abnormal quiz 3 Flashcards

1
Q

Diagnosis anorexia

A
  • Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory and physical health)
  • Either an intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain (even through significantly low weight)
  • Disturbance in the way one’s body shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight
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2
Q

types of anorexia

A
  1. Restricting type: during the last 3 months, the individual has not engaged in recurrent episodes of binge eating or purging behaviour (i.e. self-induced vomiting or the misuse of laxatives, diuretics or enemas). This subtype describe presentations in which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise
  2. Binge-eating/purging types: during the last 3 months, the individual has engaged in recurrent episodes of binge eating or purging behaviour (i.e. self-induced vomiting or the misuse of laxatives, diuretics or enemas)
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3
Q

Alternative conceptualisations: embodiment (anorexia)

A
  • The bio-psycho-social paradigm defines and categorises anorexia as a ‘disturbance in the way in which one’s body weight or shape is experienced’
  • Conceptualising anorexia within the broader construct of embodiment enables the inclusion of a range of embodied experiences
  • An embodied framework departs from the cartesian mind-body dualistic impression of human functioning to emphasize the interactions between the mind, the body, and the self within their social structures
  • Embodiment theory enables researcher to anchor enquiry into the bod by shifting the vantage point from an externally driven orientation to the subjective experience of the ‘body-subject’ that is experientially aware and connected to feelings and sensations of the corporeal body
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4
Q

Alternative conceptualisations: feminism (anorexia)

A

•Feminist approaches have sought to situate ED’s in relation to the wider social expectations surrounding western femininity, ranging from gendered discourses on appetite, sexuality, economic power to social roles
- Not about magazines
– not cultural but structural
-Who owns women’s bodies in our society?
•Anorexia can be seen as a culture-bound syndrome, understood as a cultural metaphor for issues of control, compliance and body ownership in a patriarchal system

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5
Q

Medical risks (anorexia)

A
  • neurological
  • Metabolic
  • Cardiovascular
  • Haematological
  • Renal
  • Endocrine
  • Musculo-sketal
  • Gastroenterological
  • Immunological
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6
Q

Indications for hospitalisation anorexia nervosa

A
  1. Physiological instability
    a. Severe bradycardia (heart rate < 50 beats/minute daytime; <45 beats/minute night time)
    b. Hypotension (<80/50 mmHg)
    c. Hypothermia (<35.5 degrees Celsius)
    d. Orthostatic changes in pulse (>30 beats/minute) or blood pressure (>10 mmHg)
  2. Cardiac arrhythmia
  3. Electrolyte disturbances (hypokalaemia, hyponatraemia and hypophosphatasemia)
  4. Severe malnutrition (weight <75% IBW)
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7
Q

Prognosis (anorexia)

A
  • The risk of successful suicide is 32 times that expected, compared with major depression in which death form suicide is 21 times greater than expected
  • The average duration of illness is 7 years
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8
Q

family therapy (anorexia)

A

• One exception is a family therapy for adolescents which focuses on enabling parents to refeed their child… appears promising… unclear whether this approach is superior to other types of family therapy or to individual therapy, hence it cannot be recommended as an evidence-based treatment at this point

  - Child living at home and developed anorexia
  - Therapist gets the parents to take control a home 
  - Stop the child exercising
  - Watch the child eat the whole meal
  - Make sure the parents aren’t arguing
  - Don’t blame the child 
  - Prevent hospitalisation as it can become a cycle
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9
Q

DSM- 5 criteria: bulimia nervosa

A

• Recurrent episodes of binge eating. An episode of binge eating is characterized by both o the following:
1. Eating, in a discrete period of time (e.g. within any 2-hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances
2. A sense of lack of control over eating during the episode (e.g. a feeling that one cannot stop eating or control what or how much one is eating)
• Recurrent inappropriate compensatory behaviours in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics or other medications; fasting; or excessive exercise
• The binge eating and inappropriate compensatory behaviours both occur, on average, at least once a week for 3 months
• Self-evaluation is unduly influenced by body shape and weight
• The disturbance does not occur exclusively during episodes of anorexia nervosa
• Specify if:
-In partial remission: after full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time
- In full remission: after full criteria for bulimia nervosa were previously met, none of the criteria have been met for a sustained period of time

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10
Q

Epidemiology of bulimia nervosa

A
  • came to attention of professionals in the 1970’s
  • occurs predominately in women
  • co-varies with dieting
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11
Q

comorbid conditions (bullimia)

A
  • substance abuse
  • depression
  • suicidality
  • personality disorders
  • anxiety disorders
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12
Q

CBT (bullimia)

A

•CBT: cognitive behavioural therapy

  - Usually lasts 20 weeks
  - Semi-structured 
  - Problem- orientated
  - Concerned with present and future (rather than past)
  - 3 stages of treatment 

• The aims of stage 1 - CBT

  - To establish a sound therapeutic relationship
  - To educate the patient about cognitive view on the maintenance of BN and to explain the need for both behaviour and cognitive change 
  - To establish regular weekly weighing
  - To educate about body weight regulation, adverse effects of dieting, physical consequences of binge eating, self-induced vomiting and laxative abuse
  - To reduce the frequency of overeating by introducing a pattern of regular eating and the use of alternative behaviour 
  - To reduce secrecy and enlist the cooperation of friends and relatives 

• The aims of stage 2 (sessions 9-16)

  - Tackling dieting
  - Enhancing problem-solving skills
  - Addressing concerns about shape and weight
  - Addressing other cognitive distortions 

•The aims of stage 3 (sessions 17-19)

  - 3 interviews at 2 week intervals
   - Aim is to ensure that progress is maintained
  - Relapse prevention
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13
Q

Therapist skills (bullimia)

A
  • Technical competence
  • Establishing an effective therapeutic relationship
  • Nurturing a commitment to change
  • Maintaining a specific therapeutic focus
  • Expertise and experience
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14
Q

Therapeutic relationship (bullimia)

A
  • Be credible
  • Be caring and non-judgemental
  • Develop a collaborative relationship
  • Balances empathy with firmness
  • Be positive
  • Gender issues
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15
Q

Medical complications (bullimia)

A

The clinician should never under-estimate the risk of medical complications of BN, despite apparent normal weight. Potential medical problems such as electrolyte imbalance from repeated purging, to actual damage to heart muscle and other organs should be investigated by a full medical evaluation/examination and appropriate laboratory investigations

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16
Q

The elimination of dieting (bullimia)

A
  • Stress the importance of ceasing to diet and provide education abut weight gain
  • Assess food avoidance and systematically introduce avoided foods into planned meals or snacks (therapist-assisted exposure)
  • Relax other controls over eating
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17
Q

Importance of prescribed regular eating pattern (bullimia)

A
  • It begins to break down dieting
  • It restores a sense of control
  • I disrupts learned association between urges/triggers (emotional and situational) to eat or binge
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18
Q

Sexual Abuse and Eating Disorders

A

*Sexual abuse violates the boundaries of the self so dramatically that inner sensations of hunger, fatigue, or sexuality become difficult to identify. People who have been sexually abused may turn to food to relieve a wide range of different states of tension that have nothing to do with hunger. It is their confusion and uncertainty about their inner perceptions that leads them to focus on the food.
• Many survivors of sexual abuse often work to become very fat or very thin in an attempt to render themselves unattractive. In this way, they try to de-sexualize themselves
• Sexual abuse and emotional eating both have one element in common. It is secrecy. Many eating disorder patients feel guilty about the sexual abuse in their childhoods, believing they could have prevented it but chose not to because of some defect in themselves.
• To date, no treatments have been developed specifically for clients with comorbid PTSD and eating disorders.

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19
Q

DSM-5 binge eating disorder

A

• Recurrent episodes of binge eating. An episode of binge eating is characterised by both of the following:
1. Eating, in a discrete period of time (e.g. within any 2-hour period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances
•NB. Objectively large amounts of food e.g. 1 loaf of bread, 1L of ice cream, a few bowls of cereal, a family sized chocolate block
2. A sense of a lack of control over eating during the episodes ( e.g. a feeling that one cannot stop eating or control what or how much one is eating)
- Some individuals report a ‘dissociative quality’ during or following binge-eating
• NB. Some people feel that they are ‘bingeing’ when they do not have objectively large amounts of food (e.g.. break a diet by eating a few chips or a piece of cake. If loss of control is present, this constitutes a subjective binge episode
b. the binge-eating episodes are associated with three or more of the following:
1. eating much more rapidly than normal
2. Eating until feeling uncomfortably full
3. Eating large amounts of food when not feeling physically hungry
4. Eating alone because of feeling embarrassed by how much one is eating
5.Feeling disgusted with oneself, depressed or very guilty afterward
c. Marked distress regarding binge eating is present
- Individuals with binge eating disorder are typically ashamed of their eating problems and attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as possible
d. The binge eating occurs, on average, at least once a week for 3 months

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20
Q

Bing eating disorders vs bulimia nervosa

A

e. The binge eating is not associated with the recurrent use of inappropriate compensatory behaviour as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa

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21
Q

Specifiers for binge eating

A

• Specifiers – current severity: the minimum level of severity is based on the frequency of episodes of binge eating. The level of severity maybe be increased to reflect other symptoms and the degree of functional disability

 - Mild: 13 binge-eating episodes/week
 - Moderate: 4-7 binge-eating episodes/week
 - Severe: 8-13 binge eating episodes/week
 - Extreme: 14 or more binge-eating episodes/week
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22
Q

Binge eating disorders associated with:

A
  • Early onset obesity
  • severity of obesity
  • increased rates of psychopathology
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23
Q

relationship between binge eating and obesity

A
  • 41% of overweight/obese in the comity meet the criteria for one of the binge eating illnesses
  • 52% of overweight and obese in weight loss programs meets the criteria for one of the binge eating illnesses
  • 88% individuals with binge eating disorder had obesity at some point in their lives
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24
Q

How abnormal is binge eating?

A
  • Time trends in population prevalence and burden
  • Health-related quality of life (HRQoL) impairment attenuated over time, such that those reporting recurrent binge eating scored similarly to the population norms on the measures of HRQoL
  • Weekly binge eating no longer associated with increased days out of role compared to 2005
  • And in 2015, -50% of respondents who report weekly or twice weekly binge eating report that they do not experience distress related to the act of binge eating, but distress experience is related to QoL impairment and higher number of days out of role
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25
Q

Risk factors (binge eating)

A
  • Binge eating disorder appears to run in families, which may reflect genetic influences: 17%- 39% of the variance
  • Dieting is greatest risk factor of developing binge eating disorder
  • Other risk factors: trauma (especially early-life), low self-esteem, body dissatisfaction, negative emotionality, overvaluation of the importance of weight and shape, difficulty regulating emotional states, parental substance abuse
  • Triggers for binge eating include: negative affect, interpersonal stressors, dietary restraint, boredom
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26
Q

Comorbid conditions (binge eating disorder)

A
  • Binge eating disorder similar to other eating disorders in terms of comorbidity
  • Depression and anxiety disorders most common (-54% have comorbid depression; -37% have a comorbid anxiety disorder)
  • Substance use and personality disorders are also common (-25%)
  • Few gender differences observed; men had higher lifetime rates of substance use disorders and current rates of obsessive compulsive disorder
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27
Q

Assessment tools (binge eating disorder)

A
  • SCOFF, a 5-item screening tool. Administration and scoring is very simple, but it is not binge eating disorder or binge eating-specific. It also covers other eating disorder behaviours
  • Binge eating scale (BES) is a 16-item self-report scale and scoring is slightly more complicated than the SCOFF, but it is specific to binge eating
  • BEDS-7, a 7 item diagnostic screener which follows the DSM-5 criteria for binge eating disorder
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28
Q

Treatment for binge eating

A
  • Cognitive behavioural therapy (CBT) most common (-70% studies)
  • Dialectical behavioural therapy (DBT)
  • Interpersonal psychotherapy (IPT)
  • Brief strategic therapy (BST)
  • Behavioural weight loss (BWL)
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29
Q

Hapifed definition

A

a heathy approach to weight management and food in eating disorders

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30
Q

Hapifed

A

• The problem
- Psychological therapies for binge eating disorder while impacting binge frequency do not lead to weight reduction
• The solution
- Integrate the best of behavioural weight loss with cognitive behaviour therapy
- Sustain weight loss by reducing disordered eating, enhancing psychological wellbeing and improving appetite regulation.

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31
Q

Along comes Vyvanse….

A

• Vyvanse (Lisdexamfetamine dimesylate)
• Lisdexamfetamine dimesylate (LDX) is approved for the treatment of adults with moderate to severe binge eating disorder (BED)1 in the United States, Canada and Australia
• The BED research for LDX includes:
- 3 placebo (PBO)–controlled, double-blind studies (1 forced-dose; 2 flexible-dose)2,3
- 1 PBO-controlled, double-blind, randomized-withdrawal maintenance-of-efficacy study4
- 1 open-label safety extension study
• LDX produced statistically significant and clinically meaningful reductions in binge eating days/week compared with PBO
• Time relapse significantly favoured LDX over PBO (P<0.001)
• The percentage of participants with observed relapse was:
- 32.1% (42/131) with PBO
- 3.7% (5/136) with LDX)

32
Q

Addiction:

A
  • a primary, chronic disease of brain reward, motivation, memory and related circuitry, with potential for both relapse and recovery
    - Many circuits are associated with normal behaviours (eating, drinking, sex, survival)
    • Looking at behaviour that is added to survival
33
Q

Physical and psychological dependence (substance dependance)

A
  • adaptation resulting in tolerance and withdrawal, and/or cravings/urges
    • Neuro-adaption – critical to transition to addiction but tolerance and withdrawal no longer deciding factor in whether an individual ‘has an addiction’
    • Fills a need the individual has
34
Q

Common component (substance abuse)

A
  • Salience (can no longer feel pleasure any other way)
  • Mood modification (use to change mood)
  • Tolerance (increasing doses in order to gain the same high)
  • Withdrawal
  • Conflict
  • Relapse
35
Q

Brain disease vs psychosocial factors

A

• Addiction as a brain disease
- Concerns that it minimizes important and environmental social st5ressors like loneliness, poverty, violence and other psychological and environmental
- Deflects responsibility over actions: ‘my brain made me do it!’
o Self-control and free will central to philosophical concepts
- Irresistible urge vs compulsive drive (craving as intuitive drive vs foreign urge)
- Desire centred vs control centred accounts of impaired control
• But dominant theoretical framework in addiction science is that biopsychosocial framework

36
Q

Concept of addiction (2)

A

• Multifactorial interaction between biopsychosocial factor
• Syndrome (combination of signs and symptoms) rather than unitary disorder
- Not all signs and symptoms present in all cases; some have unique features

37
Q

Addiction: reflects a motivational shift

A
  • anxiety, depression, low self esteem
  • Reward sensitivity – genetic/neurobiological
  • Environmental: poverty, lifestyle, trauma exposure
38
Q

Distal antecedents (substance abuse)

A
  • Neurobiological (reward sensitivity, genetic)

* Psychosocial intrapsychic and environmental

39
Q

Addiction models of behaviour

A

• Transition distinction between:
-Medical/disease model: impaired control over urges/cravings
o +reduced stigma, blame
o -reduced personal responsibility, trust in behaviour (prone to relapse)
- Rational choice model: characterised by voluntary behaviour under control
o + increased personal responsibility
o + increased sense of control
o Majority cease without treatment

40
Q

Disease model

A
• Drugs affect brain’s reward system:
       1. The dopaminergic system
       2. The endogeno9us opioid system 
• Concentrations of dopamine increase (directly/indirectly) following most drugs, including:
      -	Alcohol
      -	Nicotine
      -	Cannabis
      -	Opioids
      -	Cocaine
      -	Amthamines
41
Q

Opponent process theory of addiction

A
  • work towards homeostasis
  • when you take a drug there is an increase in arousal and the body is trying to bring that back to homeostasis
  • process of habituation
  • with repeated uses there is a reduced effect (tolerance)
42
Q

tolerance in substance dependence

A
  • over time homeostatic state begins to reduce
  • homeostatic state: opponent-process (b-process) balances the drug activation (a-process). It can return to the homeostatic state
  • after repeated drug use, the affective system transitions to a lower allostatic level
43
Q

I-RISA – impaired response inhibition and salience attribution

A

• drug addiction medicated by functional and structural changes in circuits modulated by dopamine
• mesolimbic: amygdala, nucleus accumbent, hippocampus
-acute reinforcing affects, memory and conditioning linked to craving, and emotional and motivation changes during withdrawal
• mesocardiac: prefrontal cortex, orbito-frontal cortex and anterior cingulate
-conscious experience of intoxication, salience, expectations, cravings, and inhibitory control/decision-making

44
Q

four clusters of behaviours involved (RISA) (substance abuse)

A
  1. intoxication/excitement
    - higher extra-cellular dopamine concentrations in limbic circuits (nucleus accumbens) and frontal lobe
  2. craving
    - classical and operant association of cues with pleasure
    - memory consolidated in amygdala and hippocampus (and thalami-orbitofrontal circuit in experience of craving)
  3. compulsive use
    - continued use when no longer perceived as pleasurable
  4. withdrawal
    - dysphoria, anhedonia and irritability contributing to relapse
    - involvement of frontal cortical circuits
45
Q

Example (substance abuse)

A

• eating a piece of cake: take a bite > VTA releases dopamine to all regions
- amygdala: “this is delicious… this makes me very happy right now”
- hippocampus: remembers experience and context
- prefrontal cortex: focus attention on cake
- nucleus accumbens: “pleasure centre” stimulated, causing you to take another bite
- reward system: reactivated with each bite
• addictive behaviours emerge if repeated too often

46
Q

Addiction as choice

A

• medical model focus on impaired control: i.e. loss of normal capacities for rationale self-control
• desire-centred models explain compulsion as an inability to resist acting on desire because the desire coerces her to choose the compulsive behavio0ur
- rationale informed stable choice
- theory of rational addiction
- self-medication model
- choice theory
- challenges notion of ‘compulsive behaviour’ as equivalent to ‘compelled behaviour’
• rationality/utility: subjective short term benefits outweigh long term costs
• but unstable preferences: repeated failure to cease consumption: self-control vs self-regulation

47
Q

Clinical approaches and challenges (substance abuse)

A

• Common barriers to successful treatment
- Psychiatric comorbidity
- Acute or chronic cognitive deficits
- Medical problems
- Social stressors
- Stigma
• Identify high risk situations and events
- including people, places, internal cues such as changes in affect)
• Reduce likelihood that these events are encountered (providing alternative activities)
• Rehearsing non-drug alternatives to cues

48
Q

Principles of effective treatment (substance abuse)

A
  1. No single treatment is sufficient
  2. Treatment readily available and accessible,
  3. Address multiple psychological, medical and social interventions and needs (CBT, naloxone, Antabuse, methadone, peer support)
  4. Comorbid conditions treated in integrated manner
  5. Mandated treatment can lead to effect change
  6. Recovery a long term process and frequently requires multiple episodes of treatment for lapses/relapse
49
Q

Briefly describe the 3 main pathways/subgroups of gambler proposed in the model:

A

(a) The behaviourally conditioned problem gambler
- availability of gambling allows people to ask it for purely socialisation initially > reinforcement schedule > habituation > chasing (dopaminergic system – winning)
- absence of premorbid psychopathology – no psychological disorders to cause the gambling

(b) The emotionally vulnerable problem gambler
- emotionally vulnerable as a result of psycho-social and biological factors – utilising gambling as a means of emotional escape
- premorbid anxiety and/or depression
- participation is motivated by desire to modulate affective states and/or meet specific psychological needs
- negative childhood experiences
- recommended to take medication to treat neurochemistry
- negative reinforcement

(c) The antisocial, impulsivity problem gambler
- ADHD, impulsivity; anti-social behaviour
- Substance abuse
- Characterised by neurochemical dysfunction
- Attention deficit
- Substance abuse, suicidality, irritability, low tolerance for boredom and criminal behaviours
- Poor compliance ra4es and poor response to intervention
- Pathological gamblers show more impulsive and manifest higher levels of affective disturbance than substance abusers
- Impulsivity believed to be independent of gambling and functions as a good predictor of severity of involvement for at least one group of gamblers
- Biological vulnerability
- Recommended to take medication to treat chemistry
- Thrill-seeking

50
Q

How could this model inform treatment of pathological gambling?

A
  • First pathway
    • Wouldn’t require medication: because they don’t have any living conditions (recondition them, aren’t other problems to solve)
  • Second pathway
    • Have multiple other issues (pre-morbidity, are emotionally vulnerable) therefore use psychotherapy, drugs and CBT. Provide alternative coping strategies
  • Third pathway
    • Treat with medication due to the chemical imbalance.
    • ADHD medication – dopamine function (psychostimulant) (amphetamine)

-The third group is the hardest to treat as it is deeply imbedded into their lifestyle and biology, the gambling is part of a pattern of risk taking (impulsive in various other ways)

51
Q

What is a transdiagnostic construct?

A

• Disorders share many core features
• Transdiagnostic processes or constructs:
a. Feature across several disorders
b. Represent a causal mechanism across several disorder

52
Q

Death anxiety

A
• Central part of the human condition
• ‘the worm at the core’ of our existence 
• We are the only species to understand our own mortality
• Throughout recorded history 
    -	Religion, ritual, myth
    -	literature, art and theatre
    -	Philosophy 
    -	Psychology
53
Q

Death anxiety: absence of theory

A

• Becker (1973)
- Motivation to live + inevitability of death = crippling fear
- Cultural theory
•Death anxiety: absence of clinical theory

54
Q

Terror management theory

A

• TMT: two buffers against death anxiety

1. Cultural worldviews
- Gain virtual immortality by buying into beliefs    2. Self-esteem 
- Gain meaning by fulfilling expectations of cultural worldview
55
Q

Panic disorder

A

• Fears of death argued to play a central role
• “I am having a heart attack”, “I am going to die”
• Panic disorder patients reported significantly higher death fears than social phobia patients and controls
- Those with comorbid disorders also reported high levels of death anxiety than individuals who only met criteria for 1 disorder

56
Q

Somatic symptoms disorder, illness, anxiety and hypochondriasis

A

• Death anxiety argued to be a central feature
• Worrying about physical health – particular physical symptoms being experienced, think this means you are unwell
* May repeatedly consult GP’s and specialists, check body (e.g. blood pressure, bruises, pulse, stools) for symptoms, or seek reassurance from others
• “is this a headache or a brain tumour?”
• Hypochondriasis patient’s vs matched medical and non-hypochondriacal psychiatric patients
• Those with hypochondriasis:
- Attended more closely to bodily sensations
- Were more likely of distrust doctor’s judgements
- Reported more fears of death and disease

57
Q

Agoraphobia and separation anxiety

A

• Many symptoms are associated with death fears
- Fears of harm when leaving home
- Increased focus on internal sensations (e.g. change in heart rate, dizziness)
- Hypochondriacal concerns
- Frequent catastrophic death-related fears
• “I can’t go out – I could be attacked”
• Onset of agoraphobia is often preceded by traumatic events (e.g. loss of a loved one or physical threat)
• Fear of death and separation anxiety are positively correlated among individuals with agoraphobia
- Suggests that fear of separation from loved ones may increase as death anxiety increases
• Increased death anxiety and separation anxiety among individuals with BPD and schizophrenia, compared to controls
- Suggest separation anxiety may mask death anxiety

58
Q

specific phobias

A

• Freud argued that fears of death underlie phobias
• Heights, snakes, spiders, water, flying – most common fears, they have potential to be fatal
• Phobias may occur when death anxiety focuses on smaller, more manageable threats
• Strachan tested whether mortality saliences could increase phobic behaviours
- 32 students who met criteria for specific phobia of spiders, 30 non-phobic
- Primed with death or control
- For those with spider phobia, reminders of death (MS):
o Increased avoidance of spider-related stimuli
o Increased perceived threat (i.e. “how likely is it that the spider in the first picture is dangerous to humans?”)

59
Q

PTSD

A

• DSM-5: the person was exposed to: death, threatened death, actual or threatened serious injury or actual threatened sexual violence
• Death anxiety argued to play a role in development and maintenance
- I can’t leave the house at night – I could be attacked again’
• Across 2 studies, of veterans and individuals with HIV, death anxiety was significantly correlated with:
- Overall PTSD symptom severity
- Re-experiencing, avoidance and hyper-arousal
• Exposure to life-threatening events argued to increase death anxiety, which may lead to PTSD symptoms and further increased death fears
• From TMT perspective, PTSD may involve disrupted anxiety buffers
- Severity of PTSD symptoms depends on both severity of trauma and prior strength of buffers
- Individuals with PTSD don’t show increased worldview defence after MS, unlike control participants
• Chatard used MS with individuals following a civil war:
- High PTSD symptoms > immediate increase in death-related thoughts
- Low PTSD symptoms > suppression of death thoughts
• Suggest severe PTSD is characterised by impaired suppression of death thoughts
- Anxiety-buffering defences are disrupted in PTSD

60
Q

depressive disorders

A

• MS study with mildly depressed individuals
- Following priming, being given opportunity for worldview defence was associated with increased belief that life is meaningful
• Bolstering worldview beliefs may increase meaning among depressed individuals
- Consistent with idea depression is associated with weaker buffers against death anxiety

61
Q

Eating disorders - death anxiety

A

• Women diagnosed with anorexia show significantly higher death anxiety than controls
• Study on non-clinical participants (164)
- Death anxiety positively correlated with disordered eating, perfectionism, and self-reports of current mental disorder
- Perfectionism was only significant predictor when death anxiety and self-esteem were excluded from the model
• Goldenberg found reminders of death led women (but not men) to:
- Perceive themselves as further from their ideal thinness
- Eat 40% less in a ‘taste-testing’ task than controls
• Death anxiety may be driving women to strive for thinness promoted by their cultural worldviews

62
Q

social anxiety disorder

A

• Social exclusion meant literal death
• Strachan used MS with student’s high vs low in social anxiety
1. Primed with MS or control
2. Allowed to decide when to join a group discussion (social avoidance)
• Reflecting on own death led socially anxious participants to wait longer before joining a group discussion
- Death priming produced significantly more social avoidance among socially anxious participants

63
Q

Obsessive- compulsive disorder

A

•verbal reports among most common subtypes suggest role of death fear
- contamination: “I could get HIV if I ouch that doorknob”
- checking: “ what if I left the stove on? We will burn”
- aggressive obsessions: “ I’m going to stab my child”
- tapping, counting: “ if I don’t, something bad will happen”
•no study investigating role of death anxiety among patients with OCD
• Thoughts of death can worsen OCD symptoms (e.g. hand washing)
• Double time spent washing

64
Q

Implications death anxiety

A
  • Results of recent research suggest we may need to rethink treatment of these conditions
  • What do treatments for anxiety look like?
  • All of these treatments produce great pre- post- measures
  • But we often assume success from a single measure of a single disorder
  • Is the problem that treatment studies are measuring the thing we’re targeting in the treatment, not necessarily the core problem?
  • Increased functionality, but are these contributing to the ‘revolving door’ of mental health?
  • We may need innovative treatments to address the underlying dread of death…
65
Q

Concept of non-substance behavioural addiction

A
  • Repetitive persistent behaviours resulting in significant harm or distress that causes functional impairment
  • Rapid escalation of behaviours becoming labelled ‘behavioural addictions’
  • New disorders medicalise/pathologize multiple reward seeking behaviours by attaching medical names, diagnostic instruments, and suggested treatments
66
Q

Changes in DSM 5

A

-Introduced new category:
o Substance-related and addicted behaviours
o Non-substance related disorder
- Reclassified pathological gambling as gambling disorder
- Internet gaming disorder included in section III (conditions for further study)
o Behavioural similarities to substance use disorders
o Has significant public health implications
o Internet gaming recognised by Chinese government as a disorder with polices and treatment services provided
- Disorder introduced as a mix of social and political: medicare wouldn’t help unless it was a disorder (in US) and scientists wanted
more funding
- Found video game addiction (area for further study) – now classified as a behaviour addiction in many countries. This is due to strong rise of internet gaming. Found in Asia, with Korean government pushing for use of technology

67
Q

DSM-5: non-substance related disorders

A

• Gambling

  • Criterion A: four or more
    1. Preoccupation (psychological dependence)
    2. Increased amount gambled (tolerance)
    3. Irritability/restlessness on cessation (withdrawal)
    4. Escape from stress (negative reinforcement and motivation)
    5. Chasing losses (erroneous and distorted cognitions)
    6. Lying
    7. Repeated failure to cease (impaired control)
    8. Illegal acts
    9. Risked significant relationships
    10. Bailout
68
Q

Range of behavioural addictions

A
•Consistently identified:
    -Gambling disorder (DSM-5)
    -	Sex addition
    -	Compulsive shopping
    -	Internet addiction
    -	Internet gaming disorder 
    -	Kleptomania 
• Less often identified:
    -	Exercise addiction
    -	Eating (food) addiction
    -	Love addiction 
    -	Work addiction 
    -	Social networking addiction
    -	Mobile/smart phone addiction
    -	Tanning 
• Occasionally identified
    -	Binge eating
    -	Pyromania
    -	Trichotillomania 
    -	Orthorexia (preoccupation with eating health food)
    -	Musicorexia (addiction to music activity)
    -	Self-mutilation
    -	Dancing fortune telling
    -	Stock markets
69
Q

Confirmatory three step approach - gambling

A
  1. Anecdotal observations consider behaviour a priori as addictive
  2. Screening instrument developed (often derived from criteria defining another disorder – substance use/gambling disorder)
  3. Identify risk factors known to play a role in the development and maintenance of substance use/gambling disorders (impulsivity, attentional biases)
  4. Ignores
    • Functional impairment
    • Stability of dysfunctional behaviour a(evidence that behaviours are transient and context specific)
70
Q

Gambling and terminology

A

• Why do people gamble?
- Excitement generated by the un-certainty but hope of winning
- Hope of winning large amounts to enhance lifestyle choices
- Fun in a social context and environment
• Why do people persist in gambling despite adverse consequences?
- Hope to recoup (chasing)
- Emotional escape
- Satisfy emotional needs (narcissism, ego)
- Manage dysfunctional affective state (depression, anxiety)

71
Q

Cognitive behavioural model

A
  • Irrational beliefs held about gambling
  • Illusions of control – think they have skills and capacity to win
  • Linked to superstitions
  • Gambler fallacy – if you have a streak of losing bets a win is due – therefore they continue to gamble
  • Biased evaluation – if you win it is due to skill, if lose it is due to an external explanation
  • 75% of gamblers have a big win at the beginning, therefore continue
72
Q

What are the model’s underlying assumptions? -pathway gambling

A

• Problem gamblers are a heterogenous population
• Symptoms and signs at presentation may be similar
BUT
• Critical pathway leading to problem gambling differs
• Differing factors and variables play crucial roles within each pathway
• Different etiological factors and by the time they merge they all appear to be the same

73
Q

pathway gambling

A
  • Psychopathology
  • Pathway one: symptoms are casual outcomes of gambling related problems: amenable to psycho-education, brief interventions and brief CBT
  • Pathway two: affective disturbances, poor coping skills and suatnce se contribute to gambling (dissociation and escape)
  • Pathway three: deficits in reward pathways (dopaminergic) and impulsive: psychopharmacology and intensive interventions
74
Q

Clinical characteristics: pathway 1

A

• Demographics
- Motivation to generate excitement, winning
- Briefer history of excessive gambling
- Childhood and family stability
• Psychopathology
- Absence of psychopathology
- Depression/anxiety: secondary to problem gambling
- Substance abuse minimal: onset after gambling problems

75
Q

Clinical characteristics: pathway 2

A
  • Comorbid conditions: anxiety, depression, lack of social support, gambling used as means of emotional escape
  • Gambling with money not FOR money
  • Motivation: gambling with money, not for money: prolong sessions to allow continued emotional escape
  • Poor stress-coping and problem solving strategies
  • Negatively reinforced
76
Q

Pathway 3

A
  • Attentional deficit disorders – impulsive control
    • Linked with substance abuse and criminality
    • Age: early onset problem gambling
    • Early history of family instability, abuse/neglect
      o Gambling reflects one of many maladaptive behaviours
    • High levels of impulsivity, anti-social behaviour
      o Poorer performance at school (inattentive, disruptive)
      o Involvement in activities with high degree of stimulation
    • Substance abuse- drugs and alcohol and broad spectrum of criminal behaviours
    • Difficult to separate popular games that one enjoys to one that is gambling
    • Key issue is that if you are going to gamble you are not going to win