Chapter 1 Flashcards

1
Q

What are the purposes of classification?

A
  • description→ highlight critical features, provide surplus info regarding patient
  • prediction→ diagnosis can be predictive
  • theory→ explore relationships of different elements to one another
  • communication→ between clinicians
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2
Q

What are th 5 key crtieria for a valid diagnosis?

A
  • clinical description→ consistent commun set of symptoms clustering together (ex: depression= insomnia + sadness BUT not mania)
  • course→ should follow a common trajectory and have similar onset
  • treatment response→ people with same disorder should respond similarly to treatments (debatable)
  • family history→ does it run in the family
  • laboratory studies→ look for biological and psychophysiological associations

Additional validating indicator→ Endophenotypic
- biomarkers or laboratory indicators, that is, “measurable components unseen by the unaided eye along the pathway between disease and distal genotype”

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3
Q

What is the Procrustean beds myth and how is it relevant to the limits of the classification system?

A

Difficulty of boundary cases
- Procrustean beds myth
- try to adapt people to the category rather than adapting the cases

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4
Q

What is the internal consistency of a mental disorder?

A

extent to which the signs and symptoms comprising a diagnosis hang together

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5
Q

What are the pros and cons of a categorical system?

A

Categorical→ nowadays
- presence OR absence of disorder
- need a threshold
- ex: either you are anxious or you are not
- speak to our natural preference to employ categories

Advantages
- easier for research
- simplify communication
- better fitted for clinical decison-making

Disadvantages
-not good at communicating nuances
-need a threshold

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6
Q

What are the pros and cons of a dimensional system?

A

Dimensional→ rank on quantitative dimension
- degree of symptoms

Advantages
- may capture functioning better/ higher correlations with external validating variables
- preserves more information (how high/low on the scale the person is)
- greater reliability (inter-rater, test re-test)
—>most personality disorder seems to be dimensional as opposed to taxonic in nature

Disadvantages
- but arbitrary cut-offs

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7
Q

What are the dates of the DSM-I and II and their novelty?

A

DSM-I→ 1952
- first attempt to write down common definitions for everyone
- standardization of diagnosis

DSM-II→1968
- few categories
- psychoanalysis was dominant at that time

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8
Q

What are the novelty brought by the DSM-III?

A

DSM-III→1980
- more biological and empirical approach
- inclusion criteria→ nature and numbers of symptoms needed to be diagnosed
- Duration Criteria
- Exclusion Criteria→ symptoms ruling out specific diagnosis

Multi-Axial Classification
1. Major Clinical Disorders (PTSD, MDD)
2. Personality Disorders (BPD, NPD)
3. Medical conditions that might be relevant to treatment
4. Psychosocial Stressors→ something with which to record environmental contexts
5. GAF (Global adaptive functioning)→ a simple rating of function/summary score for severity (0-100)

Assumptions introduced
- symptoms are most useful basis for assessment
- Nosology based on behavior and symptoms
- Locus of pathology is in the individual

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9
Q

What is the novelty of the DSM-IV?

A

DSM-IV→ 1994
- Introduced “clinically significant distress or impairment in social, occupational, or other important areas of functioning” as criteria
- added culture-bound syndrome

DSM-IV-TR→ 2000
- define broadly mental illness

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10
Q

What are the novelty of the DSM-V?

A

DSM-5→ 2013
- removed multi-baxial system
- introduced dimensional assessment criteria→ only for a small number of diagnosis
- re-classified some disorders (only 157 categories left)

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11
Q

What are the two mains challenges of categorical classification?

A

Heterogeneity
- people within boundaries of specific disorders look different from one another
- hard to find homogeneous essence of a disorder

Comorbidity→ disorders might not be distinct from each other
- ex: if diagnosed with MDD, odds are high that will be diagnosed with Anxiety disorder
- problem in research because if exclude comorbidity, don’t represent the general population of people with that disorder
- among people with DSM diagnosis, 50%qualify for more than one
- over course of lifetime→ 75%
- comorbidity have a lot of important repercussion on development, treatment…
- poorer outcomes for comorbid patients
—>it is the norm to present more than one diagnosis

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12
Q

What are the different explanations of comorbidity?

A

Chance
- MDD adult females→ 20%
- Anxiety disorders→ 20%
- just by chance→ 4% will have both

Sampling bias→ people with more disorders are more likely to seek treatment
- clinical samples are likely biased samples
- more likely to seek treatment for AUD when develop MDD
- BUT don’t account for all comorbidity
- Berksonian bias→ selection bias resulting from the tendency of people with multiple conditions to be selected for research.

Problems with Diagnostic Criteria→ criterion sets overlap
- ex: suicidal ideation in MDD, Schiz, BPD, AUD, SUD
- BUT still don’t account for totality of comorbidity

Poorly-drawn diagnostic boundaries
- multiformity→ same disorders might take different forms
- comorbid disorder might be 3rd independent disorder
- Causal explanation→ one disorder is risk factor for other disorder

Shared etiological risk factors
- ex: child maltreatment associated with every psychopathology

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13
Q

What is the difference between Prevalence, Incidence and Risk factor?

A

Prevalence→ % of people in a population with a disorder at a particular point in time
- ex: past month, year, or lifetime

Incidence→ the % of people who develop a disorder for the 1sttime during a specific time period
- 1st onset cases

Risk Factor→ for epidemiologists, a correlate (most often demographic variables) associated with different disorders / predictor, or cause

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14
Q

What are the lifetime prevalence of the different categories of disorder

A

Mood disorder-> 21%
Anxiety Disorders-> 27%
Substance Use Disorders-> 15%
Any Disorder-> 46%

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15
Q

What are the refrigerator and schizophrenogenic mothers?

A

Especially present in Freudian theories
- schizophrenogenic mother→ inconsistent mother could cause schizophrenia was popular idea
- refrigerator mother→ lack of warmth from mother caused autism

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16
Q

What does polygenic mean?

A

Polygenic→ influenced by many genes
- how many genes determined where you fall on dimension

17
Q

What is the Diathesis-Stress Model?

A

Diathesis→ underlying predisposition or vulnerability to develop a disorder
- genetically influenced
- not enough to get the disorder
- make the disorder more likely to emerge under certain conditions

Stress
- trigger the disorder’s development

18
Q

What is the etiological heterogeneity?

A

Etiological heterogeneity→ same disorders can come from different causes
- ex: MDD might be due to high levels of stress but not diathesis and vice versa
—>assume that diathesis and stress are independent which is not true
—> Gene-Environment Correlations

19
Q

What is the vulnerability-Stress correlations?

A

Vulnerability-Stress Correlations
- non independent in important ways
- Stress generation
- Scars as vulnerability→ previous disorders can become a vulnerability and a stress
- ex: cognitive vulnerabilities following MDD
—>Vulnerability may shape perception of the stress
—>Stress can influence the development of the diathesis

20
Q

What is the difference between equifinality, Final common pathway and multifinality?

A

Equifinality→ getting to same disorder via different pathways
- etiological heterogeneity

Final common pathway
- how does equifinality merge into homogenous phenotypes?
- ex: different things can shape reward processing which then lead to MDD

Multifinality→ same life events can lead to very different outcomes
- ex: child abuse can lead to many psychopathologies

21
Q

What are the different types of longitudinal designs and their characteristics?

A

Retrospective→ collect sample of people with disorder
- ask people about past experience
- ex: interview people with schizophrenia about their adolescence
- use self-report (not always reliable) or existing archival data (cannot control the quality of data you have/ not standardized)

Follow up→ follow the same people over many years
- already-ill sample
- difficult to derive etiological explanations

High-Risk→ follow people at high risk for disorders BUT before they develop the disorder
- variant to follow up
- better for etiological explanations
- identify people at risk→ Offspring of people with a disorder, biological abnormality, behavioral variable
Cons
- very costly because need lot of participants to make sure to have people developing the disorder
- attrition problem
- need to find people with the disorder and have children which can be rare
- biological risk markers are not well-proven
- behaviors→ might be a risk factor or early manifestation of the disease

22
Q

What is the sampling issue with using clinical populations to study a disorder?

A

clinical populations tend to be more severe cases and more likely to be women

23
Q

How do researchers study the genetic epidemiology using family studies?

A

Want to know if run in family
- identify proband→ people with disorder
- then assess family members
- can use Family study with interviews OR Family history study with informant report
- have to find higher rates in proband family than in general population
—>many disorders do run in families
—>can also look at symptoms and not disorder itself
—>problem of coaggregation in family

24
Q

What is an adoption study and what are its limits?

A

Parent or adoptee used as proband
- cross fostering design
- look at adoptive parents and biological parents as well
- but adoption is a rare event AND selective placement bias

25
What is the ACE model in Twin studies?
- ACE Model→ variance distributed between - A→ Additive Genetic component (0-1 (all due to genetics)) - C→ Common Environment Component (similarities just because of shared environment) - E→ Unique Environment
26
What is a gene-environment correlations (rGE)?
environment we experience is not independent from our genotype/ genetically influenced environment
27
What are the three types of rGE?
- Passive→ genes of parents influence the environment in which the child grow in - Active (=niche-picking)→ as people age, seek out environment consistent with genetics - Evocative→ people treat a person differently depending on underlying genes (ex: joyful person might get more positive interactions)
28
What is the single-gene transmission not supported as a mode of transmission?
Single-gene Transmission - would expect 50% of relatives to have disorder→ NOT THE CASE - no strong evidence
29
What account for the missing heritability in the transmission of disorders?
Gene Environment Interactions (GxE) - adverse effects of genes on mental health only expressed under certain environmental conditions Epigenetics - actions of genes can be regulated under certain environmental circumstances - alterations heritable Genotypes-Endophenotypes-Phenotypes - poorly defined phenotypes - Endophenotype→ intermediate step between microscopic genes and nerve cells and the experiential and psychological phenotype (ex: reward processing mechanism)