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
Q

alcohol effect on brain

A

amnesia, permanent memory loss or confusion, brain damage (usually motor areas)

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26
Q

alcohol effect on peripheral nerves

A

legs and optic nerves can be damaged

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27
Q

alcohol impact on GI tract

A

gastritis, peptic ulcer, fatty liver, pancreatitis

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28
Q

alcohol impact on heart and blood vessels

A

heart muscle weakening, heart disease, peripheral blood vessels dilated by alcohol, high BP

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29
Q

alcohol related illnesses

A

liver, heart, gastric, sexual (impotence, disrupted ovaries)

30
Q

FASD (Fetal Alcohol Spectrum Disorder)

A

3rd leading cause of birth defects
Distorted facial features, growth deficiency, learning disabilities…

31
Q

can you die from alcohol withdrawal syndrome, how?

A

yes, huge increase in brain activity → seizure

32
Q

Alcohol withdrawal stage 1

A

6-12 hrs after last drink
Lasts 3-5 days
Psychomotor agitation, anxiety, insomnia, decreased appetite, GI disturbances, increased HR, BP, sweating, tremors)

33
Q

Alcohol withdrawal stage 2

A

within 24hrs after last drink (up to 3 days)
Same as 1 + convulsions, hallucinations, disorientation, panic attacks

34
Q

biopsychosocial model of AUD

A

biological factors: genetics, neurochemistry
psychological factors: personality, stress, vulnerability, novelty seeking
sociocultural factors: group attitudes, accessibility

35
Q

alcoholism psychological factors

A

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
Q

alcoholism neurobiological factors

A

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
Q

alcoholism sociocultural factors

A

Group attitudes: cultures that abstain/restrict with religion → lowest alcoholism rates
Accessibility: social drinking accepted → higher alcoholism rates

38
Q

Smoking with other health-compromising behaviors:

A

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
Q

nicotine

A

highly toxic, colorless, volatile alkaloid; not well absorbed from digestive tract

40
Q

what remains after moisture and nicotine

A

carbon monoxide and tar, contains a lot of carcinogens

41
Q

starting age and education impact on smoking

A

Earlier start - harder to quit, education increases → smoking decreases

42
Q

nesbitt’s paradox

A

more arousal but less emotion

43
Q

behavioral effects of nicotine

A

Mild euphoria, increased energy, heightened arousal, reduced stress/anxiety, reduced appetite

44
Q

nicotine withdrawal

A

craving, irritability, anxiety, difficulty concentrating, memory problems, restlessness, hunger/weight gain
Calming effect in smokers, tension in nonsmokers → effect depends on history

45
Q

why teenagers take up smoking

A

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
Q

chippers

A

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
Q

secondary reinforcers for smoking

A

things in the environment that are related to smoking (coffee, etc.)

48
Q

Dual Reinforcement Model for smoking

A

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
Q

Theory for Drug Abuse 1: Primary Drives

A

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
Q

Theory for Drug Abuse 2: Family Model

A

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
Q

Theory for Drug Abuse 3: Self-Medication

A

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
Q

Theory for Drug Abuse 4: Social Learning Theory

A

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
Q

Theory for Drug Abuse 5: Developmental-Genetic Model

A

Integrative perspective - Devor (1994)
Dynamic interaction of genetic and environmental factors over the course of development

54
Q

Developmental-Genetic Model: primary genetic risk factors

A

history of substance abuse in the family

55
Q

Developmental-Genetic Model: secondary genetic risk factors

A

genetic determinants for comorbid disorders

56
Q

Developmental-Genetic Model: tertiary genetic risk factors

A

other genetic polymorphisms

57
Q

Developmental-Genetic Model: external environmental factors

A

trauma, loss, etc.
lead to epigenetic changes in gene expression and changes in temperament

58
Q

treatment for addiction: AA helps overcome

A

shame and guilt

59
Q

CBT

A

cognitive behavioral therapy used for addiction

60
Q

MI (motivational interviewing)

A

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
Q

OARS approach for MI

A

Open-ended questions, Affirming, Reflective listening, and Summarizing

62
Q

antabuse for alcoholism

A

results in sickness after drinking - effectiveness varies with user’s motivation to quit

63
Q

first hurdle in alcoholism treatment

A

denial

64
Q

enablers of alcoholics

A

family and friends that repair the damage caused by the drinker and making excuses for their behavior, preventing them from experiencing the consequences

65
Q

detoxification treatment for alcoholism

A

Benzodiazepines given to prevent alcohol withdrawal symptoms
usually combined with psychosocial rehabilitation programs

66
Q

nicotine dependence treatment: behavioral interventions

A

anti-smoking appeals in the media, health warnings on packages, high taxes

67
Q

Most common pharmacological intervention for nicotine dependence: nicotine replacement therapy (NRT)

A

nicotine gum and lozenges, transdermal patch, nasal spray and inhalers
needs to gradually decrease

68
Q

other pharmacotherapies for nicotine dependence

A

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
Q

key factors for response to addiction treatment

A

social support and stress management/relapse prevention

70
Q

counseling for nicotine dependence

A

individual or group can be successful