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PSY333 > L3: Substance Abuse > Flashcards

L3: Substance Abuse Flashcards

1
Q

health-compromising behaviors examples

A

substance abuse, overeating, unsafe sex

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2
Q

characteristics of health-compromising behaviors

A

Adolescent vulnerability
Image (peer culture)
Reinforcement
Gradual development
Predicted by conflict and stress

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3
Q

substance use disorders

A

Anything that can stimulate the brain and have psychoactive impacts

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4
Q

behavioral definition of addiction

A

a chronically relapsing disorder maladaptive to user’s life characterized by: (4C’s) - compulsion, loss of control, consequences, craving

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5
Q

4Cs of addiction

A

Compulsion to seek and take drug
Loss of control in limiting intake
Continued use despite consequences
Craving

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6
Q

route of administration

A

The method used to ingest the drug
Effects how addictive it is

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7
Q

route of administration order of how fast

A

Inhalation (5 sec) > injection (15 sec) > oral (30-45 mins) > subcutaneous

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8
Q

faster peak for substance use means…

A

faster high and faster decline, more addictive

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9
Q

“set” in addiction

A

user’s state of mind at time of use

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10
Q

“setting” in addiction

A

physical environment at the time of use (with people/alone, strangers/friends)

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11
Q

cravings

A

an insistent search for an activity (distinctive feature of addictions)
PFC (impulse control) also disrupted
Nucleus accumbens linked to craving

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12
Q

tolerance

A

decrease in effect as an addiction develops
Drug tolerance is learned - can be weakened through extinction (environmental and social cues important)

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13
Q

withdrawal

A

body’ reaction to absence of the drug
Drug can relieve withdrawal (negative reinforcement)

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14
Q

DSM-5 Substance use disorder

A

2-3/11 → mild
4-5/11 → moderate
6+/11 → severe

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15
Q

the mesolimbic dopamine system

A

brain reward system
VTA, NAc, FC

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16
Q

the mesolimbic dopamine system: Nucleus Accumbens

A

depression → less activity → more vulnerable to addiction

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17
Q

the mesolimbic dopamine system: Ventral Tegmental Area

A

reinforcement of reward

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18
Q

genetic influences for addiction

A

Twin studies confirm strong genetic influence on vulnerability
Many addiction-linked genes, each with a small effect

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19
Q

environmental influences for SUD

A

Prenatal environment (stressed mother, use of substance)
Childhood environment
G x E

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20
Q

behavioral predictors of SUD

A

Sons of alcoholics: show less than average intoxication after drinking a moderate amount of alcohol

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21
Q

is alcohol a depressant or stimulant

A

depressant, irritating as well as sedative properties, can have a negative effect on every tissue in the human body

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22
Q

can alcohol cross placenta

A

yes, leads to FASD

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23
Q

how is ethanol produced

A

fermentation of sugars by yeast

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24
Q

BAC

A

blood alcohol concentration
0.45 - coma, lethal for 50% of population

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25
alcohol effect on brain
amnesia, permanent memory loss or confusion, brain damage (usually motor areas)
26
alcohol effect on peripheral nerves
legs and optic nerves can be damaged
27
alcohol impact on GI tract
gastritis, peptic ulcer, fatty liver, pancreatitis
28
alcohol impact on heart and blood vessels
heart muscle weakening, heart disease, peripheral blood vessels dilated by alcohol, high BP
29
alcohol related illnesses
liver, heart, gastric, sexual (impotence, disrupted ovaries)
30
FASD (Fetal Alcohol Spectrum Disorder)
3rd leading cause of birth defects Distorted facial features, growth deficiency, learning disabilities…
31
can you die from alcohol withdrawal syndrome, how?
yes, huge increase in brain activity → seizure
32
Alcohol withdrawal stage 1
6-12 hrs after last drink Lasts 3-5 days Psychomotor agitation, anxiety, insomnia, decreased appetite, GI disturbances, increased HR, BP, sweating, tremors)
33
Alcohol withdrawal stage 2
within 24hrs after last drink (up to 3 days) Same as 1 + convulsions, hallucinations, disorientation, panic attacks
34
biopsychosocial model of AUD
biological factors: genetics, neurochemistry psychological factors: personality, stress, vulnerability, novelty seeking sociocultural factors: group attitudes, accessibility
35
alcoholism psychological factors
Response to stress: alcohol - reinforcing effects - chronic stress → increased consumption Novelty seeking and risk taking: high → greater activation of mesolimbic DA pathway Anxiety: increased vulnerability, family history of alcoholism → greater cortisol response
36
alcoholism neurobiological factors
Genetics: close relatives of alcoholics 4-8x greater risk for alcoholism Neurochemistry: an acute low sensitivity to alcoholism is a risk factor for alcoholism
37
alcoholism sociocultural factors
Group attitudes: cultures that abstain/restrict with religion → lowest alcoholism rates Accessibility: social drinking accepted → higher alcoholism rates
38
Smoking with other health-compromising behaviors:
Weight: nicotine stimulates release of fatty acids Stress: nicotine increases HR and BP Exercise: less physical activity in smokers Cancer: 50% increased cancer risk Mental health: smoking considered cause for depression
39
nicotine
highly toxic, colorless, volatile alkaloid; not well absorbed from digestive tract
40
what remains after moisture and nicotine
carbon monoxide and tar, contains a lot of carcinogens
41
starting age and education impact on smoking
Earlier start - harder to quit, education increases → smoking decreases
42
nesbitt's paradox
more arousal but less emotion
43
behavioral effects of nicotine
Mild euphoria, increased energy, heightened arousal, reduced stress/anxiety, reduced appetite
44
nicotine withdrawal
craving, irritability, anxiety, difficulty concentrating, memory problems, restlessness, hunger/weight gain Calming effect in smokers, tension in nonsmokers → effect depends on history
45
why teenagers take up smoking
Feelings of independence and maturity Self-image, social acceptance Counteracting stress or boredom (nicotine is a CNS stimulant) Curiosity Young people emphasize positive, deny negative aspects
46
chippers
long-term smokers who smoke <5 cigs per day and don't become dependent but develop tolerance → suggests dependence and tolerance produced by different processes
47
secondary reinforcers for smoking
things in the environment that are related to smoking (coffee, etc.)
48
Dual Reinforcement Model for smoking
Three processes, dual reinforcement Primary reinforcement Non-nicotine related stimuli acquire secondary reinforcing properties through classical conditioning “Reinforcement enhancing” properties of nicotine - making the effect of sensory cue stronger
49
Theory for Drug Abuse 1: Primary Drives
4 primary drives: hunger, thirst, sex, desire to alter consciousness Users have positive beliefs that drugs open avenues to unconscious issues, help user to resolve conflicts, give new awareness or perception Addiction: unrealistic/neurotic beliefs Our innate drive to alter consciousness: boredom, impulsivity and disinhibition: drug use involves taking risks in using
50
Theory for Drug Abuse 2: Family Model
Addiction affects all family members - environment and genetic Modeling for children very poor (parents with addiction) - very ineffective parents Poor parenting → poor sense of self / self concept (most frequently generalized risk for drug problems) → leads to under-achievement, shyness, aggressive and antisocial behavior
51
Theory for Drug Abuse 3: Self-Medication
Drug use is not random, purposeful attempt to: assuage painful feelings, manage psychological problems, manage personality traits and disorders Crucial for therapists to explore this motive Dopamine & CRH linked increased stress → increased CRF → less dopamine signaling → cravings CRF/CRH gets up-regulated by dopamine neurons
52
Theory for Drug Abuse 4: Social Learning Theory
social learning aspect of drug use - socially acquired, learned behabior pattern maintained by: Antecedent cues (cc, expectancies) Consequent reinforcers (reward, tension reduction) Cognitive factors Modeling influences Interaction of behavioral and genetic influences
53
Theory for Drug Abuse 5: Developmental-Genetic Model
Integrative perspective - Devor (1994) Dynamic interaction of genetic and environmental factors over the course of development
54
Developmental-Genetic Model: primary genetic risk factors
history of substance abuse in the family
55
Developmental-Genetic Model: secondary genetic risk factors
genetic determinants for comorbid disorders
56
Developmental-Genetic Model: tertiary genetic risk factors
other genetic polymorphisms
57
Developmental-Genetic Model: external environmental factors
trauma, loss, etc. lead to epigenetic changes in gene expression and changes in temperament
58
treatment for addiction: AA helps overcome
shame and guilt
59
CBT
cognitive behavioral therapy used for addiction
60
MI (motivational interviewing)
Uses brief, individual counseling to help patients explore their motivation to change and their ambivalence about change Patient-centered: focuses on eliciting and understanding the patient's view choice to change is voluntary: patient is more committed to recovery if they choose, change is the patient's responsibility OARS approach
61
OARS approach for MI
Open-ended questions, Affirming, Reflective listening, and Summarizing
62
antabuse for alcoholism
results in sickness after drinking - effectiveness varies with user’s motivation to quit
63
first hurdle in alcoholism treatment
denial
64
enablers of alcoholics
family and friends that repair the damage caused by the drinker and making excuses for their behavior, preventing them from experiencing the consequences
65
detoxification treatment for alcoholism
Benzodiazepines given to prevent alcohol withdrawal symptoms usually combined with psychosocial rehabilitation programs
66
nicotine dependence treatment: behavioral interventions
anti-smoking appeals in the media, health warnings on packages, high taxes
67
Most common pharmacological intervention for nicotine dependence: nicotine replacement therapy (NRT)
nicotine gum and lozenges, transdermal patch, nasal spray and inhalers needs to gradually decrease
68
other pharmacotherapies for nicotine dependence
Bupropion (SSRI) - noncompetitive antagonist at brain nicotinic receptors Varenicline- partial agonist at high-affinity alpha4beta2 nicotinic receptors expressed in VTA and other brain areas → reduces nicotine cravings High variability in people’s response to treatment
69
key factors for response to addiction treatment
social support and stress management/relapse prevention
70
counseling for nicotine dependence
individual or group can be successful

PSY333 (5 decks)

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