Final Exam Flashcards
Topics: Substance Use Disorder, Psychosis and Schizophrenia, Childhood Disorders, Personality Disorders
What can excessive use of substance lead to?
Dangerous behaviours
Continued use despite persistent problem
What is substance dependence?
Substance abuse resulting in tolerance and/or withdrawal
Define tolerance
Physiological need for increased substance for the same effects
Define withdrawal
Physical symptoms that result from stopping use (e.g., nausea, sweating, tension, headaches, tremors)
What are the stages of substance abuse?
Positive attitude leads to experimentation which leads to regular use then heavy use which leads to physical dependence/abuse
How does the DSM-5 define substance use/alcohol use disorder?
Problematic pattern of ETOH use leads to impairment
How does the DSM-5 diagnose substance use/alcohol use disorder?
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
What does the WHO describe as harmful alcohol use?
Heavy episodic drinking
≥ 6 drinks
≥ 1x/month
What is the prevalence of harmful drinking patterns?
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
What is BAC and what affects it?
Amount ingested in a particular period of time
Food eaten, sex, age, medications
What are some short-term effects of heavy alcohol use?
Stimulating, then depressant action
Interference with complex thought and motor coordination
Interacts with several neural systems
Effects strongly tied to expectations
How does heavy alcohol use interact with neural systems in short-term use?
Stimulates GABA receptors (tension and motor coordination goes down)
Increases 5-HT and DA (motivation for pleasure/craving, addictive)
Inhibits glutamate receptors (cognitive effects)
Biopsychosocial model of Substance Use: Etiology: Bio
Genes
Alcohol risk personality
Ability to tolerate/metabolize alcohol
Motivation for substance use (decrease tension vs increase pleasure)
Biopsychosocial model of Substance Use: Etiology: Psycho
Stress, tension reduction, (negative) reinforcement
Expectations of social success
Perceived benefits outweigh the costs
Sensation (novelty) seeking
Drinking motives
What are the drinking motives?
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
Biopsychosocial model of Substance Use: Etiology: Social
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
Biopsychosocial model of Substance Use: Treatment: Bio
Medication: block desire to drink (operant conditioning)
e.g., Antabuse, naltrexone
Lower side effects of withdrawal (e.g., valium)
Transtheoretical Model (TTM)
What are the 6 stages of change in the transtheoretical model?
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)
Biopsychosocial model of Substance Use: Treatment: Psycho
CBT and Behavioural
Aversion conditioning
Skills training
Self-control
Motivation enhancement
Controlled drinking vs abstinence
Biopsychosocial model of Substance Use: Treatment: Social
Group therapy
Forced to confront problem
Alcoholics Anonymous (AA)
Environmental intervention (e.g., halfway houses)
What is the treatment efficacy for substance use?
Wide range
Depends on everity of substance abuse (duration, amount of tolerance), and type of treatment
All treatment types are equally effective
List drugs that are associated with addiction
Narcotics
Sedatives
Stimulants
Includes ADHD meds
Anti-anxiety drugs
Pain medication
Hallucinogens
What are some short term biological effects of opioids?
Decreased physical pain
Relaxation
Decreased anxiety
Euphoria
What are some long term biological effects of opioids?
Physiological craving
Withdrawal symptoms
Physical deterioration
Immune system, organ damage
Consequences of poor health, dangerous behavior
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
Explain reward deficiency syndrome
Addiction = genetic deviation in reward pathway
Less satisfaction from natural rewards are more likely to become addicted once exposed
What is comorbidity of opioid abuse?
70% other psychological disorders
50% other substance abuse
36% history of trauma
Depression
Anxiety
Antisocial personality disorder
What are different types of stimulants?
ADHD meds
Cocaine
Amphetamines (meth)
Caffeine
Nicotine
What are symptoms of amphetamine abuse?
Intense fatigue
Psychological and physically addictive
Brain damage, amphetamine psychosis
Suicde, homicide, violence
Highly activating
What are different types of hallucinogens?
LSD
Mescaline
Psilocybin
MDMA (ecstasy, molly)
What are some short-term effects of MDMA use?
Rush of pleasure
Sense of wellbeing
Depressed mood (for days after use)
What are some long-term effects of MDMA use?
Brain damage (frontal and temporal lobes)
Memory deficits
Hallucinations
What are some short-term effects of cannabis use?
Relaxation, sense of wellbeing, euphoria `
Hallucination
Increased perceptual acuity
What are some therapeutic effects of cannabis use?
Decrease nausea and pain
Increase appetite and sleep
What are some long-term effects of cannabis use?
Psychosis/schizophrenia (if have the diathesis)
Memory loss
What is psychosis?
Significant loss of contact with reality
Hallmark of schizophrenia
Delusions
Hallucinations
Disorganized speech and/or behaviour
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
What are the hallmark symptoms of schizophrenia?
Delusions
Hallucinations
Disorganized speech and/or behaviour
*have to have at least 2
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
Describe delusions
Erroneous (incorrect) beliefs
Highly unusual thought content
Firmly held belief despite evidence
Examples:
Thought insertion
Broadcast thoughts
Thought withdrawal
Made feelings
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
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)
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
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
What are the 3 phases of schizophrenia?
- Prodromal:
Obvious deterioration in role functioning
Personality change (schizotypal PD) - Active:
Psychosis - Residual:
Improvement in positive symptoms
Continued negative symptoms
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)
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
Biopsychosocial model of Schizophrenia: Treatment: Social
Family therapy
Communication skills
Decreased expressed emotion
Case management
Social and living skills training
Vocational rehabilitation
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