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PSYC 337 (psychopathology) > midterm 1 > Flashcards

midterm 1 Flashcards

1
Q

what is etiology?

A

the study of the origins of psychopathology

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2
Q

why is it important to define mental illness?

A
  • knowing the issue makes it easier to treat and standardize treatments
  • destigmatization (within the self and among others)
  • allows us to predict the course of the disorder based on common trends
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3
Q

where does the concept of syndromes come from?

A
  • put forth by Thomas Sydenham (c. 1600s)
  • borrowed from the medical model of physical illness (clusters of symptoms that present together)
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4
Q

what is a syndrome?

A
  • a measurable entity that expresses itself as clusters of symptoms that present together
  • symptoms either occur at the same time or have a predictable course
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5
Q

what does it mean when we say that mental disorders are taxonic in nature?

A
  • they are measurable, real-world entities
  • can be treated/classified like physical ailments
  • categorical in nature (you have it or you don’t)
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6
Q

in what ways do we accept/reject the medical model of psychopathology today?

A
  • accept the idea of syndromes
  • accept that mental disorders are measurable and can be treated like physical ailments
  • reject the idea that they are categorical in nature (we know now that boundaries are blurred and different severities exist)
  • medical models have evolved over time to acknowledge illness as multifactoral and multiply determined
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7
Q

list the four kinds of approaches to differentiating between normative vs psychopathological behaviour

A
  1. medical model
  2. harmful dysfunction
  3. mental disorders as constructs
  4. multimodal approach
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8
Q

what is harmful dysfunction? who pioneered it?

A
  • Wakefield (1992)
  • looks to natural selection as the basis for mental disorder classification
  • biological component: the brain is designed to perform many basic functions; problems with these functions indicates disorder
  • social component: to be considered a disorder, dysfunction must cause harm/impairment within the social context
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9
Q

what is Lillienfeld’s critique of Wakefield’s harmful dysfunction approach?

A
  • what constitutes a “natural function” is hard to define, since it’s difficult to differentiate between adaptations, adaptively neutral byproducts, and secondary adaptations
  • natural selection depends on variability
  • some disorders may represent adaptations, not maladaptations
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10
Q

what is an adaptively neutral byproduct?

A
  • an ability that may be beneficial in certain social circumstances but which is not necessary for evolutionary continuation
  • eg. ability to do art
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11
Q

define dysfunction

A

an organ system performing contrary to its design/intended purpose

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12
Q

what is the main point of the mental disorders as a construct approach to measuring psychopathology? who pioneered it?

A
  • Widiger
  • a construct is something that exists and has real world consequences but is arbitrarily delineated or categorized
  • there is no single all-encompassing definition of psychopathology–the ways of conceptualizing it is constantly evolving
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13
Q

according to the multimodal approach to psychopathology, what are psychiatric disorders?

A

psychiatric disorders are…
- complex latent constructs
- multiply determined
- represent the sum of environmental influences + genetic susceptibility or biological abnormality

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14
Q

according to the multimodal approach to psychopathology, how can we measure disorders?

A

requires multiple modes of measurement:
- self-report
- neural functioning
- physiological responses
- behavioural responses

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15
Q

why is it important to have a classification system for disorders?

A
  1. description (highlights critical features, avoids subjectivity)
  2. prediction (informs about the course, treatment and response, and etiology of the disorder)
  3. theory (postulates how/why certain symptoms occur together and whether there is an underlying mechanism of illness)
  4. communication (eg. between clinicians; allows for standardization of treatment and understanding of ailments)
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16
Q

what do we mean when we say “diagnosis is prognosis”?

A

standardized diagnostic practices and categorization of mental disorders may allow for predictions about the course of the illness, possible treatments, response to treatment, and its etiology

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17
Q

what are the limitations of the classification system of diagnosis?

A
  • loss of uniqueness (emphasizing common features more than the ways in which individuals vary)
  • difficulty of boundary cases (i.e., people who sit right at the threshold)
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18
Q

what is a procrustean bed?

A
  • comes from a story of an inn-keeper who only had one size of bed and would chop of the limbs that hung over the end
  • used to describe the limits of the classification system of diagnosis when it comes to boundary cases
  • illustrates the debate: should we fit the diagnoses to people, or fit people into to the diagnoses?
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19
Q

what 5 criteria do Robins and Guze propose for determining valid classification of disorders?

A
  1. clinical description: must be characterized by a common set of symptoms that cluster together
  2. course: people with the disorder should have a common trajectory and onset
  3. treatment response: valid disorders have similar treatment responses
  4. family history: heritability speaks to the validity of the diagnosis (operating on the medical model assumption)
  5. lab studies: useful in looking for biological, psychophysiological, and behavioural associations with the disorder
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20
Q

what are the advantages of a dimensional system of classification?

A
  • everybody falls somewhere
  • preserves more info about the individual
  • high inter-rater and test-retest reliability
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21
Q

what are the disadvantages of a categorical system of classification?

A
  • diagnostic criteria cut-offs tend to magnify small differences between patients
  • lower inter-rater and test-retest reliability than dimensional systems
  • difficulty with boundary cases/cases just below the threshold
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22
Q

what are the advantages of a categorical system of classification?

A
  • simplifies clinical communication
  • potentially better-suited for making clinical decision (eg. hospitalize/treat or don’t)
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23
Q

what is inter-rater reliability?

A

measures consensus among different people who rate the same patient

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24
Q

what is test-retest reliability?

A

measures consistency when testing a patient over a period of time

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25
Q

when was the first edition of the DSM released?

A

1956

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26
Q

when was the DSM-II released?

A

1968

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27
Q

what were the main differences between the DSM-I and the DSM-II?

A

the DSM-II attempted to establish a scientifically grounded, standardized, and shared definition of mental illness for the first time, as well as broad descriptions of disorders

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28
Q

when was the DSM-III released?

A

1980

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29
Q

what were the main differences between the DSM-II and the DSM-III?

A
  • DSM-III = biological empirical approach; DSM-II = psychoanalytic approach
  • addition of inclusion criteria (what symptoms you need to have and how many) and exclusion criteria (what symptoms rule out a diagnosis), and duration criteria (how long you need to exhibit these symptoms)
  • addition of multi-axial classification
  • big jump in the amount of categories
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30
Q

describe the multi-axial classification system

A
  1. major clinical disorder (MDD, PTSD)
  2. personality disorders (BPD, NPD)
  3. medical conditions that might contribute to or be relevant to treatment
  4. psychosocial stressors (environmental context)
  5. global assessment of functioning (GAF) - summary score out of 100 for severity
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31
Q

what assumptions are implicit in the DSM-III?

A
  • biological empirical approach is the most valid
  • symptoms are the most useful basis for assessment (as opposed to freudian etiology)
  • locus of pathology is in the individual rather than social/environmental
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32
Q

what is nosology?

A

diagnostic system

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33
Q

when was the DSM-IV introduced?

A

1994

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34
Q

in what ways did the DSM-III and the DSM-IV differ?

A

DSM-IV introduced “clinically significant distress or impairment in social, occupational, or other important areas of functioning” as a requirement for diagnosis

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35
Q

when was the DSM-IV-TR released?

A

2000

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36
Q

what were the main differences between the DSM-IV and the DSM-IV-TR?

A
  • DSM-IV-TR provided more info about each diagnosis
  • DSM-IV-TR provided a broad definition of mental illness for the first time
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37
Q

when was the DSM-V introduced?

A

2013

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38
Q

how did the DSM-V differ from the DSM-IV(-TR)?

A
  • DSM-V removed the multi-axial system
  • re-introduced dimensional assessment to certain disorders (as opposed to categorical) (eg. ASD)
  • re-classified some disorders and removed others (eg. OCD from anxiety disorders to OC and related disorders; PTSD from anxiety disorders to trauma and stressor related disorders); removed nearly half the categories
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39
Q

which version of the DSM removed nearly 150 categories of diagnoses?

A

DSM-V

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40
Q

which version of the DSM first provided a broad definition of mental illness?

A

DSM-IV-TR

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41
Q

which version of the DSM first considered diagnosis based on impairment to daily life/functioning?

A

DSM-IV

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42
Q

which version(s) of the DSM included the multi-axial system?

A
  • DSM-III (-R)
  • DSM-IV (-TR)
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43
Q

which version of the DSM first shifted the focus of diagnosis from etiology to symptomology?

A

DSM-III

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44
Q

which version of the DSM first incorporated inclusion criteria?

A

DSM-III

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45
Q

which version of the DSM first incorporated duration criteria?

A

DSM-III

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46
Q

which version of the DSM first incorporated exclusion criteria?

A

DSM-III

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47
Q

which version of the DSM saw dramatic changes from its predecessors based on popular demand for a more biological and empirical approach?

A

DSM-III

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48
Q

which version of the DSM was dominated by the psychoanalytic paradigm?

A

DSM-II

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49
Q

what does heterogeneity mean, in regards to diagnosis and classification? what is its implication?

A
  • heterogeneity illustrates how different people with the same diagnosis may have different symptom profiles
  • represents a challenge to the categorical classification symptom, as people within one category do not look alike, and may experience symptom overlap with other disorders
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50
Q

what are the two main challenges to the categorical system of diagnosis present in the DSM-V?

A
  • heterogeneity
  • comorbidity
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51
Q

what are the consequences associated with comorbidity?

A
  • affects the course, development, presentation, and treatment response of a disorder
  • comorbid patients tend to have worse outcomes
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52
Q

how common is comorbidity?

A
  • of people who currently meet criteria for one disorder, 50% qualify for more than one
  • lifetime prevalence of comorbidity (for those already meeting one diagnosis) is as high as 75%
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53
Q

list the theories as to why comorbidity exists

A
  1. chance
  2. sampling bias
  3. problems with diagnostic criteria
  4. poorly drawn diagnostic boundaries
  5. causal explanations
  6. shared etiological risk factors
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54
Q

explain the theory that says that comorbidity exists due to chance. what evidence supports/refutes this?

A
  • odds of acquiring two different disorders may overlap in the same person (eg. 20% chance of MDD and 20% chance of anxiety disorder -> 4% chance of having both)
  • but, comorbidity arises at a greater rate than chance alone would suggest, indicating that this is not a strong enough explanation
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55
Q

explain the theory that says that comorbidity exists due to sampling bias. what evidence supports/refutes this?

A
  • individuals with more (severe) symptoms are more likely to seek treatment
  • but, we find high rates of comorbidity in community samples as well, not just clinical samples, indicating that sampling bias cannot account for all comorbidity
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56
Q

explain the theory that says that comorbidity exists due to problems with diagnostic criteria. what evidence supports/refutes this?

A
  • the idea is that many criterion sets may overlap, leading to diagnosis of more than one disorder
  • eg. suicidal ideation is a symptom of MDD, schizophrenia, BPD, AUD, and SUD
  • still can’t totally account for such high rates of comorbidity
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57
Q

explain the theory that says that comorbidity exists due to poorly drawn diagnostic boundaries. what evidence supports/refutes this?

A
  • multiformidy: disorders can express themselves in many ways–some of which can mimic other disorders
  • eg. people with MDD frequently have panic attacks
  • evidence that comorbid disorders may in fact reflect a third independent disorder
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58
Q

what is multiformidy?

A

the idea that disorders can express themselves in many ways–some of which can mimic other disorders (eg. people with MDD frequently have panic attacks)

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59
Q

explain the theory that says that comorbidity exists due to causal explanation. what evidence supports/refutes this?

A
  • claims that one disorder is a risk factor for another disorder
  • eg. GAD sometimes leads to MDD
  • eg. conduct disorder may lead to substance disorder
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60
Q

explain the theory that says that comorbidity exists due to shared etiological risk factors. what evidence supports/refutes this?

A
  • claims that multiple disorders may arise from one event or risk factor, which is why comorbidity exists
  • eg. childhood maltreatment is a strong predictor for many forms of psychopathology
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61
Q

what are two alternative approaches to the DSM-V’s categorical system that have been proposed?

A
  • hierarchical system (eg. HiTOP)
  • RDoC (research domain criteria) approach
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62
Q

describe the hierarchical system of diagnosis. who proposed it?

A
  • put forth by Achenbach
  • proposed alternative to the categorical system
  • looks at symptoms/disorders that often co-occur in an effort to explain comorbidity
  • eg. HiTOP
  • two underlying dimensions: internalizing and externalizing
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63
Q

what are the main criticisms regarding a hierarchical approach to disorder classification?

A
  • neglects to address disorders that don’t fit into the structure
  • internalizing and externalizing symptoms/disorders are frequently correlative and overlapping
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64
Q

describe the research domain criteria (RDoC) approach to diagnostic classification

A
  • proposed alternative to the categorical system
  • talks about dysfunctions of core systems that are thought to be central to human functioning, rather than focusing on diagnosis (aka transdiagnostic approach)
  • better for research than for treatment
  • domains include negative valence systems, positive valence systems, cognitive systems, systems for social processes, and arousal and regulatory systems
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65
Q

what is a transdiagnostic approach to classification

A
  • an approach that focuses on dysfunction across diagnoses
  • eg. RDoC
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66
Q

what are the domains present in the RDoC approach to classification?

A
  • negative valence systems
  • positive valence systems
  • cognitive systems
  • systems for social processes
  • arousal and regulatory systems
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67
Q

what is epidemiology?

A
  • study of the frequency and distribution of traits in a population
  • looks at demographic correlates of disorders
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68
Q

what is prevalence? how does this differ from incidence?

A
  • prevalence: percent of people in a pop with a disorder during a specific time period
  • incidence: percent of people in a pop who develop a disorder for the first time during a specific time period
  • prevalence = incidence x chronicity
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69
Q

which class of disorders are the most common in terms of lifetime prevalence?

A

anxiety disorders (27%), closely followed by mood disorders (21%)

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70
Q

describe the environmental model of etiology

A
  • learning experiences/environment are responsible for the emergence of psychopathologies
  • based in Freudian theories (schizophrenic or refrigerator mother)
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71
Q

describe the notion of the refrigerator mother

A
  • freudian/environmental model of etiology
  • idea that a mother who lacked genuine warmth causes autism
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72
Q

describe the notion of the schizophrenic mother

A
  • freudian/environmental model of etiology
  • idea that a mother who is alternating between overprotective and rejecting is responsible for the emergence of schizophrenia
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73
Q

describe the genetic model of etiology

A
  • genes are not deterministic but are probabilistic
  • researchers have identified dozens of genes that, in certain combinations, lead to symptoms of different forms of psychopathology (i.e., polygenic symptoms)
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74
Q

what does polygenic mean?

A
  • influenced by many genes
  • according to the genetic model of etiology, the amount of specific genes you have determines where you fall on the spectrum of vulnerability or of the expression of a disease
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75
Q

describe the diathesis-stress model of etiology

A
  • combines nature and nurture
  • diathesis = predisposition or vulnerability (often genetic)
  • stress = exposure to experiences or factors to an organism’s ability to maintain homeostasis
  • stress + diathesis = unwell; presence of only one = well
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76
Q

what are the main critiques of the diathesis-stress model of etiology?

A
  • doesn’t acknowledge etiological heterogeneity
  • assumes diathesis and stress are independent, though evidence shows that a gene-environment correlation exists
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77
Q

what is diathesis?

A
  • predisposition of vulnerability
  • often genetic but not always
  • eg. neural response patterns, attachment styles, etc.
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78
Q

describe the vulnerability-stress correlations model of etiology

A
  • stress and vulnerability are non-independent in important ways
  • vulnerable people may behave in ways that produce stress (eg. excessive reassurance seeking)
  • vulnerability may shape the perception of stress
  • “scars” (i.e., having been ill in the past) can exist as a vulnerability factor by changing the way you think about things
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79
Q

what is equifinality?

A
  • when many people get the same diagnosis through multiple pathways or root causes
  • makes the study of etiology very difficult and complex
  • can be due to comorbidity and heterogeneity of disorders
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80
Q

what is the notion of a final common pathway?

A
  • the idea that multiple etiological factors converge into one final step or final cause of a disorder
  • suggests a potential intervention point for treatment
  • eg. family history OR stress patterns -> specific neurological processes -> MDD
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81
Q

what is multifinality?

A
  • the idea that a single risk factor can lead to many different outcomes
  • eg. child abuse is associated with almost all forms of psychopathology
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82
Q

describe the difference between classification and diagnosis

A
  • classification: the overarching taxonomy of mental illness
  • diagnosis: the act of placing an individual into a category within the existing taxonomy
  • classification is a prerequisite for diagnosis
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83
Q

what is the difference between signs and symptoms?

A
  • signs = observable indicators
  • symptoms = subjective indicators
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84
Q

describe the difference between pathology and etiology

A
  • pathology: the underlying pathophysiology (the abnormal changes in body functioning) that may accompany a condition
  • etiology: the cause of a condition
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85
Q

what is the difference between syndrome vs disorder vs disease

A
  • syndrome: constellations of signs/symptoms that co-occur across individuals or that point to an underlying etiology
  • disorders: syndromes that cannot be explained by other conditions
  • diseases: disorders in which pathology and etiology are understood
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86
Q

according to Robins and Guze, what are the 4 requirements for establishing the external validity of psychiatric diagnoses?

A
  1. clinical description
  2. lab research
  3. natural history
  4. family studies
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87
Q

what is the statistical model or disorder? what are its shortcomings?

A
  • equates disorder with statistical rarity
  • but, it offers no guidance as to where to draw the line between normality and abnormality, no guidance as to which dimensions are relevant to abnormality, and misclassifies high scores on certain adaptive dimension (intelligence, creativity, etc) as being inherently abnormal
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88
Q

what is the subjective distress model of disorder? what are its shortcomings?

A
  • psychological pain is the key feature distinguishing disorder from non-disorder
  • but, it fails to recognize that some disorders cause minimal psychological distress, since people with these conditions could see nothing wrong with their behaviour
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89
Q

describe the biological model of disorder and its shorcomings

A
  • disorder is defined in terms of its biological/evolutionary disadvantage that it poses to the individual
  • but, while many disorders do support this model, many counterexamples exist in which the disorder poses no threat to longevity, and many non-illnesses can pose this threat
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90
Q

what is the need for treatment model of disorder? what are its shortcomings?

A
  • disorders are a class of conditions characterized by a perceived need for medical intervention
  • but, many counterexamples exist that require medical intervention but are not disorders (eg. pregnancy)
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91
Q

what is the roschian analysis model of disorder?

A

belief that disorders are intrinsically undefinable, since their features and boundaries are necessarily vague and blurry

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92
Q

what is theoretical agnosticism? what version of the DSM pioneered this approach?

A
  • when diagnosis does not require ties to a specific etiology
  • first introduced in the DSM-III, as many freudian approaches were left behind
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93
Q

which version of the DSM introduced culturally specific disorders?

A

DSM-IV

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94
Q

what are the four main criticisms that the DSM-V faces?

A
  1. extensive comorbidity (symptom overlap can lead to diagnostic overshadowing or underdiagnosis)
  2. medicalization of normality (due to lower diagnostic thresholds)
  3. does not address the attenuation paradox (i.e., that higher reliability can lead to lower validity)
  4. unsupported retention of a categorical model (claims that no disorder is completely discrete, yet it follows a categorical model)
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95
Q

what is the attenuation paradox?

A

higher reliability can lead to lower validity

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96
Q

what are retrospective studies?

A
  • type of longitudinal study
  • involves collecting a sample of people with a disorder and then trying to determine what preceded it
  • through self-report or existing archival data
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97
Q

what are follow-up studies?

A
  • type of longitudinal study
  • follows people with the disorder over time to see what happens
  • uses an already-ill sample
  • useful for examining the course of a disease, but difficult to derive etiological explanations
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98
Q

what are high-risk studies?

A
  • type of longitudinal study and type of prospective study
  • identifies people who are likely to develop a disorder and follow them over time
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99
Q

what is the difference between a case control design and a cohort design? when is each one useful?

A
  • case control involves comparing one group of people with a disorder to a second group without the disorder (most useful when looking at a rare disorder)
  • cohort involves a single large sample of people, some of whom have the disorder (preferable when the disorder is fairly common, as it allows for comparison to multiple possible control groups)
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100
Q

how do patient samples tend to differ from community samples?

A

patient samples tend to be more severe, have more comorbidities, more chronic course, and are more likely to be female, and have higher SES

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101
Q

what’s the difference between healthy controls and psychiatric controls?

A
  • HC: people without the disorder
  • PC: people with a different disease than the one you’re studying
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102
Q

what are the three steps in determining genetic epidemiology?

A
  1. family studies
  2. adoption studies
  3. twin studies
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103
Q

how are family studies conducted?

A
  1. identify proband and ask about their family and their potential symptoms
  2. assess family members to see if they also fave the disorder (interview or informant report)
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104
Q

what is a proband?

A

someone who has the disorder at hand; often used in reference to family studies/genetic epidemiology

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105
Q

what is coaggregation (in reference to genetic epidemiology)?

A
  • when a family may show higher rates of other related disorders than the general population
  • provides evidence that there is a genetic transmission of shared vulnerability that may manifest in different ways in different people
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106
Q

what do general findings from family studies tell us about the role of genes in determining disorders?

A
  • subthreshold and coaggregation found in family studies can suggest a genetic role of a disorder, though it doesn’t necessarily prove it
  • points to genetic transmission of shared vulnerability, that may manifest differently
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107
Q

list the three types of adoption studies

A
  1. biological parents as proband
  2. adoptee as proband
  3. cross-fostering design
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108
Q

describe the “biological parent as proband” type of adoption study

A

involves finding the biological parent and assessing them for the disorder of interest, then looking at whether their biological children have the same disorder or symptoms

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109
Q

describe the “adoptee as proband” type of adoption study

A

involves assessing adopted child for the disorder of interest, then tracking down both the biological and adoptive parents to determine nature vs nurture for the disorder

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110
Q

describe the “cross-fostering design” type of adoption study

A

involves comparing two groups to determine which group of children is at greater risk for developing the disorder:
1. children of biological parents without the disorder raised by adoptive parents with the disorder
2. children of biological parents with the disorder raised by adoptive parents without the disorder

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111
Q

which of the three types of adoption studies is the most difficult to conduct?

A

cross-fostering design

112
Q

describe the three kinds of gene-environment correlations?

A
  1. passive (the people who give you your genes are also the ones who parent you)
  2. active/niche-picking (we behave in ways and gravitate toward environments based on our genetic makeup)
  3. evocative/reactive (genotype may determine the response we elicit from the people in our environment)
113
Q
A
114
Q

what is the Flynn effect? what is its significance?

A
  • IQ has increased across the 20th century, while the tests have gotten harder
  • mostly seen in developing countries
  • shows that IQ is malleable, while also being 80% heritable
115
Q

what is the genotype-phenotype gap?

A
  • begs the question: how does the additive genetic component contribute to the observed phenotype?
  • people are looking for an endophenotype to explain this phenomenon
116
Q

how was anxiety classified/understood in the DSM-I and -II?

A
  • anxiety was grouped in with somatoform and dissociative disorders
  • thought to be related to either neurosis or psychosis
  • caused by disturbance in the central nervous system
117
Q

which aspect of anxiety in particular was studied extensively by Freud?

A

distinction between fear and anxiety

118
Q

which version of the DSM first introduced the class of anxiety disorders?

A
  • DSM-III
  • before that, it was grouped in with somatoform dissociative disorders, as per the psychoanalytic tradition
119
Q

how do we define fear?

A
  • response to a real or perceived, objective, current threat
  • very quick response
  • prepares us for action
  • characterized by increases in heart rate, blood pressure, cortisol and adrenaline, breathing rate, as well as muscle tension
120
Q

how do we define panic?

A
  • false alarm: fear response evoked in the absence of any real current or future threat
  • characterized by increases in heart rate, blood pressure, cortisol and adrenaline, breathing rate, as well as muscle tension (mimics fear response)
121
Q

how do we define anxiety?

A
  • future-oriented; feeling threatened by a potential occurrence
  • in the absence of a current threat
  • many symptomatic overlaps with fear and panic
122
Q

what are the three categories/chapters of anxiety-related disorders in the DSM-V?

A
  1. anxiety disorders
  2. obsessive-compulsive and related disorders
  3. trauma and stressor-related disorders
123
Q

according to the HiTOP model of classification, what are the two potential pathways that anxiety disorders may follow?

A
  1. internalizing -> fear (includes specific phobias, SAD, panic disorder, OCD)
  2. internalizing -> distress (includes GAD, PTSD)
124
Q

what are the 5 most common types of specific phobias?

A
  1. animal-type
  2. natural environment-type
  3. blood/injection/injury-type
  4. situational-type
  5. residual other category
125
Q

what is the sex prevalence ratio for phobias?

A

2F : 1M

126
Q

which other disorders are most often comorbid with phobic disorders?

A

anxieties and depression

127
Q

in terms of their course, what makes phobic disorders different from other anxiety disorders?

A

most children outgrow specific fears and don’t become phobic adults, while this is not true of other anxiety disorders

128
Q

what is Mowrer’s two-factor theory regarding the etiology of phobias?

A
  • behavioural: fears are acquired through classical conditioning and maintained through operant conditioning
  • negative reinforcement: feelings of anxiety related to the conditioned fear stimulus leads to increased avoidance behaviour
129
Q

what is the evolutionary preparedness theory regarding the etiology of phobias?

A
  • we have evolved a sensitivity to certain stimuli, and the effects of this selection are still with us
  • certain fears were adaptive at one point, and these fears were thus selected for
  • this is why we are more likely to fear snakes or heights than flowers
130
Q

what were the main takeaways from Cook and Mineka’s experiment on phobia acquisition?

A
  • certain fears are easier to condition than others, likely due to their adaptive quality
  • heritability and temperament play a role in phobia acquisition
131
Q

describe the diagnostic criteria for panic disorder

A
  1. characterized by recurrent and unexpected panic attacks
  2. at least one panic attack followed by a month or more of persistent concern about panic attacks
  3. not better accounted for by another disorder
  4. discrete period of fear of discomfort meeting at least 4 of the 13 symptom criteria (symptoms must develop abruptly and peak in intensity within 10 min)
132
Q

according to Klein, how does panic disorder develop?

A
  • originally results from anxiety paired with a negative stimulus (i.e., panic attack)
  • then avoidance occurs
  • through avoidance, anxiety is negatively reinforced
133
Q

what does differential diagnosis mean?

A

attempt to identify whether an individual’s symptoms are better explained by another disorder label

134
Q

what is the sex prevalence ratio of panic disorder?

A

2F : 1M

135
Q

what is the median age of onset for panic disorder?

A

24 years, though it has a narrow range: rarely before adolescence or after middle age

136
Q

what is Goldstein and Chambliss’ theory of panic disorder?

A
  • “fear of fear”
  • dominant theory of the disorder today
137
Q

what is Clark’s theory of panic attacks?

A
  • panic attacks are due to catastrophic misinterpretations of certain bodily sensations
  • symptomatic experiences then become magnified, leading to more arousal symptoms (vicious cycle)
138
Q

what is Reiss and McNally’s theory of panic disorder?

A
  • anxiety sensitivity is an important etiological factor
  • people who are high on anxiety sensitivity are more likely to panic when they experience physiological sensations of anxiety
139
Q

what are two culture-specific symptoms of panic attacks?

A

uncontrollable crying and sore neck

140
Q

agoraphobia diagnosis requires a fear of which situations?

A

at least 2 of the following:
- public transport
- open spaces
- enclosed places
- being outside the home alone
- standing in line or being in a crowd

141
Q

how common is it for people with panic disorder to have nocturnal panic attacks?

A

roughly half of people with panic disorder have them

142
Q

what edition of the DSM was the first to include panic disorders?

A

DSM-III

143
Q

what are the behavioural features of panic disorder?

A
  1. avoidance of particular situations where panic attacks are likely to occur
  2. avoidance of activities that induce panic-like sensations (interoceptive avoidance)
  3. safety behaviours
  4. experiential avoidance
144
Q

what are the common cognitive features of panic disorder?

A
  • more likely to interpret bodily sensations in a catastrophic fashion
  • more likely to attend more to words that represent physical threat
  • more likely to attend to heartbeat information
145
Q

what are the emotional features of panic disorder

A

associated with…
- neuroticism
- negative affectivity

146
Q

how heritable is panic disorder?

A

30-40%

147
Q

what brain structures/pathways are associated with panic disorder

A

pathway between ventromedial prefrontal cortex (vmPFC) and amygdala: underactivity of vmPFC -> diminished inhibitory inputs to amygdala and related subcortical regions

148
Q

what is the most researched anxiety disorder?

A

panic disorder

149
Q

how does the HiTOP model differentiate between SAD and GAD?

A

SAD = internalizing -> fear
GAD = internalizing -> distress

150
Q

how was GAD presented in the DSM-II? what about the DSM-III?

A
  • DSM2: lumped into broad category of anxiety neurosis
  • DSM3: left as a residual category
151
Q

what version of the DSM began to place the emphasis on worry as a primary symptom of GAD?

A

DSM-III-R

152
Q

how long does one have to worry in order to be diagnosed with GAD?

A

6 months or longer

153
Q

what diagnosis meets the following symptomatic criteria?

restlessness, fatigue, difficulty concentrating, irritability, muscle tension, sleep disturbance, excessive worry about multiple events

A

GAD (must meet at least 3 of the symptoms + worry)

154
Q

for people who have tried to get rid of GAD as a DSM diagnosis, what alternate explanations do they propose?

A
  • otherwise explained by negative affectivity, which when combined with other environmental factors can trigger other pathologies
  • could be a vulnerability marker or a pre-symptomatic state of another disorder
155
Q

what is the sex ratio for GAD?

A

2F:1M

156
Q

how high is comorbidity for GAD?

A

90%, mostly comorbid with mood disorders

157
Q

when does GAD usually onset?

A
  • median age is 30, but with lots of variability
  • symptoms usually emerge earlier in life
158
Q

based on family studies, which disorder seems to have a stronger genetic component: GAD or panic disorder?

A

GAD

159
Q

what mechanisms of GAD make it distinct from MDD?

A
  1. attentional biases and intolerance of uncertainty more common in GAD
  2. low positive affect and memory biases more common in MDD
  3. precipitating stressors: MDD usually triggered by humiliation events; GAD triggered by danger events
  4. response to lab stressors: emotional context insensitivity in MDD; hyper-responsivity in GAD
  5. temporal course: GAD often precedes MDD
160
Q

according to Borkovec’s cognitive theory, how does worry arise?

A
  • worry is a form of low cognitive avoidance in which people’s concern about low probability events is negatively reinforced
  • worry inhibits emotional processing, and is therefore a form of cognitive avoidance
  • inability to control sorry creates a vicious cycle in people with GAD
161
Q

according to Borkevic’s cognitive theory, why is worry so challenging to intervene on?

A

it is a cognitive, verbal, and mental operation

162
Q

what is the difference between worry and rumination?

A
  • rumination: fixation on the past; more common in SAD
  • worry: future-oriented; more common in GAD
163
Q

what is the criterion A for SAD?

A

A: marked fear about at least one social situation in which individual is exposed to possible scrutiny

164
Q

what is the sex ratio for SAD?

A

2F:1M
gender differences emerge in adolescence

165
Q

what is the median age of onset for social phobia/SAD?

A

16; relatively late compared to other phobic disorders

166
Q

what are the ethnic differences found in SAD epidemiology?

A
  • prevalence is lower in East-Asian countries as well as ethnicity in North America
  • in NA samples, Hispanic and Black ethnicity is also associated with lower prevalence
167
Q

what is Clark and Wells’ cognitive theory of social phobia/SAD?

A
  1. social situation activate a core set of values regarding one’s social competencies, and they believe others will view them negatively. these schemas interfere with their ability to make accurate interpretations of social situations
  2. they begin to see social danger and threat everywhere
  3. self-focus on making sure social situations will go well helps to maintain the disorder, which can make them less socially competent
  4. biased memory for negative experiences reinforces negative self-expectation
168
Q

what is metacognition, in the context of GAD?

A

worrying about worrying

169
Q

what is the first line of pharmacological therapy for GAD?

A

SSRIs

170
Q

what is the HiTop model of OCD?

A

internalizing -> fear

171
Q

what is the HiTop model of PTSD?

A

internalizing -> distress

172
Q

what is the oldest standalone anxiety disorder in the DSM?

A

OCD

173
Q

what is the criterion A for OCD diagnosis?

A

presence of obsessions, compulsions, or both

174
Q

what are the specifiers associated with OCD diagnosis?

A
  1. good or fair insight, poor insight, or absent insight/delusional beliefs
  2. tic-related
175
Q

how long must obsessions/compulsions last in order to receive a diagnosis of OCD?

A

at least 1 hour per day

176
Q

what are the 6 most common types of obsessions present in OCD?

A
  1. contamination (most common)
  2. uncertainty
  3. aggressive
  4. symmetry/exactness
  5. sexual
  6. somatic (health-related)
177
Q

how do OCD obsessions manifest in children usually?

A
  • less likely to have sexual obsessions
  • more likely to have aggressive obsessions
178
Q

what are the 5 most common categories of compulsions in OCD?

A
  1. decontamination
  2. checking/reassurance seeking
  3. repeating
  4. ordering and arranging
  5. mental rituals
179
Q

what is the sex ratio in OCD?

A

slightly more common in women than men

180
Q

when is the avg onset of OCD?

A
  • 19
  • usually gradual
181
Q

what are the cognitive models of OCD?

A
  1. negative feedback loop: people w OCD have inflated sense of personal responsibility and self-blame. negative affect increases the rate of negative thoughts, increasing distress, and thus requiring ritualization to reduce anxiety
  2. OCD is due to deficits in short-term memory, requiring constant checking
  3. OCD is due to intolerance of uncertainty and perceived lack of sufficient coping skills
182
Q

what is thought-action fusion (TAF)

A
  • aka magical thinking
  • moral TAF: belief that unwanted thoughts about disturbing actions are equivalent to the actions themselves
  • likelihood TAF: belief that thinking about a disturbing event makes the event more probable
  • common in OCD
183
Q

according to the study conducted by Rachman and Shafran et al, how is neutralization linked to anxiety?

A
  • neutralization regardless of timing reduces anxiety
  • the desire to neutralize remains high in time delay conditions, despite already lowered anxiety, showing that the two are somewhat separate
184
Q

what is the disgust proneness theory of OCD put forth by Olatunji?

A
  • a trait associated with both nature and nurture factors, focusing on themes of contamination
  • OCD may reflect a false-contamination alarm, where people are more likely to believe something is contaminated
185
Q

in what version of the DSM did PTSD first appear?

A

DSM-III

186
Q

what is the criterion A for PTSD diagnosis?

A
  • exposure to traumatic event
  • includes actual or threatened death, serious injury, or sexual violence
  • can be through direct experience, witnessing in person, learning that something happened to a close family member (must be violent or accidental), or experience repeated or extreme exposure to aversive details of the event (eg. first responders)
187
Q

what is the sex ratio for PTSD?

A

2F:1M

188
Q

following trauma, how many people develop PTSD?

A

9% (twice as likely for women than men)

189
Q

what types of traumas are most likely to lead to development of PTSD?

A

violence or assault

190
Q

what are the cross-cultural findings of PTSD diagnosis?

A
  • rates are higher in developing countries
  • symptoms may vary by culture
191
Q

what are the risk factors for PTSD development following trauma?

A
  1. nonspecific familial psychopathology
  2. internalizing symptoms in early childhood
  3. aversive childhood experiences
  4. lower IQ
  5. lack of social support
192
Q

what variables regarding the traumatic event tend to predict PTSD development after trauma exposure?

A
  1. proximity
  2. duration
  3. intention (deliberate -> PTSD more likely)
  4. psychological processes occurring during and after event
  5. dissociation
193
Q

what two disorders are equally likely to occur following exposure to a traumatic event?

A

MDD and PTSD

194
Q

what were the findings of a study conducted using a Vietnam war-era twin registry regarding PTSD?

A
  • for Mz twins, even without combat exposure, one twin was more vulnerable to PTSD if their twin had it, suggesting a strong genetic component of the disorder
  • and yet, Mz twin who served in combat was much more likely to have PTSD than their non-veteran twin, indicating that environmental effects are crucial
195
Q

what biological abnormalities have been observed in people with PTSD?

A

hippocampus:
- reduced volume
- reduced neuronal integrity
- reduced functional integrity

196
Q

what did the findings of prospective twin studies show regarding the relationship between hippocampus volume and PTSD?

A

small hippocampus is heritable, representing a pre-existing familial vulnerability
- may predispose individuals to acquire stronger or more persistent conditioned emotional responses
- may predispose individuals to stronger hormonal stress responses

197
Q

do people with PTSD recover?

A
  • “disorder of non-recovery”
  • no, they tend to stall out at a certain point (differ from people with non-PTSD trauma exposure)
198
Q

which version of the DSM moved PTSD out of the anxiety disorders category?

A

DSM-V

199
Q

how long do symptoms need to present before PTSD diagnosis?

A

one month

200
Q

what are the subtypes of PTSD?

A
  1. for children younger than 6
  2. with strong dissociative symptoms
201
Q

what are the differences in presentation of PTSD in children vs adults?

A
  • young children display less avoidance and negative alterations in cognition and mood symptoms
  • in kids, symptoms are more rooted in behaviour (eg. social withdrawal)
202
Q

how common is comorbidity in PTSD?

A

one of the highest!! over 90%

203
Q

what are the three unofficial subtypes of PTSD proposed by the textbook?

A
  1. simple (low on internalizing and externalizing)
  2. externalizing (higher comorbidity with personality and substance disorders)
  3. internalizing (higher comorbidity with mood and anxiety disorders)
204
Q

according to Brewin et al’s proposed dual representation theory of PTSD, how are traumatic experiences stored?

A
  1. verbally accessible memories (VAM): autobiographical memories of the event which include before, during, and after, that have been transferred to long term memory
  2. situationally accessible memories (SAM): contain extensive unconscious and nonverbal info about the event that cannot be deliberately accessed; can be triggered with flashbacks, nightmares, or intrusive images
    - successful emotional processing of a traumatic event requires activation of both
205
Q

according to Brewin et al’s proposed dual representation theory of PTSD, what are the two types of emotional reactions?

A
  1. primary emotions: conditioned during a traumatic event (eg. helplessness, fear, horror)
  2. secondary emotions: result from post hoc consideration of the event (eg. shame, sadness, anger)
206
Q

what is Ehlers and Clark’s paradox of memory in people with PTSD?

A

someone with PTSD may have trouble intentionally accessing their memory of the event, but have involuntary intrusions of parts of it

207
Q

what are the risks of maladaptive coping strategies in people with PTSD, such as avoidance behaviours or rumination?

A
  1. may increase symptoms
  2. may prevent change in negative appraisals
  3. may prevent change in the traumatic memory
208
Q

what are Janoff-Bulman’s 3 major assumptions that may be shattered in the face of a traumatic event?

A
  1. personal invulnerability
  2. the world as a meaningful and predictable place
  3. the self as positive and worthy
209
Q

according to Resick, what are the three possible reactions to when a traumatic event conflicts with prior beliefs?

A
  1. assimilation (altering interpretation of event to maintain previous beliefs)
  2. accommodation (slightly altering beliefs to accommodate new info)
  3. overaccommodation
210
Q

what is Hobfoll’s conservation of resources (COR) theory of stress, in relation to PTSD?

A
  • people strive to obtain, retain, and protect what they value; stress occurs when resources are threatened, lost, or don’t increase adequately
  • traumatic stress results in the sudden and rapid loss of resources, such as trust in self and others, perception of control, and sense of well-being
211
Q

what is the frontline treatment approach for PTSD?

A
  • CBT
  • or sertraline and paroxetine for pharmacological treatment
212
Q

what are the 4 subtypes/dimensions of OCD?

A
  1. contamination
  2. responsibility for harm and mistakes
  3. incompleteness
  4. unacceptable, taboo, violent, sexual, or blasphemous thoughts
213
Q

according to the behavioural model of OCD, what are its two stages?

A
  1. development through classical conditioning
  2. maintenance through operant conditioning
214
Q

what are the cognitive deficit models of OCD?

A
  1. memory deficit -> cognitive checking
  2. difficulties with reality monitoring -> cognitive checking
  3. inhibitory defects -> obsessional fears
215
Q

what is Beck’s cognitive behavioural model of OCD?

A

obsessions and compulsions arise from incorrect interpretations of normal intrusive thoughts as having serious consequences

216
Q

what are the neurobiological models of OCD?

A
  1. serotonin hypothesis: due to hypersensitivity of postsynaptic serotonegeric receptors (hence why SSRIs are most effective)
  2. structural models: due to functional abnormalities in orbitofrontal-subcortical circuits
217
Q

what did Hippocrates first call what we now know as depression?

A

melancholia

218
Q

according to hippocrates, what caused melancholia?

A

too much black bile

219
Q

how did Emile Kraepelinan reform depression diagnosis?

A

refined what used to be a unitary concept of psychosis by classifying it as 2 distinct syndromes:
1. manic depressive illness (later split into MDD and Bipolar)
2. dementia praecox (later labelled as schizophrenia)

220
Q

who first proposed the unipolar-bipolar distinction for depression?

A

Karl Leonhard

221
Q

what was MDD called int he DMS-II?

A

“depressive reaction”, referring to a response to adverse life events

222
Q

in what version of the DSM did the label MDD first appear?

A

DSM-III

223
Q

how long must symptoms be presenting for a MDD diagnosis?

A

2 weeks

224
Q

what are the two cardinal symptoms of MDD?

A

(must meet one of two)
1. dysphoric mood)
2. anhedonia

225
Q

how much more common is MDD than bipolar?

A

10-20x

226
Q

what is the sex ratio of unipolar vs bipolar depression?

A

MDD = 2F:1M
bipolar = M:F

227
Q

how does the course and onset differ between unipolar and bipolar depression?

A
  • bipolar has earlier and more abrupt onset
  • bipolar people have more episodes (more severe and chronic)
  • bipolar has a more pernicious course
228
Q

what are the subtypes of MDD?

A
  1. psychotic MDD
  2. recurrent depression
  3. melancholia (more biological than related to external stressors; profound anhedonia)
  4. atypical depression (intact mood reactivity)
  5. chronic MDD (episodes last 2+ years)
  6. seasonal affective disorder
  7. postpartum depression
  8. PDD (milder sustained form; 2+ years)
229
Q

according to Watson and Clark’s tripartite model, what are the main similarities and differences of depression and anxiety disorders?

A
  • similar: general distress and negative affect
  • unique to depression: anhedonia
  • unique to anxiety: physiological hyperarousal
230
Q

what are the cultural/regional/ethnic differences present in MDD/PDD?

A
  • MDD rates significantly lower in East Asia
  • PDD higher in industrialized countries
  • Black Americans report lower lifetime prevalence but more chronic course
  • more somatic presentation in Asia, Latin America, and North Africa
231
Q

what is the avg age of onset for MDD?

A

teens-mid 20s

232
Q

how often is MDD preceded by PDD?

A

25%

233
Q

how long do depressive episodes usually last in people with MDD?

A

5-6 months

234
Q

what are the predictors of longer MDD episodes?

A
  • comorbid personality disorder
  • non-mood comorbid disorders
235
Q

according to the results of twin and family studies, which is more heritable: MDD or Bipolar?

A

Bipolar

236
Q

according to the Parental Bonding Instrument (PBI) put forth by Parker, what are the two dimensions of caregiving? what are the implications for MDD?

A
  • care/nurturance and overprotection/control
  • interaction of low care and high control seem to pose a heightened risk for depression, according to the stress and adversity model
237
Q

what is the passive gene-environment correlation between parenting and depression?

A

depression in parents -> poor parenting -> depression in children

238
Q

what is the evocative gene-environment correlation between parenting and depression?

A

kids who will become depressed elicit more negative parenting

239
Q

what is the reward and positive reinforcement model of depression put forth by Skinner et al?

A
  • behavioural view
  • depression is related to a reduction in behaviours that are positively reinforced (vicious cycle)
240
Q

what is Beck’s cognitive triad of depression?

A
  • negative views about world -> about future -> others -> world
  • depressogenic schema contributes to negative automatic thoughts though which our experience of the world is filtered
241
Q

how does Seligman’s learned helplessness theory apply to depression?

A
  • depression occurs because bad things happen to us and we learn that we are completely helpless in the face of adversity
  • later revised to incorporate 3 dimensions of attributions: internal vs external, global vs specific, and stable vs unstable
242
Q

how are memory biases tested in the lab?

A

through SRET

243
Q

how are attentional biases tested in the lab?

A

stroop task, visual search task, dot-probe task, dichotic listening task

244
Q

which disorder is ranked as the most common disability for US citizens 15-44 years old?

A

depression

245
Q

what are the specifiers for MDD?

A
  1. single episode or recurrent form
  2. level of severity
  3. mixed features
  4. with anxious distress
246
Q

what are the specifiers for PDD?

A
  1. pure dysthymic syndrome
  2. persistent depressive episode
  3. intermittent major depressive episode, with current episode
  4. intermittent major depressive episode, without current episode
247
Q

what is the behavioural deficits theory of depression?

A

underactive behavioural activation system (which is responsive to reward cues) leads to anhedonia, amotivation, and avoidance, which perpetuate depressive episodes

248
Q

what are the three components to Beck’s cognitive model of depression?

A
  1. negative self-statements/automatic thoughts
  2. cognitive errors
  3. underlying schemas/core beliefs
249
Q

according to the hopelessness theory, depression is more likely to occur when…

A
  1. negative events that are important to the individual are attributed to global and stable causes
  2. negative events are predicted to lead to additional negative consequences
  3. the individual makes a causal attribution about the relationship between negative events and their inherent deficiencies
250
Q

what are the 2 dominant biological models of depression?

A
  1. monoamine hypothesis (caused by deficiency in CNS concentration in norepinephrine and serotonin)
  2. abnormal functioning in endocrine system (excess secretion of cortisol, excess of stress-induced white blood cells)
251
Q

what is the criterion A for a bipolar diagnosis?

A

manic episode lasting at least 1 week (or until they are hospitalized)

252
Q

what are the 3 possible main characteristic of a manic episode?

A
  1. elevated expansive mood
  2. extreme irritability
  3. persistently increased goal-directed energy
253
Q

what’s the difference between bipolar 1 and 2?

A
  • bipolar 1: full blown mania + MDD episodes
  • bipolar 2: hypomania + depression (milder, no psychosis, stimulus-seeking)
254
Q

what is cyclothymia?

A
  • form of bipolar
  • hypomania + short depressive episodes that would not necessarily meet MDD criteria
  • at increased risk for bipolar 1
  • can be triggered by antidepressant meds
255
Q

what is the main specifier for bipolar?

A

rapid cyclers (4+ episodes in a year)

256
Q

what are the psychotic symptoms associated with bipolar?

A
  • mood congruent in mania: delusions of grandeur
  • mood congruent in depression: extreme feelings of guilt/sin, nihilistic delusions
  • mood incongruent in mania: thought insertion, mind control
  • mood incongruent in depression: anything happy (rare)
257
Q

how does the DSM-V resolve overlap in psychotic disorders?

A
  • mood disorder with psychosis: if psychotic symptoms occur during a manic or depressive episode but never outside
  • schozoaffective disorder: if symptoms occur outside a mood episode
258
Q

what is more common: bipolar 1/2 or cyclothymia?

A

cyclothymia, just slightly

259
Q

what treatments are used for bipolar?

A

mood stabilizers (lithium)
anti-convulsants

260
Q

what is the average age of onset in bipolar disorder?

A

20-30 (half the time the first episode is manic, half is depressive)

261
Q

what are the poor prognostic indicators for bipolar disorder?

A
  • mixed states
  • rapid cycling
262
Q

how do suicide rates compare among unipolar vs bipolar depression?

A

risk of death by suicide is…
- 15x the gen pop for bipolar
- 4x the gen pop for MDD

263
Q

what are the risk factors for suicide?

A
  • younger age
  • recent illness onset
  • male
  • prior attempts
  • family history of suicide
  • comorbid alcohol/substance abuse
  • rapid cycling course
  • social isolation
264
Q

what are the 3 main etiological models for bipolar disorder?

A
  1. stress and adversity
  2. kindling (progressive hypersensitization to stress)
  3. sleep deprivation as a predictor of mania
265
Q

what are the top 4 stressors for Canadians?

A
  1. work
  2. money
  3. relationships
  4. health
266
Q

who originally determined the connection between psychological stressors and physical health?

A

hippocrates

267
Q

what is the difference between stress and stressor?

A
  • stressor = external demand that creates a threat to a person’s equilibrium
  • stress = how the organism reacts to the stressor
268
Q

describe the physiological stress response

A
  1. hypothalamus
    2a (fast response): SAM stimulation -> release of adrenaline and noradrenaline -> fight or flight activation -> physiological response
    2b (slow response): HPA axis stimulation -> release of CRH, ACTH, and cortisol -> activation of fight or flight
269
Q

what is allostatic load?

A

how much strain the system must be under in order to accomplish stress response

270
Q

what effect does chronic stress have on the hippocampus?

A

results in decreased hippocampal volumes due to low dendridic arborisation

271
Q

what brain structures are affected by chronic stress?

A
  • hippocampus volume
  • PFC volume
272
Q

what properties of stressors predict psychopathology development?

A

those perceived as…
1. uncontrollable
2. unpredictable
3. severe
- timing also matters

273
Q

what is fetal programming in the context of stress?

A
  • maternal stress may be transmitted to the fetus as cortisol passes through the placenta
  • can cause the infant to develop a hypersensitive stress response system
274
Q

what was a unique finding of Yong Ping et al’s study on maternal stress and fetal programming?

A

effect of fetal programming is only seen in girls

275
Q

what are empirically supported steps to reducing stress?

A
  1. social support
  2. exercise
  3. mindfulness and controlled breathing
  4. sleep

PSYC 337 (psychopathology) (8 decks)

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