Exam 1 Flashcards

1
Q

What is developmental psychopathology and how does it differ from a symptom-focused classification of mental disorders?

A

• DP is theory that proposes the trajectory of psychopathology multifactorial systems process.
• DP is multidisciplinary
• Multiple vulnerabilities and risk factors interact and transact into case specific yet predictable ways
• Psychopathology unfolds across entire lifespan
• DP is complex conception vs simplistic or linear
◦ Ex: interactions between G and E make psychopathology multifactorial
◦ Linear perspectives seek to blame psychopathology on family or on individual weakness
◦ Static perspectives erroneously lump together illnesses with substantially different etiological pathways > labeled as same condition

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2
Q

Normal vs atypical development

A

• Without understanding the processes of normal/health processes, such as attention, memory, impulse control,for example, understanding the development of atypical Bx such as ADHD would be incomplete > no sample to determine the range of Bxs

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3
Q

Continuities and discontinuities

A

• Homotypic continuity: unfolding of a single class of Bx/ emotional disturbance over time
◦ Ex: aggression
• Heterotypic continuity: development of different (but related) internalizing or different externalizing Bxs or disorders across lifespan
◦ Ex: tantrums and hyperactivity (toddler) + ODD (preschool) + CD (elementary) + SUD (adolescence)
• Discontinuity: Bxs that desist over time
◦ Ex: child biting

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4
Q

Risk and protection (and resilience)

A

• Risks and vulnerabilities > variables that precede and predict dysfunction
◦ Malleable and potentially casual > but not inevitably predictable
• Impairment waxes and wanes over time
• Not all vulnerabilities and risk factors lead to develop pathology
• Resilience: good outcomes despite vulnerability and risks
• Protective factors or processes that mitigate risks and vulnerabilities, promote successful outcomes
• Understanding protective factors help w/intervention and preventive measures (deflect pathology) and understanding atypical Bxs just as the study of normative Bxs do

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5
Q

Transactional models

A

• Open systems functioning > interaction and transactional patterns are multidirectional overtime
◦ Ex: children influenced by teachers, fathers and peers who in turn each shape development of child

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6
Q

Multi-level analysis

A

• RDoC: levels of analysis include they ways in which we measure units of
◦ Genes: bio markers that indicate normal or abnormal development
◦ behavior: behavioral tasks (working memory), or observational (toddler Bx)
◦ self reports: interview based scales, or self report measures that indicate normal or abnormal Bx

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7
Q

Equifinaility and multifinality

A
  • equifinality: multiple and different trajectories can lead to development of atypical conditions or outcomes
  • Multifinality: similar risk factors and/or vulnerabilities can lead to different conditions or outcomes
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8
Q

How has the DSM changed overtime? How has it improved? What problems and criticisms remain?

A

• DSM 1 ‘reactions’ to stress
• DSM 2: homosexuality removed: diagnostic systems reflect social values
• DSM 3: more scientific and empirical evidence vs professional consensus of prior DSM. Diagnosis requires reliability
• Current DSM: specification of operational criteria, standardize data on Sxs, structured interviewing, improve validity, dimensional indices, ADHD into neurodevelopment, addition of non suicidal self injury
• Criticisms: with changes made to DSM 5 > years of research to asses validity of diagnosis
◦ Evidence suggests PDs can be diagnosed in adolescence reliably > DSM 5 states PD diagnosis for age 18 younger is dangerous
◦ No evidence for ABC clustering in PD disorders
◦ DSM obscures etiological connection between ADHD and CD > moving ADHD into neurodevelopment
◦ Drop of multiaxial system: downplays importance of environment in shaping Bx even in the face of genetics

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9
Q

What are empirically derived classification systems and how do they differ from the DSM?

A

• Empirically based assessment: inductive (bottom up) assessment > derived from factor analysis of large sample sets of Sxs of psychopathology > result in hierarchal latent structure of mental illness. Two higher order factors (internalizing and externalizing) account for covariation among first order factors
◦ Raters not forced to chose between dichotomous diagnostic decisions > scales scores can be evaluated from national norms (flag for concern those in the 85th percentile, 95th percentile considered clinically impaired
◦ Does not force clinicians to chose one disorder over another > elevated scores both across and within internalizing and externalizing domains are observed and expected
◦ More sensitive to capturing heterotypic comorbidity (primarily externalizing Sxs, with subclinical internalizing Sxs)

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10
Q

What is the RDoC and how does it differ from the DSM?

A

• RDoC is a framework to investigate new approaches to mental disorders
(Research Domain Criteria)
◦ Not seeking to replace diagnostic guidelines
◦ Goal > Integrate multiple levels of integration (microsystem, mesosystem, exosystem, macrosystem) to understand basic functioning of human Bx from normal to atypical
◦ RDoC believes multiple units of analysis will yeild more valid phenotypes and better understanding of causes and Txs of mental disorders

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11
Q

What is gene-environment interaction and why is it important?

A

◦ Environment moderates effect of genes on Bx or genes moderate effects of environment on Bx

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12
Q

What is gene-environment correlation and why is it important? What are the different types of gene-environment correlation

A

• Situations in which (a) heritable traits of parents affect their child’s exposure to adverse environments (b) heritable traits of children affect their own exposure to adverse environments
◦ Active: heritable vulnerability influences selection of environment > propensity to seek risky environment
‣ Ex: schizophrenia seeking substance abuse
• Passive: parents pass 50% of genes and influence of specific environment
◦ Intelligent parent purchases books for child + lots of reading = greater opportunity
• Evocative: genetic propensity evokes and elicits reaction from others (environment) > increase severity of vulnerability
◦ Ex: musically orientated > parents maintain high exposure to musical environment

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13
Q

What do we know about the genetics of comorbidity? (are genes specific risk factors for types of psychopathology or general risk factors for psychopathology?

A

• Homotypic comorbidity: co-occurance of multiple externalizing or internalizing Dxs w/in individual
◦ Ex: ADHD + ODD, CD, ASPD, SUD (externalizing)
◦ Ex: Depression, Dysthymia, anxiety Dxs (internalizing)
• Heterotypic comorbidity: co-occurance of at least one internalizing Dx and at least one externalizing Dx w/in individual
◦ CD + Depression rates higher than expected
• Most Dxs share common heritable vulnerability > but shared variance strongly influenced by environment > genetic predispositions manifest differently depending on environment influence
• Comorbidity as covariation of related syndromes that stem from common heritable vulnerability

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14
Q

What do we know about the genetics of continuity?

A
• Homotypic continuity: unfolding of a single class of Bx/ emotional disturbance over time
	◦ Ex: aggression 
• Heterotypic continuity: development of different (but related) internalizing or different externalizing Bxs or disorders across lifespan
	◦ Ex: tantrums and hyperactivity (toddler) + ODD (preschool) + CD (elementary) + SUD (adolescence)
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15
Q

What are the stages of case formulation?

A
1. Primary characteristics of child’s Px?
	A. Normative expectations
	B. Assessment of disorder and etiology
2. How does clinician perform in depth assessment of Px?
	A. Family Hx
		a. Genetic 
		b. Events, crisis, trauma
3. How does clinician decide on Tx?
	A. Evidence based Tx
	B. Evaluation of Tx effectiveness
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16
Q

• Be able to demonstrate an emerging ability understand an example case from at least two theoretical perspectives (i.e., I may ask you to use theories discussed in this chapter to aid in your interpretation/understanding of the development and maintenance problematic behavior – stage 2 of Wilmhurst’s model)

A

• Biological perspective: genetics, secretion of hormones, brain development influence etiology of human Bx
◦ Medications may be used in Tx, which help to regulate the low levels of activity in the prefrontal cortex in ADHD, and regulate neurotransmitters like serotonin implicated in those suffering from depression
• Attachment theory: early secure child - caregiver attachment results in ability to regulate emotion and integrate cohesive self of self > insecure attachment leads to dis regulation of emotions into adulthood and fragmented and in cohesive sense of self
◦ Through characteristics of PACE, intersubjective experiences w/ therapist (as caregiver) from present and past, individual learns to regulate emotion, integrate new meaning into cohesive sense of self

17
Q

What do we know about ASD:

A

Prevalence
• Prevalence 1%
• Highly heritable
o Patterns of comorbidity
• More than 70% of individuals w/ ASD have cooccuring conditions that tend to persist into adolescence
• The more cooccuring conditions the greater the disability
o Causes
• Advanced maternal or paternal reproductive age
• Paternal germline mutation
• Parents who reproduce later in life may do so because they have broader autism phenotype
• 2x higher in cities where information- technology sector
• Gestational factors effecting neurodevelopment during pregnancy and exposure to chemical
• Compromises to perinatal and neonatal health
o Prognosis
• Mortality rate 2x8 times higher > due to co-occurring medical conditions
• Adults have poor outcomes of independent living, education, employment, peer relationships
o Early developmental signs
• Deficits or delays in joint attention (shared focus on object) and pretend play
• Atypical implicit perspective taking
• Deficit in reciprocal affect behavior
• Decreased response to own name
• Decreased imitation
• Delayed verbal and nonverbal communication
• Motor delay
• Repetitive unusual Bxs
• Atypical visuomotor exploration
• Inflexibility in disengaging visual attention
• Extreme variation in temperament
• Higher functioning (especially females) more difficult to detect early
• Differential variation in presentation
o Behavioral and Pharmacological Treatment
• No biomedical Tx shown to reliably improve social communication
• Creation of autism friendly environment crucial
• Multidimensional and multidisciplinary Tx
• Improving social skills and communication
• Reduction disability and comorbidity
• Promotion of independence
• Support for family
• Fulfilling potential areas of strength

18
Q

What are some early indicators of risk for ASD?

A
• Sensory motor
	◦ Reduced motor activity
	◦ Delayed motor milestones
	◦ Atypical development trajectory
	◦ Unusual mannerisms/ repetitive Bxs
	◦ Various sensory sensitivities 
• Attention
	◦ Selective deficit in attentional disengagement
	◦ Difficulty regulating emotional state
• Social- emotional
	◦ Reduced positive affect and reciprocal social smiling 
	◦ Reduced social orienting
	◦ Atypical face processing
• Communication 
	◦ Reduced verbal and nonverbal communication (lack of eye gaze, pointing to shared objects)
	◦ Diminished use of gestures
	◦ Reduced babbling and reduplication
	◦ Delayed receptive word learning
	◦ Few words used meaningfully
19
Q

What are some early intervention targets for kids who are at-risk for ASD?

A
  • Early targeting of 4 risk indicators
  • Community interventions > cost effective and sustainable
  • Comprehensive behavioral for preschoolers
  • Parent- mediated > applied behavior analysis
  • Naturalistic learning > infants and toddlers > child directed, highly motivating
20
Q

Why is early intervention important for this population?

A
  • Identifying key target Bxs likely has a collateral effect on multiple domains + evidence based intervention = effective and efficient sustainable Tx very early in development
  • Very early Tx has trickle down effect, potentially influencing secondary prevention on less optimal conditions
21
Q

A/RFID

A
  1. prevalence: 1-2%
  2. compromise of efficient effective eating
  3. comorbid with anxiety, ASD, OCD, ID
  4. etiology:
    - environmental: too much diversity, lack of diversity, inconsistency, external stimuli during feeding time
    - genetic
    - gross/ fine motor skills
    - emotional
  5. assessment
    - family Hx
    - observational
    - interviews
    - rating scales
    - food inventory
  6. Tx
    - continuous and consistent parental structure
    - positive reinforcement: praise for touching food, kissing, licking
    - extinction: ignore Px Bx, non removal of spoon, physical redirection
    - physical guidance: promote autonomy (self feed, partial assistance)
    - distraction free environment: scheduled meals, small bites
    - appetite manipulation: reduction of free feeding
22
Q

Enuresis

A
  1. Prevalence
    - 7 yr old: 10% at night
    - 7 yr old: 1-3% daytime
  2. Developmental age: 5
  3. Etiology
    - genetic: risk higher w/parental enuresis
    - environment: limited toilet training, psychosocial stress
  4. Assessment:
    - family Hx
    - Interview
    - rating scale
    - physical exam
    - psych Hx
  5. Tx
    - psycho education
    - tracking accidents: scheduling
    - behavior reinforcement: nocturnal bell in pad
23
Q

Encopresis

A
  1. Elimination of waste at inappropriate times/ locations
  2. Prevalence:
    - 7 yr olds 1-3%
  3. Developmental age
    - 5
  4. Etiology
    - genetic: constipation
    - environment: psychosocial stress
  5. Assessment
    - family Hx
    - Interview
    - rating scale
    - physical exam
  6. Tx
    - Psychoeducation
    - tracking accidents: scheduling
    - Medication: laxatives, suppositories, psyc Med education
    - behavior reinforcement
24
Q

ID

A

1.

25
Q

Statistical deviance

A
  1. Normal is bell curve
  2. Ab-normal determined in part by statistical model
    - 2 standard deviations from mean seen as maladaptive (zone of concern)
  3. Compare target Bx, emotion, thought to normative sample
  4. Issues?
    - how many Sxs is too much
    - where do we draw the line between normal and abnormal?
    - are we comparing skewed reference points?
    - what makes an adequate normative sample?
26
Q

Sociocultural norms

A
  1. Essential to understand the context and individual values in which the target behavior, cognition, or emotion is expressed
  2. Within context is Bx atypical?
27
Q

Moral model

A
  1. Extension of social norm model into religious and ethical domains
  2. Outmoded?
    - homosexuality: conversion Tx
    - female Bx dress
28
Q

Impairment

A
  1. For Dx must have
    -impairment
    Ex: hyperactivity vs. hyperactivity + impairment
29
Q

Ecological perspective

A
  1. Goodness of fit between individual and context
30
Q

Validity

A
  1. Whether the classification gives us true-to-life, meaningful information
    - Internal validity: About etiology or core patterns
    - External validity: About the implications of the disorder
    - must have reliability to have validity
31
Q

Reliability

A
  1. Whether different clinicians classify children into the same categories
    - Interrater reliability: Two or more mental health care
    providers come to the same conclusion.
    - Test-retest reliability: A child is similarly classified by the
    same clinician over time.
32
Q

Multiple methods assessment strategy

A
  1. Multiple measures used with each information/source
    - Interview
    - rating scales
    - observation
33
Q

Child assessment measures

A

Interviews (unstructured, semi-structured or structured)
– Strengths: Systematic, flexible, comprehensive, dx
– Limitations: Time consuming, no norms, training
• Rating Scales
– Strengths: Great for screening, broad-band, narrow-band, efficient, norms,
different perspectives, possible tx targets
– Limitations: $, not adaptable, noise in responses
• Observations
– Strengths: Convenient
– Limitations: Novel setting
• Record Review/speaking with other providers
– Strengths: Good way to get a history, may provide glimpse of stability/change
over time, may have rec’s, may provide assessment of systems you are not trained in
– Limitations: Relevance to presenting problem, reliance on others