Final Exam Flashcards

Topics: Substance Use Disorder, Psychosis and Schizophrenia, Childhood Disorders, Personality Disorders

1
Q

What can excessive use of substance lead to?

A

Dangerous behaviours
Continued use despite persistent problem

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2
Q

What is substance dependence?

A

Substance abuse resulting in tolerance and/or withdrawal

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3
Q

Define tolerance

A

Physiological need for increased substance for the same effects

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4
Q

Define withdrawal

A

Physical symptoms that result from stopping use (e.g., nausea, sweating, tension, headaches, tremors)

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5
Q

What are the stages of substance abuse?

A

Positive attitude leads to experimentation which leads to regular use then heavy use which leads to physical dependence/abuse

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6
Q

How does the DSM-5 define substance use/alcohol use disorder?

A

Problematic pattern of ETOH use leads to impairment

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7
Q

How does the DSM-5 diagnose substance use/alcohol use disorder?

A

2+ symptoms within 12 months
More ETOH than planned
Desire to control use
Time spent in ETOH pursuits
Craving
Use leading to interpersonal problems
Use despite above, interpersonal problems
Activities given up because of use
Use in physically dangerous situations
Use despite physical/psychological problems to to ETOH
Tolerance
Withdrawal

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8
Q

What does the WHO describe as harmful alcohol use?

A

Heavy episodic drinking
≥ 6 drinks
≥ 1x/month

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9
Q

What is the prevalence of harmful drinking patterns?

A

30% Canadian undergraduates vs 17% of the population
People who use a lot of alcohol in university does not mean they will continue to do so in adulthood

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10
Q

What is BAC and what affects it?

A

Amount ingested in a particular period of time
Food eaten, sex, age, medications

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11
Q

What are some short-term effects of heavy alcohol use?

A

Stimulating, then depressant action
Interference with complex thought and motor coordination
Interacts with several neural systems
Effects strongly tied to expectations

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12
Q

How does heavy alcohol use interact with neural systems in short-term use?

A

Stimulates GABA receptors (tension and motor coordination goes down)
Increases 5-HT and DA (motivation for pleasure/craving, addictive)
Inhibits glutamate receptors (cognitive effects)

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13
Q

Biopsychosocial model of Substance Use: Etiology: Bio

A

Genes
Alcohol risk personality
Ability to tolerate/metabolize alcohol
Motivation for substance use (decrease tension vs increase pleasure)

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14
Q

Biopsychosocial model of Substance Use: Etiology: Psycho

A

Stress, tension reduction, (negative) reinforcement
Expectations of social success
Perceived benefits outweigh the costs
Sensation (novelty) seeking
Drinking motives

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15
Q

What are the drinking motives?

A

Positive Internal: Enhancement (highest risk)
Sensation seeking
I am feeling great
Negative Internal: Coping (highest risk)
Stress, tension reduction, reinforcement
How do I deal with this?
Positive External: Social
Expectations of social success
I want to enjoy people more
Negative External: Conformity
Perceived benefits outweigh costs
I don’t want to be judged so I am going to do it to fit in
Most common at highschool and university age

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16
Q

Biopsychosocial model of Substance Use: Etiology: Social

A

Culture
What you see is what you do
Attitudes/use patterns
Tradition of aggression
Religion
Family
Parent use/guidance
Family/marital problems
Older siblings
Exposure and learning
Availability of substance
Peer/social influences
Media

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17
Q

Biopsychosocial model of Substance Use: Treatment: Bio

A

Medication: block desire to drink (operant conditioning)
e.g., Antabuse, naltrexone
Lower side effects of withdrawal (e.g., valium)
Transtheoretical Model (TTM)

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18
Q

What are the 6 stages of change in the transtheoretical model?

A

Pre-contemplation: no mention of changing behavior
Contemplation: start thinking about change
Preparation: intend to take action
Action: start making changes and developing new behavior
Maintenance: sustaining changes and developing new behavior
Relapse: return to old ways (common)

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19
Q

Biopsychosocial model of Substance Use: Treatment: Psycho

A

CBT and Behavioural
Aversion conditioning
Skills training
Self-control
Motivation enhancement
Controlled drinking vs abstinence

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20
Q

Biopsychosocial model of Substance Use: Treatment: Social

A

Group therapy
Forced to confront problem
Alcoholics Anonymous (AA)
Environmental intervention (e.g., halfway houses)

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21
Q

What is the treatment efficacy for substance use?

A

Wide range
Depends on everity of substance abuse (duration, amount of tolerance), and type of treatment
All treatment types are equally effective

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22
Q

List drugs that are associated with addiction

A

Narcotics
Sedatives
Stimulants
Includes ADHD meds
Anti-anxiety drugs
Pain medication
Hallucinogens

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23
Q

What are some short term biological effects of opioids?

A

Decreased physical pain
Relaxation
Decreased anxiety
Euphoria

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24
Q

What are some long term biological effects of opioids?

A

Physiological craving
Withdrawal symptoms
Physical deterioration
Immune system, organ damage
Consequences of poor health, dangerous behavior

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25
Explain the DA theory of addiction
Addiction = dysfunction of DA reward pathway Drugs lead to heavy dopamine dump which leads to no dopamine for normal activities All addiction comes from motivation for pleasure
26
Explain reward deficiency syndrome
Addiction = genetic deviation in reward pathway Less satisfaction from natural rewards are more likely to become addicted once exposed
27
What is comorbidity of opioid abuse?
70% other psychological disorders 50% other substance abuse 36% history of trauma Depression Anxiety Antisocial personality disorder
28
What are different types of stimulants?
ADHD meds Cocaine Amphetamines (meth) Caffeine Nicotine
29
What are symptoms of amphetamine abuse?
Intense fatigue Psychological and physically addictive Brain damage, amphetamine psychosis Suicde, homicide, violence Highly activating
30
What are different types of hallucinogens?
LSD Mescaline Psilocybin MDMA (ecstasy, molly)
31
What are some short-term effects of MDMA use?
Rush of pleasure Sense of wellbeing Depressed mood (for days after use)
32
What are some long-term effects of MDMA use?
Brain damage (frontal and temporal lobes) Memory deficits Hallucinations
33
What are some short-term effects of cannabis use?
Relaxation, sense of wellbeing, euphoria ` Hallucination Increased perceptual acuity
34
What are some therapeutic effects of cannabis use?
Decrease nausea and pain Increase appetite and sleep
35
What are some long-term effects of cannabis use?
Psychosis/schizophrenia (if have the diathesis) Memory loss
36
What is psychosis?
Significant loss of contact with reality Hallmark of schizophrenia Delusions Hallucinations Disorganized speech and/or behaviour
37
What is schizophrenia?
Disorder characterized by major disturbances in thought, emotion, and behaviour Disordered thinking Flat emotions or in appropriate reactions Highly unusual motor activity
38
What are the hallmark symptoms of schizophrenia?
Delusions Hallucinations Disorganized speech and/or behaviour *have to have at least 2
39
What's the difference between positive and negative schizophrenia symptoms?
Positive: Excess or distortion in typical range of behaviour and perception (more, added on) Negative: Deficit of typically present behaviours, reduced expressive behaviour, reduced motivation/pleasure (taken away) *Usually get more negative symptoms the older you get/farther along in diagnosis
40
Describe delusions
Erroneous (incorrect) beliefs Highly unusual thought content Firmly held belief despite evidence Examples: Thought insertion Broadcast thoughts Thought withdrawal Made feelings
41
Describe hallucinations
Sensory experience (any sensory modality) Seems real despite no external stimulus Examples: Voices talking about person Unusual images Sensations of things crawling on skin
42
Describe disorganized speech/behaviour
Speech: Context - grammatically correct form, but does not make sense (loose associations) Form - grammatically incorrect (clang association) Behavior: Catatonia Unusual complex movements Waxy flexibility (immobile posture)
43
What were the positive and negative symptoms from the in class case study?
Positive symptoms: Delusions (grandiose, persecutory) Ideas of reference Disorganized thinking Negative symptoms: Blunted affect Asociality Anhedonia
44
What is the typical age of onset/life expectancy for schizophrenia?
18-30 Shorter life expectancy Increased risk for suicide 20-40% attempt suicide 105 complete suicide
45
What are the 3 phases of schizophrenia?
1. Prodromal: Obvious deterioration in role functioning Personality change (schizotypal PD) 2. Active: Psychosis 3. Residual: Improvement in positive symptoms Continued negative symptoms
46
What are some risk factors/affecting factors towards schizophrenia?
Conceived with a dad over 50 Parents in dry cleaning business Severity: males > females Age of onset (younger = more severe) Premorbid functioning Cognitive ability Access to treatment (3-5 years)
47
Biopsychosocial model of Schizophrenia: Etiology: Bio
Most important ~ 80% Environment affects expression of symptoms Genetic markers Brain structure and function Original vs revised DA hypothesis Dopaminergic pathways Glutamate hypothesis Neurodevelopment hypothesis Later environment stressor Multiple HIT model
48
Explain genetic markers in regards to the development of schizophrenia
Identical twins have a 50% risk of both having it which means there is an environmental piece to it Can be a biological environment Behavioral markers Smooth-pursuit eye movement Tracking deficits People with SCZ and relatives
49
Explain brain structure and function in regards to the development of schizophrenia
Pyramid Decreased brain volume Enlarged ventricles Reduced volume of the thalamus Abnormalities in the temporal lobe areas Hypofrontality Temporal cortex, language areas
50
Describe the stages in the brain structure and function pyramid from bottom to top
Disorganized cytoarchitecture: Cells line up with each other but with schizophrenia they tend to not have as uniformed of a structure Disrupted brain development in adolescence: Things are going wonky Loss of gray matter: Cell bodies are dying, neurodegeneration Loss of white body: Fewer connections Attentional and working memory deficits: As the cells start deteriorating it is much harder for them to get their jobs done Impaired social cognition: Not understanding what is happening socially
51
What effect does reduced volume of the thalamus have?
Gateway for processing all incoming sensory info Call center director Relays information less effectively, can't understand Likely due to disorganized (difficulty with) perception and thoughts
52
What effect does hypofrontality have ?
Reduced neural connectivity Excessive synaptic pruning (use it or lose it) Major DA pathway (PFC inhibits DA in limbic system) Working memory Representing sensory info to guide behavior Disorganized behavior and speech, thought disorder
53
What effect does the temporal cortex have?
Broca’s area: speech production Wernicke’s area: language comprehension Broca's area is active during an auditory hallucination since it is producing the voice
54
Explain original DA hypothesis in regards to the development of schizophrenia
Schizophrenia ↔ DA excess Drugs ↑ DA Result in schizophrenia like behavior E.g., amphetamine, L-Dopa for Parkinson’s disease Drugs ↓ DA Reduce schizophrenia like behavior E.g., neuroleptics Do not treat negative symptoms *Drugs that increase DA increase schizophrenia and drugs that decrease DA decrease schizophrenia
55
Explain revised DA hypothesis in regards to the development of schizophrenia
Negative symptoms ↓ DA in cortical regions Underactivity at D1 receptors Positive symptoms ↑ in DA subcortical regions Pre synaptic Too much produced and released into synapse → overactivity at D2 receptors Post synaptic Some findings of too many D2 receptors
56
What's the primary difference between the original and revised DA hypotheses?
The original believes the too much DA increases schizophrenia where too little decreases it but only in regards to positive symptoms The revised accounts for both positive and negative symptoms
57
Explain dopaminergic pathways in regards to the development of schizophrenia
Mesolimbic pathways (positive symptoms) Nucleus accumbens (NA) Ventral tegmental area (VTA) Where a ton of the DA is produced and it is sending it to the NA Excess activity here in positive symptoms Mesolimbic pathways (negative symptoms) The VTA sends DA to the frontal cortex and when there is more DA there it the limbic system can’t tell it to stop Both pathways are reversed
58
Explain glutamate hypothesis in regards to the development of schizophrenia
↓ Glutamate PCP and ketamine → schizophrenia like behavior Underactivity at NMDA receptors DA receptors also inhibit glutamate activity so too ↑ DA activity leads to too ↓ glutamate activity which increases schizophrenia symptoms Glutamate plays a role in learning, memory, neural processing Explains problems with attention, working memory, excessive function
59
Explain neurodevelopment hypothesis in regards to the development of schizophrenia
Silent lesion Neuromotor, cognitive and behavioral abnormalities: Smaller head circumference at birth Slower to reach developmental milestones Higher rates of left-handedness Congenital minor physical and craniofacial anomalies: Velocardiofacial syndrome Gestational and perinatal exposures: Viral infection Early nutritional deficiencies and maternal stress Pregnancy and birth complications Maternal starvation (1st trimester Hypoxia (less oxygen) Maternal viral infections
60
Explain the silent lesion hypothesis
Abnormalities lie dormant until normal developmental processes expose problems Brain makes up for the loss and in adulthood you realize you are missing a piece Related to prefrontal cortex development Problems in the neural system are present way before you actually see the symptoms
61
Explain later environmental stressor in regards to the development of schizophrenia
People with schizophrenia are 2x as likely as the general population to smoke cannabis An extensive study found if people consumed a lot of weed at the age of 14 that increased risk later in life Could be caused from cell death due to weed Diathesis-stress COMT gene Breaks down proteins
62
What relationship do COMT alleles have to risk of schizophrenia and weed usage?
Met → high DA There is no difference in schizophrenia development if you use weed in adolescents with 2 met genes Val → lower DA People with one met and one val gene have a increased risk of schizophrenia if they consume weed and a very low risk if they do not
63
Biopsychosocial model of Schizophrenia: Etiology: Psychosocial
Multiple HIT model Psychological stress Increased relapse rate Migration: 2nd generation migrants have double the risk than 1st generation migrants Urbanization Lowest SES Sociogenic hypothesis Social selection theory (downward drift) From developing vs developed countries: 3.3 From areas with predominantly black population: 4.8 Family Outdated - schizophrenogenic mother Current - expressed emotion - relapse much more Criticism Hostility Emotional over-involvement
64
Explain multiple HIT model in regards to the development of schizophrenia
Brain development from conception to early adulthood How are cells are forming Anatomical and functional disruption in neuronal connectivity and communication Cognitive dysmetria (dysregulation of information processing in the brain) Impairments in higher-order cognitive processes (e.g., attention, memory, language, emotion) Symptoms of schizophrenia (e.g., hallucinations, delusions, negative symptoms, disorganized speech)
65
Biopsychosocial model of Schizophrenia: Treatment: Response
33% continue to have symptoms and problems even after treatment 12% need long term institutional care 38% function well 15-25 years later (can manage symptoms) 10-15% fully recover Symptoms remit > 2 years, good social functioning No cure
66
Biopsychosocial model of Schizophrenia: Treatment: Bio
Historical: Prefrontal lobotomy Institutionalization Insulin coma ECT Current: Antipsychotic medication Mechanism: block DA receptors 1st generation (more complications/side effects): Conventional antipsychotics 2nd generation: Atypical antipsychotics *Need the meds
67
What is the range of response for schizophrenia treatment?
1+ psychotic episodes: Episode has relatively rapid return to normal functioning Good prospects for recovery Years of recurrent psychotic relapses: Periods of remission Varying degrees of residual impairment Failure to respond
68
Biopsychosocial model of Schizophrenia: Treatment: Psycho
CBT: Create space for consideration that what they are experiencing may not be true Reframe positive symptoms Identify triggers for symptoms Improve social skills Reduce relapse (not helpful for negative symptoms) Cognitive remediation: Improve cognitive functioning Other individual: CBT + life skills
69
Biopsychosocial model of Schizophrenia: Treatment: Social
Family therapy Communication skills Decreased expressed emotion Case management Social and living skills training Vocational rehabilitation
70
What is developmental psychopathology?
How childhood disorders are discussed Some sort of maladaptation (biological, psychological, and/or socially) happening over the course of typical development Origins and course of individual maladaptation in context of typical growth process
71
What is the epidemiology of childhood disorders
~15% Anxiety is more common Likely underestimate since often don't line up with diagnostic criteria Half (most) have more than 1 disorders 25% (very few) get treatment Treatments have long wait times
72
What is the median onset ages for different childhood disorders?
6 - anxiety 11 - behavioural 13 - mood 15 - substance use
73
What are the most common mental health problems in children?
Anxiety, irrational fears Depression Aggression, rule violation *Attention deficit/hyperactivity disorder (ADHD)
74
What are common questions regarding childhood disorders?
How is functioning different? How might differences influence disorders thinking and behavior? How are children more vulnerable to developing psychopathology?
75
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Bio
Brain: Incomplete development of the PFC (the brakes) leaves amygdala (the gas) unchecked Difficulty stopping when impulse takes control Aggression, fear, lack of impulse control Leaves the functioning to make one more likely to behave in certain ways Ability to control plan and stop ourselves Real loud in childhood Engage in unhealthy behavioral habits Synaptic pruning : What you practice is what you keep Automatic cognitions → strong connections Childhood views shape your adulthood views
76
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Psycho
Lack of experience: Do not have the resources to rely on to change attributions Theory of mind: Not knowing how everyone sees things What I think is how everyone thinks Self = cause of others behaviors: Believing oneself is the center of everything Could be related to narcissism Simplistic view of self/world: Black and white Not seeing the contexts of things Immediate threats seem very important: Threat is life ending
77
Biopsychosocial model of Childhood Disorders: Etiology/presentation: Social
Relationships Dependence on others For survival Lack of control over environment Level of stress in environment Maltreatment 235000 reported investigations (2003) ½ substantiated Agreed that it happened Most abuse does not have evidence Increase odds of developing psychological disorder Causal Do not have to have the gene to develop
78
Biopsychosocial model of Childhood Disorders: Treatment
Evidence based treatments CBT IPT Family systems Other common treatments Psychodynamic therapy Play therapy Standard More value in using as an assessment tool vs treatment
79
What are issues for treatment in childhood disorders?
Child can’t seek treatment Adults can get kids into treatment Early intervention Kids don’t know the help that they need Need to treat parents/family Family and parents can have a lot of influence on how treatment goes Can continue lessons in the home Counteracting treatments Not changing behavior Shift the way the parent acts can shape the environment the child is in
80
How are anxiety and depression related in childhood?
Internalizing disorders High comorbidity: Anxiety often develops first, which then causes depression to emerge As you start to avoid things, there is less meaning in life which often leads to depression Environmental triggers Anxiety: threat, risk Depression: loss, high and chronic stress Learned helplessness
81
What is the epidemiology of anxiety and depression in childhood?
~6% of children (ages 5-17) High comorbidity among anxiety disorders Girl > boys (2:1) Boys are more likely to display behavioral/disruptive behaviors Genes Temperament: behavioral inhibition Tendency to avoid novel and unfamiliar situations (e.g., toys, people) Difference in autonomic (sympathetic nervous system) reactivity More easily conditioned to anxiety
82
Biopsychosocial model of Childhood Anxiety: Etiology: Social
Early relationships Higher anxiety and lower adaptive coping skills Parents : anxiety sensitizers vs suppressors E.g., a child wakes up Parent helicopters and treat them like a fragile kid Parent who teaches them skills to cope with the feelings Environment Unusual level of stress, threat, exposure E.g., dangerous neighborhood, war/bombings, maltreatment
83
Biopsychosocial model of Childhood: Treatment: Bio
Bio SSRIs (+CBT)
84
Biopsychosocial model of Childhood Anxiety: Treatment: Psychosocial
Behavioral therapy Child CBT + parent/family treatment 2x effective as child alone E.g., parent-child interaction therapy CBT skill Problem solving, finding a whole bunch of solutions Identify numerous solutions Adult supports child to solve herself
85
What are the problem solving STEPS?
Situation Think of the possible solutions Evaluate the solutions Pick one See if it worked
86
What is the epidemiology of childhood depression?
Age: Preschool (1%) Grade school (2-4%) Adolescence (8-15%) Sex: Childhood - approximately equal Adolescence - girls > boys = 2:1 Course: Average MDE 7-9 months Average 2 years, 90% recovered Recurrent
87
Biopsychosocial model of Childhood Depression: Etiology: Psycho
Same as adults Perfectionism Super rewarded to be good Stifles people because they have a fear of failure
88
Biopsychosocial model of Childhood Depression: Etiology: Social
Depressed parent 2-3x more depression 15% to 45% lifetime risk Critical parent Particularly important More critical more hopeless Others same as for adults
89
Biopsychosocial model of Childhood Depression: Presentation: Psycho
Formal operations Abstract, complex thoughts Egocentrism Cognitive inflexibility Metacognition How I am as a person Beliefs about themselves Children: Somatic complaints, psychomotor retardation Physioal Slower movement, speech, thinking Greater overlap with anxiety Adolescence: Hopelessness, hypersomnia, weight changes Depression and suicide: Ages 12-17: second leading cause of death Ages 5-14: fifth leading cause of death
90
Biopsychosocial model of Childhood Depression: Treatment: Bio
SSRIs Can increase suicide risk in youth Side effects Family history
91
Biopsychosocial model of Childhood Depression: Treatment: Psycho
CBT Behavioral activation Increase mastery
92
Biopsychosocial model of Childhood Depression: Treatment: Social
Interpersonal therapy Parent child relationship Getting them to react differently Ways to connect with people
93
What is the epidemiology of ADHD in childhood?
1-7% of population Increasing in past 5 years 4:1 boys : girls 60% persistent (ADHD as adults) Mild hyperactivity symptoms that may grow out of
94
What is the difference in how ADHD presents itself between girls and boys?
Girls tend to be compliant Boys tend to be problematic ADHD usually leads to other disorders
95
What are the childhood ADHD subtypes in the DSM?
Inattentive Hyperactive-impulsive Combination
96
What are the childhood ADHD DSM symptoms?
Hyperactivity Forgetfulness Poor impulse control Distractibility Run by a motor
97
What are Russell Barkley's reconsidered symptoms of ADHD?
ADHD is a disorder of: Self regulation Executive function Presentation: Issue is performance (not skill) Low response inhibition Time blindness Periods of hyper focus (DA) Difficulty with transitions
98
What is the nature of ADHD?
Chronic neurological “disorder” Variety of treatments to manage symptoms Also benefits of ADHD Calmer feeling during crisis
99
Biopsychosocial model of Childhood ADHD: Etiology: Bio
Genes >30% have family members with ADHD NTs Low DA Much more likelihood of getting into trouble (sensation seeker) Pre-perinatal stress Cocaine use Birth complications Really its genetic
100
Biopsychosocial model of Childhood ADHD: Etiology: Psychosocial
Not much Family adversity and disorganization (weak correlation)
101
Biopsychosocial model of Childhood ADHD: Presentation: Bio
Hyperactivity-impulse control: Poor connections between amygdala and PFC (impulse control) Underactive Behavioural Inhibition System (BIS) Under arousal theory Inconsistent attention: Striatum + frontal lobes + posterior periventricular region (controlling and directing attention) Interconnected with sensory cortices Act as a gate Important information registers Irrelevant noise filtered out They are underactive so there is attention everywhere, very open to stimuli Sensory cortices flooded with incoming messages which lead to high blood flow
102
Biopsychosocial model of Childhood ADHD: Treatment: Bio
Medication is most effective in managing symptoms Methylphenidate (ritalin, concerta): Redistributes blood flow in brain Increases function of striatum, frontal lobes, and posterior periventricular region Increase availability of DA Increased focus, inhibitory control, regulation of extraneous motor behaviour (e.g., fidgeting) Reduce symptoms of in 60-80% of school age children
103
Biopsychosocial model of Childhood ADHD: Treatment: Psychosocial
Cognitive: Externalize executive functioning (schedule, reminders) Behavioural: Reward systems, frequent breaks Environmental adjustment and accommodation necessary Behavioral parent (and teacher) training Behavioural programs emphasizing: Time-limited attention, emotion regulation, and rule following
104
What is conduct disorder?
Baby antisocial personality disorder Violation of rules and disregard for basic rights of others Aggression to people and animals Destruction of property Deceitfulness or theft Serious violation of rules Lack of remorse
105
What is the epidemiology of conduct disorder?
Comorbidity ADHD (likely based on emotion dysregulation or arousal seeking) Substance use Anxiety and depression (common) Prevalence (ages 4-16) 8% of boys 3% of girls Course Childhood onset: boys > girls Life course persistent (sticking around, traits) Adolescent onset: boys = girls Adolescence limites (maturity gap)
106
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Bio
Genes: 50% heritability (antisocial behavior) MAOA gene - the warrior gene Breaks down 5-HT, SE, DA when you do not have this gene you tend to be more aggressive Gene x environment correlations: Passive rGEs (parent created) that is more likely for the kid to behave in certain ways Active rGEs (kid created) they are going to seek out certain environments Callous-unemotional style Executive dysfunction Poor problem solving and planning that leads to poorly thought out, maladaptive reactions to distress and conflict
107
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Psycho
High emotional reactivity Sensation seeking Chronic underarousal which leads to stimulus seeking Empathy and perspective taking deficits Hostile attributional bias
107
Biopsychosocial model of Childhood Conduct Disorder: Etiology: Social
Modeling Inter parent discord Overly harsh discipline (worse things tend to get) Inconsistent contingencies (e.g., based on mood) in how people parent do not make sense to the kid Low involvement, weak bonding , poor monitoring Differential attending/rewarding (coercive process)
108
Biopsychosocial model of Childhood Conduct Disorder: Treatment: Bio
Antipsychotics Stimulant medication
109
Biopsychosocial model of Childhood Conduct Disorder: Treatment: Social
Harsh discipline increased delinquency Family intervention (fundamental piece) Parent management training Multisystemic treatment (MST) Involves child, family, school, peer group Often used instead of incarceration
110
How does parent management training work?
Relationship-building (1:1 time) Attending (and active ignoring things like swearing) Effective instructions Praise and reward system (shaping) Consequences (privilege removal, removing attention)
111
What is multisystemic treatment (MST)?
Aspects of CBT, case management, family systems treatment Fit between problem and systemic context Encourage responsible behavior in family members Require daily/weekly effort from family
112
What is the pattern of behaviour of personality disorders?
*In DSM-5, must be over 18 Chronic (throughout life): Early onset (childhood or adolescence) Stable and longstanding Pervasive across life areas Identity (central to the person's identity): Inflexible Deviate from cultural expectations Clinical distress or impaired functioning: Cognition (thinking) Affect (emotions) Interpersonal functioning Impulse control
112
Explain cluster A personality disorders
Paranoid: suspicious, mistrustful, expect attacks Schizoid: inability to form attachments (and no interest) Schizotypal: strange (often magical) thinking; perception and speech interferences with communication Overall characteristics: odd, eccentric, avoid social contact
113
Explain cluster B personality type
Antisocial: disregard and violation of others rights, serious violation of social norms; deceitful, manipulative; conduct disorder in childhood Histrionic: dramatic, (mainly sexual) attention seeking (temper outbursts if cannot achieve); emphasis on attractiveness More common in women Borderline: impulsive; extreme emotional reactivity; drastic mood shifts; self-injury/suicicde attempts Narcissistic: grandiosity; attention seeking; lack of empathy; self promoting Overall characteristics: dramatic, erratic, punitive, hostile
114
Explain cluster C personality type
Avoidant: shy, hypersensitive to rejection, extreme social insecurity, self conscious and self critical Dependent: extreme discomfort being alone; suppress own needs to keep relationships; indecision Obsessive-compulsive: excessive concern with order, rules, and trivial details; rigidity; perfectionism; lack of warmth Overall characteristics: anxious, fearfulness
115
What is the prevalence of personality disorders?
10-12% meet criteria for more than 1 personality disorder Cluster A: ~4 Cluster B: ~4% Cluster C: ~7%
116
What are some difficulties in studying personality disorders?
Criteria is not sharply defined Categories are not mutually exclusive Personality characteristics are dimensional (what's the cutoff) Lack of agreement on assessment measures
117
What are the categories in the 5 factor model?
Openness: openness to experience (feelings, ideas, actions, ideas) Conscientiousness: order, duty, achievement, self-discipline Extraversion: warmth, excitement seeking, positive emotions Agreeableness: trust, compliance, altruism Neuroticism; anxiety, anger-hostility, depression, self consciousness
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What makes personality disorders difficult to treat?
Varied goals People aren’t open to treatment Clients belief in need to change Client response Relationships are hard to develop Cilnican motivation and patience 37% (alot) drop out early, since there is not immediate results
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What are the main characteristics of borderline personality disorder?
Impulsivity: Impulsive reaction to dysphoria/distress leads to self-injury, substance abuses, etc. Affective instability: Rapid mood changes (often mistaken for bipolar disorder)
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What are the differences between BPD and bipolar?
BPD: Dysthymic and emptiness Anger and anxiety Highly responsive to environmental changes Minutes to hours (based on what's happening) Bipolar disorder Neutral Depends on phases in cycle Weeks to months
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What are the domains and symptoms of dysregulation?
Emotional: High emotional reactivity Unstable mood (depression, anxiety, irritability, anger) Interpersonal: Rejection sensitivity is the underlying driver Fears of abandonment Unstable and intense relationships Behavioral: Extreme impulsivity related to intense emotion NSSI, suicidal behavior Self: Feelings of emptiness Unstable sense of self Stress related paranoia/dissociation
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What is the course of BPD?
Young adulthood there is greater impairment and suicide risk but as they get older there is more stability Over half of people with BPD do not meet full criteria 10 years later even without treatment It is not stable
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What is the prevalence of BPD?
1-2% of population High among psychiatric inpatients (20%) Women = men (show different behavioral patterns)
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What is the comorbidity of BPD?
Mood disorders (85%) Anxiety disorders (83%) Substance use (78%) Eating disorders PTSD Other cluster B personality disorders *Very likely to have more than one
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Biopsychosocial model of Borderline Personality Disorder: Etiology: Bio
Traits (negative emotional responsiveness): Neuroticism Impulsivity 5x more common among first degree relatives Relatives - impulse spectrum disorders (e.g., ASPD, substance abuse)
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Biopsychosocial model of Borderline Personality Disorder: Etiology/Presentation: Bio
Decreased orbitofrontal volume which leads to impulsivity, aggression, mood instability Decreased hippocampal volume which leads to stress overreactivity (anxiety), increased fear responses Amygdala hyperactivity, easier conditioning to fear, affective lability Lower 5-HT leads to impulse behavior, disinhibition
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How is amygdala hyperactivity related to BPD?
Hypervigilance Emotional dysregulation Neutral = threatening
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Biopsychosocial model of Borderline Personality Disorder: Etiology/Presentation: Psycho
Emotion Perceived rejection leads to intense rage (fight) Misperception of anger, usually is actually fear Cognition Thinking mistakes Black and white thinking, catastrophizing (similar to anxiety and depression) Result of fear of abandonment and rejection
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Biopsychosocial model of Borderline Personality Disorder: Etiology: Social
Invalidating environment Early adverse events Trauma/maltreatment (8x higher risk for cluster B) 90% childhood physical, sexual abuse, and/or neglect Early separation or loss (lack of safety) Abnormal parenting Bonding Neglectful and overprotective
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What is the biosocial theory?
Diathesis to stress Biological diathesis for emotional reactivity plus invalidating environment leads to BPD Invalidating environment: Efforts to communicate inner experience disrespected or punished (being shut down) Child suppresses emotions leads to explosion to get parents attention which reinforces the outburst
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Biopsychosocial model of Borderline Personality Disorder: Treatment: Bio
Comorbid mood disorders: SSRIs Mood stabilizers Psychotic/dissociative symptoms Antipsychotics
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Biopsychosocial model of Borderline Personality Disorder: Treatment: Psycho
Dialectical behavior therapy (DBT): Intensive (2 sessions a week, diary cards daily, for a year ) Expensive Mentalization: Client-therapist relationship Perspective taking, cognitive flexibility Transference-based psychodynamic psychotherapy: Client-therapist relationship Expensive Takes years
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What are the DBT principles?
Acceptance: ACT Validation, why are you doing what you're doing Change: CBT Problem solving Dialectics: Balancing the two
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What are the assumptions of DBT?
Acceptance: Individuals are doing the best they can They want to improve Change: At the same time; They need to do better, try harder, be more motivated to change They may not have caused all of their problems; they have to solve them anyway Their lives are often unbearable as they are currently being lived They must learn new behaviors in many contexts
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What is the format of DBT?
Individual therapy Skills group: Mindfulness (awareness and attention) Emotional regulation Distress tolerance Interpersonal effectiveness Dialectics (walking the middle path)
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What are the main characteristics of antisocial personality disorder?
Inadequate conscience development Ability to impress and exploit others Irresponsible and impulsive behavior
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What are the symptoms of ASPD?
Disregard for and violation of the rights of others Deceitfulness Impulsivity Aggressiveness Reckless disregard for safety of self or others Consistent irresponsibility Lack of remorse *Don't have to have all, have to have some
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What is the comorbidity of ASPD?
Substance abuse Other cluster B personality disorders
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What is the prevalence of ASPD?
Community: 3% men 1% women Prison: 47% (half) men 21% (some) women Younger adults Lower SES
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Biopsychosocial model of Antisocial Personality Disorder: Etiology: Bio
PFC dysfunction: Poor executive control Genes: Low MAOA (warrior gene) Enzyme that breaks down 5-HT, NE, DA Structural and functional changes in brain On X chromosome Traits: Aggressiveness Impulsivity Low anxiety
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Biopsychosocial model of Antisocial Personality Disorder: Etiology: Psychosocial
Low income Low parental supervision Parent psychopathology Delinquent sibling/papers Neglect Abuse (physical or sexual) Harsh discipline
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Explain the course of ASPD
Strong risk ODD (age 6) leads to conduct disorder (age 9) leads to ASPD ADHD + CD leads to ASPD (possibly psychopathy
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What is the difference between ASPD and psychopathy?
ASPD: Broader category More behavioural symptoms (criminality) Psychopathy: Narrow Personality structure Born this way Developmental risk factors ASPD: Difficulty learning to regulate emotions High emotional reactivity (aggressive, antisocial) in response to stress Psychopathy: Fearlessness Low anxiety Poor conscience Premeditated aggression
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What are the dimensions of psychopathy?
Core: Interpersonal - Superficial charm Pathological lying Affective - Lack of remorse, guilt, empathy Behavior: Lifestyle - Need for stimulation, impulsivity Antisocial - Poor behavioral control Criminality
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Biopsychosocial model of Antisocial Psychopathy: Etiology: Bio
Genes: ~50% variance Callous/unemotional traits (heritable) Brain structure: Amygdala volume (more often in unsuccessful psychopathy) Brain function: PFC dysfunction (more often in unsuccessful psychopathy)
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Biopsychosocial model of Antisocial Psychopathy: Etiology/Presentation: Psycho
Callous/unemotional traits Low levels of fear/poor conditioning of fear (opposite of BPD) Cognitive encoding, don’t encode things as dangerous Low physiological and emotional encoding High reward sensitivity Attentional directedness (tunnel vision)
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Biopsychosocial model of Antisocial Psychopathy: Etiology: Social
Early parental loss Parental loss or rejection Callous/unemotional traits evoke negative negative parenting responses: Anger Frustration Harsh discipline
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Biopsychosocial model of Antisocial Psychopathy: Treatment
Punishment is ineffective Treatment is very difficult Early intervention is critical (not completely shut down) Focus on social skills they get better at manipulating and use other peoples trauma stories Better to work toward redirecting their skills toward prosocial goals, get them what they want
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What does early intervention look like for psychopathy?
If not callous/unemotional: Reduce Hostile attributions Resentment, shame (key element) Increase Closeness in relationships Kind responses to self/others Lean into softer primary emotions fear/sadness vs anger/shame Predict limits Compassion in caregivers
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What is the purpose for laws in psychology?
Rules governing clinicians actions to protect vulnerable persons Anyone with a disorder is automatically vulnerable
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What are the risks in psychology?
Un or under qualified clinicians Clinicians treating outside areas of expertise Treatments without empirical support
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What are the two local ethic boards?
Canadian Psychological Association (CPA) - Code of Ethics College of Health and Care Professionals of BC (CHCPBC) - Code of Conduct
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What are the CPA code of ethics principles?
Respect for the dignity of persons (confidentiality, informed consent) Responsible caring (clinical competence, treatment must maximize benefit and minimize harm) Integrity in relationships (unbiased by affiliations, guided only by clinical judgment) Responsibility to society (recognize how actions affect society, in addition to clients rights)
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What are the three legal and ethical issues?
Confidentiality Involuntray confinement Deinstilutionalization
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What are the important items in psychology?
Guarantee of right and freedoms No arbitrary detainment or imprisonment Equality before law No discrimination
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What is the difference between privilege and privacy in confidentiality?
Privlidge: Right to refuse to disclose information to legal system (in all circumstances) E.g., lawyer-client communication Privacy: Right to choose information being shared (in most circumstances) E.g., clinician-clinet communication
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What does confidential communication mean in clinician-client communication?
Communication is private Client chooses whether and to whom info can be disclosed (in most circumstances) Law against breaching confidentiality
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What are the expectations to clinician-client confidentiality?
Imminent risk to self or others Suspected harm to a child or dependent adult (and guardian will not protect) Driving while intoxicated Court subpoena
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What allows the CPA code to breach confidentiality?
Clinician must breach confidentiality when and 3rd party identifiable victim or class of victims is believed to be at risk
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What are some issues in confidentiality?
Clinican efforts to reduce liability: Asking fewer (important) questions Vaugue language in session motes so you cannot be held reliable Who is the client? Organization vs patient Parent vs child Infant act, if you believe the child can consent
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What are the 2 types of involuntary confinement?
Criminal commitment Civil commitment
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What is criminal commitment?
Confining person who commits crime due to mental illness to psychiatric institution
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What is M'Naughten Rule?
Insanity defense: Ability to know an act is wrong Legally not allowed Morally (standards of society) Intellectual ability to know right from wrong Ability to apply that knowledge rationally in the situation (policeman at the elbow), would you be able to stop yourself if there was a cop beside you
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What is the irresistible impulse rule (1887)?
Functional Knowledge of right vs wrong Nonfunctional Impulse to act is irresistible
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What is neurolaw?
Evidence of disorder neural structure and function = sufficient to alter sentence (held less responsible) Activation in areas consistent with impulse urges vs inability to control urges
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Explain volitional control vs irresistible urges in murderers
Neural systems - checks and balances Lower self-reflective PFC More active impulse from amygdala Impulsive murderers had high subcortical and low PFC, less brain matters Predatory murderers high subcortical and normal PFC, control and plan
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What is civil commitment?
Confining a person to psychiatric institution No laws broken Mental illness results: Dangerous to self or others Incapable of providing for their basic physical needs Unable to make responsible decisions about hospitalization In need of treatment or care in hospital
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What are the types of civil commitment?
Informal commitment (no court order) Formal commitment (court order) Community commitment (Conditional Treatment Order - CTO)
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Explain the dangerousness model
Only to prevent physical harm Denying personal freedom is serious Softer standards discriminate against people with mental illness and are paternalistic
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Explain the treatment model
Prevent physical harm or serious deterioration Dangerousness is difficult to predicit Need to protect vulnerable persons
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How do you predict dangerousness?
Strongest predictors: Psychopathy scores Elementary school maladjustment score (bias) Good at predicting: General recidivism (reoffend) Sexual and violent recidivism Extreme violent recidivism Correlation = .44
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What was institutionalization like pre vs post 1960s?
Pre 1960 People with mental disorders were often placed in institutions indefinitely Post 1960 Massive release of patients to stress No alternative care provided Resulted in homelessness, substance addiction, jail
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What are Scott Simmie's potential solutions for deinstitutionalization?
Home care for people with serious mental illness Community mental health centres as access points Increase forensic beds Increase mental health workers in jails Most effective medications first Increased early detection and defragment intervention in children 24hr information/crisis line for appropriate referrals
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What are André Picard's potential solutions for deinstitutionalization?