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ukmla 2026

Bulimia Nervosa

Eating disorder characterised by recurrent episodes of binge eating followed by compensatory behaviours (purging, fasting, excessive exercise) — typically normal or overweight BMI

Psychiatryless-commonchronic
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Condition details
Psychiatry
less-common
6 min read
reviewed 2026-04-05
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About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

  • Recurrent binge eating (eating large amounts with loss of control) followed by compensatory purging (vomiting, laxatives, diuretics, fasting, excessive exercise)
  • BMI typically NORMAL or above normal — distinguishes from anorexia binge-purge type (which has low BMI)
  • Self-evaluation is unduly influenced by body shape and weight
  • First-line treatment: bulimia nervosa-focused guided self-help (CBT-ED based). If ineffective → individual CBT-ED
  • Pharmacotherapy: fluoxetine 60 mg/day (higher than antidepressant dose) — reduces binge-purge frequency
  • Metabolic complications of purging: hypokalaemia (metabolic alkalosis from vomiting, metabolic acidosis from laxatives)

Overview

Bulimia nervosa is an eating disorder characterised by recurrent episodes of binge eating (consuming objectively large amounts of food with a subjective loss of control) followed by inappropriate compensatory behaviours to prevent weight gain. Compensatory behaviours include self-induced vomiting (most common), misuse of laxatives, diuretics, or enemas, fasting, and excessive exercise. Unlike anorexia nervosa, individuals with bulimia nervosa typically maintain a normal or above-normal BMI, which can make the condition less visually apparent. Self-esteem is excessively influenced by body shape and weight. The binge-purge cycle is typically secretive and associated with intense shame and guilt.

Epidemiology

Bulimia nervosa has a lifetime prevalence of approximately 1–2% in young women. The female:male ratio is approximately 10:1. Typical onset is late adolescence to early adulthood (18–25 years), slightly later than anorexia nervosa. Risk factors include family history, dieting behaviour, childhood adversity, low self-esteem, perfectionism, and sociocultural pressure regarding body image. Comorbidity with depression (~50%), anxiety, substance misuse, and personality disorders is common. Mortality is lower than anorexia nervosa but still elevated compared to the general population.

Clinical Features

Symptoms
Binge eating: consuming large quantities of food rapidly with loss of control — often in secret
Compensatory purging: self-induced vomiting, laxative/diuretic misuse, fasting, excessive exercise
Preoccupation with body shape and weight — drives self-evaluation
Shame, guilt, and distress about eating behaviour — often secretive
Irregular menstrual periods (but typically not amenorrhoea unless underweight)
Sore throat, acid reflux, abdominal bloating
Suicidal ideation or self-harm
Signs
Normal or slightly above-normal BMI (≥17.5) — distinguishes from anorexia binge-purge type
Russell sign: calluses/scars on dorsum of hand from self-induced vomiting
Dental erosion: enamel loss on palatal surface of upper teeth (perimolysis)
Parotid/salivary gland enlargement ("chipmunk cheeks")
Signs of dehydration, peripheral oedema

Investigations

First-line
U&EsHypokalaemia is the most important finding — risk of cardiac arrhythmia. Vomiting → metabolic alkalosis; laxative misuse → metabolic acidosis
ECGIf hypokalaemia or cardiovascular symptoms — check for QTc prolongation, U waves, arrhythmia
BMITypically ≥17.5 — if <17.5 with binge-purge behaviour → anorexia binge-purge type, not bulimia
Second-line
FBC, LFTs, glucose, amylaseRaised amylase (from salivary gland inflammation, not pancreatitis). Mild transaminitis possible
Screen for comorbiditiesDepression (PHQ-9), anxiety, substance misuse — high comorbidity rates
Specialist
Dental assessmentReferral if evidence of dental erosion from vomiting
1
Adults
  • First-line: bulimia nervosa-focused guided self-help (based on CBT-ED) — with professional support over 4–9 sessions, 16 weeks
  • If guided self-help ineffective or declined: individual CBT-ED (16–20 sessions over 20 weeks)
  • Fluoxetine 60 mg/day (HIGHER than antidepressant dose) — reduces binge-purge frequency independent of depression
  • Can combine CBT-ED with fluoxetine if individual treatments alone insufficient
2
Children and adolescents
  • First-line: bulimia nervosa-focused family therapy (FT-BN)
  • If FT-BN not available/appropriate: individual CBT-ED adapted for age
  • Fluoxetine may be considered in adolescents alongside psychological therapy
3
Medical management
  • Correct electrolyte abnormalities: potassium supplementation if hypokalaemic
  • Advise against further purging (risks of Mallory-Weiss tear, oesophageal rupture, aspiration)
  • Dental referral if erosion present — advise not to brush teeth immediately after vomiting (worsens erosion)

Complications

  • Hypokalaemia: From vomiting or laxative misuse — cardiac arrhythmia, muscle weakness, renal tubular damage
  • Metabolic alkalosis: From vomiting (loss of HCl). Metabolic acidosis from laxative misuse (bicarbonate loss)
  • Dental erosion: Irreversible enamel loss from gastric acid exposure — palatal surface of upper teeth
  • Mallory-Weiss tear: Oesophageal mucosal tear from forceful vomiting — upper GI bleed
  • Oesophageal rupture (Boerhaave syndrome): Rare but life-threatening surgical emergency
  • Parotid enlargement: Sialadenosis from recurrent vomiting
UKMLA Exam Tips
  • 1Bulimia = binge-purge cycle with NORMAL BMI. Anorexia binge-purge type = binge-purge cycle with LOW BMI (<17.5)
  • 2Vomiting → loss of H⁺ and Cl⁻ → hypokalaemia + metabolic ALKALOSIS. Laxatives → loss of HCO₃⁻ → metabolic ACIDOSIS
  • 3Fluoxetine for bulimia is given at 60 mg/day — HIGHER than the 20 mg used for depression
  • 4Russell sign (knuckle calluses) and dental erosion (palatal surface of upper incisors) are classic exam findings
  • 5Raised amylase in bulimia = SALIVARY (parotid) origin, not pancreatic. Do not misdiagnose as pancreatitis
  • 6Guided self-help (CBT-ED based) is FIRST-LINE, not full CBT — step up if insufficient

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Verified Sources & References

NICE NG69 — Eating disorders: recognition and treatment
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