says up to 30 days, but heavy smokers, esp women, have reported longer timeframes

322
Q

How long can nicotine cravings last

A

up to 6 months

323
Q

how effective is nicotine replacement therapy

A

about 25%

324
Q

what nicotine therapy drug can be up to 50% effective

A

Bupropion (wellbutrin)

325
Q

what is buropion

A

a NDRI antidepressant that increases midbrain DA levels and block psychoactive effects of stimulants, including nicotine

326
Q

what are the behavioral nicotine mechanisms, as described by smokers

A
  • pleasurable
  • helpful for concentration
  • calming
  • stress relieving
  • anxiolytic
327
Q

what kind of receptor is nicotine

A

a nicotine acetylcholine receptor (nAChR) agonist

328
Q

where are nAChR found

A

throughout brain and body
muscles: alpha 1, beta 1, gamma, delta, epsilon
CNS: alpha 2 through alpha 6, beta 2 through beta 4

329
Q

why is Beta 2 nAChR agonists imporotant

A

they are important for reinforcing effects

330
Q

Neurobiological effects of nicotine (what occurs at a neuro level)

A

neuronal nAChRs activate other neurons by opening the Ca ion channels using other mechanisms

331
Q

T or F: the break point for animal self administration of nicotine is higher than for cocaine

A

False, Cocaine break point is higher than nicotine

332
Q

How does nicotine reduce pain

A

Nicotine has analgesic effects that are due to the activation of alpha4beta2 and alpha7 nAChR receptor subunits which will then increase opioid peptide levels in the Nucleus accumbens

333
Q

how is rat behavior effected at low/high doses of nicotine

A

low doses: facilitates social behavior
high doses: dampens behavior

334
Q

How do nicotine acute reinforcing effects occur

A

Through DA release in the mesolimbic DA system (VTA and NAcc) via the Beta2 subunit

335
Q

where are nAChRs located on the VTA

A

on both cell bodies and dendrites of DA neurons

336
Q

what type of mouse will not self administer nicotine

A

Beta 2 knockout mice

337
Q

how does nicotine effect glutamate, GABA, and DA levels

A
  1. raises glutamate levels (alpha 7)
  2. reduces GABA levels (alpha4beta2) in the VTA
  3. increases DA release
338
Q

What does alpha 7 nAChRs activate

A

Glutamate long term activation which leads to increase of DA

339
Q

What does alpha4beta2 nAChRs do

A

This cholinergic afferent will reduce GABA levels (GABA is a DA inhibitor) leading to increase in DA release

340
Q

What are cannabinoids

A

drugs that contain tetrahydrlcannabinol or similar pharmacologic actions

341
Q

how many types of cannabinoids exist

A

over 100 types, including naturally occurring and synthetic

342
Q

where is cannabis naturally found

A

a hemp plant indigenous to Altai and Tien-Shan mountains

343
Q

how long has cannabis been cultivated

A

6000 years

344
Q

what everyday material can be made out of cannabis

A

rope

345
Q

when was cannabis first used as an anesthetic

A

2000 years ago

346
Q

Where does marijuana come from

A

plant called cannabis sativa

347
Q

what are the different cannabis administration methods

A
  • joint
  • water pipe aka a bong
  • blunt
  • hash
  • hash oil (very concentrated)
  • butane honey oil (BHO)
348
Q

how is hash oil made

A
  1. soak cannabis flower buds in isopropanol (an alcohol)
  2. remove all plant material
  3. heat mixture to evaporate isopropanol
349
Q

difference between hash oil and butane honey oil?

A

butane is used instead of isopropanol for extraction

350
Q

what are the THC levels the different administration levels

A

Marijuana 4.5%
Sinsemilla 11%
Hashish 12.7-15.6%
Hashish oil 14.1-19.5%
BHO 60-90%**

351
Q

How many non-psychoactive chemical constituents does cannabis contain

A

hundreds

352
Q

what are the 2 main gene pools of cannabis

A

C sativa or c afghanica “indica”

353
Q

what cannabis products are made from c. sativa

A

fiber/seed (low THC, mid-high CBD)
marijuana (high THC, low CBD)
hashish (high THC, low-mid CBD

354
Q

What cannabis product is made from indica

A

hashish w/ high THC, low-high CBD

355
Q

Is marijuana associated with lung cancer

A

no

356
Q

What is the correlation between testicular cancer in epidemiologic studies

A

increased rates (up to 2x) of testicular cancer

357
Q

what are the main 2 types of cannabinoids

A

naturally occurring and synthetic

358
Q

how many naturally occurring cannabinoids exist

A

70+

359
Q

are the 3 naturally occurring psychoactive cannabinoids

A
  1. delta 9- tetrahydrocannabinol
  2. delta 8- tetrahydrocannabinol (67% as potent as 1)
  3. delta 9-tetrahydrocannabidivarin (25% as potent as 1)
360
Q

What are some examples of synthetic cannabionids

A
  1. spice
  2. K2
361
Q

what doe cannabinoid receptors in synthetic cannabionoids bind to?

A

THC

362
Q

synthetic compounds of cannabis are known as

A

JWH designations after John huffman who first synthesized them

363
Q

what does delta 9-tetrahydrocannabinol and synthetic cannabis have in comon

A

they are both cannabinoid receptor 1 and 2 agonists

364
Q

what is the most commonly used illegal drug in US

A

marijuana

365
Q

what percent of people 12+ have used marijuana

A

42%

366
Q

what percent of people in the last month have used marijuana

A

15%

367
Q

what is the pattern of cannabis prevalence seen since 1978 to 2016 based on past month use

A

Gradual decrease from 34% to 9% from 1978 to 1992, but around 2000, the rates of use has slowly begun to increase and in 2016 were at 15%

368
Q

what is interesting about the rate of marijuana usage and marijuana use disorder

A

Rates of use have increased since 2000, but the rate of marijuana use disorder has not

369
Q

what has been the average prevalence of marijuana use disorder percentage seen in adults

A

2%

370
Q

what 2 drug usage hit historic highs in 2021

A

marijuana 13.2% increase
hallucinogen 4.7% increase from 2011 to 2021

371
Q

what percent of cannabis users in the past year demonstrate dependence

A

9%

372
Q

what drug is most regularly used psychoactive drug for kids and teens

A

marijuana, they use that more than alcohol and tobacco

373
Q

what are marijuana well confirmed clinical effects

A

refractory nausea, vomiting, anorexia, appetite loss, HIV/AIDS, canceer cachexia

374
Q

what are the less well confirmed clinical effects of marijuana

A

spasticity due to spinal cord injury, multiple sclerosis, neurogenic pain, neuropathy, allodynia, movement disorders (Tourette’s syndrome, dystonia, dyskinesia), bronchodilation effects, glaucoma

375
Q

what are the unexplored clinical effects of marijuana

A

epilepsy, hiccups, bipolar disorder, alzheimer’s disease, alcohol dependence

376
Q

what are the behavioral effects of marijuana

A

intoxicating, includes euphoria, happiness, dream-like state, and at high doses, tiredness and fatigue

377
Q

what are some other, not as common, behavioral effects of marijuana

A

more social, or less social (depends on dose), worse concentration, memory becomes poor, simple tasks require excess efforts, slowed perception of time

378
Q

what is the most common administration method for marijuana

A

almost always smoked, (oral admin is not very effective)

379
Q

how long after consumption does peak blood levels occur for marijuana

A

3-10 min

380
Q

what are the effects of marijuana on the heart rate

A

When smoked, heart rate will decrease from 87 down to 75
when oral, heart rate will go from 72 to 80 then back down to 75

381
Q

How does the rate high for marijuana differ among different administration methods

A
  • IV has the most intense reported high with the peak occurring within the first 10 minutes and high wearing off after 4 hours
  • Smoked has 2nd highest rated high with peak occurring same as IV and wearing off after 4 hours
  • Oral has lowest rated high and has gradual increase and peaks around hour 3 before gradually decreasing and wearing off after 6 hours
382
Q

what percent of the delta 9-THC has entered the brain when the behavioral/psychoactive effects occur

A

1%

383
Q

What happens to the rest of the delta 9-THC that did not enter the brain

A

it is stored in body fat and broken down by the liver

384
Q

How is THC broken down

A

THC is broken down into 8 beta-OH-THC and 11-OH-THC. 8 Beta-OH-THC then breaks down into to conjugates while 11-OH-THC breaks down into 11-OXO-THC, Conjugates and 8 alpha, 11-OH-THC which is then broken down into conjugates

385
Q

what are the psychoactive metabolites seen during breakdown of THC

A

THC, 8 beta-OH-THC, 11-OH-THC, and 11-OXO-THC

386
Q

how long does the elimination of all active metabolites take

A

5 to 6 days

387
Q

what can be detected due to the slow elimination of half lives

A

active metabolites in Cannabis can be detected in urine for over a month due to slow half-life

388
Q

when was a dependence syndrome identified for cannabis

A

1980s when THC making methods had greater concentrations

389
Q

what were symptoms of the 1980 cannabis dependence syndrome

A

fear of health consequences, blunted emotional expression, emotional alienation from loved ones, low achievement, low grade depression

390
Q

what is the typical course of progression for cannabis dependence

A

pleasurable social use then tolerance then more frequent use then social withdawal then function impairment at work/school

391
Q

how many types of cannabis dependece are there

A
  1. type 1
  2. type 2
392
Q

what are the characteristics of type 1 cannabis dependence

A
  • multiple times a day
  • significant self perceived dependence
  • moderate withdrawal symptoms
  • high rate of relapse
  • dependence metabolites include delta 9-THC, 11-hydroxyl-delta 9-THC
393
Q

what are the characteristics of type 2 cannabis dependence

A
  • every 24-48 hours
  • minor/moderate self perceived dependence
  • mild withdrawal symptoms
  • high rates of relapse
  • dependence metabolites include 11-nor-delta 9-THC-carboxylic acid
394
Q

what other drugs have similar dependence symptoms to cannabis

A

alcohol and cocaine

395
Q

what does tolerance look like for cannabis users

A

tolerance to physical (HR acceleration) and psychological effects builds rapidly, even for light users

396
Q

what causes tolerance to build in cannabis

A

neuroadaptations (cannabinoid receptors are profoundly downregulated)

397
Q

what are the cannabis withdrawal symptoms

A
  1. irritability, anger, or aggression
  2. nervousness or anxiety
  3. sleep difficulty
  4. decreased appetite/weight loss
  5. restlessness
  6. depressed mood
  7. abdominal pain, shakiness/tremors, sweating, fever, chills, headache
398
Q

how many withdrawal symptoms must an individual show in order to get diagnosed with cannabis withdrawal syndrom

A

at least 3 or mor symptoms

399
Q

how are alcohol and cannabis effects on performance similar

A

have similar psychomotor performance and memory

400
Q

what are the effects of cannabis that can impair driving and pilot skills

A
  • slow rxn time, poor detection of peripheral stimuli, poor oculomotor tracking, space and time distortion, impaired coordination, brake and accelerator errors, poor speed control, poor judgement, increased risk of overtaking, impaired attention, impaired short term memory, additive effects w/ alcohol and other drugs
401
Q

how did THC affect word recal test

A

decreased ability to recall words, same as alcohol

402
Q

how does marijuana play a role in motor accidents

A

doubles the risk

403
Q

what is the relation of marijuana use and individuals w/ psychotic disorders

A

cannabis rates are high among people who are predisposed to or suffer from psychotic disorders

404
Q

how does cannabis effect brain of teens

A

has detrimental effects on prefrontal cortex development

405
Q

what is reduced prefrontal volumes based on cannabis use associated with

A

decision making, memory, long-term palnning deficits

406
Q

what is the neurobiological effect of cannabis

A

potency of cannabinoids correlates strongly with the CB1 and CB2 receptor binding affinity

407
Q

where are cannabinoid receptors expressed densely

A

Basal ganglia and cerebellum

408
Q

what regions of the basal ganglia have dense number of cannabinoid receptors

A

N. Acc, cuadate, putamen, thalamus, globulus pallidus

409
Q

what is the function of the cerebellum

A

important for motor control and coordination of neural activity across the cortex

410
Q

in what regions of the brain are there low levels of cannabinoid receptors

A

hippocampus
amygdala
cortex

411
Q

function of hippocampus

A

memory consolidation and part of preoccupation/anticipation stage of addiction

412
Q

function of amygdala

A

implicated in withdrawal/negative affect and the preoccupation/anticipation stages of addiction

413
Q

function of cortex

A

imp for sensory, attentional, and executive functions and implicated in the preoccupation/anticipation stage of addiction

414
Q

what is the role of CB1 receptors

A

found throughout the brain and mediate psychoactive effects of cannabinoids

415
Q

What did CB1 knockout mice show

A
  1. no behavioral effects of delta9-thc admin
  2. did not self administer delta 9-THC
  3. did not show withdrawal syndrome after prolonged delta 9-admin
416
Q

what is the role of CB2 receptors

A

found in the periphery and small areas of brain, and function is to exert some effects on the mesolimbic DA system

417
Q

what are the reinforcing effects of delta 9-THC seen in animals during the binge/intoxication stage

A
  1. conditioned place preference
  2. IV self admin
  3. conditioned place aversion during withdrawal
418
Q

how can reinforcing effects during the binge/intoxication stage of cannabis be blocked

A

use cannabinoid receptor antagonists

419
Q

can you cross substitute cannabis with other drugs

A

no

420
Q

what is released by both delta 9-THC and canabionoids

A

DA is released in N. Acc shell
and endogenous opioid peptides are also released

421
Q

How does DA release between heroin and THC compare

A

Heroin has 175% compared to baseline release of DA in NAcc shell while THC has a 150% release aka heroin releases more DA

422
Q

What is the Neurocircuit drug reward pathway of cannabinoids

A

Interneurons and opioid peptides are activated by cannabinoid receptors and found in the VTA, AMG, and NAcc activate the areas, VTA then release DA to FC, NAcc, and Amygdala regions

423
Q

what is the effect of chronic delta 9-THC admin during the withdrawal/negative affect stage

A

produces tolerance to behavioral, analgesic, motor, and memory effects

424
Q

how long does it take for tolerance to form during chronic use of THC in the withdrawal stage

A

tolerance to behavioral and analgesic effects begin in 3 days
tolerance to memory effects takes weeks

425
Q

how does tolerance to THC occur

A

through down regulation of CB1 receptor densities throughout the brain, but will return to normal after a month of abstinence

426
Q

what is the withdrawal stage of THC characterized by

A

excessive anxiety

427
Q

what factor levels increase during THC withdrawal

A

Corticotropin releasing factor (CRF) levels rise during acute withdrawal which indicates a physiological stress response

428
Q

animal model for THC preoccupation/anticipation stage

A

not well developed

429
Q

what does marijuana use reinstate

A

it reinstates drug-seeking for cocaine, alcohol, nicotine, and heroin

430
Q

what are the 2 appraoches to non-pharmacological treatment

A

behavioral and self help

431
Q

what are the 2 appraoches to non-pharmacological treatment

A

behavioral and self help

432
Q

what are the stages of change

A

Pre-contemplation
Contemplation
Preparation
Action
Maintenance
Relapse or permanent exit

433
Q

what occurs at each stage of change for addiction treatment

A

Pre-contemplation: does not recognize need for cange or does not actively consider it
Contemplation: recognizes problem and considers change
Preparation: getting ready to change
Action: initiating change
Maintenance: adjust to change and practice new skills and behaviors to sustain change
Relapse: may occur and start cycle again

434
Q

what is readiness to change

A

the brief, transient, short lived recognition that change is needed, often follows adverse events
ex: dui, overdose, partner leaves

435
Q

what kind of treatment shows efficacy in treating addiction

A

behavioral treatment

436
Q

what is the premise of motivational interviewing

A

it helps clients identify their own intrinsic reasons to change

437
Q

when is motivational interviewing most effective

A

it is designed to work around denial and resistance, often used in acute settings such as ER but can be useful elsewhere

438
Q

in what conditions is motivational interviewing most effective

A

it is designed to work around denial and resistance, often used in acute settings such as ER but can be useful elsewhere

439
Q

what is an example of motivational interviewing

A

READS
Rolling w/ Resistance (R): work w/ assistance instead of opposing, balance the perspective
Express Empathy (E): identify and understand reasons for resistance w/o judging, create trust and show you are on patient’s side
Avoid Arguing (A): avoid adding additional resistance, feelings are not arguable, confront do not argue
Develop Discrepancy (D): strategy to create dissonance, motivate change by creating discrepancy bw patient behavior and personal goals/values
Support Self Efficacy (S): point out positives, praise patient for what they are doing to make change

440
Q

What is an example of motivational interviewing technique

A

READS

Rolling w/ Resistance (R): work w/ resistance, balance perspective

Express Empathy (E): identify and understand reasons for resistance w/o judging, create trust and show you are on patient’s side

Avoid Arguing (A): avoid additional resistance for pt, feelings are not arguable, confront do not argue

Support Self Efficacy (S): point out positives, praise patient for effort put in to change

441
Q

what is motivational interviewing effective for

A

reducing marijuana use and alcohol intake among heavy drinkers

442
Q

what the limitations of motivational interviewing

A
  • often delivered in single sessions
  • efficacy for treating addiction is poor
443
Q

What is the conclusion for motivational interviewing

A

useful, low cost method but by itself is not a viable strategy for treating addiction

444
Q

what is the premise of contigency managment

A

reward patients for meating treatment goasl (clean drug screens)

445
Q

Ex of contigency management

A

vouchers redeemable for goods and services, contigent on cocaine free urine screens

446
Q

what is contingency management effective for

A

improving retnetion and abstienence in outpatient opioid detoxification
reude smling and illicit substance use among opioid adicts in methadone maintenance
reduce frequency of marijuana use
improve compliance among opioid-dependent pts treated w/ naltrexone maintenance

447
Q

what are the limitations of contingency management

A

unsustainable clinical practice
promotes external attributions of success
effects weaken/disappear after contingency is stopped

448
Q

Conclusion of contingency management

A

probably a short term solution to be used as an adjunct to other approaches

449
Q

premise of cognitive behavior therapy (CBT)

A

high risk behaviors (using) and feelings (craving) can be modified through cognitive strategies and restructuring
- automatic, catastrophic thinking and assumptions must be changed

450
Q

Ex of CBT

A

cravings do not inevitably lead to using, “play the tape all the way through”
A-B-Cs reciprocal feedback emphasis
Affect: craving, anxiety, excitement
Behavior: drug seeking
Cognitions: hopelessness, resignation

451
Q

What is easier to change than feelings or behaviors

A

cognitions

452
Q

what is CBT effective for

A
  • alcohol use disorders
  • outpatient treatment of cocaine dependence
  • treat depressed cocaine users
  • treat benzodiazepine addiction
  • increase effectiveness of certain pharmacotherapies (such as disulfiram)
  • teach skills needed for long term abstinence
  • induce internal attributions of success
453
Q

limitations of CBT

A

requires expert clinicians and is more effective with higher functioning educated clients

454
Q

conclusion of cbt

A

components of cbt such as the changing attributions, teaching cognitive strategies, changing faulty cognitions are seen in all treatments, including self help

455
Q

premise of couples and family therapy

A

treat addiction by altering family/social context within which it is embedded

456
Q

example of couples and family therapy

A

see graph on notes

457
Q

what is couples and family therapy effective for

A

reducing attrition
helps participating family members (improve kids psychosocial outcomes)
more effective than individual therapy for cocaine and opioid dependence

458
Q

what are the limitations of couple and family therapy

A

very diverse set of treatments w/ wide range of efficacy

459
Q

conclusion for couple and family therapy

A

many who are addicted do better when families are included in inpatient, outpatient, aftercare and extended therapy

460
Q

most popular example of self help approach

A

AA

461
Q

Premise of self help

A

recovery from addiction requires help of others and adoption of new way of life
addicts must surrender to their addiction, thereby accepting loss of control
addicts should find sponsor w/ significant clean time to advise them
w/ their sponsor, addicts should work an active 12 step program of recovery, including amends to those they’ve hurt

462
Q

Premise of self help

A

recovery from addiction requires help of others and adoption of new way of life
addicts must surrender to their addiction, thereby accepting loss of control
addicts should find sponsor w/ significant clean time to advise them
w/ their sponsor, addicts should work an active 12 step program of recovery, including amends to those they’ve hurt

463
Q

example of self help

A

traditional 12 steps
see slides for all the steps

464
Q

what is self help effective for

A

encouraging abstinence, encourage social networking, recovering from shame

465
Q

how many people are currently estimated to be abstinent in AA

A

2 million

466
Q

limitations of self help

A

less effective for those with comorbid mental health issues
off-putting to those who do not believe in God and are not made aware of secular gorups
some in scientific community are against AA bc it is rooted in teachings of single religion (christianity) and bc it is difficult to study

467
Q

conclusion of self help

A

collectively, those who attend AA show better outcomes in a dose-response fashion

468
Q

Steps to developing drug treatments

A
  1. serendipity
  2. systematic research with animals, then humans
  3. once approved for human research, drug efficacy is evaluated using clinical trials
469
Q

what are clinical trials

A

any prospective study comparing effects and value of interventions against a control in human beings
include intervention and control groups that are followed forward in time and evaluated/compared for treatment response

470
Q

what is an intervention group

A

patients who get the new drug

471
Q

what is an intervention group

A

patients who get the new drug

472
Q

what is the control group

A

patients who get a placebo or treatment as usual (TAU)

473
Q

what are the 4 phases of clinical trials

A

phase 1: large pharma studies, examine drug tolerance and interactions, pharmacokinetics and max tolerated dose

phase 2: therapeutic efficacy studies, examine diff doses and measures outcome

Phase 3: therapeutic confirmation studies, demonstrate clinical use and safety profile

Phase 4: therapeutic use studies, examine broad and special populations, and identify uncommon adverse events

474
Q

who must approve for an investigational new drug before clinical trials can begin

A

FDA

475
Q

what are the 3 stages of animal model that categorize medication developments

A
  1. binge/intoxication
  2. withdrawal/negative effect
  3. preoccupation/anticipation
476
Q

existing drugs used to treat addiction among humans in the binge/intoxication stage

A

disulfiram
naltrexone
methadone
buprenorphine
naloxone
varenicline
bupropion

477
Q

existing drugs used to treat addiction among humans in the withdrawal/negative effect stage

A

methadone
buprenorphine
nicotine patch
varenicline

478
Q

existing drugs used to treat addiction among humans in the preoccupation/anticipation stage

A

acamprosate
bupropion

479
Q

what is disulfiram used for

A

blocks conversion of acetaldehyde to acetic acid, raising acetaldehyde levels 5 to 10 times the normal amount when metabolizing alcohol alone
effective in preventing alcohol use if taken

480
Q

limitation of disulfiram

A

can reduce one’s confidence to abstain

481
Q

what is naltrexone

A

a mhu, delta, kappa opioid receptor antogonist

482
Q

what does naltrexone treat

A

alcohol and opioid dependence, but is more effect for alcohol (not known why)

483
Q

limitations of naltrexone

A

reduces, but does not eliminate euphoric properties of use
extended release injections, which circumvent adherence problems, cost over 1200 per month

484
Q

limitations of naltrexone

A

reduces, but does not eliminate euphoric properties of use
extended release injections, which circumvent adherence problems, cost over 1200 per month

485
Q

what is methadone

A

a less potent longer acting opioid than heroin

486
Q

what is methadone used for

A

substitution therapy for heroin addiction and for analgesic effects

487
Q

limitations of methadone

A

carries abuse potential itself
longer withdrawal than heroin

488
Q

how many deaths per year due to methadone

A

5000

489
Q

what is buprenorphine

A

a less potent longer lasting opioid than heroin and methadone, it is a partial mhu opioid receptor agonist

490
Q

what is naloxone

A

a mhu opioid and kappa opioid receptor antagonist

491
Q

what is buprenorphine used for

A

maintenance therapy for heroin addiction and for analgesic effects

492
Q

limitations of burprenorphine

A

carries abuse potential itself
risk of respiratory depression and death, especially if paired with benzodiazepines
black market had developed
longer withdrawal than heroin (up to a month)

493
Q

what is buprenorphine called when naloxone is added

A

suboxone

494
Q

what is the suboxone withdrawal timeline

A

first 72 hours: worst physical symptoms
1 week: body aches and pains, insomnia, mood swings
2 weeks: depression
1 month: cravings and depressions end but several symptoms can last several months

495
Q

buprenorphine withdrawal symptoms

A

nausea, vomiting, body aches, insomnia, drowsiness, indigestion, anxiety, depression, irritability, cravings, fever, chills, sweating, headache, difficulty concentrating

496
Q

buprenorphine withdrawal symptoms

A

nausea, vomiting, body aches, insomnia, drowsiness, indigestion, anxiety, depression, irritability, cravings, fever, chills, sweating, headache, difficulty concentrating

497
Q

buprenorphine withdrawal symptoms

A

nausea, vomiting, body aches, insomnia, drowsiness, indigestion, anxiety, depression, irritability, cravings, fever, chills, sweating, headache, difficulty concentrating

498
Q

what is varenicline

A

a partial alpha4beta2 nicotinic acetylcholine (nACH) receptor agonist that releases DA into the NAcc and results in reduction of nicotine cravings

499
Q

limitations of varenicline

A

potential to increase suicide ideation, not allowed by FDA

500
Q

what is bupropion

A

norepinephrine and dopamine reuptake inhibitor (NDRI) antidepressant
will increase DA levels in ventral striatum (VS), reduce cravings
HAS NO PSYCHOACTIVE PROPERTIES

501
Q

what is bupropion used for

A

blocks the high associated w/ nicotine and strong stimulants (cocaine and meth)

502
Q

Limitations of bupropion

A

increases blood pressure and lowers seizure threshold, banned in Europe due to hypertensive effects

503
Q

what is nicotine patch

A

less potent longer acting form of nicotine

504
Q

what are limitations of a nicotine patch

A

heavily marketed
intuitive appeal but unsupervised weaning more often than not is ineffective, regardless of addictive substance
effectiveness is usually assessed by smoking cessation, not addiction to nicotine

505
Q

what is acamprosate

A

a glutamate receptor, NMDA receptor, and Ca channel modulator

506
Q

what is acamprosate used for

A

used to treat alcohol dependence, works best for people motivated to quit drinking

507
Q

limitations of acamprosate

A

FDA labels include warnings about increase in suicidal behavior, major depressive disorder, and kidney failure

508
Q

what are limitations of drug treatments

A
  1. effect sizes are more often small and effectiveness is overstated by drug companies who sell to physicians
  2. rodent models are great for assessing effects of addiction on subcortical functions, but limited for assessing effects of addiction on cortical functions
  3. IMP: neither acquisition of nor recovery from addiction can be understood at any single level of analysis, including neurobiology, we live in an era of biological reductionism
509
Q

what are limitations of drug treatments

A
  1. effect sizes are more often small and effectiveness is overstated by drug companies who sell to physicians
  2. rodent models are great for assessing effects of addiction on subcortical functions, but limited for assessing effects of addiction on cortical functions
  3. IMP: neither acquisition of nor recovery from addiction can be understood at any single level of analysis, including neurobiology, we live in an era of biological reductionism
510
Q

what is an example of the first drug treatment limitation

A

effect sizes for naltrexone and acamprosate in treating alcohol dependence (61 studies)
- treatment and control groups overlap more than they differ

511
Q

Explanation of 3rd drug treatment limitation

A

emotion is missing from many of our models
animal models cannot address the roles that emotion paly in recover from addiction
ex: depression, guilt, shame, self doubt
Culture is missing from many models
ex: culture norms, fallacies, stigma

512
Q

Model of systemic research w/ animals chart

A

novel analogs lead to screening animal studies, with mult models for reference compounds
and
new use of approved drugs lead to human lab studies, with mult. dependent variables for reference compounds
these reference compounds interact with each other

psychology of addiction (3 decks)

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