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PSYC 337 > L01 - Intro to Psychopathology > Flashcards

L01 - Intro to Psychopathology Flashcards

conceptual models - assessment, classification, and diagnosis

1
Q

medical models/syndromes of psychopathology

A

syndrome borrowed from medical models of illness

taxonic

medical models have evolved over time

acknowledge illness as multifactorial/multiply-determined

Clinical Psychology working to catch up

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2
Q

According to Wakfefield, what is harmful dysfunction?

A

dysfunction: “an organ system performing contrary to its design”
- importantly, not at the peak of its design
- Wakefield argues that the brain is designed to perform a number of functions
– thinking
– feeling
– emotion regulation
- problems with any other these functions indicates a disorder
- presumes we understand the function and design of the brain, personality, emotions, etc.

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3
Q

What is Lillienfeld’s critique to Wakefields argument?

A

What is “natural function”?

natural selection depends on variability

some disorders may represent adaptations, not maladaptations

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4
Q

What was Widiger’s proposal to Wakefield and Lillienfeld’s thoughts?

A

mental disorders are constructs

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5
Q

What are the purposes of a classification system?

diagnosis and diagnostic systems

A

Description: highligh critical features of a diagnosis
- e.g., schizophrenia: what are the important symptoms?

Prediction: may tell you something about course, treatment response, etiology

Theory: provides a set of postulates about relationships of different elements to one another

Communication: e.g., between clinicians

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6
Q

What are the 5 criteria proposed for valid classification of disorders?

A
  1. Clinical Description: the disorder has to be characterized by a common set of symptoms that cluster together and are characteristic of the disorder
  2. Course: people with the disorder should follow a common trajectory, and have a similar onset
  3. Treatment response: if a disorder is valid, most people will respond similarly to similar treatments
  4. Family history: does the disorder run in families? if so, speaks to validity of a diagnosis
  5. Laboratory studies: look for biological and psychopathological associations
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7
Q

What are the limitations of a classification system?

and what is a procrustean bed?

A

Loss of uniqueness: diagnosis implies that common features are more important than the ways in which individuals vary

Difficulty of boundary cases: what do you do about the people who are on the boundary? Do we arbitrarily decide which group they’re more similar to? (sometimes we do both)

procrustean beds: we fit people to our diagnosis rather than fitting
diagnosis to the people in front of us

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8
Q

What are categorical and dimensional systems?

A

Categorical
- presence/absence of a disorder
– either you are anxious or you are not anxious

Dimensional
- rank on a continuous quantitative dimension
– degree to which a symptom is present
– How anxious are you on a scale from 1 to 10?

Dimensional systems may better capture an individual’s functioning

Categorical approach has advantages for research and understanding

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9
Q

What are the advantages of a categorical approach vs. a dimensional one?

A

Categorical
- simplifies communication
- in dimensional model, everybody falls SOMEWHERE
- natural preference among people to employ categories in speech
- categories better-suited for clinical decision-making:
– hospitalize or don’t?
– Treat or don’t?
– Dimensional: arbitrary cut-offs

Dimensional
- preserves more information
- greater reliability - inter-rater, test re-test
- cutoffs in categorical system tend to magnify small differences

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10
Q

In what year was DSM-I published, and how many diagnostic categories did it include?

A

1952

106 categories

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11
Q

In what year was DSM-II published and how did it differ from DSM-I?

A

1968

  • few categories (182 categories)
  • no requirements for # of symptoms
  • psychoanalysis was the dominant paradigm
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12
Q

In what year was DSM-III published and how did it differ from DSM-II?

A

1980
- 265 categories
- demand for a more biological, empirical approach

Inclusion criteria: what symptoms do you need to have, and how many?

Duration criteria: how long do you need to exhibit these symptoms?

Exclusion criteria: what symptoms rule out a diagnosis?

Multi-axial classification

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13
Q

What is the mulit-axial classification?

(DSM-III)

A
  1. Major Clinical Disorders (e.g., MDD, PTSD)
  2. Personality Disorders (e.g., BPD, NPD)
  3. Medical conditions that might contribute or be relevant to treatmetn
  4. Psychosocial Stressors - something with which to record environmental contexts
  5. GAF - a simple rating of function/summary score for severity
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14
Q

How many diagnostic categories did DSM-III-R have?

A

292

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15
Q

How many diagnostic categories did DSM-IV-TR have?

A

297

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16
Q

How many diagnostic categories does DSM-5 have?

A

157

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17
Q

What were the assumptions introduced in DSM-III?

A

symptoms are the most useful basis for assessment
- nosology based on behaviour and symptoms

locus of pathology is in the individual
- what about family systems?
- social systems?

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18
Q

When was DSM-IV published and what did it introduce?

A

1994

introduced “clinicall significant distress or impairment in social, occupational, or other important areas of functioning”

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19
Q

When was DSM-IV-TR published and how did it differ from DSM-IV?

A

2000

did not introduce new diagnoses or specific criteria

provided more information on each diagnosis

provided a broad definition of mental illness

20
Q

When did DSM-5 come out and how does it differ from DSM-IV-TR?

A

2013

removed multi-axial system

introduced dimensional assessment criteria for some diagnoses

re-classified some disorders

removed others

21
Q

What are some challenges to categorical classification?

A

Heterogeneity
- same diagnoses, but different symptoms

Comorbidity
- of people who currently meet criteria for one disorder, 50% qualify for more than one
– over the course of their lifetime, 75%
– comorbidity affects course, development, presentation, treatment response, etc.
– comorbid patients tend to have poorer outcomes
- research implications: anything you find to be associated with one disorder may actually be a result of the comorbid disorder
– if you don’t consider any comorbidities they might have, you are missing a huge part of the diagnosis

22
Q

Why does Comorbidity exist?

A

Chance
- odds of MDD for adult females = 20%
- odd of anxiety disorder for adult females = 20%
– 4% will have both
– some comorbidity is just chance
- but comorbidity greater than chance alone would indicate

Sampling bias
- each disorder associated with a chance of being treated
- individuals with more disorders (i.e., more severe individuals) are more likely to seek treatment
- clinical samples, likely biased samples
- BUT, we find high rates of comorbidity in community samples as well
– not just clinical samples
– sampling bias doesn’t account for all

Problems with diagnostic criteria: many criteron sets overlap
- suicidal ideation in MDD, schizophrenia, BPD, AUD, SUD
- sleeplessness in MDD and GAD
- Worry in GAD and MDD, etc.
- still can’t totally account for high rates of comorbidity

Poorly-drawn diagnostic boundaries
- Multiformity:
– possible that some disorders manifest themselves in the same way
– people with MDD frequently have panic attacks
– comorbid disorders may in fact reflect a 3rd, independent disorder
- Causal explanation: one disorder is a risk factor for another disorder
– Conduct disorder in youth may lead to adult Substance Use Disorder by affecting the peers youth is exposed to
- Shared etiological risk factors:
– etiology: the origins of the disorder
– may also explain some of the comorbidities

23
Q

What are some alternative, dimensional/hierarchical models to diagnosis?

A
  1. one early attempt
    – factor analysis: you put a bunch of variables in a dataset together, and then you run a factor analysis to see which symptoms/diagnoses clump together (share variance) and which ones do not to identify factors in this structure of psychopathology
    - Internalizing:
    – MDD, GAD, and Panic Disorder all load onto internalizing
    – people who cause distress to themselves (FALSE, but people do mention this)
    - Externalizing:
    – ODD, SUD, Psychopathy load onto externalizing
    – they are distinct and relatively independent
    – people who cause distress to others (FALSE, but people do mention this)
  2. HiTOP
  3. RDoC
24
Q

Why are MDD and GAD more like one another?

A

because they are more related to anxious misery and load onto internalizing

25
Q

Why are Panic disorder and Social phobia more like one another?

A

because they are more fear-based disorders that load onto internalizing

26
Q

Which disorder do not load onto anything in a factor analysis model?

A

OCD
PTSD
BPD

27
Q

What is HiTOP?

A

Hierarchical Taxonomy of Psychopathology

They introduced thought disorder

Separated externalizing into 4 different categories
- result of factor analysis

some people are more at risk for or more likely to have psychopathology that can manifest in mulitple ways

poses some challenges

28
Q

What is RDoC?

A

Research Domain Criteria

funding initiative

dysfunction of core systems that animals have evolved to have

trans-diagnostic approach

not for treatment, just for research definitions
- really agnostic about where we need to go

29
Q

What does prevalence mean?

A

% of people in a population with a disorder at a particular point in time
- e.g., past month, year, or lifetime

30
Q

What does incidence mean?

A

% of people who develop a disroder for the 1st time during a specific period
- 1st onset cases
- prevalence = incidence x chronicity

31
Q

What does risk factor mean?

A

for epidemiologists, a correlate (most often demographic variables) associated with different disorders
- psychologists use this term to mean predictor, or cause

32
Q

What is the 1-year prevalence and the average age of onset of Major Depression?

A

6.7%

14-15, 30s

33
Q

What is the 1-year prevalence and the average age of onset for Persistent Depressive Disorder?

A

1.5%

30s

34
Q

What is the 1-year prevalence and the average age of onset for Bipolar disorder?

A

2.6%

25

35
Q

What is the 1-year prevalence and the average age of onset for Panic disorder?

A

2.7%

24

36
Q

What is the 1-year prevalence and the average age of onset for OCD?

A

1.0%

child-adolescent

37
Q

What is the 1-year prevalence and the average age of onset for Social Anxiety Disorder?

A

6.8%

13

38
Q

What is the 1-year prevalence and the average age of onset for GAD?

A

3.1%

31

39
Q

What is the 1-year prevalence and the average age of onset for PTSD?

A

3.5%

any age

40
Q

What is the lifetime prevalence for mood disorders, anxiety disorders, substance use disorders, and any other disorders?

A

Mood disorders: 21%
Anxiety Disorders: 27%
Substance Use Disorders: 15%
Any disorders: 46%

41
Q

What is the 1-year prevalence for 19-25-year-olds for Anxiety disorders, Mood disorders, Alcohol Use Disorder, any other disorders, and mental health usage?

A

Anxiety Disorder:
- college students: 11.9%
- not college students: 12.7%

Mood Disorder:
- college students: 10.6%
- not college students: 11.9%

Alcohol Use Disorder
- college students: 20.4%
- not college students: 17%

Any disorder:
- college students: 45.8%
- not college students: 47.7%

Mental Health Usage:
- college students: 18.5%
- not college students: 21.5%

42
Q

In etiological models, what is an environmental model?

A

environmental/learning experiences

Freudian theories

“Schizophrenogenic mother”
- the idea that a mother that was alternating between an over-protective and a distance behaviour led to schizophrenia

“Refrigerator mother”
- the idea that a mother who lacked genuine warmth and positivity caused autism

we are genetically related (in most cases) to the people who parent us
- always important to consider the difference between environemnt and genes, but they’re often related to each other

43
Q

In etiological models, what are genetic models?

A

genes are not deterministic
- genes did it
- if you have a genetic risk for a mental disorder
- psychopathologies run in families
- subejct to genetic influence/genetic contributions
- no evidence, to date, show that disorders are entirely heritable

most genes are **probabilistic **
- make small contributions (with other genes) to create the ultimate outcome
- research identifying dozens of genes that, in certain combinations, lead to symptoms of different forms of psychopathology

Polygenic: influenced by many different genes
- how many genes you have determines where you fall on a spectrum of vulnerability or expression of a disease

44
Q

What is the diathesis-stress models?

A

TABLE:
- stress present/diathesis present: ILL
- stress present/diathesis absent: WELL
- stress absent/diathesis present: WELL
- stress absent/diathesis absent: **WELL*

Rosenthal & Neal (early 1960s)
- natura vs. nurture –> they interact with each other
- diathesis is a vulnerability or predisposition of developing a disorder
– examples: parenting styles, attachment styles, patterns of neural response, etc.
- stress –> exposure to experienes or factors that overwhlem ability of homeostasis

etiological heterogeneity
- many different pathways to the same disorder
- all pathways are complex and differently determined

assumes diathesis and stress are independent

Gene-environment correlation

45
Q

What are vulnerability-stress correlations?

A

often non-independent in important ways

stress generation
- e.g., excessive reassurance seeking

“scars” as vulnerability
- cognitive vulnerabilities following MDD ep
- having been ill can change the way you think about things
– may lead you to view the world in a negative way –> exacerbate certain other factors

vulnerability may shape perception of the stress

stress can influence the development of the diathesis
- gestational stress and mental illness

46
Q

What are some important terms in etiology?

A

equifinality

final common pathway

multifinality

PSYC 337 (2 decks)

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