Brainscape's Knowledge GenomeTM

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


See full index

PS2028 - Mental Health & Clinical Psychology > EDs & obesity > Flashcards

EDs & obesity Flashcards

1
Q

how many people were obese in England and Wales in 2021?

A

26%

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

what is the role of the media?

A
  • media bombard us with a standard of beauty
  • media promotes the ‘thin ideal’
  • media forms associations between beautiful (thin) people with happy lives and high moral standards
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the clinical features of an ED?

A
  • persistent disturbance of eating, or eating-related behaviour
  • impaired physical health and psychological wellbeing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some feeding and eating disorders identified by the DSM-5?

A
  • pica
  • anorexia nervosa
  • bulimia nervosa
  • rumination disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the etymology of the word “anorexia”?

A
  • an = without
  • orexis = appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the characteristics and of AN?

A
  • restriction of energy intake relative to requirements, leading to significantly low body weight
  • intense fear of gaining weight
  • disturbance in the way one’s body weight or shape is experienced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the subtypes of AN?

A
  • restricting
  • binge-eating/purging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the psychological symptoms of AN?

A
  • intense fear of weight gain
  • irritability & anxiety
  • low self-esteem
  • pre-occupation with food, calories, weight, size
  • impaired memory, attention, concentration
  • not recognising the seriousness of the condition
  • distorted or unhelpful thinking styles
  • distorted body image
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the behavioural symptoms of anorexia?

A
  • avoidance or restriction of eating
  • excessive exercising
  • lengthy/frequent toilet visits
  • overt or secret
  • drinking excessive fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the characteristics of BN?

A
  • recurrent episodes of binge eating; Feel a lack of control overeating
  • recurrent, inappropriate compensatory behaviours to prevent weight gain
  • binge eating and compensatory behaviours occur, on average, 1/week for 3 weeks
  • self-evaluation unduly influenced by body shape and weight
  • not experiencing anorexia nervosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the subtypes of BN?

A
  • purging
  • non-purging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the characteristics of BED?

A
  • recurrent episodes of binge eating
  • 3+ of the following:
  • eating more rapidly than normal
  • large amounts of food when not hungry
  • eating alone due to embarrassment
  • distress
  • at least once a week for three months (on average)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are some comorbidities of EDs?

A
  • depression
  • OCD
  • substance use disorders
  • personality disorders
  • autism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the diagnostic crossovers between EDs?

A
  • crossover between both types of AN
  • crossover between AN (binge/purge subtype) and BN
  • crossover between BN and BED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T,B,PE

transdiagnostic CBT-model for EDs: what are the key features of AN?

A
  • thoughts
  • behaviours: restriction of food/energy intake
  • physiological effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T,B,E

transdiagnostic CBT-model for EDs: what are the key features of BN?

A
  • thoughts
  • behaviours: binge-eating and compensatory weight control behaviours
  • emotions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the prevalence of EDs: AN, BN and BED?

A
  • AN = 0.9% women and 0.3% men
  • BN = 1%
  • BED = 2%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

is the prevalence of EDs changing over time?

A
  • (mistakenly) thought to be a modern condition
  • AN stable for past decades, incidence among those <15 years old has increased
  • BN increase 1970s to 1990s; declining
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why is the prevalence of EDs hard to estimate?

A
  • not everyone gets/is able to get a diagnosis
  • some people may not want to be diagnosed
  • some people may not know they should be diagnosed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the average ages of onset for AN, BN and BED?

A
  • AN = age 16-20
  • BN = age 21-24
  • BED = age 30-50
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what role does gender play in EDs?

A
  • gender ratio previously thought to be 10:1, but recent estimates suggest 3:1
  • men experience more sociocultural pressure to have toned/muscular bodies
  • gay and bisexual men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

why are EDs underdiagnosed in men?

A
  • seen as a ‘women’s disorder’
  • bias in diagnostic criteria: emphasis on desire to be thin (vs. lean, muscular), methods of weight control (dieting)
  • leads to risk of misdiagnosis, less likely to receive appropriate, specialist treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why are EDs multi-determined?

A

lots of factors affect them:
- biological factors
- individual risk factors
- family influences
- sociocultural factors

24
Q

H,NF

what are the biological factors in EDs?

A
  • tendency to develop an ED runs in families
  • findings related to specific genetic factors are mixed, but a susceptibility to EDs may be inherited along with a diathesis for other psychological conditions
  • hormones: set-point theory; the idea that our bodies resist marked variation may play a role - onset near puberty
  • neurological factors may play a role
25
Q

is there a genetic contribution in EDs?

A
  • start by looking at family rates since one would predict higher rates in relatives
  • example: Strober (2000) found EDs at least 3x more common among relatives of individuals with AN or BN than among relatives of individuals without AN or BN
  • indicative of some element of familial transmissibility
26
Q

what are the conclusions of AN in relatives of individuals with and without AN?

A

AN is over 10 times more common in relatives of AN sufferers

27
Q

what does research suggest about genes and their role in EDs?

A
  • a strong (but not 100%) genetic contribution
  • if there is a genetic mechanism underlying the familial patterns, then it is not an all-or-nothing mechanism – more consistent with increased susceptibility
28
Q

DoBWSS,DoBC,DoPT

how is the genetic influence on EDs mediated?

A

3 obvious ways (or underlying mechanisms):
- via the determination of body weight/shape/size
- via the determination of brain chemistry
- via the determination of personality traits (incl. neurocognitive and socio-emotional profile
- not necessarily mutually exclusive

29
Q

H,FC

which brain structures are involved in EDs?

A
  • hyopthalamus (satiety and appetite)
  • frontal cortex (TC involved in body image perception and OFC involved in monitoring stimuli pleasantness)
30
Q

which hormones are involved in EDs?

A

serotonin
- most popular neurotransmitter in AN research due to involvement in mood, obsessions, appetite regulation and impulse control
- patients with AN have low levels of serotonin metabolites (5-HIAA)
- following recovery, patients with previous AN or BN have higher levels of 5-HIAA than controls
- dopamine (role in reward systems)

31
Q

hormones and EDs: what is the set point theory?

A

hormones involved in appetite and weight regulation

32
Q

what is the satiety hormone and what does it do?

A
  • leptin
  • reduces food intake
33
Q

what is the hunger hormone and what does it do?

A
  • grehlin
  • increases food intake
34
Q

which hormone is disturbed in AN patients and how?

A

leptin secretion is profoundly disturbed in AN and the degree of hypo-leptinaemia in acute AN is an indicator of the severity of the disorder

35
Q

what is the role of puberty and sex hormones in EDs?

A
  • puberty is a key risk period for the development of EDs
  • before puberty, genetic influences account for ~0% of the variability in disordered eating, whereas genetic factors account for over 50% during and after puberty
  • oestradiol is potent regulator of gene transcription in CNS and recent theories propose that ovarian hormones may “activate” genetic risk for disordered eating in girls during puberty
36
Q

what are some activities to promote positive body image and body acceptance?

A
  • curate body positive and inclusive messages
  • exercise for pleasure, strength, and accomplishment
  • make a gratitude list
  • challenge negative body talk
  • practice self-kindness
37
Q

what are the individual risk factors of EDs?

A
  • negative body image
  • internalisation of thin ideal
  • personality factors (perfectionism)
  • neurocognitive impairments (rigidity, attention to detail)
  • dieting
  • negative emotionality (e.g., alexithymia)
38
Q

how does perfectionism relate to EDs?

A
  • EDs are characterised by high-levels of perfectionism, which endures after recovery, and appears to be familial in nature
  • some examples of potential mechanisms: self-validation (via weight and social feedback) or rumination
39
Q

what are some limitations of studies looking into EDs?

A
  • most studies cross-sectional
  • don’t have long-term follow-ups
  • recruitment from treatment settings only
  • limits the generalisability of the findings, and the understanding of causal relationships
40
Q

what are some neurocognitive impairments as an Endophenotype for AN?

A
  • AN is strongly associated with obsessive-compulsive thinking style, perfectionism, and difficulties with social communication
  • these difficulties may be an intermediate phenotype (observable traits) triggered by a specific neurocognitive profile
  • adults with AN show poor set-shifting (i.e., inflexibility between strategies, rules, or behaviours) and weak central coherence (i.e., bias to detail at expense of global integration)
  • weight restored individuals show intermediate and attenuated profile
  • unaffected relatives show similar profile, suggesting genetic component
41
Q

what are the family influences on EDs?

A
  • individuals with AN report that family dysfunction contributed to the development of their eating disorder
  • parents beliefs about the desirability of thinness, dieting, and good physical appearance
  • criticism of child’s appearance and weight strong predictor of BN symptoms
  • has led to recommendations for family therapy approaches
42
Q

what are the media influences on EDs?

A
  • body dimensions of models, actresses and cultural icons have become thinner over the last few decades
  • influence of social media on body image/satisfaction
  • diet/weight normative content is increasing in media
43
Q

what are the peer influences on EDs?

A
  • girls who engaged more frequently in social media photo activities (selfie- taking and sharing) reported greater overvaluation of shape and weight, more body dissatisfaction, and more dietary constraint
  • photo investment and manipulation was unique predictor of overvaluation of shape and weight, and dietary restraint
  • relationship between social media and body-related/eating concerns may be bi-directional and mutually reinforcing
44
Q

what was Becker et al.’s (2002) study on eating behaviours and attitudes following prolonged exposure to television among ethnic Fijian adolescent girls?

A
  • the impact of Western TV on disordered eating in Fiji on relatively media-naïve adolescent girls studied via a naturalistic experiment
  • attitudes to body image changed drastically with the coming of TV in 1995 – only one channel – American teenage programmes
45
Q

do EDs only occur within specific cultures?

A
  • BN only occurs within specific cultures/cultural contexts
  • AN is not culturally specific (e.g., there are far more historical examples of AN; AN is actually found in wide range of cultures, sometimes lacking Western influence)
  • this fits with stronger genetic basis of AN
  • heritability estimates for BN show greater variability cross- culturally than heritability estimates for AN
46
Q

what are some treatment for AN?

A
  • emergency procedures to restore weight
  • antidepressants or other medications
  • family therapy
  • cognitive-behavioural therapy (CBT)
47
Q

what are some treatments for BN?

A
  • antidepressants or other medications
  • cognitive-behavioural therapy (CBT)
48
Q

What are the targets for CBT?

A
  • encourage healthy eating and reaching healthy body weight
  • create a personalised treatment plan based on processes that appear to maintain the eating problem
  • enhance self-efficacy
49
Q

LS,T,P,B,E

how can the transdiagnostic CBT-model be used in CBT to help patients with an ED?

A

-life stressors ( stress management skills/ study skills)
- thoughts (cognitive restructuring)
- physiological (routinely and regularly eating)
- behaviours (meal planning and monitoring)
- emotions (coping strategies to help regulate negative emotions)

50
Q

what is family-based treatment (FBT)?

A
  • specific treatment for eating disorders that involve the full family
  • parents/carers empowered to support their child’s recovery
  • no blame: the Eating Disorder is seen as separate from the patient and externalised (reduce parent/carer blame on child and vice versa)
  • importance of early intervention
51
Q

what is obesity?

A
  • defined by BMI
  • major public health concern: high cholesterol, diabetes, heart disease, arthritis, cancer
52
Q

are obesity rates increasing?

A

YES

53
Q

is obesity included in the DSM-5?

A
  • from a diagnostic perspective, obesity is not an ED, and obesity is not included in DSM-5
  • central problem is the habit of over-eating
  • obesity is seen by some as a “food addiction”
  • the idea that obesity is a “brain disorder” is controversial
  • there is increasing acceptance that key brain areas involved in motivation to eat, as well as those involved in reward processing and inhibitory control (serotonin, dopamine) play a part
54
Q

what are the risk and causal factors for obesity?

A
  • genetic influences (runs in families)
  • neurotransmitters and hormones (leptin, grehlin)
  • socio-cultural influences
  • family influences
  • stress and “comfort food”
55
Q

family influences: how can family behaviour patterns impact obesity?

A
  • high-fat, high-calorie diet
  • eating to alleviate distress or show love
  • overfeeding
  • “socially contagious” obesity
56
Q

how does stress and ‘comfort food’ impact obesity?

A
  • stimuli, conditions and cues that trigger things such as: watching TV/movies, attending parties or becoming anxious, angry or bored
57
Q

what are some treatments for obesity?

A
  • lifestyle modifications
  • medications
  • bariatric surgery

PS2028 - Mental Health & Clinical Psychology (13 decks)

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