Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychopathology > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Why do we define mental illness/why do we diagnose?

A
  • Knowing what the issue is makes it easier to treat it
  • Helps with self-stigmatization (explains behaviour to the individual and provides clarity)
  • Can standardize treatments so everyone with that illness gets the same treatment
  • Can help others understand how to interact with an individual who is mentally ill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are arguments against defining mental illness or diagnosing?

A
  • Some think it stigmatizes people
  • Some believe it removes the individuality of mentally ill people and “puts them in a box”
  • It can be difficult to arbitrate what is and what isn’t mental illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What’s the DSM?

A
  • Diagnostic and Statistical Manual
  • Manual in North America that we use to define and classify mental disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the purposes of a classification system?

A
  • Description: highlight critical features of a diagnosis -> ex: what are the important symptoms of schizophrenia?
  • Prediction: may tell you something about course, treatment response, etiology
  • Theory: Provides a set of postulates about relationships of different elements to one another (important for research into psychopathology)
  • Communication: for example between clinicians (you want every clinician to have the same definition of different disorders)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the limitations of a classification system?

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?
  • Ex: similar to procrustean beds -> we fit people into the diagnosis rather than fit the diagnosis to the people in front of us
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are categorical systems?

A
  • Identifies the presence/absence of a disorder -> you either have the disorder or you don’t (you’re anxious or you’re not)
  • Advantageous for research and understanding
  • Simplifies communication (provides a lot of info relatively quickly)
  • Natural preference among people to employ categories in speech (heuristics)
  • Categories better-suited for clinical decision-making (Hospitalize or don’t? Treat or don’t?)
  • Cutoffs in categorical system tend to magnify small differences
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are dimensional systems?

A
  • Rank on a continuous quantitative dimension
  • Degree to which a symptom is present
  • Ex: how anxious are you on a scale of 1 to 10?
  • May better capture an individual’s functioning
  • Everybody falls somewhere
  • Arbitrary cut-offs
  • Proposes thresholds for diagnoses
    -Preserves more info
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the invention of the DSM

A
  • DSM I was first introduced in 1952
  • The 1st and 2nd DSM were very similar
  • First attempts to standardize definitions of psychopathology
  • People were trying to establish a scientifically grounded shared set of definitions for psychopathology
  • With standardized definitions you can determine how common or rare something (ex: a behaviour) is
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the DSM-II

A
  • 1968
  • Very similar to DSM-I
  • Few categories
  • No requirements for # of symptoms
  • Psychoanalysis was the dominant paradigm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the DSM-III

A
  • 1980
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are disorders in the DSM determined?

A

Often these diagnoses are determined by a small group of experts determining a consensus on definitions of disorders and their validity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s the Multi-Axial Classification?

A
  • Axis I (first axis you use). Major Clinical Disorders (ex: MDD, PTSD)
  • Axis II. Personality Disorders (ex: BPD, NPD)
  • Axis III. Medical conditions that might contribute or be relevant to treatment
  • Axis IV. Psychosocial Stressors (something with which to record environmental contexts) -> may interfere with treatment
  • Axis V. Global Assessment Functioning (GAF) –> a simple rating of function/summary score for severity
  • The primary problem would always be if someone has an Axis 1 problem and Axis 2 was used after to determine if using the right treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the differences in the number of diagnostic categories per edition of DSM

A
  • Large difference between DSM-I and DSM-II (~75 more)
  • Large difference between DSM-II and DSM-III (~80 more)
  • Smaller difference between DSM-III and DSM-III-R (~30 more)
  • Even smaller difference between DSM-III-R and DSM-IV-TR (5 more)
  • Less categories in DSM-5 than in DSM-IV-TR (140 less)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the assumptions that were introduced in DSM-III?

A
  • Symptoms are the most useful basis for assessment
  • Nosology based primarily on behavior and symptoms and not on etiology
  • Beforehand it was focused on etiology
  • Locus of pathology is in the individual (not the system that the individual is a part of)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the DSM-IV

A
  • 1994
  • Didn’t make a lot of changes
  • Introduced “clinically significant distress or impairment in social, occupational, or other important areas of functioning”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the DSM-IV-TR

A
  • 2000
  • DMS-4-TEXT REVISION
  • The revision process of this one was much more public and research-based
  • Did not introduce new diagnoses or specific criteria
  • Provided more info on each diagnosis
  • Provided a broad definition of mental illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the DSM-5

A
  • 2013
  • Removed multi-axial system
  • Introduced dimensional assessment criteria for some diagnoses (spectrum of varying degrees of a disorder)
  • Re-classified some disorders (ex: OCD and PTSD no longer classified as anxiety disorders)
  • Removed others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some challenges to the categorical classification system?

A
  • Heterogeneity
  • Comorbidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the heterogeneity challenge to the categorical classification system

A
  • Ex: if depression is in one category and anxiety is in a different one then we would assume that people within each category look like one another and different from the people in the other categories
  • However we find heterogeneity in some of these categories
  • Different people with the same diagnosis will look differently
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the comorbidity challenge to the categorical classification system

A
  • Comorbidity: simultaneous presentation of more than one disease
  • Ex: MDD and Anxiety are often comorbid
  • If someone presents with more than one diagnosis, do you treat both simultaneously or on a case by case basis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe comorbidity

A
  • For people who currently meet criteria for one disorder, 50% qualify for more than one and over the course of their lifetime 75%
  • Comorbidity is the norm (suggests the categories are probably not working that well)
  • Comorbidity affects course, development, presentation, treatment response, severity of the symptoms, etc.
  • Comorbid patients tend to have poorer outcomes (ex: short lives and poor quality of life)
  • Not accounting for comorbidity can lead to a lack of info in understanding a patient’s condition
  • Most people with MDD also have a comorbidity
  • Research Implications: anything you find to be associated with one disorder may actually be a result of the comorbid disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some reasons for why comorbidity exists?

A
  • Chance
  • Sampling bias
  • Problems with diagnostic criteria
  • Poorly-drawn diagnostic boundaries
  • Causal explanation
  • Shared etiological risk factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Explain why chance is a reason for why comorbidity exists

A
  • Some comorbidity is just chance
  • Ex: odds of MDD for adult females = 20%
  • Ex: odds of anxiety disorder for adult females = 20%
  • By chance alone, 4% will have both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Explain why sampling bias is a reason for why comorbidity exists

A
  • Each disorder associated with a chance of being treated
  • Individuals with more disorders (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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain why problems with diagnostic criteria is a reason for why comorbidity exists

A
  • Many criterion sets overlap (same symptoms appear in different disorder sets)
  • Ex: Suicidal ideation in MDD, Schiz, BPD, AUD, SUD
  • Ex: Sleeplessness in MDD and GAD & Worry in GAD and MDD
  • Can’t totally account for high rates of comorbidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Explain why poorly-drawn diagnostic boundaries is a reason for why comorbidity exists

A
  • Multiformity (disorders can express themselves in multiple ways)
  • People with MDD frequently have panic attacks -> if only looking at panic attacks, you may assume someone with MDD has panic disorder
  • Comorbid disorders may reflect a 3rd, independent
    disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Explain why a causal explanation is a reason for why comorbidity exists

A
  • One disorder is a risk factor for another disorder
  • Ex: Conduct Disorder may lead to adult Substance Use Disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Explain why shared etiological risk factors is a reason for why comorbidity exists

A
  • Etiology: origins of disorder
  • Childhood maltreatment is a risk factor for almost every disorder
  • Biological commonalities can also be risk factors -> not much research on this
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the Dimensional/Hierarchical Models of pathology

A
  • Tom Achenbach conducted a factory analysis to see which symptoms or diagnoses clump together (share a variance) and which don’t, to try to identify factors
  • In this system you have 2 factors -> internalizing and externalizing
  • These are distinct and relatively independent but correlate within themselves
  • He believed that this explains comorbidity (what are the factors that explain the similarities within diagnostic categories)
  • Internalizing: people that cause distress to themselves
  • Externalizing: people that cause distress to others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the internalizing factor of the dimensional/hierarchical models

A
  • Split in 2 sub-categories: Anxious misery and fear
  • Anxious misery is comprised of MDD and GAD
  • Fear is comprised of Panic and Social Phobia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the externalizing factor of the dimensional/hierarchical models

A
  • Split in 2 sub-categories: addiction and aggression
  • Addiction is comprised of Alcohol Abuse and Drug Dependence
  • Aggression is comprised of ODD and CD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some problems with the dimensional/hierarchical models of pathology?

A

○ There are more disorders that don’t fit in these models
- Internalizing and Externalizing forms of dysfunction often correlate with themselves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the Hierarchical Taxonomy of Psychopathology (HiTOP)

A
  • The most recent way of thinking about these hierarchical ways of describing psychopathology
  • Introduced a thought disorder category
  • Included some personality disorders
  • Method used for this is factory analysis
  • This isn’t a causal model, it’s just describing the structure of psychopathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe RDoC (Research Domain Criteria)

A
  • Funding initiative
  • Wanted to forget diagnoses altogether and focus on dysfunctions of core systems since many disorders can fit into these
  • Trans-diagnostic approach
  • This isn’t used for treatment this is just used for research on descriptions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What’s prevalence?

A
  • % of people in a population with a disorder at a
    particular point in time
  • Ex: past month, year, or lifetime
  • Prevalence = incidence x chronicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What’s incidence?

A
  • % of people who develop a disorder for the 1st time during a specific time period
  • 1st onset cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What’s a risk factor?

A
  • For epidemiologists, a correlate (most often demographic variables) associated with different disorders
  • Psychologists use this term to mean predictor, or cause (should not be a causality)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the relativity of the 1-year prevalence rates of the different psychological disorders (highest to lowest)

A
  1. SAD (6.8% -> highest prevalence rate)
  2. MDD (6.7% -> close 2nd highest)
  3. PTSD (3.5% -> 3rd highest (Half less than SAD & MDD)
  4. GAD (3.1% -> close 4th)
  5. Panic (2.7% -> close 5th)
  6. Bipolar (2.6% -> close 6th)
  7. Persistent Depressive Disorder (1.5%)
  8. OCD (1% -> lowest prevalence rate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe the relativity of the onset of the different psychological disorders (youngest to oldest)

A
  1. PTSD (any age)
  2. OCD (child/adolescent)
  3. SAD (13)
  4. Major Depression (14-15 or 30s)
  5. Panic (24)
  6. Bipolar (25)
  7. Persistent Depressive Disorder (30s)
  8. GAD (31)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the relativity of the lifetime prevalence rates between mood disorders, anxiety disorders, substance use disorders and any disorder (highest to lowest)

A
  • Any disorder (46%, almost 1/2 -> highest) -> 46% will meet criteria of a DMS diagnosis within their lifetime
  • Anxiety disorders (27% -> 2nd highest)
  • Mood disorder (21%, about 1/5)
  • Substance use disorders (15% -> lowest)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe the relativity of the 1-year prevalence rates for 19-25 yr old college (CS) & non-college students (NCS) for mental health usage, mood disorders, anxiety disorders, substance use disorders and any disorder

A
  • Any disorder: CS = 45.8% and NCS = 47.7% (higher for NCS)
  • Anxiety disorder: CS = 11.9% and NCS = 12.7% (higher for NCS)
  • Mood disorder: CS = 10.6% and NCS = 11.9% (higher for NCS)
  • Alcohol Use Disorder: CS = 20.4% and NCS = 17% (higher for CS)
  • Mental Health Usage: CS = 18.5% and NCS = 21.5% (higher for NCS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What’s etiology?

A
  • The scientific study of the causes of things
  • Etiology of mental disorders -> why do people become mentally ill, what are the causes?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are etiological perspectives on psychopathology?

A
  • Environmental causes
  • Genetics causes
  • Diathesis-Stress Model
  • Vulnerability-stress correlations
  • Developmental pathways (equifinality and multi finality)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are some environmental causes of psychopathology?

A

*Environmental/ learning experiences
*Freudian theories:
- “schizophrenogenic mother” -> popular in the 40s-70s , the idea that a mother that often switches between being overbearing and neglectful can cause schizophrenia
- “refrigerator mother” -> idea that a mother that lacked genuine warmth and positivity caused autism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are some genetic causes of psychopathology?

A
  • Genes are not deterministic -> most are probabilistic (if your family is tall, you’re more likely to be tall)
  • Make small contributions (with other genes) to create the ultimate outcome
  • Single gene association doesn’t exist (ex: “this is the gene for schizophrenia”
  • Researchers identifying dozens of genes that, in certain combinations, lead to symptoms of different forms of psychopathology
  • Polygenic - influenced by activity of many genes -> How many genes you have determines where you fall on dimension/spectrum
  • There’s strong evidence of psychopathology running in the family -> MDD in the family could make someone more likely to get MDD
  • No mental illness to this day is perfectly heritable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the Diathesis-Stress model

A
  • Diathesis model tries to drop the nature vs nurture debate, it’s trying to bring these ideas together (gene-environment correlation)
  • The diathesis is a vulnerability or predisposition to develop psychopathology
  • Stress is exposure to experiences or things that overwhelm an organism
  • Only when both stress and diathesis is present that one becomes mentally ill (not when stress absent/diathesis present, stress absent/diathesis absent or stress present/diathesis absent)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the reworking of the Diathesis-Stress model

A
  • Etiological heterogeneity
  • Assumes diathesis and stress are independent
  • Say that it’s not do you have the diathesis or stress or do you not, now it’s to what degree do you have either or?
  • Now, no diathesis is not perfectly protective -> people without a diathesis that are exposed to high levels of stress could develop a disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are some challenges to the reworking of the Diathesis-Stress model

A
  • There’s not just a single etiological pathway
  • We have a lot of evidence for gene environment correlations showing these are not independent of one another
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe vulnerability-stress correlations

A
  • Often non-independent in important ways
  • Stress Generation -> ex: excessive reassurance seeking
  • “Scars” as vulnerability -> ex: cognitive vulnerabilities following MDD episode
  • Vulnerability may shape perception of the stress
  • Stress can influence the development of the diathesis -> ex: gestational stress (can change brain development that can make people more vulnerable to developing psychopathology) and mental illness
  • It’s not just exposure to stress that leads to depression, people that have depression behave in ways that leads to more stress
  • Parents that have a genetic risk for externalizing behaviours pass that onto their children but they may also through their parenting create externalizing behaviours in a child
  • Dynamic relationship with lots of correlation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What’s equifinality?

A
  • Final common pathway
  • People who get a disorder, get it from different causes
  • Getting to the same point from many different pathways
  • Equifinality explains how multiple different pathways converge on the same point
  • Most disorders that we encounter are representative of equifinality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What’s multifinality?

A
  • Final different pathways
  • A single risk factor can lead to many outcomes
  • Ex: experiences of child abuse are associated with almost all forms of psychopathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the different types of longitudinal designs?

A
  • Retrospective
  • Follow-up
  • High Risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the retrospective longitudinal design

A
  • A study that looks back into history
  • Collect a sample of people with a disorder
  • Try to determine what factors preceded the onset of the disorder
  • Data collected through self-reports and existing archival data (looking at home videos or school reports to identify abnormalities -> ex: when looking at home videos of schizophrenic individuals, people could identify motor abnormalities that could predict schizophrenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the main limitation with retrospective longitudinal designs

A
  • Problem with relying on recall
  • Memory is not always accurate
  • Mood states can affect the way people recall things (depressive episodes can lead to people reporting things more negatively)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the follow-up studies longitudinal design

A
  • Follow people with the disorder over time
  • See what happens to them (trying to observe the course of the disorder overtime)
  • Already-ill sample
  • Difficult to derive etiological explanations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Describe the high risk studies longitudinal design

A
  • Variant of follow-up
  • Identify people who are likely to develop a disorder
  • Ex: offspring of people with a disorder (genetic), biological abnormality, behavioural variable
  • Follow them over time (prospective longitudinal study)
  • This is difficult because you need a very large sample to be able to make statistical inferences
  • More statistical power when using people who are more likely to develop a disorder for sample
  • These are powerful designs but there are a lot of challenges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the limitations of high risk studies

A
  • Genetic: Need to find people who have the disorder and also have children (people with schizophrenia often don’t have offspring)
  • Biological: associations not well-proven
  • Behaviors: may be a risk factor, or may be early manifestation of the disease
  • If you recruit the offspring of someone with a disorder, you may not have a representative sample
  • It’s hard to get someone to come to the lab, let alone a person and their child
  • These studies are uncommon because they’re hard to do and are expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the characteristics of a vulnerability marker?

A
  • Should be trait-like, not state-related
  • If a marker only appears when people are ill, then it isn’t a vulnerability marker (it should be present before the illness, during and after)
  • Ex: negative attribution bias as vulnerability marker, you would want to see this before the disorder, during episodes of depression, and after
  • Has to be correlated with the disorder, but has to persist beyond the end of the episode -> if a marker isn’t evident prior but persists after the offset of a disorder, this could be considered a scar -> not considered a vulnerability marker
  • Has to be present in a high-risk population (not a vulnerability marker if it’s not present in people who are at higher risk for developing it)
  • Has to pre-date disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What’s case control?

A
  • Compare one group of people with disorder to a second group without the disorder
  • Case control tends to be most informative and useful if you’re looking at a disorder that’s rare because you have to recruit a lot of people
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What’s a cohort?

A
  • A single large sample of people, some of whom have the disorder
  • Cohort is preferable when the disorder is not that rare because you can compare your control group to multiple groups of people with different disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Describe the patients vs community issue with psychopathology

A
  • Patient populations not representative of people with the disorder in the community -> a lot of people don’t seek treatment so patient populations aren’t very representative
  • Clinical populations tend to be more severe, have more comorbidities, more likely to be female (women are more likely to seek treatment than men), higher SES, chronic -> represent people seeking treatment
  • General population, get a sense of disorder “in the wild” -> general population tend to be milder and lead to misdiagnosis
  • Very expensive (because large samples)
  • We need info from both designs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are controls?

A
  • Healthy Controls (HC): often “super healthy controls” because this group is a smaller % of the population because most people at some point in their life will meet criteria for a psychiatric dysfunction
  • Psychiatric Controls (PC): people from a psychiatric population with a different disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What’s genetic epidemiology?

A

Trying to understand to what extent there are genetic contributions to pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are family studies?

A
  • Does the disorder run in families? If not, then no genetic contribution
  • Why does it run in families?
  • First identify proband (someone that has the disorder)
  • Assess family members to see who in the family also has a disorder
  • Interview -> Family Study
  • Informant report -> Family History Study
  • Many disorders run in families -> rates of illness in family members of the proband must be higher than in general population (or of family members of the controls) to state that the depression runs in the family
  • Subthreshold/symptoms -> family members may show symptoms but not have the disorder (ex: we don’t inherit the disorders but we inherit the traits that make us vulnerable to these like magical thinking or paranoia
  • Coaggregation: if looking at depression in a proband, their family will not only have higher rates of depression but also of anxiety disorders than in the general population (depression and anxiety tend to coaggregate together)
  • Suggest genetic role, does not prove it (because family members are similar to one another due to shared experiences, environments and culture)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are adoption studies?

A
  • Natural experiment (observation of people already in these situations) attempting to isolate the effect of genes on psychopathology
  • Parent as proband
  • Adoptee as proband
  • Cross-fostering design
  • Typically we want to look at parental psychopathology in these studies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe the cross-fostering design in adoption studies

A

Children of parents without schizophrenia adopted into a household of parents with schizophrenia and children of parents with schizophrenia adopted into a household of parents without schizophrenia -> which of these groups is at a higher risk of developing schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the parent as proband design in adoption studies

A
  • Group of parents, some of whom have the disorder and others who don’t all of which have given their children up for adoption
  • The people who gave you your genes are not the ones that raised you -> removes the environmental and experience similarities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe the adoptee as proband design in adoption studies

A

Track down and assist the biological and the adoptive parents (ex: child has depression, are the biological or/and adoptive parents more at risk to develop depression?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe the limitations to adoption studies

A
  • Adoption is a rare event
  • Adoptive parents are very carefully screened -> typically not allowed to adopt a child if you have a history of psychopathology
  • Creates an unrepresentative sample for these studies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What’s fear?

A
  • Response to a current present threat -> real or perceived
  • Something that is either present or is perceived to be in the presence of the person
  • Fear response: response to keep us safe from threats (to enable fight or flight)
  • Fear is fast (rapid fear response)
  • This response is not necessarily mediated by conscious thought -> immediate physiological and behavioural response
  • The fear is to the present object
  • Usually calms down pretty quickly once the stimuli is removed
  • Physiological responses -> all thought to emerge to aid the organism in surviving when encountering a threat
  • Fear response exists/evolved to keep us safe (it’s our friend)
  • Preparation for adaptive action
  • The neural systems that allow us to see danger are very primitive and fast -> when using these systems, you’re not differentiating between dangerous animals and non-dangerous animals (ex: you don’t have time to differentiate between a tarantula and a non-dangerous spider)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the physiological responses related to fear?

A
  • Increased heart rate
  • Blood pressure increases
  • Increases in hormones like cortisol and adrenaline
  • Muscle tension
  • Increased breathing rate
  • Etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What’s panic?

A
  • Extreme fear response that is evoked even if there’s no threat
  • False alarm -> there is no threat present
  • Activates a very powerful fear response
  • Physiological components are similar to fear
73
Q

What are the physiological responses related to panic?

A
  • Increased heart rate
  • Blood pressure increases
  • Increases in hormones like cortisol and adrenaline
  • Muscle tension
  • Increased breathing rate
  • Etc.
74
Q

What’s anxiety?

A
  • Future oriented (affective state where someone feels a threat from a potential outcome in the future)
  • May have some of the same symptoms as fear and panic
  • In the absence of a current threat (threat is not actually present)
  • Anxiety disorders are disorders of anxiety and panic -> disorders in which fear anxiety and panic reach a level where they interfere with the individual’s ability to live a valued life
  • Fear is our friend, but anxiety is a maladaptation of our fear response
75
Q

What’s the difference between panic and anxiety?

A

Anxiety is much more future oriented and the physiological response is usually less intense than with panic

76
Q

What’s the prevalence of anxiety disorders?

A

As a class, among the most common psychological disorders (lifetime prevalence of around 30-40%)

77
Q

In the DSM-5, anxiety-related disorders are categorized into what 3 distinct chapters?

A
  • Anxiety disorders (panic disorder, agoraphobia, specific phobia, social anxiety disorder, and generalized anxiety disorder)
  • Obsessive-Compulsive and related disorders (OCD)
  • Trauma and stressor-related disorders (PTSD)
  • These groupings (3 chapters) are meant to reflect the connections between the disorders -> in terms of functionality or treatments
  • OCD and PTSD used to be in the same chapter as the anxiety disorders -> in DSM-5 they are separated
78
Q

What are the internalizing disorders according to HiTOP?

A
  • Bipolar I & II
  • MDD
  • Dysthymia
  • GAD
  • PTSD
  • Social phobia
  • Agoraphobia
  • SAD
  • Panic disorder
  • OCD
  • Specific phobia
  • BPD
  • Eating disorders
  • Sexual problems
79
Q

What are the fear disorders according to HiTOP?

A
  • Social phobia
  • Agoraphobia
  • Specific phobia
  • SAD
  • Panic disorder
  • OCD
80
Q

What are the distress disorders according to HiTOP?

A
  • MDD
  • Dysthymia
  • GAD
  • PTSD
  • BPD
  • The ways these are alike each other is more important than how they are related to others
81
Q

What are twin studies?

A
  • Monozygotic (Mz) twins: twins that are genetically identical (identical twins)
  • Dizygotic (Dz) twins: twins that share on average 50% of their genes
  • Are monozygotic twins more similar with disorders vs dizygotic twins?
  • With these groups you can control for other factors since they have the same experiences, age and environments
  • Heritability estimates can vary from 0 to 1
  • A = Additive Genetic Component -> how much more alike are monozygotic than dizygotic twins
  • C = Common Environment Component -> how much are they alike across both types of twins (because they share an environment, they are more alike)
  • E = Unique Environment -> how much does each twin differ from one another due to unique environmental factors/experiences
82
Q

What are the heritability estimates found in twin studies?

A
  • A= 2(rMZ – rDz) -> magnitude of the correlation
  • MZ concordance = 50%
  • Dz concordance = 25%
  • Difference (D) = 25%
  • 2D = 50%
  • Sample specific
  • Heritability estimates differ according to the different environments
  • Higher with less environmental variance
83
Q

What are some problems with twin studies?

A
  • The assumption underlying this study design is that the environment of MZ twins is as alike as that of DZ twins -> this is false since MZ twins may have an environment that’s even more alike
  • MZ twins often share a placenta (shared placenta has implications for gene expressions over the lifetime, even at conception, the environment of MZ twins is more similar than DZ twins)
  • MZ twins treated more similarly to one another
  • Heritability = estimated genetic contributions to observed phenotype -> not deterministic (doesn’t tell us what causes the trait), they’re probabilistic
  • Often don’t model G x E (don’t consider the environment that much)
84
Q

What are Gene-Environment correlations (rGE)?

A
  • Our genetic makeup is not independent of the environments that we experience throughout our lifetime
  • Currently, all rGE attributed to G
  • Have to be cautious when interpreting genetic contributions
85
Q

What are the different types of Gene-Environment correlations (rGE)?

A
  • Passive: the same people that give you your genes, are also often the ones that provide you with your early-rearing environment (can be addressed in adoption studies) -> passive because it doesn’t depend on what a child does (depends on parents)
  • Active: people are not just passive perceptible of their environment, we behave in certain ways based on our genetic makeup, as kids grow older, they choose their environment (friend group) -> niche-picking
  • Evocative (reactive): we are treated differently based on our genetic makeup, our genotype can determine the response that we elicit (ex: attractive people are treated differently than unattractive people and highly impulsive people often aggravate others which will lead to different responses from others)
  • Active and evocative hard to measure –> need better understanding of how environment shapes traits
86
Q

Describe the genetics of intelligence

A
  • IQ is highly heritable: ~80%
  • IQ also malleable -> Flynn effect (intelligence as measured by IQ tests increased across the 20th century, despite the tests getting harder overtime)
  • Flynn effect occurs more in developing countries since access to education increases
  • Higher IQ = seek out “more stimulating” environments -> are available w/ more development
87
Q

Describe how heritability varies as a function of the environment

A
  • Heritability of IQ increases across development (IQ in kid twins looks less heritable but more heritable when they’re older)
  • Among affluent (wealthy) families in high SES environments, heritability of IQ estimated at 0.72 -> suggesting that genes are emitting a stronger influence in these more affluent environments
  • Among less affluent families, little observed additive genetic influence (heritability of 0.10)
  • Heritability of alcohol use for those residing
    in a neighbourhood with 10 or more alcohol outlets was 74%, compared with 16% for
    those in a neighbourhood with 0 outlets
  • Eating disorder symptoms show minimal heritability before puberty but significant genetic effects (greater than 50%) during and after puberty
  • The environment in which you exist, influences the extent to which your genotype affects your phenotype
88
Q

When we say something is heritable, do we know what’s the mode of transmission?

A
  • No, it doesn’t necessarily mean that we have pinpointed the mode of transmission
  • Difficulty of making the link from genotype to phenotype
89
Q

Describe the Genotypes-Endophenotypes-Phenotypes relationship

A
  • Difficulty of making the link from genotype to phenotype (genotype-phenotype gap) -> we often don’t know how the genotype leads to the phenotype
  • Phenotypes are very complex phenomena, multiply-determined, often poorly defined (don’t have great boundaries to be defined properly)
  • Endophenotype: intermediate step between microscopic genes and nerve cells and the experiential and psychological phenotype
90
Q

What are the characteristics of endophenotypes?

A
  • must segregate with illness in the population
  • must be heritable
  • must not be state-dependent (manifests whether illness is active or in remission)
  • 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 be specific to the illness of interest (almost never the case but this is the ideal criteria)
91
Q

What are specific phobias?

A
  • A circumscribed fear of a specific object or activity
  • Phobia is not just a fear (ex: fear of speaking)
  • Phobia is a fear that interferes with people’s ability to live their lives day to day -> some aspect of the phobia must interfere with normal functioning
  • There are 5 sub-types of phobia disorders
  • Each of these is diagnosed as a specific sub-type of phobia
  • Marked persistent and excessive or unreasonable fear when in the presence or when anticipating to be in the presence of the object -> the person has to realize themselves that the fear is excessive
  • In all cases, fear is not of the object itself
  • Instead, fear is of some dire outcome of interacting with the object (ex: fear of being bitten by a snake or being stuck in an elevator)
92
Q

What are the 5 sub-types of phobia disorders?

A
  • Animal-Type (rodents, reptiles, insects)
  • Natural Environment-Type (storms, heights)
  • Blood/injection/injury type
  • Situational Type (tunnels, bridges, elevators, flying)
  • Residual “other” category (very common - choking, vomiting, illness, loud noises, falling down)
93
Q

Why is the nature of the fear in phobia key to diagnosis?

A
  • Fear of airplanes can be diagnosed as 2 different phobias, depending on the reasoning behind the fear
  • Ex: Anna is afraid of airplanes because she fears falling from the sky and dying -> airplane phobia
  • Ex: Sam is afraid of airplanes because he fears he will be trapped and unable to escape if he suddenly starts to feel dizzy or nauseated -> agoraphobia because he fears places where he feels he won’t be able to escape if he needs to
94
Q

What’s the Epidemiology, Onset and Course of phobia disorders?

A
  • Phobias are relatively common
  • Specific phobia prevalence: 12.5%
  • Agoraphobia prevalence: 1.5%
  • 2F:1M
  • Comorbidity very high (very often comorbid with other anxieties and depression)
  • Most children outgrow specific fears
  • Most don’t become phobic adults
  • Not true of other anxiety disorders (onset in childhood will often persist in adulthood)
  • All specific phobias tend to have onsets in childhood
  • Agoraphobia often onsets in adulthood
95
Q

What’s classical conditioning?

A
  • Process of associating 2 stimuli
  • Ex: associate lighting to the sound of thunder
  • Fear learning/conditioning process
  • Conditioned fear response to thunder from the lightning
96
Q

What are the types of conditioning?

A
  • Classical conditioning
  • Operant conditioning
97
Q

What’s operant conditioning?

A
  • Process of associating a response and its consequence
  • Ex: pulling a candy machine lever leads to the delivery of candy bar (reward)
98
Q

Fill in the blanks: Reinforcement _____ behaviour and punishment _____ behaviour

A
  • Reinforcement increases behaviour
  • Punishment decreases behaviour
99
Q

Describe the punishment vs negative reinforcement consequence matrix

A
  • Appetitive (positive) stimulus & supply a stimulus = Positive reinforcement
  • Appetitive (positive) stimulus & remove a stimulus = punishment (ex: time-out)
  • Aversive (negative) stimulus & supply a stimulus = punishment
  • Aversive (negative) stimulus & remove a stimulus = negative reinforcement
  • Anytime a stimulus is introduced into the environment -> positive
  • Anytime a stimulus is removed from the environment -> negative
100
Q

Describe Orval Hobart Mowrer’s psychological theory of phobias

A
  • Mowrer posited a 2-factor theory of phobias
  • He said fears are acquired from some classical conditioning but they are maintained through operant conditioning
  • Ex: if I’m afraid of something, I begin to avoid the thing (increasing avoidance behaviour to decrease exposure to feared stimulus -> negative reinforcement pattern)
  • Maybe the origins are in classical conditioning but with regards to treatment, we target operant conditioning
101
Q

If Learning Theory of phobias is true, then what should their etiology look like?

A
  • Onset of phobias should be linked to some sort of traumatic experience with the feared object
  • However, only 50% of individuals with phobia disorder report encountering a traumatic experience with the feared object
  • This could be caused by forgetting about traumatic experience
  • Could be caused from vicarious transmission -> we learn very well by watching other people, you can learn to fear something by watching someone else have a negative experience with it or being afraid of it
  • Why don’t all traumatic experiences lead to phobias?
102
Q

What’s the Evolutionary Preparedness Theory?

A
  • We have evolved a sensitivity to certain stimuli (Seligman)
  • Certain fears were adaptive at one point for our survival
  • These fears were selected for and the effects of that selection are still with us
  • Explains why people are more afraid of snakes than flowers
  • Also explains why we are more scared of sharks than of electrical outlets, despite there being more deaths caused by electrical outlets than by sharks
  • There are very few phobias pertaining to outlets or electricity
  • Outlets are relatively newer in our environment than sharks
  • Could explain that we’ve evolved to be scared of sharks
103
Q

Describe Cook & Mineka (1990) study on Evolutionary Preparedness

A
  • Study of monkeys
  • One group watched videos of other monkeys that are afraid of snakes but playing with flowers
  • Another group watched videos of other monkeys that are afraid of flowers but playing with snakes
  • The results show that the monkeys that have been conditioned to be afraid of snakes spend less time with snakes after watching the video
  • The results for the monkeys that have been conditioned to be afraid of flowers spend about the same time with flowers after watching the video
  • Why is it easier to condition a monkey to be scared of a snake rather than flower -> this is because of evolutionarily experiences, we are ready to be afraid of snakes
104
Q

What’s the immunizing effect with phobias?

A

If you have many learning experiences with an outlet that are not dangerous (ex: you don’t get shocked whenever you charge your phone) then you are less likely to be scared of it overtime

105
Q

What’s stimulus-bound panic vs situationally-bound panic?

A
  • Stimulus-bound panic= Phobias -> respond reliably to the stimulus (w/ panic)
  • Situationally-bound panic = agoraphobia -> cued so not inevitable, but this is why they tend to avoid certain places
106
Q

In Panic Disorder, panic must be _______

A
  • In Panic Disorder, panic attacks must be uncued -> must be spontaneous
  • Ex: If you panic whenever you see a spider, it is not a panic disorder
107
Q

What are the DSM-5 criteria for Panic Disorder?

A
  • Recurrent unexpected panic attacks -> at least one followed by a month or more of a persistent concern about having panic attacks
  • Panic not better accounted for by another disorder (ex: stimulus-bound phobia) -> can occur with or without agoraphobia
  • A discrete period of fear or discomfort w/ 4 out of 13 symptoms
  • Develops abruptly in an uncued way and peak in intensity within 10mins -> then decreases very rapidly
  • Lots of cardiovascular, autonomic symptoms & some cognitive
  • If you have panic attacks and you aren’t worried about them then it’s not considered a disorder -> worrying about having another panic attack, worrying about the implications of panic attack
108
Q

What is Klein’s perspective on Panic Disorder?

A
  • Originally anxiety paired with a negative stimulus (i.e., panic attack)
  • Avoidance occurs (agoraphobia) -> we start to avoid things that we think will be associated with a panic attack
  • Through avoidance, anxiety is negatively reinforced -> rather than extinguished through facing fears and seeing no negative response
109
Q

What is the key difference between social & simple phobia?

A
  • Social or simple phobia can involve avoidance of similar situations
  • Motivation is different
  • Simple phobias, may be afraid a bus will crash
  • Social phobias, may be afraid of a bus because they want to avoid crowds b/c they fear embarrassing themselves
110
Q

What’s differential diagnosis?

A

Trying to identify whether someone has one disorder or another

111
Q

What’s the epidemiology of Panic Disorder?

A
  • ~ 4-6% lifetime prevalence
  • 2F:1M
  • no significant associations with race/education
  • median age of onset – 24
  • range of age of onset – narrower
  • Rarely before adolescence, or after middle age -> usually between 14-34
  • Onset is very abrupt, go from nothing to panic symptoms -> doesn’t start with mild anxiety and then a panic attack, it’s usually an abrupt panic attack
  • Symptoms typically remain pretty consistent throughout different panic attacks
112
Q

Describe David Clark’s psychological theory of panic

A
  • Theory called fear of fear
  • Believes panic attacks due to catastrophic misinterpretations of certain bodily sensations
  • Heart palpitation = heart attack
  • Magnify
  • Vicious cycle
  • Symptoms usually internally-generated, but could come from caffeine, cocaine, anger (because of physiological changes)
113
Q

Describe Reiss & McNally’s psychological theory of panic

A
  • Anxiety Sensitivity -> important trait for panic
  • Trait-like differences in how fearful one is about physiological sensations of anxiety
  • People high on trait more likely to panic when they experience anxiety
  • In the middle of the course of panic disorder, the symptoms don’t have to be interpreted as a heart attack, you just have to believe that if you keep having those symptoms you’ll have a heart attack
  • Panic disorder is to some extent related to how sensitive you are to physiological changes (even small ones)
114
Q

Describe the history of panic disorder

A
  • Introduced in 1980 (DSM-III)
  • Prior to 1980, only “anxiety neurosis”
  • Pulled apart GAD and panic (1st attempt to differentiate fear and distress/anxious apprehension)
  • DSM-III introduced 2 types of Agoraphobia: 1 with Panic & 1 without
  • DSM III-R removed agoraphobia from category of phobias -> classified it as a complication of panic
  • DSM-IV expanded the notion of panic: must include not just panic, but also apprehension around the panic,
  • now apprehension is a necessary component of the disorder (can’t have a diagnosis of panic disorder w/out apprehension)
115
Q

Describe Bouton, Barlow and Mineka’s learning theory model of panic disorder

A
  • Interoceptive Conditioning
  • Spontaneous panic attacks
  • Paired with awareness of early symptoms of panic
  • Low level sensations become conditioned stimulus
  • Appears spontaneous, but the conditioned link was there (subconscious)
116
Q

Describe Stress in Canada

A
  • According to Statistics Canada (2017), 23% of people between ages 18 and 34 reported that most days are “quite a bit” or “extremely” stressful
  • In this age bracket 25% of women and 21% of men are experiencing stress (more women than men)
  • Top Stressors:
    1. Work
    2. Money
    3. Relationships
    4. Health
117
Q

What is stress?

A
  • Modern understanding comes from someone working at McGill, Hans Selye, who borrowed the term stress from engineering
    ○ Idea that in engineering stress is forces acting upon a structure that make it crumble (bridge is experiencing stress)
  • Hans: The way the body responds to external demands on the body
118
Q

What’s the difference between a stressor and stress?

A
  • Stressor: things/events that challenge to maintain homeostasis or maintain organism’s equilibrium (ex: actual dangers in environment -> being chased by bear or good/positive things -> having a baby or new job)
  • Stress: how the organism reacts (physically and psychologically) to the stressor
  • Stress response: holding the same event and threat level constant, diff people will react differently to the event
  • Stress reflects the interaction of the organism and its environment
119
Q

Describe the physiological cascade that occurs once a stressor happens

A
  • Starts with the hypothalamus (receives info about threat from the brain & signals to the organism to respond)
  • Hypothalamus triggers either the SAM or the HPA-Axis
120
Q

Describe the physiological cascade that occurs in the SAM once a stressor happens

A
  • Hypothalamus triggers the Sympathetic Adrenomedullary System (SAM) -> fast response system (comes online almost immediately after stressor exposure)
  • SAM triggers fight or flight and releases adrenaline and noradrenaline
  • These hormones lead to physiological changes, such as heart rate increase, pupils dilating, blood pressure increase, digestion slows, glucose consumption increase
  • All of this is thought to be in service of allowing organism to survive
121
Q

Describe the physiological cascade that occurs in the HPA AXIS once a stressor happens

A
  • Hypothalamus-Pituitary-Adrenal (HPA) Axis -> slower but plays important role in stress response
  • HPA releases the hormone CRH, which stimulates the pituitary gland and this triggers ACTH which then releases cortisol
  • Cortisol doesn’t always mean stress
  • Cortisol aids in fight or flight response and inhibits the immune system
  • Ex: If injury occurs, the healing will be slower
  • Cortisol tends to peak between 20-30 mins after exposure
  • All of this is adaptive and important for survival
122
Q

What’s the cost for using the SAM & HPA Axis stress response systems?

A
  • These eventually lead to allostatic load
  • These systems are designed for the short-term, good for short-term stress
    ○ Chronic stress is much more detrimental to both physical and emotional health
123
Q

Explain how appraisals play into the stress response

A
  • A stressor is something that is actually or perceived to be threatening
  • There’s threat value to neutral expressions
  • Stimuli don’t necessarily have a valence -> appraisals of stimulus make it stressful
  • Hypothalamus doesn’t make judgments -> it’ll activate the system if it receives signals of threat
  • Perception (appraisal) affects severity of activation
124
Q

What are the functions of cortisol?

A
  • Critical for our daily lives
  • We need an increase of cortisol in the morning to get out of bed
  • Critical for terminal maturation and remodelling of axons and dendrites
  • Too little cortisol -> cell death
  • Too much cortisol -> cell damage
  • We need enough cortisol for daily functioning
125
Q

Describe the relationship between the hippocampus and stress

A
  • Critical to memory and stress regulation
  • Shares reciprocal connections with the hypothalamus (major control center for endocrine system)
  • High concentrations of cortisol receptors (sensitive to cortisol)
  • Acute stress suppresses hippocampal activity
  • Chronic stress results in decreased hippocampal volumes (shrinkage)
  • Decreased dendritic arborisation (dendrites that branch off from a neuron to another neuron)
  • Altered function
  • Can result in cortisol hyper secretion (which could result in hippocampal damage)
126
Q

Describe the relationship between the prefrontal cortex and stress

A
  • PFC is important for decision-making, working memory, self-regulatory behaviors, mood, impulse control
  • Slow to develop
  • Repeated stress exposure causes dendritic shortening
  • Chronic stress exposure associated with decreased volume of prefrontal cortex (through cell death or decreased connections)
  • In adolescence, much more rapid development in the limbic system of the brain
  • When a system is developing, it’s easier for damage to occur (much more vulnerable)
  • PFC is vulnerable to stress exposure during developmental period
127
Q

What properties of stressors may be more closely linked with disease risk?

A
  • Stressors that are perceived as:
    1. Uncontrollable
    2. Unpredictable
    3. Severe
  • These properties have been more strongly linked to the development of some psychiatric disorders (ex: depression)
128
Q

Describe the important characteristics of stressors

A
  • Temporal nature of different stressors: stressors can be acute or chronic
  • Type: some types of stressors are more strongly associated with some forms of disease than others (ex: interpersonal stress and depression -> interpersonal stress is a strong predictor of depression)
  • Timing of stress also matters -> early vs later life stress exposure (early life stress has a huge effect on later outcomes -> when brain is developing, exposure to stress will have more effect on remodelling)
129
Q

What are the 5 general patterns observed with regard to Early Life Stress (ELS) and mental disorders in the population?

A
    1. ELS is common (very prevalent)
    1. ELS increases risk for developing a lifetime mental
      disorder compared to no ELS
    1. ELS is associated with virtually all commonly occurring forms of psychopathology – it appears to be non-specific
    1. ELS is associated with increased vulnerability to psychopathology that persists across the life course
    1. ELS explains a substantial proportion of mental disorder onsets in the population (~30%)
  • Also, ELS can alter the brain but the psychological outcomes are varied
130
Q

Describe the ELS study of the orphanage

A
  • Orphanage where group studied infants that had been abandoned at a young age -> they had an acute level of ELS (poor hygiene, poor nutrition)
  • Some of these orphans were placed in adoptive homes
  • Effect of ELS persisted later in life -> they still had an increased risk of developing psychopathology, even when adopted
131
Q

What are some potential mechanisms of risk for ELS?

A
  • Early life is a critical period of brain development and
    stress exposure may disrupt this development
  • Ex: maternal cortisol production can affect how the brain develops (affects infant brain development)
  • Exposure to stress in early life may lead to persistent dysregulation of stress response systems (including HPA-axis and ANS function)
132
Q

Describe fetal exposure to maternal stress

A
  • Growing interest in understanding whether our first contact with stress may make us more vulnerable to psychopathology in later life (this begins in utero)
  • Maternal stress during pregnancy increases risk for post-natal complications, as well as emotional and behavioral problems in infants, children and adolescents
  • Maternal gestational stress exposure does predict psychopathology later in life
  • This risk may be passed from mother to child via
    fetal programming
133
Q

What’s fetal programming?

A
  • Maternal (gestational) stress may be transmitted to the fetus via high levels of glucocorticoids (ex: cortisol)
  • Cortisol may pass through the placenta, and/or stimulate receptors on the placenta to increase cortisol production
  • Infants may develop stress response systems that are hypersensitive to threat -> will be more reactive when they encounter stressor or threat
  • Basal cortisol levels and cortisol reactivity are greater in infants exposed to higher levels of maternal stress
  • Susan King studying what happened to the offspring of pregnant women during ice storm in Montreal (1990s)
134
Q

Describe the study by Yong Ping et al. (2015) on fetal exposure to maternal stress

A
  • They examined effects of prenatal maternal stress from a natural disaster on offspring cortisol reactivity
  • 2008 Iowa Flood (rated as one of the top disasters in US history)
  • Recruited pregnant mothers who had experienced the flood (experienced some close proximity to the effects of flood)
  • Rated mothers’ objective exposure (did you lose power, did your house flood?) to stress and collected perceived stress
  • Collected saliva samples from their toddlers before and after a mother-baby separation task
  • The more severe the mothers’ objective exposure and subjective stress from a major flood during pregnancy, the greater the child’s cortisol reactivity increase in response to stress (particularly true for the girls in the study)
  • Maternal subjective stress had no effect on boys, but in girls greater subjective stress predicted greater cortisol reactivity
135
Q

Multiple studies from around the world reporting increases in symptoms of
what disorder across the course of the pandemic

A
  • Multiple studies from around the world reporting increases in symptoms of
    depression across the course of the pandemic
  • But there’s some evidence that these increases were not evenly distributed across the population
  • Ex: in a sample of 10,368 adults in the US -> risk for increased depression associated with several variables:
  • Social Isolation
  • Female gender
  • Food insecurity
  • Hispanic ethnicity
  • Unemployment
  • Some of these variables are general predictors of depression independently
136
Q

Describe the study on COVID Stress and Neural Responses to Rewards

A
  • Longitudinal sample of McGill undergrads (follow-up visit after 1-3 yrs)
  • Neural responses to rewards (pre-pandemic and in Fall 2021)
  • COVID group and non-covid group (both mostly female)
  • Quasi-experimental design
  • COVID group given a Pandemic Stress Questionnaire
  • Use of ERP
  • Results show that the covid group demonstrated a significant decrease of neural sensitivity to reward in the follow-up study
  • Suggests the stress of the pandemic may have had an effect on sensitivity to rewards
137
Q

What are the top 5 stressors in the Pandemic Stress Questionnaire

A
  1. My work/school has been disrupted due to COVID-19 – 89.7%
  2. People around me have been more frightened than usual due to COVID-19 - 89.7%
  3. I was unable to be with close family, friends, or partners because of the coronavirus pandemic – 71.8%
  4. I had less contact with good friends because of the coronavirus pandemic – 71.8%
  5. People around me have been complaining more than usual due to COVID-19 – 69.2%
138
Q

What are some empirically-supported steps to promote well-being?

A
  • Social support
  • Exercise
  • Mindfulness
  • Controlled breathing
  • Sleep
139
Q

Describe how social support can promote well-being

A
  • Humans are social creatures
  • Social support linked to 50% reduction in mortality risk
  • Loneliness associated with higher blood pressure, increased waking cortisol levels
  • Social Support helps people recover faster from recent life stress exposure
  • Helps with social evaluative stress
140
Q

Describe the studies conducted on the social buffering of stress

A
  • To provoke stress response in people -> social evaluative stress
  • Trier Social Stress Test (TSST) -> facing panel of judges who tell you you have to prepare a speech for big audience, make you count backwards by 7s from 1000 to judges with neutral looks on their faces that tell you stop and start again if you get it wrong
  • In these studies, it was found that for children, being in the presence of a parent appears to buffer their stress response
  • Men showed higher cortisol levels in TSST task
  • Men supported by opposite sex partner showed less cortisol
  • Social buffering by romantic partner worked for men in TSST task but for women presence of their partner increased cortisol levels
  • Women receiving physical contact from their partner acted as buffer (reduced their stress in task)
  • In TSST task where people had the option to be alone, be with a friend or be with a stranger dog -> Alone = cortisol peak, with friend = social buffering of cortisol, biggest social buffer of cortisol was doing the task with the dog
141
Q

Describe the effect that pets have on the social buffering of stress

A
  • Pet ownership may buffer stress -> allows you to cope with/regulate stress response
  • Pet-owning coronary patients have higher one-year survival rates
  • Elderly people with pets make fewer visits to the physician
  • People with pets show less HR (heart rate) reactivity during lab stressors
142
Q

Describe the effect of exercise on stress

A
  • Physical exercise can protect against hippocampal degeneration associated with chronic stress
  • Regular exercise associated with reduced physiological reactivity to psychological stressors
  • Exercise can improve mood -> has a stronger effect for people who start out in poorer physical health
  • Some evidence that walking for 2-4 hours/week can significantly improve mood
  • Mood improvements observed after even 10 mins of self-selected high intensity exercise (exercise that you determine as intense)
  • Trier task has reduced physiological reactivity for people doing exercise
143
Q

Describe the findings of the study linking exercise to the TSST

A

○ Inactive group show much more heart rate reactivity to the trier task
○ Moderately exercising group show less heart rate reactivity to the trier task
- Vigorously active group show the least heart rate reactivity to the trier task (close to moderately active)
- All of this is independent of mood, only focused on physiological responses

144
Q

Describe the effect of controlled breathing on stress

A
  • Trains people to turn attention to their breath
  • A lot of evidence shows that it’ll slow physiological responses to stress -> even if doing it just a few times throughout the day
145
Q

Describe the effect of sleep on stress

A
  • Sleep deprivation increases allostatic load -> increases blood pressure, increases evening cortisol levels (we need cortisol to drop in the evening so we can go to sleep and then it goes up again in the morning)
  • Chronic sleep deprivation can affect hippocampal volumes
  • Alters mood, cognitive control, affects concentration
  • Associated with increased rates of illness, accidents, lower life expectancy
  • 7 to 9 hours a night is considered optimal for 18-64-year-olds
146
Q

What’s sleep hygiene?

A
  • Reducing frequency with which people are engaging in poor sleep behaviours
  • Improvement of sleep hygiene can improve sleep quality and sleep duration
147
Q

Describe the relationship between stress and cognitive function

A
  • Acute stress can interfere with goal pursuit/learning
  • Stressed participants tend to fall back on habitual behavior
  • Greater working memory capacity at baseline can protect against these effects
148
Q

Where are SAD and GAD located in HiTOP?

A

Both are in internalizing disorders but SAD is in the fear section and GAD is in the distress section

149
Q

What’s the DSM II to DSM-III-R history of the definition of GAD?

A
  • DSM-II lumped into broad category of “Anxiety Neurosis”
  • In DSM-III, GAD broken out as a residual category (people who had anxiety symptoms but not necessarily phobia or panic related)
  • DSM-III-R GAD changed to have more of its own identity
  • Worry begins to play a larger role
  • Pathological worry -> worrying about everything all the time and not being able to control it (has to be about everyday situations, not just about another disorder)
  • Sometimes difficult differential diagnosis (ex: GAD and OCD can sometimes be a tricky differentiation)
150
Q

Describe the DSM-IV description of GAD

A
  • Simplified the criteria
  • Excessive anxiety and worry
  • More days than not
  • At least 6 months
  • About multiple events, activities, objects
  • Difficult to control the worry
  • Cannot occur exclusively during a mood episode
  • Worry interferes with ability to sleep, do their work, relationships (ex: arguments)
151
Q

What’s the DSM criteria for GAD?

A
  • Restlessness, feeling on edge
  • Easily fatigued
  • Difficulty concentrating
  • Irritability
  • Muscle tension
  • Sleep disturbance
  • Must cause significant distress or impairment
  • Overlap with depression?
152
Q

What’s the controversy behind GAD?

A
  • Almost always comorbid with something else (more than other disorders)
  • NA (Negative Affect)? -> some have suggested maybe it’s not a diagnosis but just negative affectivity that predisposes you to have other forms of psychopathology
  • Vulnerability marker? -> maybe it’s pre-symptomatic state of another disorder
153
Q

What’s the prevalence of GAD?

A
  • 5-6% lifetime
  • 12-month prevalence: 3.1%
  • 2F:1M
  • Most commonly diagnosed Axis I disorder in primary care
  • 90% of diagnosed cases meet criteria for another disorder
  • 80% of diagnosed cases meet criteria for a mood disorder
  • Also comorbid with panic disorder, SAD, personality disorders
  • A lot of people who have stomach problems (gastrointestinal distress) will meet criteria for GAD
  • Maybe this is a non-specific thing that makes ppl vulnerable to lots of other disorders
154
Q

What’s the most commonly diagnosed Axis I disorder in primary care?

A

GAD

155
Q

What are problems related to GAD?

A
  • Associated with increased health care utilization -> more frequent visits to doctor
  • Increased health care costs
  • Greater chance of concurrent physical illness (chronic constant worry takes a toll on physiological health -> muscle problems, jaw problems, gastrointestinal disease, headaches and migraines)
  • Significant social, academic, and vocational impairment (ex: days lost at work/school and damage to relationships)
156
Q

What’s the course of GAD?

A
  • Symptoms often evident in adolescence or earlier
  • These symptoms emerge pretty early on in one’s life -> people with GAD often can’t remember when they ever weren’t worried
  • Median age of onset in the 30s
  • But can onset at any time
  • Gradual onset (usually due to having a trait)
  • Chronic course
  • Sort of like a personality disorder -> chronic
  • 12-year follow-up study, the recovery rate is 58%
  • Of those who recover, the recurrence rate is high -> people will fluctuate in and out of symptomatic state (cyclical for some people)
157
Q

Describe the familial transmission of GAD

A
  • Trait anxiety highly familial -> anxiety traits run in families
  • Strong genetic component (ex: twin studies)
  • GAD also runs in families
  • Family Studies show:
  • Increased rates of GAD in
    families of probands with GAD
  • Higher rates than in probands with panic disorder
  • Suggests some specificity
158
Q

What are some distinctions between GAD & MDD in the mechanisms of the disorders?

A
  • Attentional biases -> people with GAD are more likely to have attentional biases towards threat than people with MDD
  • Memory Biases -> people with MDD are more likely to show memory biases (remember things as worse than they were)
  • Intolerance of Uncertainty
    -> prominent feature of GAD
  • Low PA -> Low positive affect/emotionality is much more common in MDD. GAD don’t necessarily show differences in positive affect -> they have high negative affect, MDD has low PA and high NA
159
Q

Describe the validity and reliability of GAD diagnosis

A
  • Reliability of GAD diagnosis (good inter-rater and test-retest reliability)
  • Predictive Validity -> diagnosis of GAD can tell us something about the course of their disorder
160
Q

What are some distinctions between GAD & MDD in the precipitating stressors and the response to laboratory stressors?

A
  • Precipitating Stressors: humiliation in MDD (ex: getting fired) and danger/threat events in GAD
  • Response to laboratory stressors: ECI (emotion-context insensitivity -> respond with the same kind of flat response to positive, neutral and negative things) in MDD and hyperresponsivity (hyperresponsive to threats but have normal responses to neutral or positive things) in GAD
161
Q

What are some distinctions between GAD & MDD in the temporal course of the disorders?

A
  • Different onsets and patterns of chronicity
  • Someone who has MDD episode could develop GAD and someone with GAD episode could develop MDD
  • Extreme goal focus (GAD) to motivational disengagement (MDD)
  • Uncertainty (GAD) to certainty about the negativity of future events (MDD)
  • Beliefs of helplessness (GAD) to beliefs of hopelessness (certainty that things are terrible and will always be terrible - MDD)
  • People with GAD are prevention focused -> making sure bad things don’t happen by thinking about every bad thing that could happen and worrying through it not happening -> leads to burnout which could lead to MDD
  • Within a week, people can go back and forth between these states (MDD and GAD)
  • MDD to GAD (MDD is an extreme stressor and GAD can show up from fear of not experiencing MDD again)
162
Q

What are the object of fears behind GAD?

A
  • GAD doesn’t have a very concrete object of fear
  • Often the fear is their own emotions and negative thoughts
  • Negative thoughts are a threat
  • Afraid of being afraid -> afraId of being overwhelmed by anxiety
  • Tend to catastrophize
  • Cognitive avoidance in GAD -> people think about worry as a form of cognitive avoidance
  • Thinking of multiple solutions (cognitive series of operations) when a negative thought comes up
163
Q

What’s the most prominent current theory of GAD?

A
  • Theory from Tom Borkovec
  • Worry = cognitive avoidance
  • We worry about low probability events
  • Often with worry in GAD, people think worry is effective so they will keep worrying to prevent things from happening
  • People worry to reduce their feelings of anxiety which reinforces the worry when their feelings temporarily subside
  • Worry = cognitive, verbal mental operation
  • Buffers GAD from high emotional arousal
  • Don’t get vivid imagery -> with exposure treatment, you need the imagery to become emotionally aroused
  • If never get aroused, never change your fear structure
  • Worry inhibits emotional processing
  • Also evidence that GAD tries to control or suppress the worry
  • Vicious cycle: inability to control worry increases sense of lack of control -> increases intrusiveness of the thoughts
  • Cycle perpetuates itself
  • Ex: “don’t think of a White Bear”
  • Thought suppression leads to increase in worries and struggles and increases intrusive thoughts -> not effective
164
Q

What are some cognitive factors of GAD?

A
  • Evidence that people with GAD are more likely to show attentional biases for threatening stimuli
  • More likely to show negative biases toward neutral stimulus -> more likely to see this as threatening
  • This has been demonstrated through ambiguous word stems and the stroop test
165
Q

What’s the difference between worry and rumination?

A
  • Rumination: tendency to think about things and how you can change them over a long period of time (seen more in MDD) -> focused on the past, how to fix it
  • Worry: fears of what will happen, how to prevent it -> future-oriented (seen more in GAD)
166
Q

Describe SAD

A
  • 2nd most common anxiety disorder
  • 3rd most common psychiatric disorder
  • Impairment: romantic and other social relationships, career, and education
  • Has a lot of worry and rumination
  • Criteria hasn’t changed much over the years
  • Used to be social phobia
167
Q

What are the DSM-5 criteria for SAD?

A
  • For SAD diagnosis you have to meet all 5 of these
  • A: “Marked fear or anxiety about one or more social situations in which the individual is exposed to possible scrutiny by others” (have to meet this one to be eligible for diagnosis)
  • B: person “fears that he or she will act in a way or show anxiety symptoms that will be negatively evaluated (will be humiliating or embarrassing, will lead to rejection or offend others)” (new to DSM-5)
  • C: social situations almost always provoke fear or anxiety
  • D: these situations are avoided (to reduce people’s distress) or endured with great distress
  • E: fear or anxiety is out of proportion to the actual threat posed by the social situation and to the sociocultural context
168
Q

Describe the fears that characterize SAD

A
  • Fears often involve specific situations:
  • Speaking in public
  • Eating in public
  • Writing in front of other people
  • Using public bathrooms (common fear for SAD - slightly more common for men)
  • Generalized Social Anxiety Disorder –> multiple situations are feared or avoided
169
Q

What’s the epidemiology of SAD?

A
  • Prevalence: 12% (pretty common)
  • 2F:1M
  • Gender diff emerges in adolescence (prior to adolescence, there’s similar rates in both genders)
  • Comorbidity very high
  • Social Phobia: high standards, very self-critical, tend to scrutinize themselves
    *High self-criticism in Depression (can explain overlap with depression)
170
Q

What are some racial/ethnic differences in SAD?

A
  • Rates similar in N and S America
  • Prevalence far lower in East Asian countries (less than 1% 1‐year prevalence -> 6-7% in N. America)
  • East Asian race/ethnicity associated with low prevalence in N. America as well
  • In N. American samples, Hispanic or Black ethnicity/ race also associated with lower risk compared to non‐Hispanic white
  • Genuine differences in psychopathology or insufficient consideration of cultural aspects of the DSM criteria, assessment instruments, or influence of features associated with race, ethnicity, and culture?
171
Q

What’s the age of onset of SAD and other phobias (animal, blood & injury, dental)?

A
  • Animal phobias -> mean age of onset: 7
  • Blood and injury: 9
  • Dental Phobias: 11
    *Social Phobia (SAD): 16 (during adolescence -> period of dramatic social changes and reorientation)
172
Q

Describe cognitive theories of social phobia

A
  • Social situations activate core set of values or beliefs (social competencies)
  • Believe others will view them negatively
  • Schemas interfere with interpretation of social situations (David Clark and Adrien Wells)
  • Begin to see danger and threat
  • The more anxious they feel, the more likely they think rejection is
  • Makes them more anxious
  • Self-focus factor that maintains the disorder (pay attention to everything they do/say and only focus on themselves during interactions and not the actual conversation)
  • Functions as “safety”/ avoidance behavior (something that someone with anxiety does thinking it helps them cope but actually functions as avoidance)
  • Used to forestall social disasters
  • Even after situation -> biased memory for negative experiences
  • Reinforces negative expectation of
    self
  • Vicious cycle -> less socially competent because too focused on themselves to make proper social responses, people consequently enjoy interactions with them less and less likely to want to spend time with them, reinforces the negative schemas and next time they go into a social situation they can use their schemas and past situations as “proof” that it won’t get better
173
Q

What is the research in support of theories of social phobia

A
  • Stroop studies
  • Dot-probe
  • Discrepancies
  • Vigilance-Avoidance
  • Stimulus duration
  • Social vignettes
174
Q

What are the criteria necessary for a DSM-5 diagnosis of Bipolar Disorder?

A
  • Diagnosed based on the presence of a manic episode, lasting at least one week (most of the day, nearly every day) -> must be distinct period (distinct change from normal functioning)
  • Manic episode can consist of “elevated, expansive mood” or “extreme irritability”
  • Persistently increased goal-directed activity or energy
  • If only irritable, need to meet more criteria
  • Inflated self-esteem or grandiosity
  • Decreased need for sleep (irritability often stems from inability to down-regulate/ slow down)
  • More talkative than usual (pressured speech)
  • Flight of ideas/racing thoughts (Jump from one idea to the next, appears similar to loose associations in Schizophrenia, thoughts are racing and they can’t keep up)
  • Distractibility (reported or observed, can contribute to the flight of ideas, can lead to diagnostic difficulties with ADHD)
  • Increase in goal-directed activities (can be social -> talk to strangers, call at all hours of the night, working on several projects at once but never finish)
  • Increased libido
  • More active or agitated (can’t sit still)
  • Excessive involvement in pleasurable activities with a high potential for painful consequences (shopping sprees, sexual indiscretions)
  • Not attributable to physiological effects of a substance (ex: drugs) or another medical condition
175
Q

What are the different specifiers of unipolar depression?

A
  • Psychotic MDD
  • Recurrent Depression
  • Melancholia
  • Atypical (intact mood reactivity)
  • Chronic Major Depression
  • Seasonal Affective Disorder
  • Persistent Depressive Disorder (PDD; formerly Dysthymic Disorder)
176
Q

What are the DSM-5 criteria for OCD?

A
  • A. Presence of obsessions, compulsions, or both
  • B. Obsessions or compulsions are time-consuming (ex: more than 1 hour per day) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
  • C. Symptoms are not attributable to the physiological effects of a substance (ex: drug abuse, a medication) or another medical condition
  • D. The disturbance is not better explained by the symptoms of another mental disorder
  • Specify if: With good or fair insight, With poor insight, With absent insight/delusional beliefs:
  • Specify if: Tic-related: The individual has a current or past history of a tic disorder.
177
Q

Why do we say obsessions in OCD are ego dystonic?

A
  • Symptoms, thoughts, behaviours that are not consistent with the patient’s sense of self
  • Intrusive, unwanted and inappropriate
178
Q

What are the different types of obsessions in OCD?

A
  • Contamination (most common)
  • Uncertainty
  • Aggressive
  • Symmetry/ Exactness
  • Sexual
  • Somatic
179
Q

What’s the DSM-5 criteria for PTSD?

A
  • Need exposure to a traumatic event
  • Re-experiencing of the event in some way
  • Avoidance (behavioural or cognitive)
  • Negative alterations of cognitions and mood
  • Marked alterations in arousal and reactivity associated with the traumatic event
  • Duration of the disturbance is more than 1 month

Psychopathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions