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Psychopathology > Module 3: Anxiety and depressive disorders > Flashcards

Module 3: Anxiety and depressive disorders Flashcards

1
Q

What is the negative feedback cycle in anxiety?

A

the more anxious a person becomes, the stress response becomes heightened and people become more easily triggered by their anxiety

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2
Q

What are some behavioural symptoms of anxiety?

A

avoidance, sleep disturbance, reassurance seeking, checking of items

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3
Q

What are some cogntiive symptoms of anxiety?

A

worry, catastrophizing, depersonalisation, memory loss

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4
Q

How does the HiTop model differ to DSM categorization?

A
  1. emphasises importance of dimensional aspects of symptoms
  2. focus on underlying biology and environment that interact
  3. disorders can be understood on a spectrum on their levels of severity and intensity and extent of comorbidity with other disorders
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5
Q

What is the advantage of HiTop?

A
  1. help tailor treatments more effectively through considering unique needs of patient and underlying factors compared to applying a more generalised diagnostic criteria
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6
Q

What is the specifier for social anxiety?

A

Specifier - with or without performance (if fear is restricted to speaking or performing in public)

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7
Q

Overview of SAD:

A
  1. individual fears they will act in a way that will be negatively evaluated
  2. Social situations always almost provoke fear/anxiety out of proportion to actual threat and are either avoided or endured with intense fear/anxiety
  3. Last at least 6 months + clinically significant distress + impairment in multiple areas of life
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8
Q

Prevalence and median onset of SAD

A
  1. early age of onset around 13 yrs
  2. Lower prevalence rates in low/lower-middle income countries in African and Eastern Mediterranean regions, higher prevalence rate in higher income countries in American and the West

12 month prevalence rate in aus: 7%

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9
Q

What happens in those with early onset with SAD?

What’s the subthreshold significance?

A
  1. Early onset without treatment results in persistent and chronic symptoms

Subthreshold prevalence is also high - HiTOP can consider experience at subclinical thresholds and identity more individual with similar to those with SAD who may still need treatment

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10
Q

What is the SES link with GAD?

A
  1. found disproportionately with - -
    lower education
    lower income
    lower employment status
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11
Q

What is the 12 month prevalence and median onset?

A
  • 12 month prevalence rate is 3.8% in Australia
  • median age onset 30 years, begins in adulthood, onset before puberty is rare only around 5%
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12
Q

What is the fear response model in SAD?

A

people with SAD often have highly negative self belief and expectations about outcomes of social interactions

thus they have a heightened focus on ability to interpret social cues and find them to be more threatening or negative

This creates a negative feedback cycle leading to avoidance behaviours that leads to short term relief that reinforces social anxiety that situation is negative/threatening

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13
Q

What type of disorder does HiTOP classify GAD and SAD?

A

In the HiTOP model, GAD and SAD are internalising disorders relating to fear-processing

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14
Q

What are findings for SAD in genome wide studies?

A

Wong et al. 2017 - GENES IN CALCIUM SIGNALLING for plasticity in brain and neurotransmissions like serotonin, norepinephrine and dopamine are linked with social anxiety

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15
Q

What 4 parts of the brain are implicated in SAD?

A
  1. HYPERACTIVE AMYGDALA activation to emotional stimuli
  2. SMALLER HIPPOCAMPUS volume in severe SAD: impairs consolidation of memories
  3. Reduced activation in DORSOLATERAL PREFRONTAL CORTEX: suggests impaired cognitive control in SAD
  4. INCREASED INSULA activation in response to social exclusion linked with higher self reported social anxiety (insula is involved in subjective feelings)
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16
Q

What are some of the aetiological factors proposed in the onset of SAD?

A
  1. Genes
  2. Individual temperament
  3. Cognitive factors
  4. Negative/traumatic life events
  5. Parental style and attachment, peer experiences
  6. Cultural factors
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17
Q

What is the overview of GAD?

A

A. Excessive anxiety and worry about something that might happen in a variety of topics, events or activities

B. Difficulty of control worry

C. 3/6 of the symptoms:
Restlessness or feeling keyed up or on edge
Being easily fatigued
Difficulty concentrating or mind going blank
Irritability
Muscle tension
Sleep disturbance (difficulty falling or staying asleep, or restless unsatisfying sleep)

D-F: impaired functioning, distress and differential diagnosis

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18
Q

How can worries in GAD extent to different areas of life?

A

Free-floating anxiety can lead to impairment to other areas of life and spread to other areas of life, eg. anxiety about a car accident can turn into fears about getting to work to fears about being fired and not being able to afford rent

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19
Q

What is the genetic heritability risk rate for GAD?

A

30% estimate of moderate genetic risk

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20
Q

What is the GABA hypothesis of GAD?

A
  1. There is a functional deficiency of GABA, that reduces neurons in brain and calm down nervous system - low GABA can lead to overactivity which benzodiazepines can help
  2. Low GABA is linked with higher trait anxiety, separation anxiety, social phobia and panic disorder and comorbid with personality and MDD (explained by genetic contributions towards neuroticism)
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21
Q

What is a non-biological precursor/predisposing factor linked with GAD?

A

high levels of trait anxiety

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22
Q

What 4 brain regions are implicated in GAD?

A
  1. The anterior cingulate cortex is involved in regulating anxiety, seems to play a role in GAD
  2. SMALLER HIPPOCAMPUS, ACC AND AMYGDALA
  3. Lower functional connectivity of ACC and dorsolateral PFC - impacts emotional regulation to negative emotions
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23
Q

What is the Metacognitive Model of anxiety disorders?

A
  1. It proses 2 levels of worry: everyday events + meta-belief worrying about worry which increases stress intensity, paired with unhelpful behaviours including avoidant behaviours and seeking reassurance and validation about meta-beliefs

Trigger initiates process of worry either Type 1 Worry or Type 2 Meta-Worry

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24
Q

What 3 things the Metacognitive Model propose happen after Type 1 Worry and Type 2 Worry are activated?

A
  1. Behaviours of avoidance or reassurance
  2. Thought control to suppress, distract or avoid
  3. Worry-related emotion like irritability or anger
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25
Q

What is the intolerance of uncertainty theory of anxiety? (Dugas et al. 2004)

A

Low tolerance for unfamiliar situations and and bias on focus of ambiguous things - leading to high levels of distress, excessive worry and meta-beliefs, avoidant behaviours to eliminate uncertainty and get a sense of control

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26
Q

What kinds of beliefs do people with GAD have about worry?

What type of problem orientation and reinforcement do they have?

A
  1. positive beliefs about worry and often interacts with positive beliefs about worry and try to justify their meta-beliefs about stressors
  2. Poor problem orientation and low confidence
  3. Negative reinforcement through avoidant behaviours reinforces the perceived severity of the stress
    Facing the worry allows one to reduce the worry
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27
Q

What disorders are no longer listed in the anxiety disorder section of the DSM?

A
  1. ASD - acute stress disorder
  2. PTSD
  3. OCD
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28
Q

What is the LP for anxiety disorders across gender and indigenous people?

A

Lifetime prevalence of an anxiety condition: ⅓ women and ⅕ men

indigenous people unknown but probably higher

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29
Q

What is Acceptance and commitment therapy (ACT) and what is it for?

A

ACT is whereby the patient is encouraged to notice and accept their thoughts, avoids controlling distressing thoughts and respond to situations that are consistent with their values

  1. ACT is beneficial for GAD, SAD, and OCD, and less known with other anxiety disorders
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30
Q

What is CBT, how long and what evidence?

A
  • look at patterns of thinking (cognition) and acting (behaviour) that are unhelpful for a disorder and make changes to replace these patterns with ones that reduce anxiety and improve coping.
  • 4 to 24 weekly sessions
  • Strong empirical evidence for all types of anxiety
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31
Q

Module 3b. What was the High Functioning Anxiety video about?

A
  1. Anxiety may be lower/higher in specific situations “situational anxiety”
  2. “High functioning anxiety” = lay term where anxious people may be able to conceal symptoms so they do not appear to be dysfunctional in society
  3. Differing symptoms across different social settings may appear to be arrogant, lazy, aloof
32
Q

What are the two main affective disorders in the DSM-5?

A

depressive and bipolar and related disorders

33
Q

Difference between depressive and bipolar disorders?

A

Depressive disorders are characterised by persistent negative mood stage, while bipolar is characterised by elevated and depressed states

34
Q

Australian 12-month prevalence rate and suicide link?

A

Australia - 12-month MDD = 10.4%, 90% of suicide deaths had risk factors of MDD

35
Q

What are the 2 main significant predictors of MDD?

A
  1. Symptom severity
  2. Symptom duration
36
Q

What is the median duration of an MDD episode?

A

Median duration of MDD episode is 24 weeks,
60% will have a second, 80% of the first 60% will have a third, 90% of those will have a fourth

37
Q

What is the Kindling Effect (Poist, 1992)?

A

MDD is triggered by repeated exposure to prolonged stressors which cause neurochemical changes in the brain, as stressors and MDD progress, the combination of stress + neurochemicals causes more frequent episodes of MDD that are progressively less linked to specific factors / without clear cause = heightened depression vulnerability

38
Q

What are 3 big comorbidities with MDD?

A

Anxiety, obesity and heart disease

39
Q

What medical effect is bidirectional with MDD?

A

Link between cardiometabolic issues and MDD are bidirectional - the risk of one increases the risk of the other, resulting with a reduced quality of life, which is risk factor for relapses in MDD and poor treatment outcomes

40
Q

What are the diagnostic symptoms of MDD? (need 5 / 9 for at least 2 weeks)

A

 A1 Depressed mood—indicated by subjective report or observation by others (in children and adolescents, can be irritable mood)
 A2 Loss of interest or pleasure in almost all activities
 A3 Significant (more than 5 percent in a month) unintentional weight loss/gain or decrease/increase in appetite
 A4 Sleep disturbance (insomnia or hypersomnia)
 A5 Psychomotor changes (agitation or retardation) severe enough to be observable by others
 A6 Tiredness, fatigue, or low energy, or decreased efficiency with which routine tasks are completed
 A7 A sense of worthlessness or excessive, inappropriate, or delusional guilt (not merely self-reproach or guilt about being sick)
 A8 Impaired ability to think, concentrate, or make decisions
 A9 Recurrent thoughts of death (not just fear of dying), suicidal ideation, or suicide attempts.

41
Q

Is MDD homogenous or heterogenous in presentation?

How many different types of clinical presentations of MDD are estimated?

A

There is substantial heterogeneity in symptom profiles, accounting for one symptom as low mood/anhedonia, dichotomous presentation of appetite/weight/sleep/psychomotor and suicidal ideals

  1. 227 potential presentations that would qualify as MDD, due to complex interaction between aetiological factors, stress, environment
42
Q

What are the two depressive subtypes of MDD?

A
  1. Melancholic, 67%, more males
  2. Atypical, 15-50%, more women
43
Q

What are the symptoms of melancholic depressive subtype?

A
  1. Non-reactive mood
  2. Consistent anhedonia
  3. Blunted emotions
  4. Appetite and weight loss
  5. Insomnia
  6. Loss of libido
44
Q

What are the symptoms of atypical depressive subtype?

A
  1. Low mood reactivity
  2. appetite and weight GAIN
  3. hypersomnia
  4. leaden paralysis
  5. sensitivity to rejection
45
Q

What’s unique about each depressive subtype?

A

Melancholic - diurnal variations from mood changes in day, higher suicide risk comorbidity with psychosis, overactive HPA axis and higher stress

Atypical - underactive HPA axis, lower cortisol

46
Q

Which type of depressive subtype will become more common in the future?

A

Atypical subtype prevalence increasing to likely surpass melancholic MDD, attributed to more increase in obesogenic environments & chronic health conditions (anxiety, metabolic syndrome, obesity)

47
Q

How does MDD assessment change through the lifespan?

Scales are tailored to reflect clinical presentation

A
  1. Changes as a function of age to reflect changes of MDD presentation
  2. common symptoms change depending on age:
    older adults = anhedonia/withdrawal, children = irritability
    adults = low mood
48
Q

Whats the difference between aetiology and pathogenesis?

A
  1. Aetiology = why a disorder develops
  2. Pathogenesis = processes that maintain a disorder
49
Q

What is Beck’s Cognitive Model, 1967?

A

MDD symptoms are byproduct of systematic negative schemas which stem from difficult experiences that cause a distorted perception of reality, negative mood, and repeated activation of these schemes causes attentional biases towards negative stimuli

50
Q

What is the learned helplessness theory of depression? Seligman 1970

A
  1. When we belief that we do not have any control over our environment, they behave as if they are helpless, which is not an innate trait but a learned behaviour
51
Q

What are the different types of learned helplessness + how does this affect mood?

A

Universal helplessness - nothing can be done about the situation, finding external reasons for problems

Personal helplessness - other people could fix their situation but not me, leading to internal attributions of being helpless

Both types cause low self esteem and mood, and maintain helplessness because they believe nothing can change

52
Q

What is the Rumination theory of MDD? (Nolen-Hoeksema, 1991)

A
  1. Rumination is the continuous mental replaying of negative feelings and events, including thinking over and over about the meaning and outcome of events

In MDD, it increases attention towards the negative, prevents interpersonal problem solving, reduces motivation to act

53
Q

What is the Monoamine Hypothesis of MDD? (Schildkraut, 1965)

A
  1. Theory that the depletion of monoamine neurotransmitters - serotonin, norepinephrine and dopamine, lead to MDD symptoms

Norepinephrine = energy,
dopamine = reward, anhedonia, serotonin - mood, appetite, anxiety, suicidal ideation

54
Q

Why does the monoamine hypothesis have low validity?

A
  1. Hard to prove because monoamine can not be measured directly in brain but only indirectly and invasively through CSF in postmortem studies

Ethics - Half-life of monoamines means the taking of CSF needs to be taken within minutes of a person dying

Low Validity - CSF show levels post neurotransmission and not pre neurotransmission

55
Q

What is the HPA Axis + hormones theory on MDD?

A
  1. HPA consists of feedback loops with brain, pituitary and adrenal glands that manage immune, stress and metabolism
  2. HPA axis manages stress by modulating cortisol and other endocrine factors, and activates in response to physical and psychosocial stresses, eg. low self esteem or injury - and levels are modulated by the perceived coping mechanisms of the individual
56
Q

How is HPA linked with MDD?

A

HPA activity significantly impacted by hormones linked with MDD, including elevated cortisol (in melancholic MDD) which cause stress, fatigue and weight loss, cytokines cause insomnia and anxiety, leptin causes overeating, dopamine causes overeating, stress

57
Q

How is the prefrontal cortex implicated in MDD?

A

Implicated with MDD

  1. regulating executive function
    Higher activity in ventromedial PFC = negative emotions, low mood and fear
    Lower activity in orbitofrontal PFC = decreased emotional regulation
    Lower activity in dorsolateral PFC = deficits in memory, attention & reasoning
58
Q

What happens with continuous stress hormones on the PFC?

A
  1. Continuous exposure to stress hormones, glutamate, cortisol, neuronal damage, inefficient transmission and sometimes cell death
  2. Can lead to decreased activation and volume in dorsolateral PFC
  3. Causes deficits in working memory, attention, goal directed behaviour and abstract reasoning
59
Q

What does the ACC do? (Attention and emotional regulation)

How is the Anterior Cingulate Cortex linked to MDD?

A

The ACC regulates attention and emotions, affect regulation, selective attention, social behaviours, stress response and demanding stimuli

Looks like there is reduced volume ACC in MDD -

results in hypoactivation and causes blunted affected, increased anhedonia and lower ability to cope

60
Q

What does the hippocampus do?

How is the hippocampus linked to MDD?

A

Hippocampus works on consolidating working, declarative, spatial, episodic and contextual memory

In MDD greater activation to negative stimuli and negatively valenced memories, may contribute to negative cognitive biases

Smaller hippocampal volume found in MDD from exposure to prolonged stressors - linked to memory impairment and cognitive decline

61
Q

How is the amygdala linked to MDD?

A
  1. The amygdala gives greater activation to negative than positive stimuli
  2. MDD amygdala has larger volumes and increased blood flow and glucose metabolism are enhanced in MDD
  3. Hyperactivation manifests as a bias towards negative emotional stimuli & low mood
  4. Remains elevated after recovery - indicates MDD can cause permanent brain changes
62
Q

What’s the heritability and concordance rate?

What’s the gender and duration rate of MDD in genetics?

A

Heritability - 35%-45%,
Concordance in twins - 37%
First degree relatives = 2x3 risk
recurrent MDD is more heritable than single episodes of MDD
more females than males

63
Q

What’s the genetic biomarkers on MDD?

A

Specific genes are unable to be found due to high heterogeneity of MDD

Proposed: Serotonin transporter 5 HTT, SLC6A4, serotonin receptor 2A/HTR2A, tryptophan hydroxylase TPH2 and BDNF gene

64
Q

What are some socio demographic risks for MDD?

A

1.Sex/female
2. Age/young
3. Marital status/single
4. Culture/West
5. Education/high
6. Socioeconomic status/high/low
7. Physical environment: population density and unemployment
8. Life events: stressful or negative, or early childhood trauma, eg. abuse, neglect

65
Q

What is the interpersonal theory of MDD? (Coyne, 1976)

A
  1. People with MDD often feel rejection and low self esteem,
  2. leading to reassurance seeking from others
  3. causes other people to be stressed or frustrated by this
  4. perpetuates the symptoms of the person with MDD, leading to social withdrawal
66
Q

What is the operant conditioning theory in MDD?

How is it linked with interpersonal theory?

A
  1. Proposes that a LOSS OF POSITIVE REINFORCEMENT in one’s environment causes social isolation and low mood.

These symptoms continue because of unintentional reinforcement of external influences, eg. people with MDD may then seek out new support systems that may feel burdened and perpetuate the symptoms of the person with MDD,

eg. low-self esteem and feeling like a burden, linked with interpersonal theory.

67
Q

What are the two main metrics of efficiency in psychological treatment?

A
  1. Number of people needed to treat - estimates number of patients needed to be treated to prevent one additional bad outcome / have an impact on one person
  2. Number needed to harm (NNH) - metric of impact describing how many people need to be treated or exposed to a risk factor for one person to have a particular adverse effect
68
Q

Example of NNT and NNH?

A

Eg. Treat - NNT of 2 means 2 people need treatment for one person to be impacted, ie. 50% success rate / failure probability

Eg. Harm- lower number of NNH = greater risk of harm, NNH = 1 would mean every patient is harmed

69
Q

What are the limitations of CBT?

A
  1. Limited consideration of how biological factors may contribute/be important to MDD
  2. somatic symptoms are NOT addressed directly
  3. Revised to include how biological factors are incorporated into CBT but is mostly hypothetical and not used
70
Q

What is the NNT for CBT?

A

NNT for CBT = 2.6,
eg. almost three people need to undergo CBT for one person to experience a change in depressive symptoms, ⅔ will not have any effect at all

71
Q

What is first form of MDD medical treatment and what is it based off?

A
  1. Antidepressants are first line of pharmacological treatment in MDD
  2. Based of the monoamine hypothesis - antidepressants are one of the most relied upon treatment
72
Q

What do the 4 types of antidepresants do?

A
  1. SSRIs/SNRIs = increase amount of serotonin or norepinephrine in the brain by blocking reuptake and keeping more in the synapse
  2. Tricyclic Antidepressant (TCAs) = blocks the triad of monoamines- serotonin, norepinephrine and dopamine and acts on cholinergic, muscarinic and histaminergic pathways
  3. Monoamine Oxidase Inhibitors (MAOI) = inhibiting enzymes that break down neurotransmitters, allowing the neurotransmitters to stay in the synapses for longer and get absorbed
73
Q

What are common antidepressant side effects?

A
  1. Gastrointestinal upsets, headaches, insomnia, fatigue, weight gain, sexual dysfunction, and cardiovascular problems (specific to TCAs)
  2. Long term antidepressant use can produce too much monoamines = serotonin syndrome - fever, seizures,

Rare: increased suicidal ideation

74
Q

What is the Efficacy of SSRIs v Placebo?

A

SSRIs are much more effective than placebos, more effective at alleviating specific MDD symptoms, such as insomnia, low mood and psychomotor and anxiety

SNRIs more effective than placebo, but no overall difference suicidal behaviours and ideation,

TCAs are more effective than placebo but more data needed

MAOI seems to also be more effective in MDD than placebo, but old data

75
Q

What is the efficacy rates between different antidepressants?

A
  1. SSRI vs SNRI efficacy shows similar results, SNRIs seem to be more effective at symptoms but have more severe side effects, leading to withdrawal and drop out rates
  2. MAOI vs TCA efficacy - TCA seems to be worse off symptoms compared to MAOI, since TCAs seem to have more adverse effects,

MAOI seems to be better for treatment-naive patients, but no difference with those with past treatment

76
Q

Main problem for antidepressants and monoamine hypothesis?

A
  1. Antidepressants are linked with low remission rates and high treatments due to delayed onset of action, especially for SSRIs - up to 6 weeks to start working
  2. Delayed onset + hard to prove monoamine hypothesis = questioning SSRIs
77
Q

What are the metrics of efficacy for antidepressants?

A

Treatment / NNT

SSRI = 6.5
SNRI = 6
TCA = 8.5,

6-8 undergo these treatments for one person to experience a change in depressive symptoms

Harm / NNH
SSRI = 20-90
TCAs 4-30 (less well tolerated)

Psychopathology (9 decks)

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