Eating Disorders Flashcards

1
Q

Define anorexia nervosa.

A

A persistent pattern of reduced energy intake (restricted eating), purging behaviours (e.g. self-induced vomiting, laxative or enema misuse), and/or increased energy expenditure (e.g. excessive exercise) associated with significantly low bodyweight for height, age, and development, usually associated with fear of gaining weight.

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2
Q

Define bulimia nervosa.

A

Frequent, recurrent episodes of binge eating (e.g. once per week or move over at least 1 month), followed by repeated, inappropriate purging (to compensate for the binge). The person’s bodyweight is normal for height, age and developmental stage.

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3
Q

Define binge eating episodes.

A

Confined periodic which the person feels noticeably unable to control or stop eating.

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4
Q

Define binge eating disorder.

A

The pattern of binge eating seen in BN, often accompanied by feeling of guilt or disgust, but without compensatory purging; this can cause obesity.

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5
Q

Define avoidant/restrictive food intake disorder (ARFID).

A

Insufficient quantity or variety of food intake to meet energy or nutritional requirements, in the absence of bodyweight or shape concerns.

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6
Q

Describe the epidemiology of eating disorders.

A

Women > Men (8:1) (incidence rising in men)

Onset in mid to late adolescence, although symptoms can start in childhood and later adulthood.

Lifetime prevalence:

o AN: 0.6%

o BN: 1.0% → may be under diagnosed as people aren’t visibly underweight

o BED: 3.2%

AN mostly affects westernised societies, where black and ethnic minority groups are at lower risk than white populations

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7
Q

What is the aetiology of eating disorders based on?

A
  • Genetics
  • Neurobiological factors
  • Psychological and family theories.
  • Sociocultural
  • Psychiatric comorbidity
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8
Q

What genetic factors contribute to eating disorders?

A

o Heritability 30% to 80%

o significant genetic contribution: single nucleotide polymorphisms

o relatives of people with BN also have higher rates of obesity and depression

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9
Q

What neurobiological factors contribute to eating disorders?

A
  • Abnormal connectivity between reward centres (e.g. the striatum) and executive control (prefrontal cortex).
  • Imbalances between dopaminergic (reward) and serotonergic systems)
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10
Q

What psychological and family factors contribute to eating disorders?

A

o Likely to have a hx of obstetric complications, sleeping and feeding difficulties, and childhood abuse

o Personality traits (perfectionism, neuroticism and low self-esteem - RFs for both AN and BN

o Theory: initial WL → enhances someone’s sense of achievement and autonomy reinforcing perfectionist traits. When life feels out of control → comfort associated with controlling something (weight) may also reinforce AN

o Parental overprotecting and family ‘enmeshment’ (excessively close relationship - compromises independence) are associated with AN.

o Theory: AN as a means of avoiding stress of separation from family support or becoming an independent sexual being; AN maintains dependence on family and a peripubertal physique

o BN associated with disturbed family dynamics, parental weight concern, and high parental expectation.

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11
Q

What sociocultural factors contribute to eating disorders?

A

o Social pressure to be thin - IMPORTANT

o Promotion of dieting
o High risk in models, athletes and dancers

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12
Q

How does psychiatric comorbidity contribute to eating disorders?

A

o Usually comorbid with other mental health disorders

o Up to 75% report a hx of depression, anxiety, OCD, BDD, substance use disorders and PDs (particularly anankastia and borderline pattern) - more common.

o People with BN have hx of obesity and 50% previously suffered AN

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13
Q

What are the key similarities and differences between AN and BN?

A
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14
Q

Describe the clinical presentation of anorexia nervosa.

A

Four main diagnostic points

  • BMI <18.5 kg/m2 (or <5th per central BMI-for-age in children and adolescents)
    • Divided into AN with:
      • Significantly low body weight: BMI > 14 kg/m2
      • Dangerously low body weight: BMI < 14 kg/m2 or <0.3 percentile BMI-for-age
  • Deliberate weight loss. Methods may include:
    • Dietary restriction
    • Purging
    • Excessive exercise
    • Medication misuse e.g. appetite suppressants, thyroxine, diuretics, stimulants such as cocaine. People with T1DM will omit their insulin.
  • Distorted body image → preoccupied with body shape; see themselves as normal or overweight
  • Endocrine dysfunction

o HPG axis → amenorrhoea
o Loss of libido
o Delayed or arrested menarche/breast development

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15
Q

Describe the clinical presentation of bulimia nervosa.

A
  • Bing eating: recurrent episodes (usually secretive) of overeating.
    • Irresistible cravings
    • Loss of control - sense of urgency and compulsion
    • May consume 1000s of calories, often eating forbidden foods e.g. 20 donuts
    • May be triggered by stress
  • Purging
    • Bingeing → feeling of shame and guilt → desperate measure to undo the damage → vomiting, laxatives
  • Body image distortion → preoccupation with shame and weight and often hate their body
  • BMI >18.5 unlike AN → normal and normal endocrine function ANA wAna w
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16
Q

What are the physical complications of eating disorders?

A

Starvation- related problems are commoner in AN, while purging- related problems tend to affect people with BN. However, since purging and starvation occur in both conditions, all complications should be considered during assessments of AN or BN

Neurological

Starvation:

  • Peripheral neuropathy
  • Cognitive deficits
  • Delirium
  • Coma
  • Cerebral volume los

Purging:

  • Convulsions (hyponatraemia)
  • Peripheral neuropathy
  • Delirium
17
Q

What is the differential diagnosis of eating disorders?

A

Differential Diagnosis for AN and BN

  • Organic causes of weight loss:malignancy, chronic infection (TB, HIV), GI pathology (IBD, coeliac), endocrine dysfunction (hyperthyroidism, DM, Addison’s)
  • Affective disorders: Depression and mania
  • Anxiety disorders: OCD (contamination fears), BDD
  • Psychosis: food restriction may result from persecutory delusions e.g. poisoning or grandiose delusions e.g. no need to eat
  • ASD - rigid eating habits
  • Other specified feeding of Eating disorder (OSFED) - not quite AN or BN but similar

Differentials for BED:

  • Depression - overeating
  • Organic and genetic conditions: brain tumours (Kluver-Bucy syndrome - hyperplasia and hyper sexuality) Prader-Willi syndrome
18
Q

What are the ix for eating disorders?

A
  1. Physical obs, CBG, lying/standing BP
  2. Height, weight & BMI
  3. Sit up-Squat-stand test - SUSS (proximal myopathy) - impaired in severe AN
  4. Essential bloods
    1. Bone profile, TFTs
    2. o FBC, U&Es, phosphate, albumin, LFTs, CK, glucose
  5. ECG: bradycardia, arrhythmia, prolonged QTc
  6. Other tests indicated e.g. DEXA in AN (osteoporosis)
  7. Pregnancy test in any women with amenorrhea
19
Q

How should we think about the management for AN?

A
  1. Consider Admission
  2. Consider referral if in primary care
  3. Biological Therapies - Nutritional management and weight restoration
    1. o Realistic weekly weight gain target (usually 0.5-1 kg/week)
    2. o Set eating plan
  4. Psychological therapies
  5. Social interventions.
  6. Treat comborbid psychiatric illness - Depression, OCD and substance misuse are common
20
Q

When should we consider admission for someone with an eating disorder?

A

o May be necessary if:

o BMI < 13 or extremely rapid weight loss

o Serious physical complications
o High suicide risk

o Mental Health Act may be needed to enable compulsory feeding

21
Q

When should we consider referrals for someone with an eating disorder?

A

Referral Pathways
o Severe → Urgent referral to CEDS (community eating disorder service)

o Features: BMI < 15, rapid weight loss, evidence of system failure

o Moderate → Routine referral to CEDS

o Features: BMI 15-17, no evidence of system failure

o Mild → Monitor/advice/support for 8 weeks, recommend support from BEAT, routine referral to CEDS if failure to respond
o Features: BMI > 17, no additional co-morbidity

22
Q

What are the risks of giving nutrition?

A

• Warning: Refeeding Syndrome

o Caused by an intracellular shift of ions due to switching to carbohydrate metabolism
o Biochemical Features: low phosphate, low magnesium, low potassium, low thiamine, salt and water retention
o Clinical Features: fatigue, weakness, confusion, high blood pressure, seizures, arrhythmia, heart failure

23
Q

What is MARSIPAN?

A

People with the greatest physical health complications need nutritional stabilization on a medical ward, applying MARSIPAN guidelines

24
Q

What are the psychological therapies for AN?

A
  • Overview of 1st Line Options
    • CBT-ED
    • Maudsley Anorexia Nervosa Treatment in Adults (MANTRA)
    • Specialist Supportive Clinical Management (SSCM)
  • CBT-ED
    • Addresses control, low self-esteem and perfectionism.
    • Person learns to monitor their dietary intake, and associated thoughts and feeling in diaries.
    • Usually up to 40 sessions over 40 weeks
  • Specialist Supportive Clinical Management (SSCM)
    • Offer 20 or more weekly sessions
    • Explore the main problems that cause anorexia
    • Educate about nutrition and how eating habits cause symptoms
    • Also explore other aspects of management (e.g. improving relationships, getting back to work)
  • Maudsley Anorexia Nervosa Treatment for Adults (MANTRA)
    • Offer 20 sessions with a practitioner
    • Helps the patient understand the cause of their anorexia (focuses on what is important to the patient)
  • If any of the above options are unacceptable, offer a different one of the three.
    • or consider Eating Disorder-Focused Focal Psychodynamic Therapy (FPT) -
    • 2nd line: CBT-ED, AFP-AN (adolescent-focused psychotherapy)
  • Other aspects of treatment
    • Motivational Interviewing - Tries to engage ambivalent patents who lack insight into their disorders (or think that their illness is a good thing)
    • Family Therapy - involves the household - share problems and solutions
    • Interpersonal Therapy
      • Aims at improving social functioning and interpersonal skills
      • Better for patients with later onset or longer duration of illness
25
Q

What is the first line management in children with anorexia nervosa?

A

o 1st line: Family Therapy

o Some sessions should be for the whole family and others should be separate

o Usually, 18-20 sessions over 1 year
o Review 4 weeks after treatment, then every 3 months

26
Q

What social interventions are available for patients with AN?

A
  • Family involvement - they are offered info about the illness
  • Charities e.g. BEAT - provide info and support for people with AN and their families
  • People with severe AN - additional support to maintain or re-enter education/employment. - can be tackled through occupational therapist-let inpatient or outpatient group activities
27
Q

Summarise the management of AN.

A

Summary
o Adults – consider one of:

o Individual eating disorder focused CBT (CBT-ED)
o Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) o Specialist Supportive Clinical Management (SSCM)

o Children
o 1st line: Anorexia Focused Family Therapy o 2nd line: CBT

o Note: up to 10% will die because of anorexia nervosa

28
Q

How should you counsel patients with AN?

A
29
Q

How would you think of managing BN?

A
  1. Consider admission/referral
  2. Treat medical complications - dental care
  3. Biological Interventions
  4. Psychological Interventions
  5. Social Interventions
  6. Treat comorbid psychiatric illness
    1. Depression, self-harm and substance misuse are common
30
Q

What are the referral pathways for BN?

A

Referral Pathways

o Severe → Urgent referral to Community Eating Disorder Service
o Features: daily purging with significant electrolyte imbalance, comorbidity

o Moderate → Monitor/advice/support for 8 weeks, recommend self-help, consider SSRI, routine referral to CEDS if failure to respond

o Features: frequent binging and purging (>2/week), no significant electrolyte abnormality, some medical consequences (e.g. chest pain)

o Mild → Recommend self-help, recommend BEAT, monitor/advice/support for 3 months, routine referral to CEDS if no improvement/deterioration

31
Q

What are the biological interventions for BN?

A
  • Medical complication management
  • SSRIs (e.g. fluoxetine) → can reduce bingeing and purging by enhancing impulse control
32
Q

What are the psychological interventions for BN?

A
  • Bulimia Nervosa-Focused Guided Self-Help Programme - provide psychoeducation and CBT. They encourage exploration of thoughts and feelings which trigger binges.
  • Adapted CBT-ED may be offered if this is ineffective
  • BN-focused family therapy - for children and young adults living at home
  • Long-term psychotherapy - may be required to address underlying or comorbid difficulties contributing to BN.
33
Q

What are the social interventions for BN?

A

Same as AN

34
Q

Summarise the management for BN

A

Summary
o Referral for specialist care is appropriate in all case
o BN-focused guided self-help for adults
o If unacceptable, contraindicated or ineffective after 4 weeks, consider ED-focused CBT (CBT-ED)
o Children should be offered BN-focused family therapy (FT-BN) o Consider a trial of high-dose fluoxetine

35
Q

How should binge-eating disorder be managed?

A

Offer BED focused guided self-help programmes for adults

If unacceptable or ineffective after 4 weeks, consider group CBT-ED

If unacceptable or ineffective, consider individual CBT-ED

36
Q

What is the prognosis of eating disorders?

A

Standardised mortality ratio of AN is 5.86 (among the highest for all psychiatric disorders)

  • 20% of deaths are by suicide.
  • 50% asymptomatic after 10 yrs
  • Remaining 40% have ongoing problems and crossover to BN is common

Poor prognostic indicators

o Very low weight
o Bulimic features
o Later onset
o Longer illness duration

• After 10 yrs, 70% of people with BN recover and 1% die
o Poor prognosis with severe binging or purging, low body weight and comorbid depression

• Refeeding syndrome = recognised cause or mortality o Electrolyte imbalance

o Sudden intracellular movement due to swtich from fat to carbohydrate metabolism and associated increased secretion of insulin