Assessment, Classification, Diagnosis, Methods Flashcards
1
Q
What are the criteria for valid classification of disorders according to Robins & Guze?
A
- Clinical description
- Course
- Treatment response
- Family history
- Laboratory studies
2
Q
What does Wakefield’s ‘Harmful Dysfunction’ refer to?
A
Dysfunction: an organ system performing contrary to its design
Example: Heart not pumping blood
3
Q
What is the purpose of a classification system in psychopathology?
A
- Description
- Prediction
- Theory
- Communication
4
Q
What are the limitations of a classification system?
How do Procrustean beds relate to one of the limitations?
A
- Loss of uniqueness
- Difficulty of boundary cases
-Procrustean beds: accommodating the system, not the person
5
Q
What is the difference between categorical and dimensional systems?
A
- Categorical: Presence/absence of a disorder
- Dimensional: Rank on a continuous quantitative dimension
6
Q
What is included in the DSM’s Multi-Axial Classification?
A
- Major clinical disorders
- Personality disorders
- Medical conditions
- Psychosocial stressors
- GAF (Global Assessment of Functioning)
7
Q
True or False: The DSM-III was less explicitly grounded in theory than earlier editions.
A
True
8
Q
What assumption was introduced in DSM-III regarding symptoms?
A
Symptoms are the most useful basis for assessment
Prior to DSM-III, there was disagreement as assessment looked more at history.
9
Q
What was the focus of nosology in DSM-III?
A
Based on behavior and symptoms
10
Q
What did the DSM-IV introduce
A
The notion of clinically significant distress or impairment in social, occupational, or other important areas of functioning
Key: interference with daily life
11
Q
What did DSM-IV-TR provide regarding diagnoses?
A
More information on each diagnosis and a broad definition of mental illness
12
Q
How many diagnostic categories were in DSM-I?
A
106
13
Q
How many diagnostic categories were in DSM-III-R?
A
292
14
Q
What percentage of individuals with one disorder qualify for more than one disorder?
A
50%
15
Q
What is the lifetime comorbidity rate for individuals?
A
75%
16
Q
True or False: Comorbid patients tend to have better treatment outcomes.
A
False
17
Q
What are some reasons for the existence of comorbidity?
A
- Chance
- Sampling Bias - clinical samples are more comorbid than the general population
- Problems with Diagnostic Criteria - many criterion sets overlap
- Poorly-drawn diagnostic boundaries - multiformity
- Causal explanation - one disorder is a risk factor for another disorder
- Shared Etiological risk factors
18
Q
What does prevalence refer to in epidemiology?
A
Percentage of people in a population with a disorder at a particular point in time
19
Q
What is the incidence in epidemiological terms?
A
Percentage of people who develop a disorder for the first time during a specific time period
20
Q
What is the lifetime prevalence of mood disorders?
A
21%
21
Q
What is a vulnerability marker?
A
A trait-like characteristic that precedes the disorder and predicts onset
22
Q
What is a challenge associated with high risk studies?
A
Recruitment and attrition problems
23
Q
What does family studies assess in genetic epidemiology?
A
If the disorder runs in the family (heritability of the disorder)
24
Q
What is the main purpose of twin studies?
A
To estimate heritability by comparing concordance rates between MZ and DZ twins
25
What does gene-environment correlation (rGE) include?
* Passive
* Active (niche-picking)
* Evocative (reactive)
26
What is the main issue with single-gene transmission in psychiatric disorders?
No psychiatric disorders show the expected rates of familial transmission - we expect 50% of relatives to have the disorder
Possible single-gene transmission but expressed differently in different relatives
27
What is polygenic transmission?
Psychological phenotypes likely controlled by more than one gene
28
What is the estimated heritability formula in twin studies?
A = 2(rMZ - rDZ)
29
What is the prevalence rate for Mendelian disorders?
About 1 in 10,000
30
What is the prevalence of Mendelian disorders?
About 1 in 10,000.
31
What is the prevalence rate for most psychiatric disorders?
At least 0.5%.
32
What type of transmission is suggested for psychological phenotypes?
Polygenic transmission.
33
What can modify gene effects?
Gene-gene (GxG) interactions and gene-environment (GXE) interactions.
34
What are the heritability estimates for the Big Five personality traits?
0.40 to 0.60.
35
What is the heritability estimate for autism spectrum disorder?
0.38.
36
What is the heritability estimate for schizophrenia?
0.64.
37
What does the term 'missing heritabilities' refer to?
The genetic variation not accounted for by known genetic factors.
38
What is the diathesis-stress model?
A model suggesting that adverse effects of genes on mental health are expressed under certain environmental conditions.
39
What did the study by Caspi et al. (2003) find about life stress?
Life stress influences depression moderated by a polymorphism in the 5-HTT gene
Revealed that adverse effects of genes on mental health are only expressed under certain environmental conditions - diathesis stress model
40
What is epigenetics?
The regulation and expression of genes.
41
What is meant by genes 'turning on'?
Some genes activate at certain developmental periods or under specific environmental circumstances.
42
What is an endophenotype?
An intermediate step between genes and psychological phenotypes.
43
List the requirements for an endophenotype.
* Must segregate with illness in the population
* Must be heritable
* Must not be state-dependent
* Must co-segregate with illness within families
* Must be present at a higher rate within affected families than in the population
* Must be amenable to reliable measurement and specific to the illness of interest.
44
What is the heritability of IQ among affluent families?
Estimated at 0.72.
45
What is the heritability of IQ among less affluent families?
Estimated at 0.10.
46
How does neighborhood context affect the heritability of alcohol use?
74% heritability in neighborhoods with ten or more alcohol outlets vs. 16% in neighborhoods with zero outlets.
47
What happens to the heritability of eating disorder symptoms before and after puberty?
Minimal heritability before puberty, significant genetic effects during and after puberty.
48
What is the Flynn effect?
The observation that IQ scores have increased over time.
49
What is quantitative genetics?
The study of the genetic basis of complex traits.
50
What is the problem with single-gene transmission in psychiatric disorders?
No psychiatric disorders show the expected rates of familial transmission.
51
What distinguishes monogenic disorders from psychiatric disorders?
Monogenic disorders are distinct and rare, while psychiatric disorders are dimensional and continuously distributed.
52
True or false: the during criterion in psychopathology is not sustained
False
53
What are some of the reasons why we should define psychopathology
*traits do not mean pathology
*pathologize normal behaviour/invalidate actual pathologies
* decision on adequate treatment
54
Something that is psychopathological is ____ and statistically _____
Abnormal & rare
55
What are syndromes
Clusters of symptoms that present together in meaningful ways with uniform course
56
True or false: medical models are taxonic
True
57
What are Thomas Sydenham and Emil Craikland known for
Sydenham: syndrome and taxonic
Craikland: taxonic
58
Define taxonic
Categories that exist in the real world
59
True or false: medical models acknowledge illness as multifactorial
True
60
What are some problems with the harmful dysfunction definition proposed by Wakefield?
How to define harm - is it to oneself or to others?
61
What is Lillienfeld’s critique of harmful dysfunction
*Natural function
*Natural selection depends on variability
*Some disorders may be adaptive rather than maladaptive: anxiety may be an adaptation in a stressful situation
62
What did Widiger propose?
Mental disorders are constructs
*latent and indirectly observed - multimodal definition is needed
*opposes a taxonic approach
63
What composes the multi-modal approach of psychopathology
Genetics, environment, self-report, physiological manifest, neurological manifest, behavioural manifest
64
What are some characteristics of the categorical system?
Simplifies communication
Natural preference among people to employ categories
Better suited for clinical decision making: hospitalization, treatment etc.
65
What are some of the advantages of a dimensional approach
Preserves more information - goes beyond yes or no
Greater reliability that is not always seen in categorical models
Cutoffs in categorical system tend to magnify small differences - not in dimensional model
66
What are some characteristics of the DMS-II
Few categories, no requirement for # of symptoms, psychoanalysis was the dominant paradigm
67
What are the key features of the DSM-III
Inclusion criteria, duration criteria, exclusion criteria, multi-axial classification
68
What are Axis-1 and Axis-II disorders respectively
Axis-I: Major Clinical Disorders
Axis-II: Personality Disorders
69
True or false: According to the DSM-III, the locus of pathology is within the system
False: the locus of pathology is within the individual
70
What are the features of the DSM-5
Removed the multi-axial system
Introduced dimensional assessment criteria for some diagnoses
Re-classified and removed some disorders
71
How many categories are in the DSM-5
157
72
What are some challenges to categorical classification
1. Heterogeneity
Assumption is that people within the same boundary should look the same which is not the case - boundaries are not capturing the homogeneity
EX: people within depression may look the same as people with anxiety
2. Comorbidity
EX: lots of comorbidity between anxiety and depression
73
What is the difference between concurrent and lifetime comorbidity
Concurrent: at the moment
Lifetime: at some point in your life
74
What does comorbidity affect
Course, development, presentation, treatment response etc.
75
What percentage of any anxiety disorder is comorbid with MDD
64
76
What percentage of any mood disorder is comorbid with SOC, GAD and OCD respectfully
SOC: 29
GAD: 36
OCD: 32
77
True or false: dimensional/hierarchical models are an alternative approach to the classification systems already discussed?
True
78
What are the hierarchical models trying to explain?
How disorders relate to one another
Latent factors that manifest in different ways
An attempt to split disorders differently than the DSM
Looking at what symptoms correlate with each other in a larger group
79
How is the HiTop organized
Super spectra (general tendency of psychopathology)
Spectra (internalizing/externalizing)
Subfactors (fear, sexual problems, substance abuse etc)
Syndromes/Disorders
Components (maladaptive traits)
Symptoms
80
What is the RDoC used for and how is it organized
Used mainly for research - do not and should not diagnose someone in a clinical setting with this
Fundamental domains that could dysfunction in different disorders - way of understanding psychopathology
Agnostic and biologically influenced
Organization:
Negative/Positive Valence systems
Cognitive systems
Systems for Social Processes
Arousal and Regulatory Systems
81
What is a risk factor
A correlate associated with different disorders
82
What is the ranking of the major disorders from most to least prevalent
Social Anxiety
Major Depression
PTSD
GAD
Panic
Bipolar
Persistent Depressive Disorder
OCD
83
What is the prevalence of having any disorder in your lifetime?
46%
84
Are college or non-college students more likely to have a disorder?
Which one is more common among college vs non college students
Non college students are more likely
Most common among both: AUD
85
What is the environmental etiological model
*parental environment and family dynamic
*environmental and learning experiences
*freudian theories
*”schizophrenic mother” - inconsistent parenting style
*”refrigerator mother” - lack of genuine warmth with her child causing autism
86
What is the genetic etiological model
Genes are not deterministic - most are probabilistic
They make small contributions to create the ultimate outcome
Researchers identifying dozens of genes that in certain combinations lead to symptoms of different forms of psychopathology
Polygenic: influenced by many genes
87
According to the diathesis-stress model, what 2 conditions need to be present for the potential development of a disorder
Diathesis present AND stress present
88
What are vulnerability-stress correlations
Often non-independent in important ways
Stress generation
Scars as vulnerability
Vulnerability may shape perception of the stress
Stress can influence the development of the diathesis
89
Define equifinality, final common pathway and multifinality
Equifinality: getting to the same point in different ways - complicates study but represents reality
Final common pathway: multiple pathways converge on a final step leading to the disorder
Multifinality: the same cause gets you to a different ending
90
What is the goal of longitudinal studies and what are the different types longitudinal designs
Goal: establish temporal precedence
Types: Retrospective, follow-up and high risk
91
Describe retrospective studies
Collect a sample of people with a disorder and try to determine what preceded it
Challenges: relying on self-report and existing archival data
92
Describe follow-up studies
Follow people with the disorder over time and see what happens to them
Already-ill sample
Helpful to look at the course but difficult to determine the cause
93
Describe high-risk studies
Identify people who are likely to develop a disorder and follow them over time
High risk people: offspring of people with a disorder, biological abnormality, behavioural variable
94
What are some other cons of high-risk studies
Genetic: need to find people who have the disorder and also have children
Biological: associations not well-proven
Behaviours: May be a risk factor or may be early manifestations of the disease
Most expensive to run
95
What is the difference between case control VS cohort
Case control: compare one group of people with the disorder to a second group without the disorder - good for rare disorders like schizophrenia
Cohort: a single large sample of people with only some people having the disorder - good when the condition is common like SUD and compare with other disorders
96
What is the difference between patients VS community
Patients are usually not representative of the general populations
Expensive to run these types of studies
97
Describe family studies
Identify a proband: someone with the disorder
Assess family members - interview (family study = better) or informant report (family history study = better access but not as good)
Suggests a genetic role but it does not prove it - no direct genetic transmission
98
Describe adoption studies
Parent or adoptee as a proband
Cross-fostering design
Genetic predisposition but low-risk environment
Helps isolate the environment and genetic factors
99
What does ACE stand for in twin studies and what does it help with
A: additive genetic component
C: common environment component
E: unique environment
Proportions out the variance between zygoticies
100
What is the MZ concordance VS the Dz concordance and what is the 2D
MZ: 50%
Dz: 25%
2D: 50%
101
What are some problems with twin studies
MZ twins often share a placenta and are treated more similarly to one another
Heritability = estimated genetic contributions to observed phenotypes - measure what is associated with variability in the phenotype
Not deterministic - only give us a range
Often don’t model a G x E
102
True or false: currently, all rGE are attributed to G
True
103
What is a passive gene environment correlation
Genes are responsible for talent shape the child’s environment
The child is a passive recipient of their environment - genetically influence environment
Can be addressed in adoption studies
104
Describe active rGE
“Genes have feet”
Early in life: controlled by parents and guardians - the environment is selected for us
We have a genetic predisposition to the environment we select
Seek out environments because of their genetic influenced personality
105
What is an evocative rGE
Treat people and the environment as a genetic predisposition of their traits and environment
106
What are the two modes of quantitative genetics
Single-gene transmission and polygenic tramission
107
True or false of polygenic transmission: psychological phenotypes are controlled by only one gene
False: they are controlled by more than 1 gene
108
What are the actions of multiple genes
Additive or interactive effects
109
How are rGE different from GxE
GxE: the genotype interacts with the environment to determine the outcome
RGE: the two are correlated but not necessarily interacting
110
What did Michael Meany do?
Good rat mothering associated with better functioning of neuroendocrine stress response
Bad rat mothering = high levels of stress and cortisol
Cross fostering: swap the pups of good and bad rat mothers
Change in glucocorticoid receptor gene: babies of good mother switched to bad mother had higher cortisol - a change in gene expression
Only evident when the switch of the pups was early on
111
What is alternative explanation for missing heritability
Phenotypes are not measured precisely
112
What is an endophenotype
intermediate step between microscopic genes and nerve cells and the experiential and psychological phenotype
113
What are the “rules” that need to be followed if something is or could be an endophenotype
Must be segregated will illness in the population
Must be heritable
Must not be state-dependent (should be trait-like) - if not trait, then probably a symptom
Must co-segregate with illness within families - those who have the illness within a family are also more likely to have the endophenotype
Must be present at a higher rate within affected families than within the general population
Must be amenable to reliable measurement, and be specific to the illness of interest
